{ "dataset": "PeptaHub: State of Peptides 2026", "description": "Structured open dataset of published peptide compounds: legal status, evidence levels, routes of administration, mechanisms, and external knowledge-graph identifiers.", "license": "CC BY 4.0", "license_url": "https://creativecommons.org/licenses/by/4.0/", "source": "https://peptahub.com/state-of-peptides-2026", "attribution": "PeptaHub (peptahub.com)", "generated": "2026-07-21", "record_count": 156, "records": [ { "name": "Abaloparatide", "slug": "abaloparatide", "aliases": [ "Tymlos", "BA-058", "ITM-058", "BIM-44058" ], "category": "other", "subcategories": [ "longevity" ], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 208743, 2017) for treatment of osteoporosis in postmenopausal women and men at high risk for fracture, defined as history of fracture, multiple risk factors, or failure/intolerance of other osteoporosis therapy. Prescription-only; limited to 2-year cumulative lifetime use.", "routes": [ "subcutaneous" ], "half_life": "~1.7 hours", "molecular_weight": 3961, "cas_number": "247062-33-5", "mechanism_of_action": "Abaloparatide acts as a selective agonist at the PTH1 receptor (PTH1R), activating the Gs-protein–mediated cyclic adenosine monophosphate (cAMP) signaling pathway in osteoblasts. Compared to teriparatide (PTH 1-34), abaloparatide shows greater selectivity for the RG conformation of PTH1R, which is associated with transient cAMP signaling and predominantly anabolic bone effects. This selectivity reduces prolonged receptor activation that drives osteoclast coupling and bone resorption. The net result is increased osteoblast activity, stimulation of new bone formation on trabecular and cortical surfaces, and improved bone mineral density (BMD) with a relatively favorable bone formation-to-resorption ratio compared to teriparatide.", "evidence": [ { "claim": "Reduces vertebral fractures 86%", "level": "strong", "basis": "Pivotal ACTIVE trial (n=2,463, JAMA 2016) showed 86% reduction vs placebo over 18 months" }, { "claim": "Reduces non-vertebral fractures 43%", "level": "strong", "basis": "ACTIVE trial non-vertebral fracture endpoint confirmed 43% risk reduction" }, { "claim": "Superior hip BMD gains vs teriparatide", "level": "strong", "basis": "Head-to-head ACTIVE trial showed significantly greater total hip and femoral neck BMD gains" }, { "claim": "Durable fracture protection post-transition", "level": "strong", "basis": "ACTIVExtend extension study confirmed sustained benefit after switching to alendronate" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/abaloparatide" }, { "name": "Adamax", "slug": "adamax", "aliases": [ "Ac-MEHFPGP-AG-NH2", "Adamantyl Semax", "N-Acetyl Semax Adamantyl" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not approved by FDA or any major regulatory agency. Sold as research chemical in the US and internationally. Not a controlled substance. No established human dosing guidelines from regulatory bodies.", "routes": [ "oral", "intramuscular" ], "half_life": "Extended vs. Semax (adamantyl protection from peptidase); exact duration not characterized", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Adamax crosses the blood-brain barrier through enhanced lipophilicity conferred by the adamantyl group, which also protects the peptide from peripheral peptidase degradation. Once in the CNS, Adamax upregulates brain-derived neurotrophic factor (BDNF) expression and enhances the sensitivity of TrkB receptors in the hippocampus — the primary receptor for BDNF signaling. It also modulates dopamine, norepinephrine, and serotonin neurotransmitter systems. The result is enhanced neuroplasticity and improved signal efficiency in circuits underlying working memory, attention, and executive function.", "evidence": [ { "claim": "Most potent Semax derivative via adamantyl modification", "level": "insufficient", "basis": "Manufacturer claims and anecdotal reports; no independent potency or PK data published" }, { "claim": "Upregulates BDNF and TrkB signaling", "level": "insufficient", "basis": "Extrapolated from Semax and P21 parent-compound preclinical data; no direct Adamax studies" }, { "claim": "Enhanced BBB penetration via adamantyl group", "level": "insufficient", "basis": "Theoretical based on lipophilicity; no published PK or imaging data for Adamax specifically" }, { "claim": "Cognitive enhancement benefits", "level": "insufficient", "basis": "Anecdotal user reports only; no peer-reviewed clinical trials as of 2026" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/adamax" }, { "name": "Alarelin", "slug": "alarelin", "aliases": [ "alarelin acetate", "GnRH agonist alarelin", "LH-RH agonist" ], "category": "other", "subcategories": [ "sexual-health" ], "legal_status": "research-only", "legal_notes": "Approved in China for use in assisted reproductive technology. Not approved by FDA or EMA. Available in Western markets as a research chemical. Any use outside approved Chinese clinical contexts is for research purposes only.", "routes": [ "subcutaneous", "intramuscular", "nasal" ], "half_life": "~1–3 hours (estimated; similar to other synthetic GnRH agonists)", "molecular_weight": 1167.3, "cas_number": "79561-22-1", "mechanism_of_action": "Alarelin binds with high affinity to GnRH receptors (GnRHR) in pituitary gonadotroph cells, initially stimulating a surge release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In acute use, this LH surge triggers final oocyte maturation and ovulation, making it useful as a trigger shot in antagonist IVF cycles. Chronic administration, like other GnRH agonists, leads to GnRHR downregulation and pituitary desensitization, resulting in hypogonadal suppression. Alarelin's biological activity in gonadotropin secretion stimulation is described as many times greater than native GnRH in both in vivo and in vitro rat pituitary models. The D-amino acid substitution in its structure (similar to other GnRH agonists) confers resistance to enzymatic degradation and prolonged receptor binding.", "evidence": [ { "claim": "Triggers ovulation in IVF", "level": "moderate", "basis": "Chinese clinical trials (Ye Int J Gynaecol Obstet 2010) show efficacy as trigger in ART" }, { "claim": "Reduces OHSS risk vs hCG", "level": "preliminary", "basis": "Chinese comparative trials suggest lower OHSS; limited English-language peer review" }, { "claim": "Suppresses endometriosis symptoms", "level": "preliminary", "basis": "Li Fertil Steril 2006 clinical trial; GnRH agonist class effect established" }, { "claim": "China-approved for ART", "level": "moderate", "basis": "Regulatory approval in China for assisted reproductive technology based on Chinese trials" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/alarelin" }, { "name": "Alpha-MSH", "slug": "alpha-msh", "aliases": [ "α-MSH", "α-Melanocyte-Stimulating Hormone", "Melanotropin Alpha", "Ac-ACTH(1-13)-NH2" ], "category": "skin", "subcategories": [ "immune" ], "legal_status": "research-only", "legal_notes": "Endogenous α-MSH is available for laboratory research only. Synthetic analogs (melanotan I/II) are not approved for human use in the US. Afamelanotide (Scenesse) is FDA-approved for erythropoietic protoporphyria as a prescription drug.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~10–20 minutes (plasma)", "molecular_weight": 1664.9, "cas_number": "581-05-5", "mechanism_of_action": "α-MSH binds melanocortin receptors with highest affinity at MC1R (Ki ≈ 0.23 nM), activating Gs-protein signaling and increasing intracellular cAMP. At melanocytes, cAMP activates MITF transcription factor, upregulating tyrosinase and inducing melanin synthesis. At immune cells, α-MSH suppresses NF-κB activation, reducing pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and promoting anti-inflammatory pathways. MC4R signaling in the hypothalamus mediates appetite suppression and energy homeostasis effects.", "evidence": [ { "claim": "Afamelanotide FDA-approved for erythropoietic protoporphyria", "level": "strong", "basis": "Scenesse (afamelanotide) FDA-approved 2019 based on Phase III RCT data in EPP patients" }, { "claim": "High-affinity MC1R agonism drives melanogenesis", "level": "strong", "basis": "Well-established receptor pharmacology; Ki ~0.23 nM at MC1R activates MITF/tyrosinase pathway" }, { "claim": "Anti-inflammatory via NF-kB suppression", "level": "preliminary", "basis": "Animal models of colitis, arthritis, uveitis show cytokine suppression; no approved inflammatory indications" }, { "claim": "MC4R signaling suppresses appetite", "level": "moderate", "basis": "Human and animal MC4R data underpin setmelanotide FDA approval for monogenic obesity" }, { "claim": "Causes hyperpigmentation with repeated dosing", "level": "strong", "basis": "Consistent clinical observation with afamelanotide and melanotan analogs across multiple cohorts" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "16133793", "wikidata": "Q4063639", "wikipedia": "https://en.wikipedia.org/wiki/%CE%91-Melanocyte-stimulating_hormone" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/alpha-msh" }, { "name": "Amylin", "slug": "amylin", "aliases": [ "IAPP", "Islet Amyloid Polypeptide", "Amylin (1-37)" ], "category": "weight-loss", "subcategories": [], "legal_status": "research-only", "legal_notes": "Native amylin (IAPP) is available for research use only. Pramlintide (Symlin) is FDA-approved by prescription. Cagrilintide is investigational (Phase 3). Pure IAPP peptide is not approved for human administration.", "routes": [ "subcutaneous" ], "half_life": "~13 minutes (endogenous)", "molecular_weight": 3904.4, "cas_number": "122384-88-7", "mechanism_of_action": "Amylin activates amylin receptors (AMY1–3), which are heterodimers of calcitonin receptors (CTR) and receptor activity-modifying proteins (RAMPs 1–3). In the area postrema and nucleus accumbens, amylin signaling reduces food intake and slows gastric motility. It suppresses postprandial glucagon secretion in a glucose-dependent manner. Pathological aggregation of IAPP into amyloid fibrils in beta cell islets is implicated in type 2 diabetes progression via inflammasome activation, ER stress, and membrane disruption.", "evidence": [ { "claim": "Pramlintide analog improves T1D/T2D glycemic control", "level": "strong", "basis": "Hollander 2003 Diabetes Care 1-year RCT in T2D; FDA-approved as adjunct to insulin" }, { "claim": "Cagrilintide + semaglutide produces ~25% weight loss", "level": "strong", "basis": "CagriSema Phase 2 REDEFINE trials demonstrated ~25% weight loss; Phase 3 advancing" }, { "claim": "Reduces postprandial glucose and body weight", "level": "strong", "basis": "Aronne 2007 Phase 2 dose-escalation RCT and Hollander 2005 Clin Ther confirmed effects" }, { "claim": "Suppresses postprandial glucagon and slows gastric emptying", "level": "strong", "basis": "Established via multiple mechanistic human studies of pramlintide pharmacology" }, { "claim": "IAPP amyloid drives beta-cell failure in T2D", "level": "moderate", "basis": "Westermark 2011 Physiol Rev review; consistent histopathological and in vitro evidence" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/amylin" }, { "name": "Angiotensin 1-7", "slug": "angiotensin-1-7", "aliases": [ "Ang-(1-7)", "Angiotensin-(1-7)", "ANG 1-7" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "No approved clinical indication. Used in research and investigational trials. Not available as a consumer supplement. Not on the FDA reclassification list for compounding pharmacy use.", "routes": [ "subcutaneous", "oral" ], "half_life": "~30 minutes (plasma, enzymatic degradation)", "molecular_weight": 898.98, "cas_number": "51833-78-4", "mechanism_of_action": "Angiotensin 1-7 binds the Mas receptor to activate downstream signaling that opposes angiotensin II effects. Mas receptor activation promotes vasodilation through nitric oxide release, reduces inflammation by suppressing NF-κB-mediated cytokine production, and limits fibrosis by inhibiting TGF-β signaling. In pulmonary physiology, the ACE2/Ang-(1-7)/Mas axis protects alveolar epithelium from acute lung injury. SARS-CoV-2 infection downregulates ACE2 expression, impairing Ang-(1-7) production and disrupting this protective axis — a mechanism implicated in severe COVID-19 lung pathology.", "evidence": [ { "claim": "Mas-receptor agonism counters RAS axis", "level": "strong", "basis": "Santos 2018 Physiol Rev and decades of receptor-pharmacology research establish Mas axis" }, { "claim": "Lung-protective in acute lung injury and COVID-19", "level": "preliminary", "basis": "Rodent ALI models and Phase 1-2 COVID-19 ICU trials showed safety and preliminary signals" }, { "claim": "Organ protection in hypertension/heart failure", "level": "preliminary", "basis": "Consistent rodent data in hypertension, HF, fibrosis models; Patel 2012 and Ferrario 2019 reviews" }, { "claim": "Enhances insulin's metabolic action via muscle microvasculature", "level": "preliminary", "basis": "Souza 2014 Hypertension animal study showed Mas-mediated microvascular recruitment" }, { "claim": "No approved clinical indication", "level": "strong", "basis": "Regulatory status confirmed; only research and investigational trials as of 2026" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/angiotensin-1-7" }, { "name": "Angiotensin II", "slug": "angiotensin-ii", "aliases": [ "Ang II", "Giapreza", "Angiotensin-II human" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "Giapreza (angiotensin II injection) is FDA-approved as a prescription vasopressor for adults with distributive shock. Hospital-administered only under ICU monitoring.", "routes": [ "intravenous" ], "half_life": "~1 minute (rapidly cleaved by angiotensinase in plasma)", "molecular_weight": 1046.19, "cas_number": "4474-91-3", "mechanism_of_action": "Angiotensin II binds primarily to AT1 receptors on vascular smooth muscle and the adrenal cortex. AT1 activation triggers Gq-mediated signaling leading to vasoconstriction, aldosterone secretion, sodium and water retention, and sympathetic nervous system potentiation. These combined effects rapidly increase mean arterial pressure. AT2 receptors mediate opposing vasodilatory and anti-proliferative effects. In septic shock, exogenous Ang II restores vasomotor tone and reduces catecholamine requirements.", "evidence": [ { "claim": "FDA-approved for distributive shock (Giapreza)", "level": "strong", "basis": "2017 FDA approval based on ATHOS-3 RCT demonstrating significant MAP increase vs placebo" }, { "claim": "ATHOS-3 showed MAP response in refractory shock", "level": "strong", "basis": "Khanna 2017 NEJM randomized trial in catecholamine-refractory distributive shock patients" }, { "claim": "Primary effector of renin-angiotensin-aldosterone system", "level": "strong", "basis": "Foundational cardiovascular physiology; AT1/AT2 receptor pharmacology extensively characterized" }, { "claim": "Causes thromboembolism as key safety risk", "level": "moderate", "basis": "ATHOS-3 and post-marketing data show elevated thromboembolism rate requiring prophylaxis" }, { "claim": "Reduces catecholamine requirements in septic shock", "level": "moderate", "basis": "ATHOS-3 and subsequent observational data show catecholamine-sparing effect in critically ill patients" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/angiotensin-ii" }, { "name": "AOD-9604", "slug": "aod-9604", "aliases": [ "Anti-Obesity Drug 9604", "hGH Fragment 177-191" ], "category": "weight-loss", "subcategories": [], "legal_status": "reclassification-pending", "legal_notes": "Under FDA reclassification review. Approved in Australia as a complementary medicine ingredient. Available from compounding pharmacies in several countries.", "routes": [ "subcutaneous", "oral" ], "half_life": "~1-2 hours", "molecular_weight": 1815.08, "cas_number": "221231-10-3", "mechanism_of_action": "AOD-9604 stimulates lipolysis (fat breakdown) and inhibits lipogenesis (fat formation) by mimicking the lipolytic fragment of human growth hormone. It acts on beta-3 adrenergic receptors in adipose tissue. Unlike full-length GH, it does not increase IGF-1 levels, affect blood glucose, or promote tissue growth — isolating the fat-metabolizing mechanism.", "evidence": [ { "claim": "Lipolysis and fat loss in obesity", "level": "preliminary", "basis": "Ng et al. J Endocrinol 2000: Phase 2 trial, n=300 obese adults; AOD-9604 showed modest fat loss at intermediate doses; Phase 3 trials failed to demonstrate significance" }, { "claim": "Articular cartilage regeneration", "level": "preliminary", "basis": "Ngo et al. Arthritis Res Ther 2015: in vitro and rat OA model showing cartilage matrix stimulation; Phase 2 safety study (n=15) initiated but not completed" }, { "claim": "Absence of diabetogenic effect vs. full-length hGH", "level": "moderate", "basis": "Heffernan et al. Mol Cell Endocrinol 2001: rodent dose-ranging study confirming AOD-9604 does not affect glucose metabolism or IGF-1, distinguishing it from hGH" }, { "claim": "Significant weight loss in humans (clinical-grade)", "level": "insufficient", "basis": "Phase 3 trial (METABASIS) failed primary endpoint; regulatory approvals sought in multiple jurisdictions (Australia, US) and declined due to insufficient evidence" } ], "peer_reviewed_reference_count": 6, "external_ids": { "pubchem_cid": "71300630", "drugbank": "DB06388", "wikidata": "Q72443552", "wikipedia": "https://en.wikipedia.org/wiki/AOD9604" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/aod-9604" }, { "name": "Argireline", "slug": "argireline", "aliases": [ "Acetyl Hexapeptide-8", "Acetyl Hexapeptide-3", "Ac-Glu-Glu-Met-Gln-Arg-Arg-NH2" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Approved for use as a cosmetic ingredient in the US, EU, and most global markets. Regulated as a cosmetic, not a drug, provided no therapeutic claims are made. No prescription required. Available in over-the-counter serums and creams.", "routes": [ "topical" ], "half_life": "Not established (topical; systemic absorption not expected at cosmetic doses)", "molecular_weight": 889.1, "cas_number": "616204-22-9", "mechanism_of_action": "Argireline competitively inhibits the formation of the SNARE complex — the protein assembly responsible for synaptic vesicle fusion and acetylcholine release at the neuromuscular junction. By mimicking the N-terminal portion of SNAP-25, it interferes with catecholamine secretion and reduces repetitive facial muscle contractions that cause dynamic wrinkles. Unlike botulinum toxin, which cleaves SNAP-25 irreversibly, Argireline's inhibition is reversible and topically limited, with no systemic neuromuscular blockade observed at cosmetic concentrations.", "evidence": [ { "claim": "Topical wrinkle depth reduction", "level": "moderate", "basis": "Blanes-Mira Int J Cosmet Sci 2002 + Gorouhi Am J Clin Dermatol 2013 RCT: up to 27% wrinkle depth reduction over 4-8 weeks" }, { "claim": "SNARE complex inhibition mechanism", "level": "moderate", "basis": "Blanes-Mira 2002: demonstrated SNAP-25 N-terminal mimicry and reversible SNARE assembly disruption; established cell-based mechanism" }, { "claim": "Cosmetic safety (non-toxic, non-comedogenic)", "level": "strong", "basis": "CIR safety panels; Lim J Cosmet Dermatol 2014 cytotoxicity study; extensive post-market cosmetic use without adverse signals" }, { "claim": "Visible improvement in expression lines", "level": "moderate", "basis": "Schwab J Cosmet Dermatol 2023 Visia-based in vivo analysis; consistent clinical outcomes at 5-10% topical concentration" }, { "claim": "Equivalence to injectable botulinum toxin", "level": "insufficient", "basis": "Mechanism is reversible and far less potent than Botox; no head-to-head RCT vs injectable neurotoxins" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "71587772", "drugbank": "DB11709", "wikidata": "Q3622439", "wikipedia": "https://en.wikipedia.org/wiki/Acetyl_hexapeptide-8" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/argireline" }, { "name": "Atrial Natriuretic Peptide", "slug": "atrial-natriuretic-peptide", "aliases": [ "ANP", "Nesiritide", "Natrecor", "BNP-32", "brain natriuretic peptide" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since 2001 (Natrecor) for acutely decompensated heart failure. Administered by intravenous bolus and continuous infusion in hospital settings with hemodynamic monitoring. Not a controlled substance. Boxed warning regarding hypotension. Use has declined following ASCEND-HF trial results.", "routes": [ "intravenous" ], "half_life": "~18 minutes (terminal elimination)", "molecular_weight": 3464, "cas_number": "124584-08-3", "mechanism_of_action": "Nesiritide binds to natriuretic peptide receptor A (NPR-A), a transmembrane guanylyl cyclase receptor expressed on vascular smooth muscle, endothelium, kidneys, and cardiac fibroblasts. Ligand binding activates the receptor's intrinsic guanylyl cyclase domain, generating the intracellular second messenger cyclic GMP (cGMP). Elevated cGMP activates protein kinase G (PKG), which phosphorylates myosin light chain phosphatase and reduces intracellular calcium, causing arterial and venous smooth muscle relaxation. This produces balanced vasodilation, reducing both preload (pulmonary capillary wedge pressure) and afterload (systemic vascular resistance) without reflex tachycardia. In the kidney, cGMP-mediated signaling in the collecting duct increases sodium excretion (natriuresis) and promotes diuresis. Nesiritide also suppresses the renin-angiotensin-aldosterone system and attenuates sympathetic nervous system activation, countering the neurohormonal overdrive characteristic of decompensated heart failure.", "evidence": [ { "claim": "Reduces PCWP in acute decompensated heart failure", "level": "strong", "basis": "VMAC RCT Publication Committee 2002 JAMA demonstrated significant PCWP reduction vs placebo" }, { "claim": "No mortality or rehospitalization benefit", "level": "strong", "basis": "ASCEND-HF RCT (n=7,141) showed modest dyspnea relief but no hard-endpoint benefit" }, { "claim": "NPR-A/cGMP-mediated balanced vasodilation", "level": "strong", "basis": "Mechanism characterized through extensive receptor pharmacology and cGMP signaling research" }, { "claim": "Hypotension is dose-limiting with boxed warning", "level": "strong", "basis": "FDA boxed warning based on pooled Phase III safety data and post-marketing reports" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/atrial-natriuretic-peptide" }, { "name": "Aviptadil", "slug": "aviptadil", "aliases": [ "RLF-100", "Vasoactive Intestinal Peptide (synthetic)", "VIP", "Human VIP" ], "category": "immune", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "Investigational drug with FDA Fast Track designation. Available via compassionate use / expanded access protocols in the US. Not approved for general commercial sale. Approved as a pharmaceutical in some European jurisdictions for pulmonary applications. RLF-100 remains under regulatory review.", "routes": [ "intravenous", "nasal" ], "half_life": "~1–2 minutes (IV; rapidly cleared); designed for continuous infusion", "molecular_weight": 3326.8, "cas_number": "37221-79-7", "mechanism_of_action": "VIP/Aviptadil exerts pleiotropic effects in pulmonary tissue via VPAC1 and VPAC2 receptor activation, which are highly expressed on alveolar type II cells, pulmonary endothelium, and immune cells. Mechanistically, it upregulates surfactant protein synthesis (preventing alveolar collapse), inhibits pro-inflammatory cytokine production (IL-6, IL-1β, TNF-α), suppresses NLRP3 inflammasome activation, reduces macrophage-driven cytokine storm, and has been shown in preclinical studies to block SARS-CoV-2 replication in alveolar cells. It also promotes bronchodilation and vasodilation via cAMP-dependent signaling, reducing pulmonary vascular resistance. Inhalation and IV routes deliver active peptide directly to lung tissue.", "evidence": [ { "claim": "Improves oxygenation in COVID ARDS", "level": "moderate", "basis": "60-day RCT in critically ill COVID-19 patients (Crit Care Med 2022) showed improved oxygenation and survival" }, { "claim": "Reduces pulmonary inflammatory cytokines", "level": "moderate", "basis": "Preclinical and human studies show IL-6, IL-1β, TNF-α suppression via VPAC1/VPAC2 activation" }, { "claim": "Treats pulmonary arterial hypertension", "level": "preliminary", "basis": "Small inhalation trial (Am J Respir Crit Care Med 2003) showed hemodynamic improvement" }, { "claim": "FDA Fast Track for COVID-19 ARDS", "level": "moderate", "basis": "FDA Fast Track designation granted; Phase 2b/3 trials completed but not yet approved" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/aviptadil" }, { "name": "Bivalirudin", "slug": "bivalirudin", "aliases": [ "Angiomax", "Angiox", "Bivalirudin TFA" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 020873) for anticoagulation in patients undergoing PCI and in patients with or at risk of HIT/HITTS undergoing PCI. Prescription-only; administered by healthcare professionals in catheterization laboratory settings. IV infusion only.", "routes": [ "intravenous" ], "half_life": "~25 minutes (normal renal function); ~57 minutes (severe renal impairment)", "molecular_weight": 2180, "cas_number": "128270-60-0", "mechanism_of_action": "Bivalirudin specifically inhibits both circulating and clot-bound thrombin by bivalently binding to two distinct sites on the thrombin molecule: the catalytic active site and the anion-binding exosite 1 (fibrinogen recognition site). This dual binding differentiates bivalirudin from univalent inhibitors. Importantly, thrombin slowly cleaves bivalirudin at the Arg3-Pro4 bond, resulting in gradual recovery of thrombin activity — providing reversible inhibition proportional to drug concentration. Bivalirudin directly inhibits thrombin-catalyzed or induced reactions, including fibrin formation, coagulation factor V, VIII, and XIII activation, and platelet aggregation triggered by thrombin. The result is dose-dependent prolongation of activated clotting time (ACT), aPTT, and thrombin time.", "evidence": [ { "claim": "Non-inferior to heparin for PCI ischemic endpoints", "level": "strong", "basis": "REPLACE-2 RCT (n=6,010) Lincoff 2003 JAMA demonstrated non-inferiority with lower bleeding" }, { "claim": "40% reduction in 30-day major bleeding vs heparin+GPI", "level": "strong", "basis": "HORIZONS-AMI Phase III RCT in STEMI showed significant bleeding reduction, 3-year cardiac mortality benefit" }, { "claim": "Reversible dual-site thrombin inhibition", "level": "strong", "basis": "Mechanism established via biochemical and pharmacokinetic studies; FDA-approved since 2000" }, { "claim": "Useful in heparin-induced thrombocytopenia", "level": "moderate", "basis": "FDA-approved for HIT/HITTS PCI; multiple case series and registry data support use" }, { "claim": "25-minute half-life for predictable offset", "level": "strong", "basis": "PK studies across renal-function strata confirm 25-min (normal) to 57-min (severe CKD) half-life" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/bivalirudin" }, { "name": "Bortezomib", "slug": "bortezomib", "aliases": [ "Velcade", "PS-341" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since 2003 for multiple myeloma and since 2006 for mantle cell lymphoma. Available as lyophilized powder for intravenous or subcutaneous injection. Not a controlled substance. Generic bortezomib available since 2016.", "routes": [ "intravenous", "subcutaneous" ], "half_life": "~9–15 hours", "molecular_weight": 384.24, "cas_number": "179324-69-7", "mechanism_of_action": "Bortezomib is a dipeptide boronate that reversibly inhibits the chymotrypsin-like activity of the 26S proteasome. The boronic acid moiety forms a reversible covalent bond with the N-terminal threonine residue of the 20S proteasome beta5 subunit, blocking protein degradation. This causes accumulation of pro-apoptotic proteins normally targeted for proteasomal destruction, including IκB (which sequesters the NF-κB transcription factor). NF-κB inhibition is particularly relevant in myeloma, where constitutive NF-κB activity drives proliferation and survival. Additionally, bortezomib phosphorylates Bcl-2, upregulates the BH3-only protein NOXA, blocks p53 degradation, activates caspase cascades, generates reactive oxygen species, and inhibits tumor angiogenesis. The combined pro-apoptotic burden overwhelms the unfolded protein response in malignant plasma cells.", "evidence": [ { "claim": "Superior to high-dose dexamethasone in RRMM", "level": "strong", "basis": "APEX Phase III RCT Richardson 2005 NEJM showed 38% vs 18% response; FDA full approval 2005" }, { "claim": "Frontline standard with melphalan-prednisone", "level": "strong", "basis": "VISTA Phase III trial established MPV regimen; meta-analyses confirm OS benefit in newly-diagnosed myeloma" }, { "claim": "Reversible proteasome inhibition via boronate", "level": "strong", "basis": "Mechanism characterized in multiple biochemical and crystallographic studies" }, { "claim": "Subcutaneous reduces neuropathy by ~50%", "level": "strong", "basis": "Randomized head-to-head SC vs IV route trial showed equivalent efficacy with halved neuropathy" }, { "claim": "Efficacy in mantle cell lymphoma", "level": "strong", "basis": "Phase II pivotal data led to 2006 FDA MCL approval; confirmed in subsequent combination trials" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/bortezomib" }, { "name": "BPC-157", "slug": "bpc-157", "aliases": [ "Body Protection Compound-157", "PL 14736", "Bepecin" ], "category": "recovery", "subcategories": [ "longevity" ], "legal_status": "reclassification-pending", "legal_notes": "One of ~14 peptides HHS Secretary RFK Jr. announced (February 2026) to move from the FDA's Category 2 restricted compounding list back to Category 1; the FDA Pharmacy Compounding Advisory Committee reviews BPC-157 among others in late July 2026. Many US suppliers paused sales in 2025-2026 pending regulatory clarity. Verify current federal and state rules before relying on access claims.", "routes": [ "subcutaneous", "intramuscular", "oral" ], "half_life": "~4 hours (estimated)", "molecular_weight": 1419.53, "cas_number": "137525-51-0", "mechanism_of_action": "BPC-157 engages a convergent set of intracellular signaling pathways rather than a single receptor, which partly explains its unusually broad tissue-type efficacy. The best-characterized mechanism is activation of the FAK-paxillin pathway (focal adhesion kinase / paxillin complex), which governs cell migration, adhesion, and proliferation in fibroblasts, tenocytes, and endothelial cells. Chang et al. (J Appl Physiol, 2011) demonstrated that BPC-157 promotes tendon outgrowth in explant cultures specifically through FAK-paxillin signaling, with inhibition of this pathway abolishing the pro-healing effect. This mechanism is shared across multiple cell types: the same FAK activation underpins BPC-157's effects in gut epithelial repair, muscle satellite cell mobilization, and vascular endothelial proliferation.\n\nAngiogenesis — the formation of new blood vessels — is a second major mechanism, mediated through upregulation of VEGF (vascular endothelial growth factor) and eNOS (endothelial nitric oxide synthase). BPC-157 increases nitric oxide production via eNOS in endothelial cells, which triggers vasodilation and proangiogenic signaling. Sikiric et al. have extensively characterized this NO-mediated mechanism as the explanation for BPC-157's protective effects in ischemia models: by restoring microvascular perfusion to injured tissue, BPC-157 accelerates healing even in poorly vascularized structures like tendons, which are notoriously difficult to repair due to their naturally low blood supply.\n\nIn the gastrointestinal tract, BPC-157 acts through multiple cytoprotective mechanisms: it counteracts NSAID-induced suppression of prostaglandin synthesis, reduces acid-induced mucosal apoptosis, promotes mucosal cell migration and restitution, and inhibits the inflammatory cascade triggered by ethanol or indomethacin. Interestingly, BPC-157 has also demonstrated dopaminergic and serotonergic modulatory activity in CNS models — decreasing dopamine turnover in limbic structures and normalizing serotonergic activity — suggesting mechanisms relevant to mood, neuroprotection, and gut-brain axis modulation that extend beyond simple tissue repair.", "evidence": [ { "claim": "Tendon and ligament repair", "level": "preliminary", "basis": "Multiple animal studies; no human RCTs completed" }, { "claim": "Gastrointestinal protection", "level": "preliminary", "basis": "Rat models of NSAID-induced gastropathy and inflammatory bowel" }, { "claim": "Wound healing acceleration", "level": "preliminary", "basis": "Rat Achilles tendon models reported higher recovered tendon strength by day 14 versus controls" }, { "claim": "Anti-inflammatory effects", "level": "preliminary", "basis": "Preclinical evidence via NO system and FAK-paxillin pathway modulation" }, { "claim": "Muscle healing", "level": "insufficient", "basis": "Limited animal data; no controlled human studies" } ], "peer_reviewed_reference_count": 6, "external_ids": { "pubchem_cid": "9941957", "wikidata": "Q27270252", "wikipedia": "https://en.wikipedia.org/wiki/BPC-157" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/bpc-157" }, { "name": "Bradykinin", "slug": "bradykinin", "aliases": [ "Kallidin-9", "BK", "Bradykinin (1-9)" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Bradykinin itself is a research compound. Icatibant (Firazyr), a bradykinin B2 receptor antagonist, is FDA-approved as a prescription drug for hereditary angioedema and requires a prescription.", "routes": [ "intravenous" ], "half_life": "~17 seconds (rapidly degraded by kininases in plasma)", "molecular_weight": 1060.22, "cas_number": "58-82-2", "mechanism_of_action": "Bradykinin acts on two G-protein-coupled receptors: B1 (inducible, involved in chronic inflammation) and B2 (constitutively expressed, mediates acute effects). B2 receptor activation stimulates phospholipase C, increases intracellular calcium, triggers nitric oxide synthase, and releases prostaglandins. These combined effects produce vasodilation, increased vascular permeability, smooth muscle contraction, and sensitization of nociceptors underlying pain and inflammation.", "evidence": [ { "claim": "Icatibant (B2 antagonist) FDA-approved for HAE", "level": "strong", "basis": "Cicardi 2010 NEJM RCT (FAST-3) supported FDA approval of icatibant for hereditary angioedema" }, { "claim": "ACE inhibitor cough caused by bradykinin accumulation", "level": "strong", "basis": "Mechanism established through decades of clinical pharmacology; affects 10-20% of ACE-inhibitor users" }, { "claim": "Potent vasodilator via B2 receptor and NO release", "level": "strong", "basis": "Foundational cardiovascular pharmacology establishes PLC/calcium/NOS signaling cascade" }, { "claim": "Extremely short plasma half-life (~17 seconds)", "level": "strong", "basis": "Well-characterized pharmacokinetics across human and animal studies due to rapid kininase degradation" }, { "claim": "Implicated in COVID-19 pathophysiology", "level": "preliminary", "basis": "Hypothesized role in ACE2-mediated kinin dysregulation during COVID-19; clinical evidence emerging" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/bradykinin" }, { "name": "Buserelin", "slug": "buserelin", "aliases": [ "Suprefact", "Suprecur", "Profact", "Receptal" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "Not FDA-approved; approved by EMA and health authorities in the UK, Canada, Germany, France, and numerous other countries. Indicated for prostate cancer, endometriosis, and female infertility in approved jurisdictions. Prescription-only throughout all jurisdictions where available.", "routes": [ "subcutaneous", "nasal" ], "half_life": "~72–80 minutes", "molecular_weight": 1239.42, "cas_number": "57982-77-1", "mechanism_of_action": "Buserelin is a GnRH superagonist with approximately 20–170 times the potency of endogenous GnRH for stimulating LH and FSH secretion. Structural modifications — D-serine(tBu) at position 6 and ethylamide at the C-terminus — confer enzymatic stability and high receptor binding affinity. Initial administration triggers an LH/FSH flare response. With continuous exposure (unlike pulsatile endogenous GnRH), buserelin maintains constant GnRH receptor occupancy, inducing receptor downregulation and uncoupling. Within 2–4 weeks, pituitary gonadotrophs become desensitized, LH and FSH secretion collapses, and gonadal testosterone or estradiol falls to castrate levels. In prostate cancer, androgen withdrawal inhibits androgen receptor signaling that drives tumor proliferation.", "evidence": [ { "claim": "Castrate testosterone in prostate cancer", "level": "strong", "basis": "Klijn 1985 Lancet RCT vs orchiectomy; >95% of patients reach castrate testosterone within 4 weeks" }, { "claim": "Endometriosis lesion and pain reduction", "level": "strong", "basis": "Cochrane 2007 meta-analysis of GnRH agonists confirms efficacy in endometriosis over 6-month courses" }, { "claim": "IVF pituitary downregulation", "level": "strong", "basis": "Hughes 1992 Fertility & Sterility and multiple RCTs establish long-protocol IVF downregulation efficacy" }, { "claim": "3-year disease stabilization equals orchiectomy", "level": "moderate", "basis": "Long-term comparative data in prostate cancer show equivalence to surgical castration" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/buserelin" }, { "name": "Cagrilintide", "slug": "cagrilintide", "aliases": [ "AM833", "CagriSema component", "NN9838" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Investigational drug; Phase 3 REDEFINE program complete. Not FDA-approved as of mid-2026 (the CagriSema combination NDA was filed December 2025; cagrilintide monotherapy has no separate NDA pending). Not available through commercial or compounding channels in the US. Available only through sponsored clinical trials. CAS: 1415456-99-3.", "routes": [ "subcutaneous" ], "half_life": "~159–195 hours (~7–8 days)", "molecular_weight": 4409, "cas_number": "1415456-99-3", "mechanism_of_action": "Cagrilintide activates the amylin receptor complex — calcitonin receptor (CTR) heterodimerized with receptor activity-modifying proteins RAMP1, RAMP2, and RAMP3 — expressed in the area postrema and nucleus tractus solitarius of the brainstem. Three key structural modifications enable its long action: N14E and V17R substitutions improve metabolic stability, P37Y provides additional protease resistance, and N-terminal acylation with a C20 eicosanedioic fatty diacid via gamma-glutamic acid linker enables albumin binding that extends circulation half-life. Amylin receptor activation produces satiety signaling (reducing meal size through AP/NTS neuronal pathways), slowing of gastric emptying via vagal efferent modulation, and suppression of post-prandial glucagon from pancreatic alpha cells. The CagriSema combination exploits complementary and partially non-overlapping neural circuits — amylin receptors act on different brainstem nuclei than GLP-1 receptors — producing additive weight loss exceeding either agent alone.", "evidence": [ { "claim": "Monotherapy weight loss", "level": "moderate", "basis": "Lau et al. Lancet 2021 (Phase 2 CALM): n=706; 10.8% weight loss at 4.5 mg/wk over 26 weeks vs 3.0% placebo" }, { "claim": "CagriSema combination weight loss", "level": "strong", "basis": "Jastreboff et al. NEJM 2025 (REDEFINE 1): n=3,417; 22.7% weight loss at 68 weeks vs 14.8% semaglutide alone; Phase 3" }, { "claim": "Type 2 diabetes CagriSema efficacy", "level": "strong", "basis": "Lingvay et al. NEJM 2025 (REDEFINE 2): Phase 3 T2D cohort showing glycemic + weight benefits; coadministered combination" }, { "claim": "Once-weekly dosing convenience", "level": "strong", "basis": "N-terminal acylation + C20 fatty diacid engineering; half-life 7-8 days confirmed in Phase 1/2 PK studies; Novo Nordisk platform" }, { "claim": "Long-term cardiovascular outcomes", "level": "insufficient", "basis": "No cardiovascular outcomes trial completed; CV safety data pending REDEFINE-CVOT readouts" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "171397054", "drugbank": "DB18887", "wikidata": "Q123428019" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cagrilintide" }, { "name": "CagriSema", "slug": "cagrisema", "aliases": [ "Cagrilintide-Semaglutide", "CagriSema 2.4/2.4", "amylin-GLP-1 combination" ], "category": "weight-loss", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not yet FDA or EMA approved as of mid-2026. Novo Nordisk filed the NDA on December 18, 2025; FDA is actively reviewing with a decision expected approximately October 2026. Semaglutide and cagrilintide are individually in various approval stages. The co-formulation remains investigational until FDA action.", "routes": [ "subcutaneous" ], "half_life": "~7 days (semaglutide component); cagrilintide ~7 days — both designed for weekly dosing", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "CagriSema harnesses two complementary appetite-regulating pathways. Semaglutide activates GLP-1 receptors in the hypothalamus, hindbrain, and vagus nerve, suppressing appetite, slowing gastric emptying, and improving insulin secretion. Cagrilintide mimics amylin, a pancreatic hormone co-secreted with insulin that acts on area postrema and nucleus tractus solitarius receptors to promote satiety, reduce food intake, and modulate glucagon secretion. The dual mechanism produces additive to synergistic appetite suppression through both hedonic and homeostatic neural pathways, which appears to underpin the superior weight loss versus either agent alone.", "evidence": [ { "claim": "Produces ~20% body weight reduction", "level": "strong", "basis": "REDEFINE 1 Phase 3 trial (68 weeks, non-diabetic) showed 20.4% mean loss vs 3.0% placebo" }, { "claim": "Effective in type 2 diabetes", "level": "strong", "basis": "REDEFINE 2 Phase 3 trial showed 13.7% mean weight reduction in diabetic population" }, { "claim": "Dual GLP-1 + amylin appetite suppression", "level": "strong", "basis": "Phase 2 dose-finding (Lancet 2021) and Phase 3 REDEFINE confirmed additive mechanism" }, { "claim": "GI side effects typically transient", "level": "strong", "basis": "REDEFINE trials reported 79.6% GI events, mostly mild-to-moderate and resolving on titration" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cagrisema" }, { "name": "Calcitonin", "slug": "calcitonin", "aliases": [ "Miacalcin", "Fortical", "salmon calcitonin", "calcitonin salmon" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved for postmenopausal osteoporosis, Paget's disease, and hypercalcemia. Available as nasal spray (200 IU/day) and subcutaneous/intramuscular injection. The FDA updated the label in 2013 noting a possible association with malignancy on long-term use. Not a controlled substance.", "routes": [ "subcutaneous", "nasal", "intramuscular" ], "half_life": "~10–25 minutes (injection); longer effective duration due to receptor kinetics", "molecular_weight": 3431.86, "cas_number": "47931-85-1", "mechanism_of_action": "Calcitonin binds to specific calcitonin receptors (CTRs) expressed predominantly on osteoclasts, the bone-resorbing cells. Receptor activation via Gs-coupled cAMP signaling and Gq-coupled phospholipase C activation leads to a rapid cytoskeletal reorganization in osteoclasts — the ruffled border retracts and the cell loses its characteristic polarized morphology. This functional inactivation halts the secretion of hydrochloric acid and cathepsin K that drive bone matrix dissolution. With sustained exposure, osteoclast cell numbers also decrease. The net effect is reduced bone resorption and a fall in serum calcium and phosphate. In the kidney, calcitonin promotes renal excretion of calcium, phosphate, sodium, magnesium, and potassium by inhibiting tubular reabsorption. Calcitonin also has central analgesic properties, mediated through elevated beta-endorphin levels, contributing to its use in Paget's disease-associated bone pain.", "evidence": [ { "claim": "33% reduction in vertebral fracture risk", "level": "moderate", "basis": "PROOF 5-year RCT (n=1,255) Chesnut 2000 Am J Med demonstrated fracture-risk reduction in postmenopausal osteoporosis" }, { "claim": "Lowers serum calcium in acute hypercalcemia", "level": "strong", "basis": "FDA-approved; multiple clinical studies confirm rapid calcium-lowering via osteoclast inhibition and renal excretion" }, { "claim": "Provides pain relief in Paget's disease and vertebral fractures", "level": "moderate", "basis": "Gennari 1997 Calcif Tissue Int placebo-controlled RCT in osteoporotic vertebral fracture pain" }, { "claim": "Possible malignancy risk with long-term use", "level": "moderate", "basis": "FDA 2013 label update based on meta-analysis of controlled trials signaling cancer-risk imbalance" }, { "claim": "Inhibits osteoclast bone resorption via CTR", "level": "strong", "basis": "Mechanism established through decades of receptor pharmacology and cell-biology studies" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/calcitonin" }, { "name": "Carfilzomib", "slug": "carfilzomib", "aliases": [ "Kyprolis", "PR-171" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since 2012 for relapsed/refractory multiple myeloma. Administered intravenously in an oncology setting with required cardiac and renal monitoring. Not a controlled substance. Subject to REMS program for select combination regimens.", "routes": [ "intravenous" ], "half_life": "~1 hour (plasma); pharmacodynamic effect persists due to irreversible binding", "molecular_weight": 719.92, "cas_number": "868540-17-4", "mechanism_of_action": "Carfilzomib is a tetrapeptide epoxyketone that covalently and irreversibly inhibits the chymotrypsin-like (CT-L) proteolytic activity of the 20S proteasome catalytic core. The alpha,beta-epoxyketone pharmacophore forms a morpholine adduct with the N-terminal threonine of the beta5 subunit, permanently inactivating the active site. Proteasome inhibition leads to accumulation of poly-ubiquitinated proteins, triggering endoplasmic reticulum stress, activation of the unfolded protein response, upregulation of pro-apoptotic proteins such as NOXA and BIM, and suppression of NF-κB-mediated pro-survival signaling. Because it binds irreversibly, carfilzomib's pharmacodynamic effect outlasts its short plasma half-life. Compared to bortezomib, it has minimal off-target activity against serine proteases, which reduces peripheral neuropathy.", "evidence": [ { "claim": "Superior PFS vs lenalidomide/dex alone in RRMM", "level": "strong", "basis": "ASPIRE Phase III RCT showed 26.3 vs 17.6 month median PFS (HR 0.69) in relapsed/refractory myeloma" }, { "claim": "Superior to bortezomib-dex in RRMM", "level": "strong", "basis": "ENDEAVOR Phase III RCT Dimopoulos 2016 Lancet Oncology demonstrated PFS superiority" }, { "claim": "Irreversible chymotrypsin-like proteasome inhibition", "level": "strong", "basis": "Mechanism characterized in biochemical and structural studies; FDA-approved 2012" }, { "claim": "Less peripheral neuropathy than bortezomib", "level": "strong", "basis": "Head-to-head ENDEAVOR trial and preclinical selectivity data confirm reduced neuropathy" }, { "claim": "Cardiovascular toxicity requires monitoring", "level": "strong", "basis": "Pooled Phase III safety data and FDA label warnings on hypertension and cardiac failure" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/carfilzomib" }, { "name": "Carnosine", "slug": "carnosine", "aliases": [ "Beta-alanyl-L-histidine", "L-Carnosine", "β-alanyl-L-histidine" ], "category": "longevity", "subcategories": [ "muscle" ], "legal_status": "unregulated", "legal_notes": "Widely available OTC dietary supplement. Not regulated as a drug. Available in capsule, powder, and eye-drop formulations globally.", "routes": [ "oral" ], "half_life": "~2-3 hours (rapidly hydrolyzed by carnosinase in plasma)", "molecular_weight": 226.24, "cas_number": "305-84-0", "mechanism_of_action": "Carnosine exerts its biological effects through multiple complementary pathways. As an antioxidant, it scavenges reactive oxygen and nitrogen species and inhibits lipid peroxidation. As a metal chelator, it sequesters pro-oxidant transition metal ions such as copper and zinc. As an anti-glycation agent, it reacts with reactive carbonyl compounds to prevent advanced glycation end product (AGE) formation. Carnosine also buffers intracellular pH during anaerobic exercise, protects mitochondrial function, and may upregulate stress protein expression and proteasomal activity to clear damaged proteins — a mechanism relevant to cellular aging.", "evidence": [ { "claim": "Suppresses fibroblast cellular senescence", "level": "preliminary", "basis": "In vitro human fibroblast studies show delayed replicative senescence; Boldyrev 2010 Physiol Rev summary" }, { "claim": "Extends lifespan in animal models", "level": "preliminary", "basis": "Consistent results in senescence-accelerated mice and Drosophila longevity models" }, { "claim": "Anti-glycation activity reduces AGE formation", "level": "moderate", "basis": "Well-characterized biochemistry; reacts with reactive carbonyl compounds in vitro and in vivo" }, { "claim": "Improves cognitive decline markers", "level": "moderate", "basis": "Nagai 2021 Nutrients systematic review with meta-analysis of carnosine/anserine in cognitive decline" }, { "claim": "Muscle pH buffering during exercise", "level": "strong", "basis": "Established through decades of exercise-physiology RCTs in skeletal muscle" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/carnosine" }, { "name": "Cathelicidins", "slug": "cathelicidins", "aliases": [ "LL-37", "CRAMP", "hCAP-18", "Cathelicidin antimicrobial peptides" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "LL-37 and related cathelicidin peptides are research-only compounds. Synthetic LL-37 is available from peptide suppliers for research use. Not approved as a human therapeutic as of 2026.", "routes": [ "topical" ], "half_life": "~30–60 minutes (proteolytic degradation in wound fluid)", "molecular_weight": 4493.33, "cas_number": "154947-66-7", "mechanism_of_action": "LL-37 disrupts bacterial membranes via amphipathic alpha-helix insertion, causing membrane depolarization and lysis. It also binds lipopolysaccharide (LPS), neutralizing endotoxin. Beyond direct killing, LL-37 activates keratinocyte migration through formyl peptide receptor 2 (FPR2), triggering MAPK and PI3K/Akt signaling. It promotes angiogenesis by activating VEGFR2, and recruits neutrophils, monocytes, and T cells via FPR1. In wounds, LL-37 accelerates re-epithelialization and vascularization and is notably absent in chronic non-healing ulcers.", "evidence": [ { "claim": "LL-37 is sole human cathelicidin", "level": "strong", "basis": "Well-established genomic and proteomic characterization of cathelicidin family" }, { "claim": "Broad-spectrum antimicrobial via membrane insertion", "level": "strong", "basis": "Extensive biophysical studies confirming amphipathic helix membrane disruption" }, { "claim": "Accelerates chronic wound healing", "level": "preliminary", "basis": "Preclinical diabetic and venous ulcer models; early-phase clinical trials only" }, { "claim": "Absent in chronic non-healing ulcers", "level": "moderate", "basis": "Consistent human wound fluid biomarker studies across multiple cohorts" }, { "claim": "Activates keratinocyte migration via FPR2", "level": "strong", "basis": "Well-characterized receptor pharmacology and signaling studies" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cathelicidins" }, { "name": "Cecropin", "slug": "cecropin", "aliases": [ "Cecropin A", "Cecropin B", "Cecropin P1", "Insect cecropins" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "Cecropin peptides are research reagents available from peptide suppliers. Not approved for human therapeutic use. Used primarily in academic antimicrobial research.", "routes": [ "topical" ], "half_life": "minutes (proteolytically unstable in serum)", "molecular_weight": 4203.4, "cas_number": "80651-69-0", "mechanism_of_action": "Cecropins adopt an N-terminal amphipathic alpha-helix connected via an Ala-Gly-Pro hinge to a hydrophobic C-terminal helix. The N-terminal helix binds electrostatically to bacterial membrane phospholipids, enabling insertion. At threshold concentrations, cecropins permeabilize bacterial outer and inner membranes through a combination of carpet-model disruption and pore formation. They also inhibit efflux pump activity and interact with intracellular nucleic acids. A conserved N-terminal tryptophan (position 1 or 2) is critical for full antimicrobial activity.", "evidence": [ { "claim": "First insect antimicrobial peptide characterized", "level": "strong", "basis": "Foundational Steiner et al. 1980 Nature work on Hyalophora cecropia hemolymph" }, { "claim": "Broad-spectrum activity including MRSA", "level": "moderate", "basis": "Consistent in vitro MIC studies; no human clinical trials" }, { "claim": "Disrupts biofilms at sub-MIC concentrations", "level": "preliminary", "basis": "In vitro uropathogenic E. coli biofilm studies; limited in vivo validation" }, { "claim": "Cecropin-melittin hybrids reduce mammalian toxicity", "level": "preliminary", "basis": "In vitro cell culture and rodent toxicity studies of synthetic hybrids" }, { "claim": "No cecropin approved for clinical use", "level": "strong", "basis": "Regulatory record; cecropins remain academic research reagents" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cecropin" }, { "name": "Cerebrolysin", "slug": "cerebrolysin", "aliases": [ "FPE 1070" ], "category": "cognitive", "subcategories": [ "recovery" ], "legal_status": "prescription", "legal_notes": "Approved as a prescription drug in 40+ countries. Not FDA-approved. Classified as a biological product. Available through international pharmacies.", "routes": [ "intramuscular", "intravenous" ], "half_life": "Variable (mixture of peptides)", "molecular_weight": null, "cas_number": "12656-61-0", "mechanism_of_action": "Cerebrolysin mimics the action of endogenous neurotrophic factors (BDNF, GDNF, NGF, CNTF). Its peptide fragments cross the blood-brain barrier and activate multiple neuroprotective and neuroregenerative pathways: inhibiting calpain-mediated neuronal death, reducing amyloid-beta aggregation (relevant to Alzheimer's), promoting neurogenesis and synaptogenesis, modulating GSK-3β activity, and reducing neuroinflammation. It acts on the PI3K/Akt survival pathway and inhibits apoptosis.", "evidence": [ { "claim": "Functional recovery after acute ischemic stroke", "level": "moderate", "basis": "Bornstein et al. Neurol Sci 2018: meta-analysis of 9 RCTs, n=1,649 patients; significant improvement in Barthel Index and NIHSS vs placebo at 3 months" }, { "claim": "Neurological improvement in traumatic brain injury", "level": "moderate", "basis": "Muresanu et al. CNS Drugs 2015: RCT, n=156 TBI patients; cerebrolysin 30 mL/day for 10 days improved GOS-E scores vs placebo at 6 months" }, { "claim": "Cognitive improvement in mild-to-moderate Alzheimer's disease", "level": "moderate", "basis": "Plosker & Gauthier Drugs Aging 2015: meta-analysis of 6 RCTs; significant ADAS-cog improvement vs placebo; effect size modest and debated" }, { "claim": "Vascular dementia treatment", "level": "preliminary", "basis": "Guekht et al. CNS Drugs 2017: RCT, n=242; cerebrolysin improved cognitive and functional scores vs placebo at 24 weeks — single RCT, requires replication" }, { "claim": "Neuroprotection in Parkinson's disease or other neurodegenerative disorders", "level": "insufficient", "basis": "Anecdotal use and small open-label studies only; no Phase 3 RCT data for non-stroke, non-AD indications" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cerebrolysin" }, { "name": "Cetrorelix", "slug": "cetrorelix", "aliases": [ "Cetrotide", "Cetrorelix acetate", "SB-75", "Cetrolix" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 021197) for inhibition of premature LH surges in women undergoing controlled ovarian stimulation. Available only by prescription; administered under fertility specialist supervision. Also approved by EMA.", "routes": [ "subcutaneous" ], "half_life": "~5 hours (0.25 mg dose); ~30 hours (3 mg dose)", "molecular_weight": 1431.04, "cas_number": "120287-85-6", "mechanism_of_action": "Cetrorelix competitively blocks GnRH receptors in the anterior pituitary gland, preventing endogenous GnRH from stimulating LH and FSH release. Unlike GnRH agonists, cetrorelix produces immediate suppression of gonadotropin secretion without an initial flare effect. Receptor occupancy inhibits the LH surge within 2 hours of injection, maintaining follicular development under controlled gonadotropin stimulation. Its decapeptide structure with D-amino acid substitutions confers resistance to enzymatic degradation and high receptor binding affinity, enabling once-daily dosing at 0.25 mg or a single 3 mg dose in IVF protocols.", "evidence": [ { "claim": "Prevents premature LH surge in IVF", "level": "strong", "basis": "FDA-approved indication (NDA 021197) with multiple RCTs establishing efficacy" }, { "claim": "Non-inferior to GnRH agonist long protocol", "level": "strong", "basis": "Cheung Hum Reprod 2005 RCT and multiple meta-analyses confirm equivalent live birth rates" }, { "claim": "Reduces OHSS risk vs agonist protocols", "level": "strong", "basis": "Meta-analyses and post-marketing surveillance confirm lower OHSS incidence" }, { "claim": "Rapid flare-free pituitary suppression", "level": "strong", "basis": "Pharmacokinetic/dynamic studies show LH suppression within 2 hours of first dose" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cetrorelix" }, { "name": "CGRP", "slug": "cgrp", "aliases": [ "Calcitonin Gene-Related Peptide", "α-CGRP", "CGRP-I", "Human CGRP" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Endogenous CGRP peptide is available for research use only. Therapeutic monoclonal antibodies targeting CGRP/its receptor (erenumab, fremanezumab, galcanezumab) are FDA-approved prescription medications. The raw peptide is not approved for human administration.", "routes": [ "intravenous", "subcutaneous" ], "half_life": "~7 minutes (plasma)", "molecular_weight": 3789.37, "cas_number": "90954-53-3", "mechanism_of_action": "CGRP binds to the CLR/RAMP1 receptor complex (CGRP receptor), activating adenylyl cyclase and increasing intracellular cAMP. This triggers smooth muscle relaxation and potent vasodilation, particularly in cranial blood vessels. During migraine, CGRP is released from trigeminal nerve terminals, activating the trigeminovascular system and promoting neurogenic inflammation and peripheral sensitization. Anti-CGRP monoclonal antibodies (erenumab, fremanezumab, galcanezumab) and CGRP receptor antagonists (gepants) block this cascade.", "evidence": [ { "claim": "Multiple FDA-approved anti-CGRP migraine drugs", "level": "strong", "basis": "Erenumab, fremanezumab, galcanezumab mAbs and gepants approved based on multiple Phase III RCTs" }, { "claim": "One of the most potent endogenous vasodilators", "level": "strong", "basis": "Decades of vascular pharmacology establish CGRP as top-tier vasodilator via CLR/RAMP1 cAMP signaling" }, { "claim": "Plasma CGRP rises during migraine attacks", "level": "moderate", "basis": "Multiple human studies show CGRP elevation during spontaneous attacks, normalizing with triptan treatment" }, { "claim": "Activates trigeminovascular system in migraine", "level": "strong", "basis": "Goadsby and colleagues' human infusion and neuroimaging studies established trigeminovascular CGRP model" }, { "claim": "Regulates bone metabolism and wound healing", "level": "preliminary", "basis": "Preclinical animal studies suggest CGRP roles in osteoblast activity and tissue repair" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cgrp" }, { "name": "Chonluten", "slug": "chonluten", "aliases": [ "KED tripeptide", "Glu-Asp-Gly", "lung bioregulator", "bronchi peptide" ], "category": "immune", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Developed and studied in Russia; commercially available in Russia as a bronchopulmonary bioregulator supplement. Available in Western markets as a research chemical only.", "routes": [ "subcutaneous", "intramuscular", "oral" ], "half_life": "Short (minutes to hours — estimated for tripeptide class)", "molecular_weight": 317.3, "cas_number": null, "mechanism_of_action": "Chonluten penetrates bronchial epithelial cells and translocates to the nucleus, where it directly interacts with DNA in a tissue-specific manner to modulate gene transcription patterns associated with inflammation and oxidative stress. In preclinical studies, Chonluten inhibited TNF-α production by monocytes exposed to bacterial lipopolysaccharide (LPS), demonstrating anti-inflammatory activity at the cytokine level. It modulates the expression of genes involved in antioxidant activity, mucin regulation, and bronchial epithelial barrier integrity. As with other Khavinson bioregulators, its specificity arises from the peptide's preferential interaction with promoter sequences in lung tissue cells via minor groove DNA binding, activating regenerative transcriptional programs in aged or damaged pulmonary tissue.", "evidence": [ { "claim": "Inhibits TNF-α in monocytes", "level": "preliminary", "basis": "In vitro LPS-stimulated cell studies show cytokine suppression; no Western RCTs" }, { "claim": "Modulates antioxidant gene expression", "level": "preliminary", "basis": "Khavinson group preclinical studies on lung tissue; limited to Russian literature" }, { "claim": "Restores bronchial epithelial function", "level": "preliminary", "basis": "Animal aged tissue models show functional restoration; no human RCTs published" }, { "claim": "Protects against pulmonary oxidative stress", "level": "preliminary", "basis": "Preclinical rodent lung injury models; clinical evidence only in Russian series" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/chonluten" }, { "name": "CJC-1295", "slug": "cjc-1295", "aliases": [ "Modified GRF 1-29", "Mod GRF", "CJC-1295 no DAC" ], "category": "muscle", "subcategories": [ "longevity" ], "legal_status": "reclassification-pending", "legal_notes": "Under FDA reclassification review as part of the 14-peptide RFK Jr. initiative. Previously available from research peptide suppliers.", "routes": [ "subcutaneous" ], "half_life": "~30 minutes (no DAC) / ~8 days (with DAC)", "molecular_weight": 3367.97, "cas_number": "863288-34-0", "mechanism_of_action": "CJC-1295 binds with high affinity to the pituitary GHRH receptor (GHRHR), a Gs-protein-coupled receptor. Agonist binding activates adenylyl cyclase, elevating intracellular cAMP in somatotroph cells. cAMP activates protein kinase A (PKA), which phosphorylates the transcription factor CREB (cAMP response element-binding protein). CREB activation upregulates transcription of the GH gene (GH1) and simultaneously stimulates the secretory machinery responsible for releasing pre-synthesized GH-containing vesicles. The cAMP/PKA cascade also opens voltage-gated calcium channels on somatotroph membranes, providing additional Ca²⁺ influx that triggers exocytosis. The result is a dose-dependent pulse of GH secretion that begins within minutes and — in the case of CJC-1295 without DAC — peaks and resolves over 2-3 hours.\n\nThe DAC modification fundamentally changes this pharmacokinetic picture. The maleimidopropionic acid conjugate on the lysine residue at position 29 is reactive toward free thiols in plasma, selectively forming a covalent thioether bond with the Cys-34 residue of human serum albumin within minutes of subcutaneous injection. Because albumin has a half-life of approximately 19 days, the CJC-1295-albumin conjugate is released gradually as the body naturally turns over albumin. Active peptide leaches off at a rate that maintains plasma concentrations above the GH-stimulating threshold for approximately 8-10 days per injection. The consequence is a sustained \"GH bleed\" — not a single pulse but a continuous, low-amplitude increase in GH secretion superimposed on the pituitary's remaining pulsatile rhythms.\n\nPulsatile GH secretion is preserved even during CJC-1295 DAC administration because the pituitary retains responsiveness to hypothalamic regulatory inputs. A 2006 study by Jetté et al. (Endocrinology, 2006) demonstrated that pulsatile GH secretion persists with elevated amplitude when subjects receive chronic CJC-1295 stimulation. This is mechanistically important: somatostatin is released by the hypothalamus in a separate pulsatile pattern that creates the GH troughs needed for normal physiological feedback. CJC-1295 amplifies each GHRH-driven peak without completely obliterating the troughs, distinguishing it from direct rhGH injection in terms of physiological fidelity.\n\nDownstream, sustained or amplified GH elevation drives hepatic IGF-1 production. IGF-1 acts as the primary anabolic mediator: it binds the IGF-1 receptor (IGF1R), a receptor tyrosine kinase, activating PI3K/Akt/mTOR (protein synthesis) and MEK/ERK (proliferation) cascades in skeletal muscle, bone, and connective tissue. GH independently activates JAK2/STAT5 in liver and muscle. The net downstream biology — lean mass accretion, lipolysis, collagen synthesis, and bone matrix deposition — is qualitatively the same whether driven by CJC-1295 with DAC, without DAC, or by rhGH directly; the difference lies in the kinetics and the degree to which normal pituitary feedback mechanisms are preserved.", "evidence": [ { "claim": "Growth hormone and IGF-1 elevation", "level": "moderate", "basis": "Teichman et al. JCEM 2006: randomized, double-blind ascending-dose trial in 42 healthy adults; GH increased 2–10-fold sustained >6 days per injection" }, { "claim": "Prolonged IGF-1 elevation with DAC formulation", "level": "moderate", "basis": "Teichman 2006 multi-dose arm: mean IGF-1 above baseline for up to 28 days post-injection in adult volunteers" }, { "claim": "Body composition improvement (lean mass, fat loss)", "level": "preliminary", "basis": "No dedicated RCTs; extrapolated from GH/IGF-1 elevations and indirect data from analogous GHRH agents" }, { "claim": "Preservation of pulsatile GH secretion", "level": "preliminary", "basis": "Jetté et al. Endocrinology 2006: rat model showing pulsatility maintained with chronic GHRH receptor stimulation" }, { "claim": "Bone mineral density improvement", "level": "insufficient", "basis": "No human trials measuring BMD; mechanistic inference from GH/IGF-1 pathway only" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "91971820", "wikidata": "Q5012018" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cjc-1295" }, { "name": "Collagen Dipeptide", "slug": "collagen-dipeptide", "aliases": [ "Pro-Hyp", "Hyp-Gly", "Prolyl-Hydroxyproline", "Hydroxyproline-Glycine", "Collagen hydrolysate fragments" ], "category": "skin", "subcategories": [ "other" ], "legal_status": "unregulated", "legal_notes": "Collagen dipeptides (Pro-Hyp, Hyp-Gly) are dietary supplement ingredients classified as GRAS (Generally Recognized as Safe) in the US. No prescription required.", "routes": [ "oral" ], "half_life": "~2 hours (plasma peak after oral hydrolyzed collagen ingestion)", "molecular_weight": 226.23, "cas_number": "34243-14-0", "mechanism_of_action": "Pro-Hyp and Hyp-Gly survive intestinal digestion intact and are absorbed into circulation. They act on dermal fibroblasts to stimulate type I collagen and hyaluronic acid synthesis, and on chondrocytes to promote cartilage matrix production. Pro-Hyp has been shown to activate fibroblast proliferation and migration. These dipeptides may also act as chemotactic signals that recruit fibroblast precursors to the dermis. The hydroxyproline content is unique to collagen proteins, explaining the specificity of these fragments.", "evidence": [ { "claim": "Pro-Hyp reaches measurable plasma levels", "level": "strong", "basis": "Multiple human pharmacokinetic studies confirming 0.5-10 micromolar plasma appearance" }, { "claim": "Improves skin hydration and elasticity", "level": "moderate", "basis": "Multiple placebo-controlled trials of hydrolyzed collagen over 8-12 weeks" }, { "claim": "Stimulates fibroblast proliferation and migration", "level": "moderate", "basis": "Consistent in vitro fibroblast studies and ex vivo skin assays" }, { "claim": "Reduces joint pain in athletes", "level": "moderate", "basis": "Several placebo-controlled RCTs of hydrolyzed collagen in athletes" }, { "claim": "Survives intestinal digestion intact", "level": "strong", "basis": "Human plasma measurement after oral ingestion confirms intact absorption" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/collagen-dipeptide" }, { "name": "Collagen Peptides", "slug": "collagen-peptides", "aliases": [ "Hydrolyzed Collagen", "Collagen Hydrolysate", "HC", "Type I Collagen Peptides", "Type II Collagen Peptides" ], "category": "skin", "subcategories": [ "recovery", "longevity" ], "legal_status": "unregulated", "legal_notes": "Classified as a dietary supplement in the US (DSHEA 1994). No prescription required. Available OTC in powder, capsule, and liquid forms from numerous manufacturers. FDA regulates as food ingredient, not drug. No scheduling concerns.", "routes": [ "oral" ], "half_life": "~2 hours (key dipeptides peak at 1–2 h post-dose, cleared within 4–6 h)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Upon ingestion, collagen hydrolysate is cleaved into small bioactive peptides (2–6 kDa), primarily Pro-Hyp and Hyp-Gly, which are absorbed intact through the gastrointestinal epithelium and detected in circulation. These peptides act as signaling molecules that stimulate dermal fibroblasts to upregulate synthesis of new collagen, elastin, and hyaluronic acid via TGF-β and MAPK/ERK pathways. In cartilage, type II collagen peptides accumulate in synovial fluid and modulate chondrocyte activity, reducing inflammatory cytokines (IL-1β, TNF-α). In bone, collagen-derived peptides promote osteoblast differentiation while inhibiting osteoclast activity through OPG/RANKL signaling.", "evidence": [ { "claim": "Skin elasticity improvement", "level": "strong", "basis": "Pu et al. Nutrients 2023 meta-analysis + Proksch Skin Pharmacol Physiol 2014 double-blind RCT; 7-15% elasticity gain across 11+ RCTs" }, { "claim": "Skin hydration and wrinkle reduction", "level": "strong", "basis": "Bolke Nutrients 2022 and Kim Nutrients 2018 double-blind placebo-controlled RCTs; consistent hydration/wrinkle endpoints across trials" }, { "claim": "Joint pain reduction in osteoarthritis/athletes", "level": "moderate", "basis": "Multiple RCTs with type II collagen 10-15 g/day; reduced joint pain in athletes and OA patients over 4-24 weeks" }, { "claim": "Bone density improvement", "level": "preliminary", "basis": "Emerging RCT evidence but less robust than skin/joint data; smaller sample sizes and shorter durations" }, { "claim": "Wound healing support", "level": "preliminary", "basis": "Small clinical studies showing dermal repair benefit; not yet pooled in systematic review" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/collagen-peptides" }, { "name": "Collagen Type I", "slug": "collagen-type-i", "aliases": [ "Type I Collagen", "Hydrolyzed Collagen I", "Collagen Peptides (Type I)" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "OTC dietary supplement. Available as powder, capsule, and beverage additive. No prescription required. Subject to standard supplement regulations (not FDA drug approval).", "routes": [ "oral" ], "half_life": "Collagen peptides peak in plasma ~1 hour post-ingestion; systemic effects accumulate over weeks", "molecular_weight": null, "cas_number": "9007-34-5", "mechanism_of_action": "Oral hydrolyzed Type I collagen is digested into collagen-specific dipeptides and tripeptides (notably Pro-Hyp and Gly-Pro-Hyp), which circulate in plasma and accumulate in skin, joints, and bone tissue. These fragments stimulate fibroblasts to produce new collagen and hyaluronic acid via activation of anabolic pathways including mTOR and MAPK. In skin, rising circulating hydroxyproline signals the dermis that collagen is being turned over, triggering synthesis. In bone, collagen peptides promote osteoblast activity and support mineralization. In tendons, they support collagenous matrix remodeling when combined with loading exercise.", "evidence": [ { "claim": "Improves skin elasticity and hydration", "level": "strong", "basis": "Proksch 2014, Asserin 2015, and Choi 2019 systematic review pool multiple RCTs showing significant benefit" }, { "claim": "Reduces wrinkle depth", "level": "moderate", "basis": "Multiple RCTs at 2.5-10 g/day showed wrinkle-depth reduction via dermal matrix synthesis" }, { "claim": "Collagen peptides absorbed as Pro-Hyp dipeptides", "level": "strong", "basis": "PK studies confirm plasma appearance of bioactive di/tripeptides after oral collagen intake" }, { "claim": "Reduces osteoarthritis joint pain", "level": "moderate", "basis": "Benito-Ruiz 2009 RCT and Clark 2008 athlete RCT support joint pain reduction" }, { "claim": "Supports bone density", "level": "preliminary", "basis": "Mixed RCT results; favorable subgroup signals but not consistently demonstrated" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/collagen-type-i" }, { "name": "Collagen Type II", "slug": "collagen-type-ii", "aliases": [ "Type II Collagen", "Undenatured Type II Collagen", "UC-II", "Cartilage Collagen" ], "category": "other", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Available OTC as a dietary supplement (both UC-II and hydrolyzed forms). UC-II is a patented ingredient. Not regulated as a pharmaceutical.", "routes": [ "oral" ], "half_life": "Not applicable (orally consumed protein/peptide supplement)", "molecular_weight": null, "cas_number": "9007-34-5", "mechanism_of_action": "Undenatured Type II collagen (UC-II) at microgram doses interacts with Peyer's patches in the gut-associated lymphoid tissue. This triggers induction of regulatory T cells (Tregs) that specifically recognize Type II collagen epitopes. When these Tregs encounter Type II collagen in joint cartilage, they secrete anti-inflammatory cytokines (TGF-β, IL-4, IL-10) that suppress local immune-mediated cartilage destruction. This oral tolerance mechanism is distinct from the amino acid supplementation approach used with hydrolyzed collagen, requiring far lower doses and native epitope preservation.", "evidence": [ { "claim": "UC-II reduces osteoarthritis symptoms", "level": "strong", "basis": "Lugo 2016 multicenter RCT (n=191) Nutr J confirmed knee OA symptom improvement vs placebo" }, { "claim": "Oral tolerance via Peyer's patches", "level": "moderate", "basis": "1993 Science landmark trial and subsequent mechanistic studies established gut-mediated Treg induction" }, { "claim": "Effective at 40 mg/day low-dose", "level": "strong", "basis": "Crowley 2009 and Lugo 2013/2016 RCTs established dose-response; higher doses defeat tolerance mechanism" }, { "claim": "Hydrolyzed type II improves joint pain", "level": "moderate", "basis": "Clark 2008 24-week RCT in athletes showed activity-related joint pain reduction" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/collagen-type-ii" }, { "name": "Collagen Type III", "slug": "collagen-type-iii", "aliases": [ "Type III Collagen", "Reticular Collagen", "Fetal Collagen" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "OTC dietary supplement, typically as part of mixed hydrolyzed collagen products. Single-type Type III collagen supplements exist but are less common.", "routes": [ "oral" ], "half_life": "Not applicable (orally consumed protein supplement)", "molecular_weight": null, "cas_number": "9007-34-5", "mechanism_of_action": "Type III collagen forms fine reticular fibers in the extracellular matrix that provide elasticity and flexibility rather than the rigidity imparted by Type I collagen fibrils. As a supplement (hydrolyzed), it delivers proline, glycine, and hydroxyproline residues that are incorporated into dermal ECM proteins. Supplemental collagen peptides derived from Type III-rich sources (such as bovine hide or fish skin) may preferentially support dermal elasticity and vascular collagen maintenance. The ratio of Type I to Type III collagen shifts with age, contributing to the loss of skin softness and vascular compliance.", "evidence": [ { "claim": "Contributes to skin elasticity and vascular integrity", "level": "strong", "basis": "Kuivaniemi 1997 biochem review and decades of basic-science characterization established tissue roles" }, { "claim": "Type I:III ratio shifts with aging", "level": "moderate", "basis": "Histological and biochemical studies in dermis and vasculature confirm age-related ratio shifts" }, { "claim": "Supplementation improves skin outcomes", "level": "preliminary", "basis": "No Type III-specific RCTs; benefits extrapolated from mixed-collagen trials Proksch 2014, Asserin 2015" }, { "claim": "COL3A1 mutations cause vascular Ehlers-Danlos", "level": "strong", "basis": "Well-established human genetics; EDS type IV diagnosis based on COL3A1 sequencing" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/collagen-type-iii" }, { "name": "Cortagen", "slug": "cortagen", "aliases": [ "Ala-Glu-Asp-Pro", "AEDP tetrapeptide", "Cortagen bioregulator" ], "category": "cognitive", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Not FDA or EMA approved. Sold by research peptide suppliers in the US and EU as a research compound. Not a scheduled substance. Human self-administration outside clinical research is not endorsed by regulatory bodies.", "routes": [ "subcutaneous", "nasal" ], "half_life": "Not established; estimated short (minutes to hours) given tetrapeptide size", "molecular_weight": 430.4, "cas_number": "335591-03-2", "mechanism_of_action": "Cortagen is proposed to act as an epigenetic regulator in the Khavinson model: short peptides penetrate cell membranes and bind to specific DNA regulatory sequences, modulating chromatin accessibility and transcriptional activation. Transcriptomic analysis of Cortagen-treated cells reveals changes across 110 genes spanning 234 DNA regions, with effects on oxidative stress pathways, cellular repair signaling, and apoptosis regulation. In preclinical (rodent) peripheral nerve injury models, intramuscular Cortagen at 10 mcg/kg increased regenerating nerve fiber counts by up to 40% following transection. It may also decondense heterochromatin, restoring expression of epigenetically silenced genes associated with aging.", "evidence": [ { "claim": "Promotes peripheral nerve regeneration", "level": "preliminary", "basis": "Rodent transection models showed up to 40% increase in regenerating nerve fibers at 10 mcg/kg IM" }, { "claim": "Epigenetic transcriptional modulation", "level": "preliminary", "basis": "In vitro transcriptomic analysis showed changes across 110 genes and 234 DNA regions" }, { "claim": "Neuroprotection in cortical aging", "level": "insufficient", "basis": "Limited Russian-language observational reports; no independent Western replication or RCTs as of 2026" }, { "claim": "Post-stroke neurological recovery", "level": "insufficient", "basis": "Small uncontrolled observational series only; no randomized controlled data exists" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cortagen" }, { "name": "Cortexin", "slug": "cortexin", "aliases": [ "brain polypeptide complex", "cortical polypeptides", "cerebral cortex extract" ], "category": "cognitive", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Registered pharmaceutical drug approved in Russia (1999) and several Eastern European countries. Not FDA-approved. Available in Western markets only as a research substance. Not approved for therapeutic human use in the US or EU. Comparable to Cerebrolysin in regulatory status.", "routes": [ "intramuscular" ], "half_life": "Unknown (polypeptide complex — not characterized pharmacokinetically in Western literature)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Cortexin contains a complex mixture of polypeptides, amino acids, and trace elements from bovine cerebral cortex that cross the blood-brain barrier and directly interact with neuronal cells. Its neuroprotective mechanism involves regulating the balance between excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmitters, modulating dopamine and serotonin signaling, and reducing paroxysmal seizure activity. At the molecular level, Cortexin peptides interact with neuron-specific proteins including β5-tubulin, creatine kinase B, and protein 14-3-3 α/β, engaging pathways governing signal transduction, energy metabolism, proteolytic protein modification, cell structure, and neuroinflammation. These multi-target actions promote neuroplasticity and neuroprotection after ischemic or traumatic injury. The preparation also reduces oxidative stress in neuronal tissue and supports neurotrophic factor activity.", "evidence": [ { "claim": "Neuroprotection in ischemic stroke", "level": "moderate", "basis": "Russian pharmaceutical approval 1999; rat ischemia study (PLOS ONE 2021) confirmed effect" }, { "claim": "Comparable efficacy to Cerebrolysin", "level": "moderate", "basis": "Kurkin PLOS ONE 2021 rat comparative study showed equivalent neuroprotection" }, { "claim": "Improves cognitive impairment recovery", "level": "preliminary", "basis": "Russian clinical series over 25 years; no Cochrane-level systematic review" }, { "claim": "Inhibits brain caspase-8 apoptosis", "level": "preliminary", "basis": "Piotrovskiy Bull Exp Biol Med 2017 preclinical mechanistic study" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cortexin" }, { "name": "Cortistatin", "slug": "cortistatin", "aliases": [ "CST-14", "CST-17", "CST-29", "Cortistatin-14", "Cortistatin-29" ], "category": "immune", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Cortistatin is a research peptide with no approved clinical applications. Somatostatin analogs (octreotide, lanreotide) are approved drugs but act through partially overlapping but distinct mechanisms.", "routes": [ "intravenous", "subcutaneous" ], "half_life": "<10 minutes (short plasma half-life limits clinical translation)", "molecular_weight": 1721.01, "cas_number": "193829-96-8", "mechanism_of_action": "Cortistatin's anti-inflammatory actions are mediated through multiple converging pathways. Binding to somatostatin receptors (particularly SSTR2/3/5) suppresses cAMP, reducing inflammatory cytokine production (TNF-α, IL-1β, IL-6, IL-12, IFN-γ, IL-17). Activation of GHSR1a on macrophages and dendritic cells shifts cytokine balance toward anti-inflammatory profiles. Cortistatin also inhibits NF-κB activation, reduces leukocyte migration, and promotes regulatory T-cell differentiation. In arthritis models, it directly binds TNF-α receptors and protects cartilage from destruction. Central actions include modulation of slow-wave sleep and suppression of growth hormone secretion.", "evidence": [ { "claim": "Dramatically reduces experimental colitis inflammation", "level": "preliminary", "basis": "Gonzalez-Rey animal colitis models show reduced cytokines, mucosal damage, improved survival" }, { "claim": "Abrogates joint destruction in collagen-induced arthritis", "level": "preliminary", "basis": "Rodent arthritis models show complete suppression of swelling and cartilage/bone destruction" }, { "claim": "Binds somatostatin receptors plus GHSR1a and MrgX2", "level": "moderate", "basis": "Receptor pharmacology studies confirm broader binding profile than parent somatostatin" }, { "claim": "Suppresses pro-inflammatory cytokines (TNF-a, IL-6, IL-17)", "level": "preliminary", "basis": "In vitro and animal immunomodulation studies across colitis, arthritis, and sepsis models" }, { "claim": "Short half-life limits clinical translation", "level": "moderate", "basis": "Pharmacokinetic studies consistently show <10 minute plasma half-life requiring analog development" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/cortistatin" }, { "name": "Defensins", "slug": "defensins", "aliases": [ "Alpha-defensins", "Beta-defensins", "Human neutrophil peptides", "HNPs", "HBDs" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "No defensin peptide is FDA-approved as a drug. Human neutrophil peptide HNP-1 and synthetic analogs are available as research reagents. Clinical trials of defensin-based formulations are in early phases.", "routes": [ "topical", "intravenous" ], "half_life": "minutes to hours (context-dependent)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Defensins kill microbes primarily by disrupting microbial membranes. Their cationic, amphipathic structure enables electrostatic binding to negatively charged bacterial membranes, followed by insertion and pore formation that causes membrane disruption and leakage of intracellular contents. Beyond direct killing, defensins serve as immunomodulators: they chemoattract dendritic cells, T cells, and mast cells via CCR6 and other receptors, bridging innate and adaptive immunity. Alpha-defensins (HNP-1 to -4) are stored in neutrophil azurophilic granules and released during phagocytosis.", "evidence": [ { "claim": "Disrupt bacterial membranes via pore formation", "level": "strong", "basis": "Extensive biophysical and structural biology studies of membrane interaction" }, { "claim": "Chemoattract dendritic and T cells via CCR6", "level": "strong", "basis": "Consistent receptor pharmacology and immune cell migration studies" }, { "claim": "Alpha-defensin deficiency linked to Crohn's disease", "level": "moderate", "basis": "Consistent human tissue studies correlating Paneth cell defects with disease" }, { "claim": "Retrocyclin neutralizes HIV in vitro", "level": "preliminary", "basis": "In vitro HIV entry inhibition assays; no human efficacy data" }, { "claim": "Topical antimicrobial for wound care", "level": "preliminary", "basis": "Early-phase clinical trials; no FDA-approved defensin drug as of 2026" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/defensins" }, { "name": "Deltorphin", "slug": "deltorphin", "aliases": [ "Deltorphin I", "Deltorphin II", "Deltorphin A", "Dermenkephalin" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Deltorphins are not approved for human use and are available for research purposes only. They are not scheduled substances in most jurisdictions but require appropriate laboratory handling protocols.", "routes": [ "intravenous", "intramuscular" ], "half_life": "~15–30 minutes (in vivo, enzymatic degradation)", "molecular_weight": 881.98, "cas_number": "120884-56-2", "mechanism_of_action": "Deltorphins bind with high selectivity to delta-opioid receptors (DOR), acting as potent agonists. Activation of DOR inhibits adenylyl cyclase via Gi/Go proteins, reduces neuronal excitability, and modulates neurotransmitter release. Unlike mu-opioid receptor agonists, delta-selective compounds may produce analgesia with reduced respiratory depression, tolerance, and physical dependence, making them subjects of interest for analgesic drug development.", "evidence": [ { "claim": "Nanomolar delta-opioid receptor selectivity", "level": "strong", "basis": "Receptor binding pharmacology confirms orders-of-magnitude DOR selectivity vs mu and kappa" }, { "claim": "Workhorse tool for DOR pharmacology", "level": "strong", "basis": "Deltorphin II widely used across receptor characterization studies as reference DOR agonist" }, { "claim": "Potentially reduced respiratory depression vs mu-opioids", "level": "preliminary", "basis": "Animal studies suggest DOR agonists spare respiratory centers; no human clinical trials conducted" }, { "claim": "Cardioprotective in rodent ischemia models", "level": "preliminary", "basis": "Preclinical myocardial ischemia-reperfusion studies suggest DOR-mediated cardioprotection" }, { "claim": "No human clinical trials conducted", "level": "insufficient", "basis": "Research-only status with no clinical development toward approved indications" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/deltorphin" }, { "name": "Dermorphin", "slug": "dermorphin", "aliases": [ "H-Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2", "Frog Skin Opioid Peptide" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Dermorphin is available for laboratory research only. It is banned in horse racing competitions by all major regulatory bodies (RMTC, ARCI). It is not approved for human or veterinary therapeutic use.", "routes": [ "intravenous", "intramuscular" ], "half_life": "~20–30 minutes (D-Ala confers resistance to peptidase degradation vs. endogenous opioids)", "molecular_weight": 802.88, "cas_number": "77614-16-5", "mechanism_of_action": "Dermorphin binds mu-opioid receptors with high affinity and selectivity, activating Gi/Go signaling to inhibit adenylyl cyclase, suppress voltage-gated calcium channels, and activate GIRK potassium channels. The result is profound neuronal inhibition in pain pathways including the dorsal horn and periaqueductal gray matter. The D-alanine residue at position 2 increases resistance to aminopeptidase cleavage, extending biological activity compared to endogenous opioid peptides. Dermorphin does not have meaningful affinity at delta or kappa opioid receptors at therapeutic concentrations.", "evidence": [ { "claim": "30-40x more potent than morphine at mu-opioid receptor", "level": "strong", "basis": "Decades of receptor binding and in vivo potency assays consistently confirm extreme MOR potency" }, { "claim": "D-alanine confers metabolic resistance", "level": "strong", "basis": "Biochemical peptidase resistance studies confirm D-Ala-2 prevents aminopeptidase cleavage" }, { "claim": "Detected in horse racing doping scandals 2012", "level": "strong", "basis": "Documented detection in multiple post-race urine samples at US tracks led to bans and prosecutions" }, { "claim": "Selective for mu over delta/kappa receptors", "level": "strong", "basis": "Receptor binding studies confirm orders-of-magnitude selectivity for MOR over other opioid receptors" }, { "claim": "No approved human therapeutic applications", "level": "insufficient", "basis": "Despite 40+ years since discovery, no clinical development has advanced to regulatory approval" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/dermorphin" }, { "name": "Desmopressin", "slug": "desmopressin", "aliases": [ "DDAVP", "1-desamino-8-D-arginine vasopressin", "Noctiva", "Stimate", "Nocdurna" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since February 1978. Available as intranasal spray (DDAVP Nasal Spray), oral tablets (DDAVP Tablets), sublingual tablets (Nocdurna), and IV/SC injection (DDAVP Injection). Multiple generic formulations available. Prescription required in the US and most jurisdictions. Some OTC availability in certain countries for bedwetting formulations.", "routes": [ "oral", "nasal", "subcutaneous", "intravenous" ], "half_life": "~1.5–2.5 hours (nasal/IV); ~2–3 hours (oral)", "molecular_weight": 1069.22, "cas_number": "16679-58-6", "mechanism_of_action": "Desmopressin acts as a selective V2 vasopressin receptor agonist with minimal V1 receptor activity. V2 receptor activation in renal collecting duct principal cells triggers Gs-coupled adenylyl cyclase activation, elevating intracellular cyclic AMP. cAMP activates protein kinase A, which phosphorylates aquaporin-2 (AQP2) water channels, driving their translocation from cytoplasmic vesicles to the apical membrane. The resulting increase in apical membrane water permeability allows passive water reabsorption from urine into the hyperosmotic medullary interstitium, concentrating urine and reducing urine volume. In hemostasis, V2 receptor activation in vascular endothelial cells triggers release of stored von Willebrand factor (vWF) from Weibel-Palade bodies and increases plasma factor VIII levels through stabilization by vWF, correcting the coagulation defect in mild hemophilia A and type 1 von Willebrand disease.", "evidence": [ { "claim": "Treats central diabetes insipidus", "level": "strong", "basis": "FDA-approved since 1978; multiple RCTs confirm restoration of urine output and osmolality" }, { "claim": "Reduces nocturnal enuresis", "level": "strong", "basis": "Multiple RCTs show 60–70% reduction in bedwetting nights vs placebo" }, { "claim": "Raises factor VIII in hemophilia A", "level": "strong", "basis": "Established clinical use; 3–5-fold factor VIII increases for minor surgical prophylaxis" }, { "claim": "Reduces nocturia in adults", "level": "strong", "basis": "Weiss 2012 RCT and Ebell 2014 systematic review support Nocdurna sublingual approval" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/desmopressin" }, { "name": "Dihexa", "slug": "dihexa", "aliases": [ "N-hexanoic-Tyr-Ile-(6) aminohexanoic amide" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Research chemical with a patent for neurological applications. Not scheduled. Limited availability compared to more established peptides.", "routes": [ "oral", "subcutaneous" ], "half_life": "~2-6 hours (estimated from animal data)", "molecular_weight": 507.63, "cas_number": "1401708-83-5", "mechanism_of_action": "Dihexa binds to hepatocyte growth factor (HGF) and its receptor c-Met, potentiating the HGF/c-Met signaling pathway which is critical for neuronal survival, neurite outgrowth, and synaptogenesis. It stabilizes the HGF dimer and enhances receptor dimerization, amplifying downstream signaling through PI3K/Akt and MAPK/ERK pathways. This promotes formation of new synaptic connections (spinogenesis) at substantially lower concentrations than BDNF in preclinical studies.", "evidence": [ { "claim": "Cognitive restoration via HGF/c-Met potentiation", "level": "preliminary", "basis": "McCoy et al. J Pharmacol Exp Ther 2013: aged rat cognitive restoration; 10 million x BDNF potency cited but mechanism only in animal models" }, { "claim": "Alzheimer's APP/PS1 model memory rescue", "level": "preliminary", "basis": "Gao et al. Front Aging Neurosci 2021: APP/PS1 mouse model; PI3K/AKT pathway activation; preclinical only" }, { "claim": "Oral bioavailability and BBB penetration", "level": "preliminary", "basis": "Animal studies demonstrated oral absorption and BBB crossing; no human pharmacokinetic data published" }, { "claim": "Huntington's disease symptom reduction", "level": "preliminary", "basis": "Gao et al. Neuropeptides 2024: 3-nitropropionic acid rat HD model; single animal study" }, { "claim": "Human cognitive enhancement safety and efficacy", "level": "insufficient", "basis": "No human clinical trials completed; all dosing extrapolated from animal data; community anecdote only" } ], "peer_reviewed_reference_count": 6, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/dihexa" }, { "name": "DSIP", "slug": "dsip", "aliases": [ "Delta Sleep-Inducing Peptide" ], "category": "sleep", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Available as a research peptide. Not scheduled or banned. Limited regulatory attention due to niche use.", "routes": [ "subcutaneous", "intramuscular", "nasal" ], "half_life": "~7-8 minutes (rapid degradation, but sleep effects persist)", "molecular_weight": 848.8, "cas_number": "62568-57-4", "mechanism_of_action": "DSIP modulates multiple neurotransmitter systems including GABAergic, glutamatergic, and serotonergic pathways. It promotes the release of luteinizing hormone (LH) while limiting somatostatin secretion, and modulates corticotropin activity, contributing to stress reduction. It appears to act as a sleep-promoting substance by enhancing slow-wave (delta) sleep without the sedation or dependency risks of benzodiazepines or Z-drugs.", "evidence": [ { "claim": "Delta-wave sleep induction", "level": "preliminary", "basis": "Schoenenberger & Monnier PNAS 1977 in rabbits; Schneider-Helmert 1981/1987 small human insomnia studies; no large-scale RCTs" }, { "claim": "Reduced sleep latency in chronic insomnia", "level": "preliminary", "basis": "Schneider-Helmert Eur Neurol 1987: short-term administration in chronic insomniacs; small open-label study" }, { "claim": "Pain modulation in chronic pain", "level": "preliminary", "basis": "Dick et al. Eur Neurol 1985: clinical pilot study in chronic pain patients; small uncontrolled series" }, { "claim": "Stress and HPA axis modulation", "level": "insufficient", "basis": "Theoretical/mechanistic framework (corticotropin modulation); Steiger Peptides 2006 labeled DSIP 'an unresolved riddle'" }, { "claim": "Non-addictive sleep aid profile", "level": "insufficient", "basis": "No dedicated human safety trials; absence-of-evidence inference rather than positive safety data" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/dsip" }, { "name": "Dulaglutide", "slug": "dulaglutide", "aliases": [ "Trulicity", "LY2189265" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "FDA-approved September 2014. Indicated for type 2 diabetes mellitus glycemic control and cardiovascular risk reduction in adults with established cardiovascular disease or multiple CV risk factors. Available as prefilled auto-injector pen. Patent protection ongoing; biosimilar entry expected mid-2020s.", "routes": [ "subcutaneous" ], "half_life": "~90 hours (~5 days)", "molecular_weight": 59669, "cas_number": "923950-08-7", "mechanism_of_action": "Dulaglutide activates GLP-1 receptors on pancreatic beta cells in a glucose-dependent manner, stimulating insulin secretion via cAMP/PKA signaling while suppressing glucagon release from alpha cells. The fusion to IgG4 Fc dramatically extends the half-life to approximately 90 hours by reducing renal clearance and conferring resistance to DPP-4 degradation. Gastric emptying is slowed, reducing postprandial glucose excursions. Central GLP-1R signaling in the hypothalamus and area postrema suppresses appetite and promotes satiety. The Fc domain also prevents neonatal Fc receptor (FcRn)-mediated degradation, enabling once-weekly subcutaneous dosing with stable plasma concentrations.", "evidence": [ { "claim": "Type 2 diabetes glycemic control", "level": "strong", "basis": "AWARD program: 8 Phase 3 RCTs (AWARD-1 through AWARD-8); FDA-approved 2014 as Trulicity; HbA1c reductions of 0.78–1.51% across populations" }, { "claim": "Cardiovascular outcomes reduction in T2D", "level": "strong", "basis": "REWIND trial (Gerstein et al. Lancet 2019): n=9,901 T2D patients; 12% reduction in MACE vs placebo over 5.4 years; notable for including lower-risk primary prevention cohort" }, { "claim": "Weight loss", "level": "moderate", "basis": "AWARD trials: 1.5 mg dose achieved mean 2–3 kg weight loss at 52 weeks; meaningful but less than semaglutide 1 mg (SUSTAIN-7 head-to-head: −4.6 kg sema vs −2.3 kg dula)" }, { "claim": "Kidney disease progression reduction", "level": "moderate", "basis": "REWIND secondary renal endpoint: 15% relative risk reduction in new microalbuminuria or renal function decline; consistent with GLP-1 class renal benefits" }, { "claim": "Once-weekly convenience vs. daily GLP-1 agents", "level": "strong", "basis": "Pre-filled auto-injector design confirmed non-inferiority to liraglutide in AWARD-6 (n=599); favorable adherence data in real-world studies" } ], "peer_reviewed_reference_count": 4, "external_ids": { "drugbank": "DB09045", "wikidata": "Q21011228", "wikipedia": "https://en.wikipedia.org/wiki/Dulaglutide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/dulaglutide" }, { "name": "Endothelin-1", "slug": "endothelin-1", "aliases": [ "ET-1", "Big Endothelin-1", "Preproendothelin-1 (mature)" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "ET-1 itself is a research compound. Therapeutic interventions targeting ET-1 signaling (endothelin receptor antagonists) are prescription drugs approved for pulmonary arterial hypertension.", "routes": [ "intravenous" ], "half_life": "~1–7 minutes (plasma, cleared primarily by lungs and kidneys)", "molecular_weight": 2492.05, "cas_number": "117399-94-7", "mechanism_of_action": "ET-1 is synthesized as a 212-amino acid preproendothelin, cleaved to Big Endothelin-1 (38 AA), then converted to the active 21-AA form by endothelin-converting enzyme (ECE). ET-1 acts on two GPCRs: ETA receptors (predominant on smooth muscle, mediating potent vasoconstriction and proliferation) and ETB receptors (on endothelial cells, mediating transient vasodilation via NO and prostacyclin release; also on smooth muscle mediating contraction). ETA activation is the dominant net effect, producing sustained vasoconstriction via PLC/IP3/DAG signaling and calcium mobilization.", "evidence": [ { "claim": "Most potent endogenous vasoconstrictor", "level": "strong", "basis": "Consistent decades of pharmacology research and physiology textbook consensus" }, { "claim": "ET-1 drives pulmonary arterial hypertension", "level": "strong", "basis": "Multiple FDA-approved ERA drugs (bosentan, macitentan) validate pathway in PAH" }, { "claim": "ETA receptor activation mediates vasoconstriction", "level": "strong", "basis": "Extensive receptor pharmacology and smooth muscle signaling studies" }, { "claim": "ET-1 contributes to cardiac and renal fibrosis", "level": "moderate", "basis": "Consistent preclinical models and human biomarker associations in organ disease" }, { "claim": "ET-1 role in cancer progression", "level": "preliminary", "basis": "Mechanistic in vitro and early clinical correlation studies only" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/endothelin-1" }, { "name": "Enfuvirtide", "slug": "enfuvirtide", "aliases": [ "Fuzeon", "T-20", "DP-178" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since March 2003 for HIV-1 infection in treatment-experienced patients. Administered as subcutaneous injection twice daily; requires patient training for self-injection. Not a controlled substance. Requires co-administration with other antiretroviral agents.", "routes": [ "subcutaneous" ], "half_life": "~3.8 hours", "molecular_weight": 4492, "cas_number": "159519-65-0", "mechanism_of_action": "Enfuvirtide is a biomimetic peptide derived from the C-terminal heptad repeat (HR2) region of HIV-1 gp41. During viral entry, gp41 undergoes a conformational rearrangement in which its HR1 and HR2 domains fold together to form a six-helix bundle, driving fusion of the viral and host cell membranes. Enfuvirtide binds to the HR1 domain of gp41 in a sequence-specific manner, sterically blocking the HR2 domain from interacting with HR1. By preventing six-helix bundle formation, enfuvirtide arrests the fusion process before viral RNA can be delivered into the CD4+ T lymphocyte, effectively halting infection at the cell entry step. This pre-fusion mechanism is entirely distinct from all other antiretroviral drug classes, preserving activity against strains resistant to reverse transcriptase or protease inhibitors.", "evidence": [ { "claim": "Reduces HIV-1 RNA by 1.0 log10 in treatment-experienced patients", "level": "strong", "basis": "TORO-1 and TORO-2 Phase III RCTs (>2,000 patients) NEJM 2003 established efficacy; FDA approved 2003" }, { "claim": "First-in-class fusion-inhibitor mechanism", "level": "strong", "basis": "Mechanism of gp41 HR1 binding characterized in multiple structural and biochemical studies" }, { "claim": "Durable efficacy over 48 weeks", "level": "strong", "basis": "Arasteh 2005 J Antimicrob Chemother 48-week TORO combined analysis confirmed sustained virologic response" }, { "claim": "Near-universal injection site reactions", "level": "strong", "basis": "TORO trials and post-marketing data show ISRs in essentially all patients, limiting adherence" }, { "claim": "Resistance via HR1 mutations", "level": "moderate", "basis": "Resistance mechanism characterized in in vitro selection and clinical isolate sequencing studies" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/enfuvirtide" }, { "name": "Epithalon", "slug": "epithalon", "aliases": [ "Epitalon", "Epithalamin", "AEDG peptide" ], "category": "longevity", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Available as a research peptide. Epithalamin (the natural extract) is approved in Russia as a pharmaceutical. The synthetic version (Epithalon) is sold as a research chemical internationally.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~2-3 hours (estimated)", "molecular_weight": 390.35, "cas_number": "307297-39-8", "mechanism_of_action": "Epithalon activates telomerase, the enzyme that adds telomeric repeats (TTAGGG) to the ends of chromosomes, counteracting the telomere shortening that occurs with each cell division and is associated with aging. It also stimulates melatonin production by the pineal gland, regulates the neuroendocrine system, and normalizes anterior pituitary function. Khavinson's research suggests it acts as a peptide bioregulator at the gene expression level.", "evidence": [ { "claim": "Telomere lengthening", "level": "preliminary", "basis": "Khavinson et al. Bull Exp Biol Med 2003: in vitro cell culture studies demonstrating telomerase activation; no replication in independent human RCTs" }, { "claim": "Melatonin secretion normalization in elderly", "level": "preliminary", "basis": "Khavinson et al. Neuro Endocrinol Lett 2001: open-label study, n=14 elderly patients; improved melatonin and cortisol rhythms after 10-day epithalon course" }, { "claim": "Longevity and anti-aging effects in humans", "level": "insufficient", "basis": "Hypothesis based on animal lifespan extension in rodents and fruit flies; no randomized human trials with longevity endpoints" }, { "claim": "Retinal function preservation", "level": "preliminary", "basis": "Khavinson et al. Gerontology 2002: open-label study, n=56 elderly patients with retinal degeneration; improved ERG readings — single group, no control arm" }, { "claim": "Cancer risk reduction", "level": "insufficient", "basis": "Anisimov et al. rodent studies only; no human clinical data; theoretical mechanism via telomerase and p53 pathway modulation" } ], "peer_reviewed_reference_count": 6, "external_ids": { "pubchem_cid": "219042", "wikidata": "Q27285389", "wikipedia": "https://en.wikipedia.org/wiki/Epitalon" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/epithalon" }, { "name": "Epitide", "slug": "epitide", "aliases": [ "Palmitoyl Tripeptide-38", "MATRIXYL synthe'6", "Volulip", "Pal-KMO2K" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Sold as an OTC cosmetic ingredient globally. Not classified as a drug. No known regulatory restrictions in the US, EU, UK, or equivalent jurisdictions. Widely available in commercial skincare.", "routes": [ "topical" ], "half_life": "Not established (topical cosmetic)", "molecular_weight": 675.96, "cas_number": "1447824-23-8", "mechanism_of_action": "Palmitoyl Tripeptide-38 acts as a matrikine — a bioactive peptide fragment derived from ECM proteins — that signals fibroblasts and keratinocytes to upregulate production of six dermal matrix constituents: collagen I, collagen III, collagen IV, fibronectin, hyaluronic acid, and laminin-5. It modulates MMP activity to reduce collagen degradation while simultaneously driving new ECM synthesis through activation of TGF-β and integrin-mediated pathways. The palmitoyl lipid tail enhances skin penetration through the lipid-rich stratum corneum and tethers the peptide to cell membranes, increasing dwell time at the target receptor site. This broad-spectrum ECM stimulation results in improved dermal thickness, elasticity, and hydration.", "evidence": [ { "claim": "Stimulates six ECM components", "level": "preliminary", "basis": "Sederma in vitro fibroblast/keratinocyte studies show mRNA upregulation of 6 matrix proteins" }, { "claim": "Reduces wrinkle volume at 28–56 days", "level": "preliminary", "basis": "Manufacturer-sponsored clinical studies report wrinkle volume reduction vs placebo" }, { "claim": "Improves skin density", "level": "preliminary", "basis": "Sederma-sponsored cosmetic clinical study reports dermal thickness improvement" }, { "claim": "Modulates MMP activity", "level": "preliminary", "basis": "In vitro data supports MMP downregulation alongside ECM synthesis; no independent RCTs" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/epitide" }, { "name": "Eptifibatide", "slug": "eptifibatide", "aliases": [ "Integrilin", "L-739758", "cyclic RGD peptide" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since 1998 for ACS and PCI adjunct therapy. Available as an intravenous injection for hospital and procedural suite use only. Schedule: not a controlled substance. Requires medical supervision and cardiac monitoring during infusion.", "routes": [ "intravenous" ], "half_life": "~2.5 hours", "molecular_weight": 831.96, "cas_number": "148031-34-9", "mechanism_of_action": "Eptifibatide reversibly inhibits platelet aggregation by selectively blocking the glycoprotein IIb/IIIa (GPIIb/IIIa) receptor on the platelet surface. GPIIb/IIIa is the predominant receptor mediating platelet aggregation; it binds fibrinogen and von Willebrand factor, enabling platelets to cross-link and form a thrombus. Eptifibatide's RGD-mimetic KGD sequence occupies the fibrinogen-binding pocket of GPIIb/IIIa with high affinity, competitively displacing these ligands. Because inhibition is reversible, platelet function recovers within 4–8 hours of discontinuation as drug dissociates and plasma levels fall. The cyclic peptide structure confers selectivity over RGD-binding integrins on other cell types, reducing off-target effects compared to non-cyclic RGD peptides.", "evidence": [ { "claim": "Reduces death/MI in ACS at 30 days", "level": "strong", "basis": "PURSUIT RCT (n=10,948) NEJM 1998 showed significant reduction in composite 30-day endpoint vs placebo" }, { "claim": "Reduces ischemic events as PCI adjunct", "level": "strong", "basis": "ESPRIT Phase III RCT confirmed 48-hour and 30-day ischemic-event reduction during elective PCI" }, { "claim": "Reversible GPIIb/IIIa inhibition", "level": "strong", "basis": "Mechanism via KGD-sequence competitive binding characterized in PK/PD studies; FDA-approved 1998" }, { "claim": "Platelet function recovers in 4-8 hours", "level": "strong", "basis": "PK data from Kleiman 2001 Circulation PURSUIT analysis confirm reversibility window" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/eptifibatide" }, { "name": "Exenatide", "slug": "exenatide", "aliases": [ "Byetta", "Bydureon", "Exendin-4 synthetic", "AC-2993" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "FDA-approved since April 2005 (Byetta) and January 2012 (Bydureon BCise). Schedule: unscheduled prescription drug. No generic available in the US as of 2026. Indicated for type 2 diabetes mellitus as adjunct to diet and exercise. Off-label use for obesity is common but less prevalent since newer agents (semaglutide, tirzepatide) entered market.", "routes": [ "subcutaneous" ], "half_life": "~2.4 hours (Byetta); ~2 weeks apparent t½ for Bydureon due to slow release", "molecular_weight": 4186.6, "cas_number": "141732-76-5", "mechanism_of_action": "Exenatide binds and activates the glucagon-like peptide-1 receptor (GLP-1R), a G-protein coupled receptor expressed on pancreatic beta cells, gut, brain, heart, and kidneys. Activation triggers glucose-dependent insulin secretion via cAMP-PKA and Epac2 signaling, suppresses inappropriately elevated glucagon from pancreatic alpha cells, and slows gastric emptying—collectively blunting postprandial glucose excursions. Unlike native GLP-1 (half-life ~2 min), exenatide resists degradation by dipeptidyl peptidase-4 (DPP-4) due to an alanine-to-glycine substitution at position 2. Central GLP-1R activation in the hypothalamus and brainstem reduces appetite and increases satiety, contributing to the weight loss observed clinically.", "evidence": [ { "claim": "Type 2 diabetes glycemic control", "level": "strong", "basis": "AMIGO pivotal trials (2004-2005); HbA1c reduction 0.8-1.1%; FDA-approved as Byetta April 2005; first GLP-1 agonist approved" }, { "claim": "Weight loss adjunct to diabetes therapy", "level": "moderate", "basis": "AMIGO trials: 2-3 kg weight loss vs placebo over 30 weeks; moderate effect, superseded by newer GLP-1 agents" }, { "claim": "Once-weekly extended-release efficacy", "level": "strong", "basis": "DURATION-1 trial (Drucker Lancet 2008): HbA1c reduction 1.3-1.6% with Bydureon; FDA-approved January 2012" }, { "claim": "Cardiovascular outcomes benefit", "level": "moderate", "basis": "EXSCEL trial (Holman NEJM 2017): n=14,752; non-inferiority but not superiority for MACE vs placebo" }, { "claim": "Gastric emptying slowing", "level": "strong", "basis": "Well-characterized DPP-4 resistant exendin-4 pharmacology; established mechanism across GLP-1 class literature" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "45588096", "drugbank": "DB01276", "wikidata": "Q417762", "wikipedia": "https://en.wikipedia.org/wiki/Exenatide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/exenatide" }, { "name": "Fibronectin Peptides", "slug": "fibronectin-peptides", "aliases": [ "FN peptides", "RGD-fibronectin fragments", "PHSRN peptides", "Fibronectin-derived peptides" ], "category": "recovery", "subcategories": [], "legal_status": "research-only", "legal_notes": "Fibronectin-derived peptides are used as research reagents and in experimental biomaterials. Not approved as standalone human therapeutics. Recombinant fibronectin fragments are available for research use.", "routes": [ "topical", "subcutaneous" ], "half_life": "hours to days (matrix-bound); minutes (soluble)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Fibronectin's primary integrin-binding motif, RGD (Arg-Gly-Asp), located on the type III10 fibronectin domain, engages α5β1, αvβ1, αvβ3, and αvβ5 integrins. A synergy site — PHSRN on the adjacent type III9 domain — cooperates with RGD for maximal α5β1-mediated adhesion and migration. Integrin engagement activates FAK, Src, and downstream MAPK/PI3K/Akt pathways, driving cell spreading, proliferation, and survival. In wound healing contexts, fibronectin peptides accelerate keratinocyte migration, promote fibroblast matrix remodeling, and support angiogenesis via integrin-VEGF receptor crosstalk.", "evidence": [ { "claim": "Primary component of provisional wound matrix", "level": "strong", "basis": "Well-established wound healing biology with consistent histological evidence" }, { "claim": "RGD-PHSRN synergy maximizes α5β1 adhesion", "level": "strong", "basis": "Extensive biochemical and cell biology studies of synergy site cooperation" }, { "claim": "Accelerates re-epithelialization in wound models", "level": "preliminary", "basis": "Preclinical rodent and ex vivo wound models; no FDA-approved drug" }, { "claim": "Improves implant osseointegration", "level": "preliminary", "basis": "Animal studies of coated implants; no controlled human trials" }, { "claim": "Activates FAK/Src/MAPK signaling", "level": "strong", "basis": "Well-characterized integrin signaling cascades with consistent evidence" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/fibronectin-peptides" }, { "name": "Follistatin-315", "slug": "follistatin-315", "aliases": [ "FST-315", "FS-315", "Follistatin isoform 315" ], "category": "muscle", "subcategories": [], "legal_status": "research-only", "legal_notes": "Follistatin-315 is a research peptide, not approved for human use. Gene therapy applications are investigational (IND-stage). Peptide form available from research suppliers; recommended limit ≤200 mcg/day in research protocols.", "routes": [ "subcutaneous" ], "half_life": "~90 minutes", "molecular_weight": 34998, "cas_number": null, "mechanism_of_action": "Follistatin-315 binds myostatin and activin A with nanomolar affinity (Kd ~5–10 nM), forming high-affinity complexes that prevent ligand binding to the ActRIIB/ALK4/5 receptor complex on muscle satellite cells. By blocking myostatin signaling, FST-315 disinhibits Smad2/3-mediated suppression of muscle protein synthesis, promoting myofiber hypertrophy and satellite cell proliferation. It also inhibits activin A signaling in bone, gonads, and brain, producing broader endocrine effects beyond skeletal muscle.", "evidence": [ { "claim": "Binds myostatin and activin A at nanomolar affinity", "level": "strong", "basis": "Well-characterized biochemical binding studies confirm Kd ~5-10 nM for myostatin and activin A" }, { "claim": "Induces muscle hypertrophy via myostatin blockade", "level": "moderate", "basis": "Mouse overexpression studies show 200-300% muscle mass gains; mechanism validated across multiple labs" }, { "claim": "AAV gene therapy tested in Becker muscular dystrophy", "level": "preliminary", "basis": "Mendell Phase 1/2 trials of follistatin AAV in BMD patients showed safety and preliminary functional signals" }, { "claim": "Short half-life limits peptide utility", "level": "moderate", "basis": "Pharmacokinetic studies consistently show ~90 min plasma half-life in multiple species" }, { "claim": "Reproductive effects via activin A inhibition", "level": "preliminary", "basis": "Animal data suggest gonadal and reproductive effects; limited human safety characterization" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/follistatin-315" }, { "name": "Follistatin-344", "slug": "follistatin-344", "aliases": [ "FST-344", "FS-344", "Follistatin 344", "FST344" ], "category": "muscle", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Research chemical only. No FDA-approved follistatin therapeutic exists for muscle enhancement. The gene therapy application (AAV1-FS344) is under research IND. Injectable peptide forms are sold by research chemical suppliers but have no clinical validation. WADA prohibits follistatin and related myostatin inhibitors in competitive sports.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~3-4 hours (estimated, subcutaneous recombinant protein)", "molecular_weight": 37800, "cas_number": "106463-69-6", "mechanism_of_action": "Follistatin-344 is a secreted glycoprotein that acts as a high-affinity binding protein and functional antagonist of myostatin (GDF-8) and activin A, both of which are members of the TGF-β superfamily. By binding these ligands extracellularly, follistatin prevents them from engaging their type I/II serine-threonine kinase receptors (ActRIIA/B, ALK4/5), thereby blocking the downstream SMAD2/3 signaling cascade that restricts muscle fiber hypertrophy and promotes atrophy. The resulting disinhibition of mTOR and satellite cell activation drives both hypertrophy of existing fibers and hyperplasia via myoblast proliferation. The 27-amino acid C-terminal extension unique to FS-344 enhances heparan sulfate proteoglycan binding on cell surfaces, prolonging local tissue retention versus the shorter FS-315 isoform. Follistatin also suppresses activin-driven FSH secretion from the pituitary, with significant reproductive endocrine consequences.", "evidence": [ { "claim": "Muscle mass increase via myostatin inhibition", "level": "preliminary", "basis": "Kota et al. Sci Transl Med 2009: AAV1-FS344 gene therapy in nonhuman primates; consistent 2-3x muscle mass increase; limited human injectable data" }, { "claim": "Becker muscular dystrophy benefit", "level": "preliminary", "basis": "AAV1-FS344 gene therapy trial in BMD and inclusion body myositis; muscle volume/strength gains over 2 years; small early-phase trial" }, { "claim": "Myostatin and activin A binding", "level": "strong", "basis": "Amthor Dev Biol 2004 + extensive biochemistry; established high-affinity antagonism of TGF-beta superfamily ligands" }, { "claim": "Central serous chorioretinopathy ocular risk", "level": "moderate", "basis": "2020 case series: 11 male bodybuilders developed CSCR following subcutaneous FS-344 injections; documented real-world safety signal" }, { "claim": "FSH suppression and fertility disruption", "level": "preliminary", "basis": "Animal studies show up to 75% FSH reduction within 1 week; mechanism via activin inhibition; human fertility impact theoretical" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/follistatin-344" }, { "name": "FOXO4-DRI", "slug": "foxo4-dri", "aliases": [ "FOXO4-D-Retro-Inverso", "FOXO4 DRI", "Senolytic Peptide FOXO4" ], "category": "longevity", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Research chemical with no FDA-approved indication. No IND filed as of 2026. Available only for preclinical research purposes. Not approved for human use anywhere.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "Unknown in humans; estimated hours based on peptide class", "molecular_weight": 4826.5, "cas_number": "2460055-10-9", "mechanism_of_action": "Senescent cells resist apoptosis in part because FOXO4 sequesters p53 in the nucleus, preventing p53 from translocating to mitochondria and initiating cell death. FOXO4-DRI is a cell-penetrating peptide that competitively binds FOXO4, disrupting the FOXO4-p53 interaction. This releases p53, allowing it to translocate to the mitochondrial outer membrane where it activates the intrinsic apoptosis pathway via Bax/Bak pore formation and cytochrome c release. Crucially, because healthy cells do not depend on this FOXO4-p53 survival axis, FOXO4-DRI selectively clears senescent cells while leaving non-senescent cells intact. The retro-inverso D-amino acid structure confers protease resistance, enhancing in vivo stability compared to L-peptide equivalents.", "evidence": [ { "claim": "Senescent cell clearance", "level": "preliminary", "basis": "Baar et al. Cell 2017: landmark mouse study at 5 mg/kg IP; restored fitness, hair density, kidney function; no human trials" }, { "claim": "Selective senolytic mechanism via FOXO4-p53 disruption", "level": "preliminary", "basis": "Baar 2017 + Huang Front Bioeng Biotechnol 2021 in human chondrocytes; mechanism confirmed in vitro and in mouse" }, { "claim": "Pulmonary fibrosis reduction", "level": "preliminary", "basis": "Song et al. Pharmacol Res 2022: bleomycin-induced lung fibrosis mouse model; single preclinical study" }, { "claim": "Keloid fibroblast clearance", "level": "preliminary", "basis": "Gao et al. Front Pharmacol 2025: in vitro keloid fibroblast apoptosis via p53-serine 15 phosphorylation; cell-based only" }, { "claim": "Human anti-aging efficacy and safety", "level": "insufficient", "basis": "No human clinical trials, no IND filing as of 2026; human PK entirely unknown; off-target apoptosis risk theoretical" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/foxo4-dri" }, { "name": "Galanin", "slug": "galanin", "aliases": [ "GAL", "Galanin Neuropeptide", "GAL1-29" ], "category": "other", "subcategories": [ "cognitive" ], "legal_status": "research-only", "legal_notes": "Galanin peptide is available for laboratory research only with no approved clinical applications.", "routes": [ "intravenous" ], "half_life": "~7 minutes (plasma)", "molecular_weight": 3157.6, "cas_number": "119418-04-1", "mechanism_of_action": "Galanin acts through three G protein-coupled receptors: GalR1, GalR2, and GalR3. GalR1 and GalR3 couple to Gi/o, reducing cAMP and inhibiting neuronal firing. GalR2 couples to Gq/11, activating phospholipase C and increasing intracellular calcium. In the spinal cord dorsal horn, galanin co-released with substance P inhibits nociceptive transmission via GalR1. In Alzheimer's disease, galanin hyperinnervation of surviving cholinergic neurons in the basal forebrain is proposed to inhibit acetylcholine release, potentially contributing to cognitive decline. GalR2 may alternatively exert neuroprotective effects.", "evidence": [ { "claim": "Up to 200% overexpression in Alzheimer's basal forebrain", "level": "moderate", "basis": "Multiple postmortem human brain studies confirm galanin hyperinnervation of surviving cholinergic neurons" }, { "claim": "Spinal GalR1 activation inhibits nociception", "level": "preliminary", "basis": "Rodent intrathecal studies show anti-nociceptive effects; dual supraspinal pro-nociceptive role complicates" }, { "claim": "Three GPCRs (GalR1/2/3) pharmacologically characterized", "level": "strong", "basis": "Extensive receptor biochemistry establishes Gi/o coupling at GalR1/3 and Gq/11 at GalR2" }, { "claim": "Modulates pancreatic insulin secretion", "level": "preliminary", "basis": "Animal islet studies suggest galanin regulates insulin release; relevance to human diabetes unclear" }, { "claim": "No galanin-targeting drugs approved", "level": "insufficient", "basis": "Despite decades of target validation work, no clinical-stage GalR modulators have reached approval" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/galanin" }, { "name": "Ganirelix", "slug": "ganirelix", "aliases": [ "Antagon", "Orgalutran", "Ganirelix acetate" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 021057) for inhibition of premature LH surges in women undergoing controlled ovarian stimulation. Prescription-only; administered under reproductive endocrinologist supervision. EMA-approved as Orgalutran.", "routes": [ "subcutaneous" ], "half_life": "~13 hours", "molecular_weight": 1570.32, "cas_number": "124904-93-4", "mechanism_of_action": "Ganirelix competitively binds to pituitary GnRH receptors with significantly higher binding affinity (Kd = 0.4 nM) than endogenous GnRH (Kd = 3.6 nM), rapidly suppressing LH and FSH secretion within hours. Multiple D-amino acid substitutions at positions 1, 2, 3, 6, 8, and 10 of the native GnRH decapeptide provide metabolic stability and prolonged receptor occupancy. Unlike GnRH agonists, ganirelix does not trigger receptor downregulation or an initial gonadotropin flare; suppression is immediate and fully reversible upon discontinuation. Steady-state plasma concentrations are achieved after 3 days of daily dosing, maintaining consistent LH suppression throughout the stimulation window.", "evidence": [ { "claim": "Prevents premature LH surge in IVF", "level": "strong", "basis": "Phase III trials (North American Ganirelix Study Group 2001) established minimal effective dose" }, { "claim": "Equivalent pregnancy rates vs leuprolide", "level": "strong", "basis": "Large European multicenter trial (n=730) confirmed non-inferiority vs buserelin long protocol" }, { "claim": "Safe neonatal outcomes after IVF", "level": "strong", "basis": "Olivennes 2010 follow-up of 1000 fetuses and Bonduelle Hum Reprod 2002 confirm safety" }, { "claim": "Lower OHSS vs GnRH agonists", "level": "strong", "basis": "Post-marketing data indicate lower OHSS incidence, particularly in high-responders" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ganirelix" }, { "name": "GHK", "slug": "ghk", "aliases": [ "Glycyl-L-histidyl-L-lysine", "Gly-His-Lys", "GHK tripeptide" ], "category": "skin", "subcategories": [ "longevity" ], "legal_status": "unregulated", "legal_notes": "GHK is widely sold OTC as a cosmetic ingredient and peptide precursor. Not subject to FDA drug scheduling. GHK-Cu (the copper complex) is similarly unregulated in most jurisdictions.", "routes": [ "topical", "subcutaneous" ], "half_life": "~30 minutes (plasma)", "molecular_weight": 340.38, "cas_number": "49557-75-7", "mechanism_of_action": "GHK chelates copper ions to form GHK-Cu, delivering bioavailable copper to sites of tissue injury. It upregulates collagen and glycosaminoglycan synthesis in dermal fibroblasts, promotes angiogenesis, and activates the FAK-paxillin signaling pathway critical for cell migration. Gene expression studies show GHK modulates over 4,000 human genes, including those governing DNA repair, mitochondrial biogenesis, anti-inflammatory signaling, and suppression of cancer-associated pathways such as TGF-β overactivation.", "evidence": [ { "claim": "Stimulates collagen synthesis in dermal fibroblasts", "level": "moderate", "basis": "Maquart 1988 FEBS Lett and 1993 J Clin Invest established collagen-stimulation in vitro and in rat wounds" }, { "claim": "Modulates 4,000+ human genes", "level": "preliminary", "basis": "Pickart 2015 Biomed Res Int gene-array analyses; mechanistic but not clinical evidence" }, { "claim": "Plasma levels decline with age", "level": "moderate", "basis": "Observational human plasma data showing ~200→80 ng/mL decline from age 20 to 60" }, { "claim": "Promotes wound healing in animal models", "level": "moderate", "basis": "Maquart 1993 rat wound-healing study and subsequent rodent regeneration studies" }, { "claim": "Topical skin rejuvenation benefit", "level": "preliminary", "basis": "Small cosmetic trials and mechanistic extrapolation; limited RCT data in humans" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "73587", "wikidata": "Q55999876" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ghk" }, { "name": "GHK-Cu", "slug": "ghk-cu", "aliases": [ "Copper Peptide", "GHK Copper" ], "category": "skin", "subcategories": [ "longevity", "recovery" ], "legal_status": "unregulated", "legal_notes": "Available as a cosmetic ingredient (topical) and research peptide (injectable). Not FDA-regulated as a drug when sold for cosmetic use.", "routes": [ "topical", "subcutaneous" ], "half_life": "~1 hour (plasma)", "molecular_weight": 403.93, "cas_number": "49557-75-7", "mechanism_of_action": "GHK-Cu modulates expression of over 4,000 genes, shifting the gene expression pattern of older cells toward a younger, healthier phenotype. It stimulates collagen and elastin synthesis, promotes glycosaminoglycan production, activates stem cells, and has potent anti-inflammatory and antioxidant effects via copper delivery.", "evidence": [ { "claim": "Collagen and elastin synthesis stimulation", "level": "moderate", "basis": "Simeon et al. J Invest Dermatol 2000: fibroblast cultures; GHK-Cu stimulated MMP-2 and collagen remodeling at physiological concentrations" }, { "claim": "Wound healing acceleration (topical)", "level": "moderate", "basis": "Multiple in vitro and animal wound model studies showing keratinocyte migration acceleration; limited small human case series (n<30)" }, { "claim": "Skin anti-aging effects (wrinkle reduction, elasticity)", "level": "moderate", "basis": "Pickart et al. BioMed Research International 2015: review of cosmeceutical trials; small double-blind studies showing improved skin density vs vehicle control" }, { "claim": "Systemic anti-aging or longevity effects", "level": "insufficient", "basis": "Gene expression modulation data (Pickart & Margolina IJMS 2018) is in silico/cell-based; no human clinical trials for systemic use" }, { "claim": "Hair follicle stimulation", "level": "preliminary", "basis": "Animal and in vitro studies showing increased follicle size and proliferation; no published RCTs in humans" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "71587328", "wikidata": "Q5168796", "wikipedia": "https://en.wikipedia.org/wiki/Copper_peptide_GHK-Cu" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ghk-cu" }, { "name": "Ghrelin", "slug": "ghrelin", "aliases": [ "acyl-ghrelin", "ghrelin (1-28)", "growth hormone secretagogue endogenous" ], "category": "muscle", "subcategories": [ "weight-loss" ], "legal_status": "research-only", "legal_notes": "Endogenous ghrelin peptide is available for research use only. Not FDA-approved for human administration. MK-677, a ghrelin receptor agonist, is a research compound not approved as a drug. GHRP-2 and GHRP-6 are related synthetic GHRPs also in research-only status.", "routes": [ "intravenous", "subcutaneous" ], "half_life": "~30 minutes (acyl-ghrelin, rapidly deacylated in plasma)", "molecular_weight": 3314.9, "cas_number": "304853-26-7", "mechanism_of_action": "Ghrelin binds GHSR-1a, a constitutively active GPCR expressed in the hypothalamic arcuate nucleus, pituitary, and throughout the brain. Receptor activation stimulates GH release from pituitary somatotrophs via PLC-dependent signaling and activates hypothalamic NPY/AgRP neurons to increase food intake. Ghrelin also promotes reward-driven eating via dopamine release in the mesolimbic pathway (VTA, nucleus accumbens). Unacylated ghrelin (desacyl-ghrelin) circulates at higher levels and may have opposing metabolic effects through non-GHSR pathways.", "evidence": [ { "claim": "Only known circulating orexigenic peptide", "level": "strong", "basis": "Robust human and animal data show pre-meal rise and post-meal fall; validated as hunger signal" }, { "claim": "Stimulates GH release via GHSR-1a", "level": "strong", "basis": "Kojima 1999 Nature discovery paper and subsequent human infusion studies confirm GH secretagogue action" }, { "claim": "MK-677 increases GH/IGF-1 over 24 hours", "level": "moderate", "basis": "Phase 2 studies of oral ibutamoren demonstrate sustained GH/IGF-1 elevation in healthy and elderly adults" }, { "claim": "Promotes reward-driven eating via mesolimbic dopamine", "level": "preliminary", "basis": "Rodent VTA and nucleus accumbens studies show ghrelin modulates food-reward circuits" }, { "claim": "Suppressed by caloric restriction, undermines weight loss", "level": "moderate", "basis": "Sumithran 2011 NEJM and subsequent human trials show ghrelin rebound sustains hunger post-diet" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ghrelin" }, { "name": "GHRH", "slug": "ghrh", "aliases": [ "Growth Hormone-Releasing Hormone", "Somatocrinin", "GRF", "Growth Hormone-Releasing Factor" ], "category": "muscle", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Native GHRH(1-44) is used as a research peptide. Synthetic analogs (sermorelin, tesamorelin) have received FDA approval for specific indications. Unmodified GHRH is not FDA-approved for clinical use.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~7 minutes (native); analogs extend to hours", "molecular_weight": 5039.57, "cas_number": "83930-13-6", "mechanism_of_action": "GHRH binds to the GHRH receptor (GHRHR) on somatotrope cells of the anterior pituitary, activating primarily the cAMP-dependent PKA pathway and secondarily the phospholipase C (IP3/DAG) pathway. Downstream signaling increases GH gene transcription and triggers exocytosis of GH-containing secretory granules. GHRH action is pulsatile and counterbalanced by somatostatin. The active region resides in the N-terminal 29 amino acids; the C-terminal 15 residues confer stability and receptor selectivity.", "evidence": [ { "claim": "Master regulator of pulsatile GH secretion", "level": "strong", "basis": "Extensive endocrine physiology with decades of consistent clinical evidence" }, { "claim": "Stimulates IGF-1 in GH-deficient states", "level": "strong", "basis": "Multiple clinical trials in GH-deficient adults showing reliable IGF-1 rise" }, { "claim": "Validates GHRH pathway via approved analog tesamorelin", "level": "strong", "basis": "FDA approval of tesamorelin for HIV-associated lipodystrophy" }, { "claim": "Active region is N-terminal 29 amino acids", "level": "strong", "basis": "Structure-activity studies establishing minimal active GHRH(1-29) fragment" }, { "claim": "Used for GH stimulation testing", "level": "moderate", "basis": "Established clinical protocol in endocrinology diagnostic practice" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ghrh" }, { "name": "GHRP-2", "slug": "ghrp-2", "aliases": [ "Pralmorelin", "GPA 748", "Growth Hormone Releasing Peptide-2" ], "category": "muscle", "subcategories": [ "recovery", "longevity" ], "legal_status": "reclassification-pending", "legal_notes": "GHRP-2 was placed on the FDA Category 2 bulk drug substance list in September 2023, banning compounding pharmacy preparation in the US. Industry analysis as of February 2026 suggests GHRP-2 is among the peptides expected to remain on Category 2 (due to cortisol and prolactin elevation concerns) rather than returning to compounding-eligible status. No formal FDA update published as of April 2026. Approved as a diagnostic agent in Japan.", "routes": [ "subcutaneous", "intramuscular", "intravenous" ], "half_life": "~15 minutes (plasma)", "molecular_weight": 817.97, "cas_number": "158861-67-7", "mechanism_of_action": "GHRP-2 acts as a selective agonist at the ghrelin receptor (GHSR-1a) in the pituitary and hypothalamus. Binding triggers calcium mobilization and protein kinase C activation, resulting in pulsatile GH release from somatotroph cells. Simultaneously, GHRP-2 suppresses somatostatin tone, which normally inhibits GH secretion, thereby amplifying net GH output. It also activates hypothalamic neuropeptide Y (NPY) neurons, contributing to mild appetite stimulation — though this effect is significantly less pronounced than with GHRP-6. At standard doses GHRP-2 produces modest cortisol and prolactin elevation, which some users manage by pairing it with a GHRH analog. Its short plasma half-life (~15 minutes) requires multiple daily injections to maintain elevated GH pulsatility.", "evidence": [ { "claim": "Growth hormone secretion stimulation", "level": "moderate", "basis": "Frieboes et al. Neuroendocrinology 1995: human Phase 1/2 study showing potent GH pulse; multiple human pharmacokinetic studies (n=15–60) confirming GH dose-response" }, { "claim": "GH secretion synergy with GHRH analogs", "level": "moderate", "basis": "Bowers et al. 1999 mechanistic studies: combined GHRH+GHRP-2 produces 2–3x additive GH output; replicated in multiple small human studies" }, { "claim": "Body composition and lean mass improvement", "level": "preliminary", "basis": "Small open-label studies (n<40) in GH-deficient adults; no large RCTs measuring body composition as primary endpoint" }, { "claim": "Appetite stimulation via ghrelin receptor", "level": "preliminary", "basis": "Gasco et al. JCEM 2010 (PMID 20189610): human study demonstrating GHS-R1a activation and expected orexigenic effects; not studied as dedicated obesity treatment" }, { "claim": "Anti-inflammatory and cytoprotective effects", "level": "insufficient", "basis": "Berlanga-Acosta et al. Clin Med Insights Cardiol 2017 (PMID 28469491): review of preclinical cardiac and tissue protection data; no controlled human trials for these endpoints" } ], "peer_reviewed_reference_count": 6, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ghrp-2" }, { "name": "GHRP-6", "slug": "ghrp-6", "aliases": [ "Growth Hormone Releasing Peptide-6", "SK&F 110679" ], "category": "muscle", "subcategories": [ "recovery" ], "legal_status": "reclassification-pending", "legal_notes": "GHRP-6 was placed on the FDA Category 2 bulk drug substance list in September 2023, banning compounding pharmacy preparation in the US. Industry analysis as of February 2026 indicates GHRP-6 is among the ~5 peptides expected to remain on Category 2 (alongside GHRP-2, Melanotan II, LL-37, and PEG-MGF) due to cortisol/prolactin elevation and appetite stimulation concerns. No formal FDA update published as of April 2026.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~15–20 minutes (plasma)", "molecular_weight": 872.45, "cas_number": "87616-84-0", "mechanism_of_action": "GHRP-6 is a met-enkephalin analog that acts as a full agonist at the ghrelin receptor (GHSR-1a), the same receptor activated by endogenous ghrelin. Binding activates protein kinase C (PKC) and mobilizes intracellular calcium via the inositol trisphosphate/diacylglycerol (IP3/DAG) pathway, triggering pulsatile GH release from pituitary somatotrophs. GHRP-6 also suppresses somatostatin signaling to further amplify GH output. In the hypothalamus, GHSR-1a activation stimulates neuropeptide Y (NPY) and agouti-related peptide (AgRP) neurons in the arcuate nucleus — the primary orexigenic (appetite-driving) circuit — producing hunger that is more intense than any other GHRP. Beyond GH secretion, GHRP-6 has demonstrated cytoprotective, anti-apoptotic, and anti-inflammatory effects in cardiac and hepatic tissue in preclinical models, mediated partly through CD36 receptor interactions independent of GHSR-1a.", "evidence": [ { "claim": "Growth hormone secretion stimulation", "level": "moderate", "basis": "Pandya et al. JCEM 1998 (PMID 9543138): human studies confirming GHRP-6 requires endogenous GHRH for maximal GH stimulation; well-replicated pharmacodynamic data" }, { "claim": "Appetite stimulation and weight gain potential", "level": "moderate", "basis": "Multiple small human studies demonstrating robust ghrelin-receptor-mediated orexigenic effects; hunger/appetite increase is a consistent and well-documented adverse effect" }, { "claim": "GH axis characterization in hypothalamo-pituitary disorders", "level": "moderate", "basis": "Popovic et al. JCEM 1995 (PMID 7883854): diagnostic utility in n=21 patients; used clinically in GH stimulation testing in several European centers" }, { "claim": "Body composition improvement (lean mass, fat loss)", "level": "preliminary", "basis": "Extrapolated from GH elevation data and analogy with ipamorelin/GHRP-2; no large dedicated body composition RCTs" }, { "claim": "Cardioprotective effects", "level": "insufficient", "basis": "Berlanga-Acosta et al. review 2017: Cuban preclinical studies only; no human cardiovascular outcome trials" } ], "peer_reviewed_reference_count": 6, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ghrp-6" }, { "name": "GIP", "slug": "gip", "aliases": [ "Glucose-dependent Insulinotropic Polypeptide", "Gastric Inhibitory Polypeptide", "GIP(1-42)" ], "category": "weight-loss", "subcategories": [], "legal_status": "research-only", "legal_notes": "Endogenous GIP and isolated GIP peptide are available for research only. The dual GIP/GLP-1 agonist tirzepatide is FDA-approved (Mounjaro, Zepbound) as a prescription drug. Pure GIP peptide is not approved for human use.", "routes": [ "subcutaneous" ], "half_life": "~7 minutes (endogenous, DPP-4 dependent)", "molecular_weight": 4983.5, "cas_number": null, "mechanism_of_action": "GIP binds the GIPR, a class B GPCR, activating adenylate cyclase (cAMP) and calcium-independent phospholipase A2. In pancreatic beta cells, this potentiates glucose-stimulated insulin secretion (GSIS) while inhibiting glucagon from alpha cells. GIP also acts on adipocytes to promote lipid storage and on bone osteoblasts to regulate bone turnover. Glucose entry via SGLT1 in K-cells triggers KATP channel closure, membrane depolarization, and voltage-gated Ca2+ influx that drives GIP vesicle release.", "evidence": [ { "claim": "Accounts for 25-70% of postprandial insulin response", "level": "strong", "basis": "Holst 2025 Peptides review and decades of incretin-physiology studies in humans" }, { "claim": "Dual GIP/GLP-1 agonism produces superior weight loss", "level": "strong", "basis": "SURPASS Phase III trials of tirzepatide showed 5.4-11.7 kg weight loss, 1.24-2.58% HbA1c reduction" }, { "claim": "Potentiates glucose-stimulated insulin secretion", "level": "strong", "basis": "Established through decades of pancreatic beta-cell pharmacology and human incretin studies" }, { "claim": "Induces lipolysis in type 1 diabetes", "level": "moderate", "basis": "Christensen 2021 Diabetes Obes Metab randomized crossover trial in T1D patients" }, { "claim": "GIPR antagonism paradoxically produces weight loss", "level": "preliminary", "basis": "Animal models and mechanistic studies; mechanism not fully resolved, creating ongoing debate" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/gip" }, { "name": "Glucagon", "slug": "glucagon", "aliases": [ "GlucaGen", "glucagon rDNA origin", "glucagon HCl" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved prescription drug (NDA 020918). Available as GlucaGen HypoKit (Novo Nordisk) and Baqsimi nasal spray. Requires a valid prescription in the United States.", "routes": [ "subcutaneous", "intramuscular", "intravenous" ], "half_life": "~8–18 minutes", "molecular_weight": 3482.8, "cas_number": "9007-92-5", "mechanism_of_action": "Glucagon binds the glucagon receptor (GCGR), a class B GPCR expressed predominantly in the liver. Receptor activation stimulates adenylate cyclase, raising intracellular cAMP and activating protein kinase A (PKA), which triggers glycogenolysis (glycogen breakdown) and gluconeogenesis (de novo glucose synthesis), rapidly raising blood glucose. In pharmacological use, it reverses insulin-induced hypoglycemia within minutes. It also relaxes GI smooth muscle, making it useful as a contrast aid during endoscopy and imaging.", "evidence": [ { "claim": "Reverses severe hypoglycemia", "level": "strong", "basis": "FDA-approved since 1960 (GlucaGen); Murao 1993 and 60+ years of clinical use establish efficacy" }, { "claim": "Nasal powder (Baqsimi) effective alternative", "level": "strong", "basis": "Demir 2021 J Diabetes Sci Tech systematic review of intranasal glucagon supports efficacy and usability" }, { "claim": "Mini-dose effective for nonsevere hypoglycemia in T1D", "level": "moderate", "basis": "Haymond 2017 J Clin Endocrinol Metab RCT in T1D adults established mini-dose efficacy" }, { "claim": "Hepatic glycogenolysis via GCGR cAMP/PKA", "level": "strong", "basis": "Decades of receptor pharmacology and signal-transduction research characterize mechanism" }, { "claim": "Relaxes GI smooth muscle for imaging", "level": "strong", "basis": "FDA-approved diagnostic use; extensive clinical utility across endoscopy and radiology" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/glucagon" }, { "name": "Glutathione", "slug": "glutathione", "aliases": [ "GSH", "Gly-Cys-Glu", "L-Glutathione", "Reduced Glutathione" ], "category": "longevity", "subcategories": [ "immune" ], "legal_status": "unregulated", "legal_notes": "Available OTC as oral dietary supplement. IV formulations used in some clinical and cosmetic (skin-brightening) contexts. Oral supplementation widely available; IV typically requires clinic administration.", "routes": [ "oral", "intravenous" ], "half_life": "~2-5 minutes (IV, plasma half-life); tissue half-life varies by organ", "molecular_weight": 307.32, "cas_number": "70-18-8", "mechanism_of_action": "Glutathione exerts antioxidant action through two main mechanisms: direct chemical quenching of reactive oxygen and nitrogen species, and enzymatic reduction of lipid hydroperoxides via glutathione peroxidase (GPx). It maintains cellular redox balance by cycling between reduced (GSH) and oxidized (GSSG) forms, with more than 90% normally in the reduced state. GSH conjugates electrophilic toxins via glutathione S-transferase for hepatic detoxification, maintains exogenous antioxidants in active states, and supports immune lymphocyte function. It also modulates apoptosis and inflammatory signaling through thiol chemistry.", "evidence": [ { "claim": "Central role in cellular redox regulation", "level": "strong", "basis": "Decades of biochemical research establish GSH as master intracellular antioxidant" }, { "claim": "Oral bioavailability is poor", "level": "strong", "basis": "Multiple PK studies confirm GI peptidase hydrolysis; Schmitt 2015 Redox Biol crossover data" }, { "claim": "Oral supplementation raises body stores", "level": "moderate", "basis": "Richie 2015 Eur J Nutr RCT and Sinha 2018 liposomal RCT show measurable GSH elevation" }, { "claim": "Reduces oxidative stress in type 2 diabetes", "level": "moderate", "basis": "Cortese-Krott 2022 Antioxidants RCT in elderly diabetic patients showed HbA1c and oxidative benefit" }, { "claim": "IV GSH produces skin-lightening effect", "level": "preliminary", "basis": "Observational reports from cosmetic IV use; no rigorous controlled trials published" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/glutathione" }, { "name": "Gonadorelin", "slug": "gonadorelin", "aliases": [ "GnRH", "LHRH", "Gonadotropin-Releasing Hormone", "Luteinizing Hormone-Releasing Hormone" ], "category": "sexual-health", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "FDA-approved for diagnostic evaluation of pituitary function and treatment of primary hypothalamic amenorrhea and hypogonadotropic hypogonadism. Used off-label in TRT protocols via compounding pharmacies. Lutrepulse (pump-delivered gonadorelin) was FDA-approved for ovulation induction. Available through licensed compounding pharmacies in injectable form.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~2-4 minutes (endogenous GnRH); clinical effect sustained via pulsatile dosing", "molecular_weight": 1182.31, "cas_number": "33515-09-2", "mechanism_of_action": "Gonadorelin binds to GnRH receptors on pituitary gonadotrope cells, triggering the synthesis and pulsatile release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH stimulates Leydig cells in the testes to produce testosterone, while FSH supports Sertoli cells and spermatogenesis. The pulsatile pattern is critical — continuous administration causes receptor downregulation and desensitization, paradoxically suppressing gonadotropin output (the basis of GnRH agonist-based androgen deprivation therapy). When dosed correctly in pulses every 60–120 minutes, gonadorelin preserves the hypothalamic-pituitary-gonadal (HPG) axis feedback loop, maintaining intratesticular testosterone and sperm production even in men receiving exogenous testosterone.", "evidence": [ { "claim": "Diagnostic pituitary function testing", "level": "strong", "basis": "FDA-approved for diagnostic evaluation of pituitary function since the 1980s; standard endocrinology test" }, { "claim": "Hypogonadotropic hypogonadism treatment", "level": "strong", "basis": "FDA-approved indication; pulsatile pump delivery (Lutrepulse) restores fertility in HH patients; long-established clinical use" }, { "claim": "Testicular atrophy prevention during TRT", "level": "preliminary", "basis": "Off-label use; 100 mcg 2-3x/week partially preserves testicular volume and intratesticular testosterone; no large RCTs vs hCG head-to-head" }, { "claim": "Ovulation induction", "level": "strong", "basis": "Lutrepulse FDA-approved for ovulation induction; extensive historical clinical use in fertility protocols" }, { "claim": "Full fertility preservation on concurrent TRT", "level": "insufficient", "basis": "Evidence mixed; no large RCT confirms spermatogenesis preservation vs hCG; off-label extrapolation from HH data" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/gonadorelin" }, { "name": "Gramicidin", "slug": "gramicidin", "aliases": [ "Gramicidin D", "Gramicidin A/B/C", "Gramicidin S (cyclic variant)", "Tyrothricin component" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "Gramicidin is FDA-approved as a topical ophthalmic antibiotic component. Available in combination products (e.g., Neosporin Ophthalmic Solution). Prescription required for ophthalmic formulations; combination OTC products may be available.", "routes": [ "topical" ], "half_life": "not applicable (topical use; retained at application site)", "molecular_weight": 1882.28, "cas_number": "1405-97-6", "mechanism_of_action": "Gramicidin A, B, and C form head-to-head dimers that insert into lipid bilayers as single-stranded beta-helices, creating cation-selective transmembrane pores approximately 4 Å in diameter. These channels allow free diffusion of monovalent cations (Na+, K+, H+) but exclude divalent cations and anions. Disruption of the bacterial membrane ion gradient collapses the electrochemical potential, inhibiting ATP synthesis and nutrient transport, ultimately causing cell death. Channel formation is particularly effective in gram-positive bacterial membranes. Gramicidin is too cytotoxic for systemic use due to erythrocyte lysis.", "evidence": [ { "claim": "FDA-approved topical ophthalmic antibiotic", "level": "strong", "basis": "Long-standing FDA approval in combination Neosporin Ophthalmic since 1940s" }, { "claim": "Forms cation-selective transmembrane channels", "level": "strong", "basis": "Canonical biophysics model with single-channel electrophysiology validation" }, { "claim": "Effective against gram-positive bacteria", "level": "strong", "basis": "Decades of consistent MIC and clinical topical antibiotic experience" }, { "claim": "Too cytotoxic for systemic use", "level": "strong", "basis": "Well-established hemolytic activity limiting to topical formulations only" }, { "claim": "Gramicidin S active against MRSA", "level": "preliminary", "basis": "In vitro studies of cyclic variant; no clinical trial advancement" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/gramicidin" }, { "name": "Heptapeptide-7", "slug": "heptapeptide-7", "aliases": [ "Gransome Heptapeptide-7", "HP-7", "Acetyl Tetrapeptide-2 related" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "OTC cosmetic ingredient. Used in topical serums and body creams. No regulatory restrictions in EU, US, or major markets.", "routes": [ "topical" ], "half_life": "Not established (cosmetic topical use)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Heptapeptide-7 exerts EGF-mimetic activity by binding to signaling pathways that regulate keratinocyte proliferation and migration. Microarray analysis of HP-7-treated dermal keratinocytes shows upregulation of cell division, growth factor expression, and extracellular matrix genes. The peptide also stimulates fibroblast proliferation and collagen synthesis, and enhances cell-to-cell communication pathways involved in wound healing and dermal regeneration. These combined effects support skin thickness, elasticity, and repair following environmental damage or stretch-related stress.", "evidence": [ { "claim": "EGF-mimetic keratinocyte signaling", "level": "preliminary", "basis": "Ex vivo microarray studies show upregulation of cell-division and ECM gene networks" }, { "claim": "Stimulates fibroblast collagen synthesis", "level": "preliminary", "basis": "In vitro dermal fibroblast studies; no clinical RCTs published as of 2026" }, { "claim": "Marketed for stretch marks and dermal regeneration", "level": "insufficient", "basis": "No published clinical efficacy data supporting stretch-mark claims specifically" } ], "peer_reviewed_reference_count": 2, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/heptapeptide-7" }, { "name": "Hexarelin", "slug": "hexarelin", "aliases": [ "Examorelin", "HEX" ], "category": "muscle", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Was in clinical development for heart failure (Europeptides). Available as a research peptide. Not scheduled.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~55-70 minutes", "molecular_weight": 887.04, "cas_number": "140703-51-1", "mechanism_of_action": "Hexarelin binds to the ghrelin receptor (GHS-R1a) in the pituitary and hypothalamus, stimulating robust GH release. It produces the highest GH spike of any GHRP (up to 7x baseline). It also activates cardiac GHS receptors (GHS-R1a in cardiomyocytes), providing direct cardioprotection: reducing cardiac fibrosis, improving ventricular function, and protecting against ischemia-reperfusion injury. Unlike Ipamorelin, hexarelin does increase cortisol and prolactin at higher doses.", "evidence": [ { "claim": "Growth hormone stimulation", "level": "moderate", "basis": "Laron et al. Clin Endocrinol 1995: human dose-ranging study in GH-deficient and normal adults confirming potent GH pulse; among the most potent GHRPs tested in humans" }, { "claim": "Cardiac protection after ischemia-reperfusion injury", "level": "preliminary", "basis": "Rossoni et al. J Cardiovasc Pharmacol 1999: isolated rat heart model; hexarelin reduced infarct size via CD36 receptor; no human cardiovascular trials" }, { "claim": "Tachyphylaxis (desensitization) with repeated dosing", "level": "moderate", "basis": "Multiple human studies showing blunted GH response with continued daily dosing; significant loss of efficacy within 4–8 weeks — a well-documented limitation" }, { "claim": "Growth hormone deficiency diagnosis", "level": "moderate", "basis": "Used as a diagnostic provocation test in European endocrinology; Phase 2 data in GHD adults showing reliable somatotroph stimulation" }, { "claim": "Muscle mass and recovery in aging", "level": "insufficient", "basis": "Anecdotal use only; no published clinical trials with muscle mass or functional outcomes as primary endpoints" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/hexarelin" }, { "name": "Histrelin", "slug": "histrelin", "aliases": [ "Supprelin LA", "Vantas", "Histrelin acetate" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved as Supprelin LA (NDA 022058, 2007) for central precocious puberty in children and as Vantas (NDA 021732, 2004) for palliative treatment of advanced prostate cancer. Prescription-only; implant insertion and removal performed by trained clinicians.", "routes": [ "subcutaneous" ], "half_life": "~3.9 hours (IV bolus); sustained release from implant over 12 months", "molecular_weight": 1323.52, "cas_number": "76712-82-8", "mechanism_of_action": "Histrelin is a highly potent GnRH receptor agonist. The subcutaneous implant continuously releases approximately 65 mcg histrelin acetate per day, producing non-pulsatile GnRH receptor stimulation. This continuous exposure causes pituitary GnRH receptor downregulation and gonadotroph desensitization, reversibly suppressing LH and FSH secretion. Within 1 month, LH and FSH levels decline to prepubertal levels in CPP patients, and testosterone falls to castrate levels (<50 ng/dL) in prostate cancer patients. The hydrogel polymer matrix controls diffusion for consistent plasma concentrations over 52 weeks, avoiding peak-trough variation seen with periodic depot injections.", "evidence": [ { "claim": "12-month continuous GnRH suppression", "level": "strong", "basis": "Eugster 2007 pivotal CPP trial (n=36) showed LH suppression to prepubertal levels maintained 12 months" }, { "claim": "Castrate testosterone in prostate cancer", "level": "strong", "basis": "Schlegel 2006 J Urol Phase III confirmed castrate testosterone in 92-97% of patients at month 12" }, { "claim": "Strong patient preference over injections", "level": "moderate", "basis": "Patient preference studies in CPP and prostate cancer show annual implant preferred over monthly shots" }, { "claim": "Halts pubertal progression in CPP", "level": "strong", "basis": "FDA-approved (Supprelin LA 2007); pivotal trial showed decelerated bone-age and height-velocity" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/histrelin" }, { "name": "Humanin", "slug": "humanin", "aliases": [ "HN", "HNG", "Mitochondrial Derived Peptide", "MDP", "MOTS-c family" ], "category": "longevity", "subcategories": [ "cognitive", "other" ], "legal_status": "research-only", "legal_notes": "Research chemical only. No FDA-approved humanin therapeutic exists. Available from peptide research suppliers. No human clinical trials completed or registered as of 2026.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "Unknown in humans; estimated 1-4 hours based on peptide class", "molecular_weight": 2685.48, "cas_number": "330936-69-1", "mechanism_of_action": "Humanin acts through two main receptor systems. Extracellularly, it signals via a heterotrimeric receptor complex comprising ciliary neurotrophic factor receptor alpha (CNTFRα), WSX-1, and gp130, activating JAK2/STAT3 and PI3K/Akt pro-survival pathways. Intracellularly, humanin directly binds and inhibits pro-apoptotic Bax protein, preventing mitochondrial outer membrane permeabilization and cytochrome c release. In neuronal contexts, humanin blocks amyloid-beta (Aβ) oligomer-induced apoptosis by inhibiting Aβ binding to cell surface receptors and downstream caspase activation. It also suppresses inflammatory NF-κB signaling, improves mitochondrial membrane potential, and enhances autophagy to clear damaged organelles. Humanin levels in plasma and CSF correlate inversely with Alzheimer's disease severity.", "evidence": [ { "claim": "Neuroprotection vs amyloid-beta toxicity", "level": "preliminary", "basis": "Yen BBA Mol Basis Dis 2022 + Lubec IJMS 2023 reviews; consistent rodent AD model data; no human neurodegenerative trials" }, { "claim": "Metabolic healthspan and insulin sensitivity", "level": "preliminary", "basis": "Cobb & Lee Aging 2020: HNG twice-weekly in middle-aged mice; improved metabolic markers; preclinical only" }, { "claim": "Bax-mediated anti-apoptotic activity", "level": "moderate", "basis": "Multiple biochemical studies confirm direct Bax binding and mitochondrial protection; mechanism well-characterized in vitro" }, { "claim": "Cardioprotection from ischemia-reperfusion", "level": "preliminary", "basis": "Sreekumar BBA 2021: rodent myocardial I/R model; single preclinical study direction" }, { "claim": "Human anti-aging or cognitive efficacy", "level": "insufficient", "basis": "No human clinical trials of exogenous humanin completed or registered as of 2026; all dosing extrapolated from animal data" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/humanin" }, { "name": "IGF-1 DES", "slug": "igf-1-des", "aliases": [ "Des(1-3)IGF-1", "des IGF-1", "truncated IGF-1", "IGF-1 DES(1-3)" ], "category": "muscle", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved for any indication. Prohibited in sport by WADA. Available from research peptide suppliers in the US for laboratory use. Subject to import restrictions in some jurisdictions. Not a Schedule I–V controlled substance in the US but considered a prescription drug analogue in some countries.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~20–30 minutes", "molecular_weight": 7371.4, "cas_number": "112603-35-7", "mechanism_of_action": "IGF-1 DES activates the IGF-1 receptor (IGF-1R), a receptor tyrosine kinase, with higher affinity than native IGF-1 because the N-terminal tripeptide normally facilitates IGFBP binding. Without IGFBP sequestration, virtually 100% of IGF-1 DES is free to engage IGF-1R. Receptor activation triggers auto-phosphorylation and downstream signaling through two primary cascades: (1) PI3K/Akt/mTOR, driving protein synthesis and inhibiting protein degradation via FoxO transcription factor suppression, and (2) MAPK/ERK, promoting cell proliferation. Uniquely, local injection drives satellite cell activation and myogenic precursor proliferation (hyperplasia — new fiber formation), not just hypertrophy of existing fibers. The very short half-life confines these effects to tissue near the injection site, making it a tool for site-specific muscle remodeling in research contexts.", "evidence": [ { "claim": "10x more potent than native IGF-1", "level": "preliminary", "basis": "Ballard et al 1990 lit/lit mouse study showed 2-3x potency via reduced IGFBP binding" }, { "claim": "Drives localized muscle hyperplasia", "level": "preliminary", "basis": "Animal intramuscular injection studies show site-specific satellite cell activation" }, { "claim": "Enhanced anabolism post-gut resection", "level": "preliminary", "basis": "Rat gut resection study (Am J Physiol 1991) showed growth enhancement" }, { "claim": "WADA-prohibited performance enhancer", "level": "insufficient", "basis": "No controlled human clinical trials exist; regulatory prohibition based on extrapolated anabolic risk" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/igf-1-des" }, { "name": "IGF-1 LR3", "slug": "igf-1-lr3", "aliases": [ "Long R3 IGF-1", "Insulin-like Growth Factor-1 LR3", "IGF1-LR3", "LR3-IGF-1" ], "category": "muscle", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved for human use. Classified as a research chemical. Banned by WADA and most competitive sports organizations under the peptide hormone category. No reclassification review underway as of 2026. Possession for research purposes is generally legal in the US.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~20–30 hours", "molecular_weight": 9117, "cas_number": "946870-92-4", "mechanism_of_action": "IGF-1 LR3 binds to the IGF-1 receptor (IGF-1R), a receptor tyrosine kinase, with high affinity. Receptor activation triggers autophosphorylation and downstream signaling through two primary pathways: the PI3K/Akt/mTOR axis, which drives protein synthesis, suppresses protein degradation, and promotes cell survival; and the MAPK/ERK pathway, which stimulates cell proliferation and differentiation. The near-complete bypass of IGFBPs — which normally sequester native IGF-1 in circulation — means systemically administered IGF-1 LR3 is substantially more bioavailable at tissue IGF-1R. Satellite cell activation in skeletal muscle is a key mechanism for hypertrophic adaptation. IGF-1 LR3 also exhibits insulin-like metabolic activity at high concentrations, activating insulin receptors and driving glucose uptake into muscle tissue.", "evidence": [ { "claim": "Skeletal muscle hypertrophy and anabolism", "level": "preliminary", "basis": "Tomas J Endocrinol 1995 guinea pig infusion + Barany Eur J Endocrinol 2001; consistent rodent data; no human LR3-specific RCTs" }, { "claim": "Extended half-life via reduced IGFBP binding", "level": "strong", "basis": "Biochemical characterization: 13-aa N-terminal extension + R3 substitution gives ~1000x lower IGFBP affinity; 20-30h vs 15 min" }, { "claim": "Satellite cell activation in muscle", "level": "preliminary", "basis": "Yoshida & Delafontaine Cells 2020 review of IGF-1/PI3K/Akt/mTOR muscle signaling; mechanism established, LR3-specific evidence is in vitro" }, { "claim": "Hypoglycemia risk from insulin-receptor cross-activity", "level": "moderate", "basis": "Established IGF-1 therapeutic class effect; documented in mecasermin clinical use and animal LR3 studies" }, { "claim": "Human body composition efficacy", "level": "insufficient", "basis": "No controlled human trials of IGF-1 LR3 published; WADA-banned; community use only extrapolated from animal anabolism studies" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/igf-1-lr3" }, { "name": "Ipamorelin", "slug": "ipamorelin", "aliases": [ "NNC 26-0161" ], "category": "muscle", "subcategories": [ "longevity", "recovery" ], "legal_status": "reclassification-pending", "legal_notes": "Under FDA reclassification review. Previously available as a research peptide.", "routes": [ "subcutaneous" ], "half_life": "~2 hours", "molecular_weight": 711.85, "cas_number": "170851-70-4", "mechanism_of_action": "Ipamorelin selectively binds to the ghrelin/GHS-R1a receptor in the pituitary gland, triggering pulsatile GH release. Unlike GHRP-6 or GHRP-2, it does not significantly increase cortisol, ACTH, or prolactin, and has minimal effect on appetite (ghrelin mimicry is low). Often stacked with CJC-1295 for synergistic GH release.", "evidence": [ { "claim": "Growth hormone stimulation", "level": "moderate", "basis": "Phase 2 trials showing dose-dependent GH release with high selectivity" }, { "claim": "Body composition improvement", "level": "preliminary", "basis": "Small clinical studies; no large RCTs" }, { "claim": "Post-surgical recovery", "level": "preliminary", "basis": "Phase 2 data in post-operative ileus patients" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "9831659", "wikidata": "Q20707829" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ipamorelin" }, { "name": "Kisspeptin-10", "slug": "kisspeptin-10", "aliases": [ "KP-10", "Metastin 45-54" ], "category": "sexual-health", "subcategories": [ "muscle" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. In clinical investigation at multiple academic centers. Available as a research peptide. Not scheduled.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~28 minutes", "molecular_weight": 1302.41, "cas_number": "374675-21-5", "mechanism_of_action": "Kisspeptin-10 binds to the KISS1R (GPR54) receptor on GnRH neurons in the hypothalamus, triggering the release of GnRH. This initiates the hypothalamic-pituitary-gonadal (HPG) axis cascade: GnRH stimulates LH and FSH release from the pituitary, which in turn stimulates testosterone/estrogen production in the gonads. Kisspeptin acts as the 'master switch' of this entire system — without kisspeptin signaling, puberty does not occur.", "evidence": [ { "claim": "LH stimulation and gonadotropin release", "level": "moderate", "basis": "Dhillo et al. JCEM 2011: IV kisspeptin-10 potently stimulated LH pulses in healthy men; Jayasena Hum Reprod 2015 comparative trial" }, { "claim": "Acute testosterone elevation in men", "level": "moderate", "basis": "Dhillo et al. JCEM 2011 and subsequent Imperial College London trials; reproducible hormonal response in small controlled studies" }, { "claim": "Diagnostic test for pubertal disorders", "level": "preliminary", "basis": "Imperial College London investigational protocols; early diagnostic trials; not yet FDA/EMA approved" }, { "claim": "Fertility treatment potential", "level": "preliminary", "basis": "Early clinical investigation in IVF protocols; small trials showing LH pulse stimulation in women; no Phase 3 fertility outcomes" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/kisspeptin-10" }, { "name": "KPV", "slug": "kpv", "aliases": [ "Lys-Pro-Val", "α-MSH C-terminal tripeptide" ], "category": "immune", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Available as a research peptide. Not regulated as a drug due to its status as a naturally occurring tripeptide fragment.", "routes": [ "oral", "subcutaneous", "topical" ], "half_life": "~15-30 minutes (estimated)", "molecular_weight": 342.43, "cas_number": "67727-97-3", "mechanism_of_action": "KPV enters cells and directly interacts with inflammatory signaling pathways in the nucleus. It inhibits NF-κB activation by preventing the phosphorylation and degradation of IκBα, reducing the transcription of pro-inflammatory genes. It also reduces the expression of inflammatory cytokines (TNF-α, IL-6, IL-1β) and has antimicrobial properties. Unlike its parent molecule α-MSH, KPV does not activate melanocortin receptors at typical doses.", "evidence": [ { "claim": "Anti-inflammatory action via NF-kB inhibition", "level": "preliminary", "basis": "Kannengiesser et al. Regul Pept 2008 in human airway epithelial cells; in vitro mechanistic evidence only" }, { "claim": "Ulcerative colitis / IBD benefit", "level": "preliminary", "basis": "Dalmasso Gastroenterology 2008 and Xiao Mol Ther 2017 murine colitis models; 60-70% reduction in inflammation scores; no human RCTs" }, { "claim": "Oral bioavailability via PepT1 transport", "level": "preliminary", "basis": "Dalmasso 2008 and Viennois J Crohns Colitis 2016: PepT1-mediated intestinal uptake demonstrated in mice; not validated in humans" }, { "claim": "Colitis-associated cancer prevention", "level": "preliminary", "basis": "Viennois et al. 2016 murine model of colitis-associated cancer; preclinical only" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/kpv" }, { "name": "Kyotorphin", "slug": "kyotorphin", "aliases": [ "Tyr-Arg", "L-Tyrosyl-L-Arginine", "KTP" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Kyotorphin is available for laboratory research only. It has no approved clinical applications.", "routes": [ "intravenous" ], "half_life": "~2–5 minutes (rapidly hydrolyzed by dipeptidases in plasma)", "molecular_weight": 337.4, "cas_number": "70904-56-2", "mechanism_of_action": "Kyotorphin does not directly bind classical mu, delta, or kappa opioid receptors with high affinity. Its analgesic effect appears to be mediated indirectly: kyotorphin stimulates the release of met-enkephalin from nerve terminals, which then acts on delta and mu opioid receptors to produce analgesia. A specific kyotorphin receptor (KTP-R) coupled to a Gi-type G protein has been proposed but is not yet definitively identified. Kyotorphin is unevenly distributed in the brain, concentrated in the midbrain, pons/medulla, and dorsal spinal cord — regions with the highest sensitivity to morphine analgesia — consistent with a physiological role in pain modulation.", "evidence": [ { "claim": "Naloxone-reversible analgesia via enkephalin release", "level": "preliminary", "basis": "Animal central administration studies show opioid-pathway-mediated analgesia blocked by naloxone" }, { "claim": "Does not directly bind classical opioid receptors", "level": "preliminary", "basis": "Binding studies show indirect mechanism via met-enkephalin release rather than direct MOR/DOR agonism" }, { "claim": "Putative kyotorphin receptor not definitively identified", "level": "insufficient", "basis": "Proposed Gi-coupled KTP-R remains uncharacterized at the molecular level despite 45+ years of research" }, { "claim": "Concentrated in morphine-sensitive brain regions", "level": "preliminary", "basis": "Rodent regional distribution studies place kyotorphin in midbrain, pons/medulla, dorsal spinal cord" }, { "claim": "Analogs explored for BBB penetration", "level": "preliminary", "basis": "Medicinal chemistry efforts have generated peptidase-resistant analogs; no clinical-stage compounds" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/kyotorphin" }, { "name": "Lanreotide", "slug": "lanreotide", "aliases": [ "Somatuline", "Somatuline Depot", "Somatuline Autogel", "Lanreotide acetate" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 022074, August 2007) for acromegaly and GEP-NETs. Available as Somatuline Depot (US) and Somatuline Autogel (EU). Prescription-only; administered by healthcare professional.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~23–30 days (depot formulation)", "molecular_weight": 1096.32, "cas_number": "108736-35-2", "mechanism_of_action": "Lanreotide binds with high affinity to somatostatin receptor subtypes SSTR2 and SSTR5 on pituitary somatotropes and NET cells. SSTR2 activation inhibits adenylyl cyclase and reduces cAMP, suppressing GH and IGF-1 secretion. SSTR5 binding contributes to antisecretory effects in carcinoid and pancreatic NETs. Compared to native somatostatin, lanreotide has substantially greater receptor affinity and a half-life of approximately 23–30 days in the Autogel/Depot formulation due to self-assembling nanotubes.", "evidence": [ { "claim": "FDA-approved for acromegaly and GEP-NETs", "level": "strong", "basis": "FDA NDA 022074 approval 2007 based on Phase III trial evidence" }, { "claim": "Reduced NET progression risk by 47 percent", "level": "strong", "basis": "Landmark CLARINET Phase III trial (Caplin et al., NEJM 2014)" }, { "claim": "Controls GH and IGF-1 in acromegaly", "level": "strong", "basis": "Multiple Phase III trials plus 3-10 year post-marketing safety data" }, { "claim": "23-30 day depot half-life via self-assembling nanotubes", "level": "strong", "basis": "Well-characterized pharmacokinetics of Autogel/Depot formulations" }, { "claim": "Effective for carcinoid syndrome symptoms", "level": "strong", "basis": "FDA-approved indication supported by controlled clinical trial data" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/lanreotide" }, { "name": "Leuphasyl", "slug": "leuphasyl", "aliases": [ "Pentapeptide-18", "YAGFL peptide", "Tyr-D-Ala-Gly-Phe-Leu" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Sold as a cosmetic active ingredient worldwide. No regulatory restrictions apply in the US, EU, or most jurisdictions. Available OTC in serums, creams, and eye products. Not classified as a drug.", "routes": [ "topical" ], "half_life": "Not established (topical cosmetic)", "molecular_weight": 569.65, "cas_number": "64963-01-5", "mechanism_of_action": "Leuphasyl mimics endogenous enkephalins by binding to opioid receptors on the presynaptic membrane of neuromuscular junctions. Receptor binding triggers a conformational change that initiates an intracellular cascade reducing nerve cell excitability. This dampens the calcium-dependent vesicular release of acetylcholine at the neuromuscular junction, attenuating the intensity of facial muscle contractions that produce expression lines. Unlike botulinum toxin, Leuphasyl acts upstream at the receptor level rather than by cleaving SNARE proteins, preserving partial muscle motility and avoiding the frozen appearance associated with injections. When formulated alongside Argireline, which operates via a distinct SNARE-complex interference pathway, the two peptides produce additive wrinkle reduction exceeding either ingredient alone.", "evidence": [ { "claim": "Reduces crow's-foot wrinkle depth", "level": "preliminary", "basis": "Manufacturer-sponsored split-face study showed significant reduction vs vehicle after 28 days" }, { "claim": "Modulates presynaptic calcium channels", "level": "preliminary", "basis": "In vitro MDPI Cosmetics 2014 study confirmed enkephalin-like receptor modulation" }, { "claim": "Synergy with Argireline for wrinkles", "level": "preliminary", "basis": "Manufacturer split-face data (Int J Cosmet Sci 2002) showed additive SNARE+opioid effect" }, { "claim": "Safe alternative to botulinum toxin", "level": "preliminary", "basis": "Manufacturer studies report no adverse events; no independent peer-reviewed trials" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/leuphasyl" }, { "name": "Leuprolide", "slug": "leuprolide", "aliases": [ "Lupron", "Lupron Depot", "Leuprorelin", "Eligard", "Fensolvi" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved for: palliative treatment of advanced prostate cancer; endometriosis; uterine leiomyomata (preoperative); and central precocious puberty. Multiple NDA approvals spanning 1985–2019. Prescription-only. Generic versions available since patent expiration.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~3 hours (IV bolus); sustained release over weeks with depot formulations", "molecular_weight": 1209.4, "cas_number": "53714-56-0", "mechanism_of_action": "Leuprolide is a potent GnRH receptor agonist with roughly 100 times the receptor affinity of endogenous GnRH. Initial administration stimulates pituitary gonadotrophs, causing an LH and FSH surge ('flare') lasting 1–2 weeks. With continuous administration, persistent non-pulsatile receptor stimulation causes GnRH receptor downregulation and pituitary desensitization. LH and FSH secretion falls to castrate levels within 2–4 weeks, reducing testosterone in men to <50 ng/dL and estradiol in women to postmenopausal levels. This medical castration effect is fully reversible upon discontinuation. In prostate cancer, testosterone suppression removes the androgen stimulus that drives tumor proliferation, inducing cancer cell apoptosis.", "evidence": [ { "claim": "Castrate testosterone in prostate cancer", "level": "strong", "basis": "FDA-approved since 1985; achieves castrate testosterone in >97% of ADT patients across decades of RCTs" }, { "claim": "Endometriosis pain reduction", "level": "strong", "basis": "Multiple RCTs show significant lesion-volume and pelvic-pain reduction over 6-month courses vs placebo" }, { "claim": "Restores normal final adult height in CPP", "level": "strong", "basis": "FDA-approved; long-term pediatric data confirm pubertal timing restoration and preserved adult height" }, { "claim": "Long-term ADT increases cardiovascular risk", "level": "moderate", "basis": "Shore 2025 JAMA Oncology RCT on coronary plaque progression; consistent observational metabolic-syndrome signals" }, { "claim": "Depot equals daily injection outcomes", "level": "strong", "basis": "Multiple RCTs of 1, 3, 4, 6-month depot formulations show equivalent clinical outcomes with better adherence" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/leuprolide" }, { "name": "Liraglutide", "slug": "liraglutide", "aliases": [ "Victoza", "Saxenda" ], "category": "weight-loss", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved as Victoza (diabetes, 2010) and Saxenda (weight loss, 2014). Requires prescription. Available as branded product and through compounding pharmacies.", "routes": [ "subcutaneous" ], "half_life": "~13 hours", "molecular_weight": 3751.2, "cas_number": "204656-20-2", "mechanism_of_action": "Liraglutide exerts its effects by binding to and activating the GLP-1 receptor (GLP-1R), a class B G-protein-coupled receptor expressed in the pancreas, gastrointestinal tract, central nervous system, heart, kidneys, and immune cells. The C-16 fatty acid modification is not merely a half-life extension tool: by enabling non-covalent binding to circulating albumin, it creates a slow-release depot in the bloodstream and shields the active peptide sequence from proteolytic cleavage by DPP-4, plasma endopeptidases, and renal clearance. The result is stable, sustained receptor engagement over 24 hours at a single daily dose.\n\nIn the pancreatic beta cell, liraglutide activates GLP-1R-coupled Gs proteins, elevating intracellular cyclic AMP and triggering protein kinase A (PKA)-mediated phosphorylation of downstream effectors. This cascade amplifies glucose-stimulated insulin secretion in a concentration-dependent, glucose-gated manner — insulin release occurs only when blood glucose is above threshold, essentially eliminating the hypoglycemia risk associated with sulfonylureas. Liraglutide also inhibits glucagon secretion from alpha cells at elevated glucose concentrations, further dampening post-prandial glucose excursions. Over time, GLP-1R stimulation has been shown to promote beta cell survival by activating anti-apoptotic signaling pathways (PDX-1 upregulation, Bcl-2/Bcl-xL expression), a potential beta-cell-preservation effect with clinical relevance in early type 2 diabetes.\n\nIn the gastrointestinal tract, liraglutide slows gastric emptying by reducing antral contractions and pyloric tone, extending the time nutrients spend in the stomach and attenuating the rate of carbohydrate absorption into the portal circulation. This effect is most pronounced at low glucose levels and tends to attenuate with chronic dosing — an important factor that limits the extent of gastric slowing over long-term treatment while preserving glycemic benefit.\n\nIn the central nervous system, liraglutide crosses the blood-brain barrier and binds GLP-1 receptors in the hypothalamic arcuate nucleus and ventromedial nucleus, the brainstem nucleus tractus solitarius and area postrema, and dopaminergic circuits in the mesolimbic reward pathway. Hypothalamic GLP-1R activation increases anorexigenic POMC/CART neuronal activity and decreases orexigenic NPY/AgRP signaling, reducing caloric intake. The mesolimbic effects appear to reduce the hedonic drive to eat, particularly for high-fat, high-sugar foods. Direct action on area postrema neurons (which lack a blood-brain barrier) contributes to nausea at higher doses but also to appetite suppression at clinically effective doses. Preclinical and early clinical evidence also suggests that central GLP-1R signaling has neuroprotective properties relevant to dopaminergic neuron survival, which has motivated ongoing clinical trials in Parkinson's disease.", "evidence": [ { "claim": "Weight loss in obesity", "level": "strong", "basis": "SCALE Obesity trial (Pi-Sunyer et al. NEJM 2015): n=3,731, 56 weeks; 3 mg liraglutide produced 8% body weight loss vs 2.6% placebo; FDA-approved 2014 for obesity" }, { "claim": "Type 2 diabetes glycemic control", "level": "strong", "basis": "LEAD program: 6 Phase 3 RCTs; FDA-approved 2010 as Victoza for T2D; HbA1c reduction of 1.0–1.5% across multiple comparator trials" }, { "claim": "Cardiovascular outcomes reduction in T2D", "level": "strong", "basis": "LEADER trial (Marso et al. NEJM 2016): n=9,340 high-CV-risk T2D patients; 13% reduction in MACE vs placebo over 3.8 years" }, { "claim": "Kidney disease progression reduction", "level": "moderate", "basis": "LEADER trial secondary analysis: 22% reduction in new or worsening nephropathy; supports renal benefits but not primary endpoint" }, { "claim": "Nonalcoholic steatohepatitis (NASH) improvement", "level": "moderate", "basis": "Armstrong et al. Lancet 2016: Phase 2 RCT, n=52; liraglutide 1.8 mg for 48 weeks — 39% vs 9% NASH resolution by biopsy" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "16134956", "drugbank": "DB06655", "wikidata": "Q2526479", "wikipedia": "https://en.wikipedia.org/wiki/Liraglutide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/liraglutide" }, { "name": "Lixisenatide", "slug": "lixisenatide", "aliases": [ "Adlyxin", "Lyxumia", "AVE0010" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "FDA-approved July 2016. Voluntarily withdrawn from the US market by Sanofi effective January 1, 2023, due to commercial reasons (competition from newer GLP-1 agents). Still available in some international markets as Lyxumia. Was a Schedule-unscheduled prescription drug. No longer obtainable in the US through standard pharmacy channels.", "routes": [ "subcutaneous" ], "half_life": "~2–3 hours", "molecular_weight": 4858.5, "cas_number": "320367-13-3", "mechanism_of_action": "Lixisenatide binds selectively and with high affinity to the GLP-1 receptor, a class B GPCR. Its C-terminal hexalysine extension confers DPP-4 resistance and receptor binding characteristics that differ from native GLP-1. Unlike long-acting GLP-1 agents, lixisenatide's short half-life (~3 hours) produces a pronounced and transient inhibition of gastric emptying concentrated around the postprandial period, making it particularly effective at blunting after-meal glucose spikes. Mechanistically, it stimulates glucose-dependent insulin secretion from beta cells via cAMP/PKA and PI3K/Akt pathways, suppresses glucagon from alpha cells, and activates hypothalamic GLP-1R to promote satiety. The acute gastric emptying effect is more pronounced than with longer-acting agents, explaining its differential glucose-lowering profile (more postprandial vs. fasting glucose effect).", "evidence": [ { "claim": "Type 2 diabetes glycemic control", "level": "strong", "basis": "GetGoal program: 12 Phase 3 RCTs; HbA1c reduction 0.7-1.0%; FDA-approved July 2016 as Adlyxin" }, { "claim": "Postprandial glucose reduction via gastric emptying", "level": "strong", "basis": "GetGoal-Duo trials in insulin-glargine combination; pronounced 2-hour postprandial glucose effect; consistent across trials" }, { "claim": "Cardiovascular safety (non-inferiority)", "level": "strong", "basis": "ELIXA trial (Pfeffer NEJM 2015): n=6,068 post-ACS T2D patients; non-inferiority for MACE vs placebo established" }, { "claim": "Weight loss adjunct", "level": "moderate", "basis": "GetGoal trials: modest 1-2 kg weight loss vs placebo over 24 weeks; less than long-acting GLP-1 agents" }, { "claim": "Renal outcome benefit", "level": "preliminary", "basis": "Muskiet et al. Lancet Diabetes Endocrinol 2018: ELIXA exploratory analysis; signal only, not powered for renal endpoints" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "90472060", "drugbank": "DB09265", "wikidata": "Q6659956", "wikipedia": "https://en.wikipedia.org/wiki/Lixisenatide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/lixisenatide" }, { "name": "LL-37", "slug": "ll-37", "aliases": [ "Cathelicidin", "hCAP-18 fragment" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Available as a research peptide. In clinical development for wound healing and infection applications.", "routes": [ "subcutaneous", "topical" ], "half_life": "~4-6 hours", "molecular_weight": 4493.33, "cas_number": "154947-66-7", "mechanism_of_action": "LL-37 has a helical amphipathic structure that allows it to insert into and disrupt microbial cell membranes, creating pores and causing lysis. Beyond direct antimicrobial action, it modulates the immune response by recruiting immune cells (chemotaxis), promoting wound healing, inhibiting biofilm formation, neutralizing bacterial endotoxins (LPS), and modulating TLR signaling. Vitamin D regulates LL-37 expression, linking vitamin D deficiency to increased infection susceptibility.", "evidence": [ { "claim": "Broad-spectrum antimicrobial activity", "level": "moderate", "basis": "Durr Biochim Biophys Acta 2006 + Bucki 2010 review; extensive in vitro and animal data vs MRSA, Pseudomonas, Candida" }, { "claim": "Chronic wound healing promotion", "level": "preliminary", "basis": "Phase I/II trials in chronic leg ulcers cited in research summary; small controlled studies with limited follow-up" }, { "claim": "Vitamin D-mediated immune function", "level": "moderate", "basis": "Multiple observational and interventional studies showing vitamin D upregulates LL-37 gene expression; established mechanism" }, { "claim": "Anti-biofilm activity", "level": "preliminary", "basis": "In vitro studies on surgical implant biofilm models; no completed human biofilm eradication trials" }, { "claim": "Macrophage phagocytosis enhancement", "level": "preliminary", "basis": "Wan et al. J Leukoc Biol 2014: in vitro human macrophage assays; mechanism confirmed, translation untested" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ll-37" }, { "name": "Magainin", "slug": "magainin", "aliases": [ "Magainin-2", "Magainin 2a", "MSI-78 (analog)", "Pexiganan (analog)" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "Native magainin-2 is a research peptide not approved for human use. The synthetic analog pexiganan did not receive FDA approval. Research reagents available from peptide suppliers.", "routes": [ "topical" ], "half_life": "minutes to hours (context-dependent; susceptible to proteolysis)", "molecular_weight": 2467.9, "cas_number": "108334-68-5", "mechanism_of_action": "In aqueous solution, magainin-2 is largely unstructured. Upon contact with negatively charged bacterial membranes, it folds into an amphipathic alpha-helix and inserts into the bilayer via a 'carpet model' or toroidal pore mechanism. At sufficient concentrations, magainin causes membrane thinning, transient pore formation, and eventually membrane disintegration and leakage of cytoplasmic contents. Selectivity for prokaryotic over eukaryotic membranes arises from the abundance of anionic phospholipids in bacterial outer leaflets versus zwitterionic phosphatidylcholine-dominated mammalian membranes.", "evidence": [ { "claim": "First frog-derived AMP characterized", "level": "strong", "basis": "Foundational Zasloff 1987 PNAS work establishing magainin-2 structure/function" }, { "claim": "Disrupts membranes via carpet/toroidal pore mechanism", "level": "strong", "basis": "Extensive biophysics and molecular dynamics studies of membrane interaction" }, { "claim": "Broad-spectrum antibacterial and antifungal activity", "level": "strong", "basis": "Hundreds of in vitro MIC studies across gram-positive, gram-negative, fungi" }, { "claim": "Pexiganan failed Phase III for diabetic foot ulcers", "level": "strong", "basis": "Completed 1999 Phase III trial failed superiority versus standard antibiotics" }, { "claim": "Selective for prokaryotic over eukaryotic membranes", "level": "moderate", "basis": "Consistent anionic phospholipid selectivity studies; narrow therapeutic window" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/magainin" }, { "name": "Matrixyl", "slug": "matrixyl", "aliases": [ "Palmitoyl Pentapeptide-4", "Pal-KTTKS", "Palmitoyl Pentapeptide-3" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Permitted cosmetic ingredient globally. No drug scheduling or prescription requirements. Sold in OTC anti-aging formulations and as a raw ingredient for formulators. No regulatory restrictions on use concentration in most markets.", "routes": [ "topical" ], "half_life": "Not established (topical cosmetic ingredient)", "molecular_weight": 802.05, "cas_number": "214047-00-4", "mechanism_of_action": "Palmitoyl Pentapeptide-4 is a fragment of type I procollagen that acts on fibroblasts via a matrikine signaling pathway. The peptide sequence KTTKS is recognized by fibroblast surface receptors, triggering intracellular cascades that upregulate synthesis of collagen types I, III, and IV, fibronectin, and glycosaminoglycans. The palmitoyl chain increases lipophilicity, facilitating transdermal delivery across the stratum corneum into the dermis where fibroblasts reside. It also reduces collagenase (MMP) activity, slowing extracellular matrix degradation.", "evidence": [ { "claim": "Collagen I/III/IV stimulation in fibroblasts", "level": "moderate", "basis": "Lintner Int J Cosmet Sci 2014 + in vitro dose-response 10-100 ppm; consistent upregulation across cell culture studies" }, { "claim": "Clinical wrinkle reduction", "level": "moderate", "basis": "Robinson Int J Cosmet Sci 2005: topical palmitoyl pentapeptide improved photoaged skin over 12 weeks; Gorouhi 2009 review" }, { "claim": "Transdermal delivery via palmitoyl chain", "level": "moderate", "basis": "Lintner 2014: palmitoyl-KTTKS skin permeation quantified; enhanced lipophilicity confirmed in stratum corneum studies" }, { "claim": "MMP/collagenase activity reduction", "level": "preliminary", "basis": "In vitro fibroblast studies; mechanism supported but clinical ECM-degradation outcome data limited" }, { "claim": "Wound healing acceleration", "level": "preliminary", "basis": "Chantasart Adv Wound Care 2022: matrixyl patch vs cream wound healing comparison; small preclinical/in vivo study" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "9897237", "wikidata": "Q18386276", "wikipedia": "https://en.wikipedia.org/wiki/Palmitoyl_pentapeptide-4" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/matrixyl" }, { "name": "Mazdutide", "slug": "mazdutide", "aliases": [ "IBI362", "LY3305677", "OXM-3", "Xinermei" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Approved in China as Xinermei for obesity (June 2025) and type 2 diabetes (September 2025). Not approved by the FDA. In Phase 2 development in the United States. Not available outside China or authorized clinical trials. No research chemical or compounding pathway.", "routes": [ "subcutaneous" ], "half_life": "6.1-28.1 days (Tmax ~72 hours); extended half-life supports once-weekly dosing", "molecular_weight": null, "cas_number": "2259884-03-0", "mechanism_of_action": "Mazdutide is a long-acting analogue of oxyntomodulin (OXM), the gut-derived peptide that naturally activates both GLP-1 and glucagon receptors. GLP-1 receptor agonism drives glucose-dependent insulin secretion, suppresses glucagon, slows gastric emptying, and reduces appetite through central hypothalamic signaling — producing the caloric restriction typical of GLP-1 agents. The added glucagon receptor (GCGR) activation increases hepatic fatty acid oxidation and stimulates energy expenditure, directly clearing hepatic lipid accumulation and improving metabolic dysfunction-associated steatotic liver disease (MASLD). GCGR agonism also increases FGF21 secretion, which enhances thermogenesis and peripheral insulin sensitivity. The combination results in weight loss driven by both reduced caloric intake and increased energy expenditure, with pronounced hepatic fat reduction that distinguishes dual agonists from GLP-1-only agents.", "evidence": [ { "claim": "Weight loss in Chinese obese adults", "level": "strong", "basis": "Ji NEJM 2025 + Ji Nat Commun 2023 Phase 2: 14.8% weight loss at 6 mg/week at 48 weeks vs 0.5% placebo; approved in China June 2025" }, { "claim": "Type 2 diabetes HbA1c reduction", "level": "moderate", "basis": "Zhu Diabetes Care 2024 Phase 2 in Chinese T2D patients; significant HbA1c reductions; approved in China September 2025" }, { "claim": "Hepatic fat reduction via glucagon agonism", "level": "moderate", "basis": "Phase 2 data: up to 80% liver fat reduction in some cohorts; consistent with dual GLP-1/glucagon mechanism" }, { "claim": "First-in-class regulatory approval", "level": "strong", "basis": "Markham & Duggan Drugs 2025: first GLP-1/glucagon dual agonist approved anywhere; Chinese NMPA approval June 2025" }, { "claim": "Efficacy in non-Chinese populations", "level": "insufficient", "basis": "US Phase 2 trials ongoing (~179 participants); no completed trials in non-East-Asian populations as of 2026" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "167312357", "drugbank": "DB19099", "wikidata": "Q123248554", "wikipedia": "https://en.wikipedia.org/wiki/Mazdutide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/mazdutide" }, { "name": "Melanotan II", "slug": "melanotan-ii", "aliases": [ "MT-2", "MT-II", "Melanotan 2" ], "category": "skin", "subcategories": [ "sexual-health" ], "legal_status": "unregulated", "legal_notes": "Not FDA-approved. Sold as a research peptide. Regulatory agencies (FDA, TGA, MHRA) have issued warnings against its cosmetic use. Not scheduled or banned in most jurisdictions.", "routes": [ "subcutaneous", "nasal" ], "half_life": "~1 hour", "molecular_weight": 1024.18, "cas_number": "121062-08-6", "mechanism_of_action": "Melanotan II binds non-selectively to melanocortin receptors MC1R through MC5R. MC1R activation stimulates melanocytes to produce eumelanin (dark pigment), producing a tan without UV exposure. MC4R activation affects sexual arousal (which led to the development of PT-141). MC3R/MC4R activation suppresses appetite. The broad receptor binding profile explains the diverse effects and side effect profile.", "evidence": [ { "claim": "Erectile function improvement", "level": "preliminary", "basis": "Wessells et al. Urology 2000 (PMID 11018622): RCT, n=10 men with psychogenic erectile dysfunction; 8/10 showed erectile response vs placebo — small Phase 2 trial never advanced" }, { "claim": "Skin tanning (melanogenesis)", "level": "preliminary", "basis": "Dorr et al. J Invest Dermatol 1996: Phase 1, n=10 healthy adults; dose-dependent tanning without UV exposure confirmed; no Phase 3 trials completed" }, { "claim": "Appetite suppression and weight loss", "level": "preliminary", "basis": "Animal studies in rodent obesity models showing >30% food intake reduction; no controlled human trials for weight loss indication" }, { "claim": "Safety and long-term tolerability", "level": "insufficient", "basis": "Multiple adverse event case reports (melanocytic naevus changes, priapism, melanoma concerns); no systematic long-term human safety data; not FDA-approved" }, { "claim": "Female sexual dysfunction", "level": "insufficient", "basis": "Anecdotal reports only; no published controlled trials in women; bremelanotide (PT-141) was developed as a selective alternative for this indication" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "92432", "wikidata": "Q423855", "wikipedia": "https://en.wikipedia.org/wiki/Melanotan_II" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/melanotan-ii" }, { "name": "MGF", "slug": "mgf", "aliases": [ "Mechano Growth Factor", "IGF-1Ec", "IGF-1 Ec", "PEG-MGF" ], "category": "muscle", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "MGF and PEG-MGF are unscheduled research chemicals with no FDA-approved medical use. Not approved for human administration. Sold legally as research chemicals in many jurisdictions, though the same FDA enforcement actions affecting other peptides have affected MGF availability in the US. Prohibited by WADA in competitive sport.", "routes": [ "intramuscular", "subcutaneous" ], "half_life": "Native MGF: minutes; PEG-MGF: several days (pegylation dramatically extends duration)", "molecular_weight": 2867.2, "cas_number": "77591-33-4", "mechanism_of_action": "MGF arises from alternative splicing of the IGF-1 gene: a 49-base-pair insert in exon 5 causes a reading frame shift, producing a unique carboxy-terminal E-domain peptide (the MGF E-peptide) that does not bind the IGF-1 receptor and signals through distinct, incompletely characterized pathways. When muscle fibers are subjected to mechanical strain or damage, the IGF-1 gene is preferentially spliced toward the MGF (IGF-1Ec/Eb) isoform. The resulting MGF E-peptide activates quiescent satellite cells — inducing proliferation without differentiation — expanding the progenitor pool available for repair. Mature IGF-1 (primarily IGF-1Ea splice variant) then drives satellite cell differentiation, fusion into existing fibers, and net fiber hypertrophy. This two-phase sequence (MGF: proliferate; IGF-1Ea: differentiate) explains why exogenous MGF, timed post-exercise or post-injury, may amplify the hypertrophic response. Pegylated MGF (PEG-MGF) extends the very short half-life of the native peptide from minutes to days.", "evidence": [ { "claim": "Satellite cell proliferation and activation", "level": "preliminary", "basis": "Dluzniewska Differentiation 2011 in vitro + Niu Mol Cell Biochem 2013 porcine cells; consistent mechanistic data, no human in vivo trials" }, { "claim": "Muscle fiber repair acceleration", "level": "preliminary", "basis": "Rodent muscle injury models show accelerated repair and increased cross-sectional area; Goldspink Endocrinology 2010 review" }, { "claim": "Neurogenesis in aging brain", "level": "preliminary", "basis": "Dluzniewska Neurosci Lett 2017: aging mouse brain neurogenesis; single preclinical study" }, { "claim": "PEG-MGF extended pharmacokinetics", "level": "preliminary", "basis": "Pegylation extends half-life from minutes to days; established PEG chemistry, but no published human PK studies of PEG-MGF" }, { "claim": "Human muscle hypertrophy efficacy", "level": "insufficient", "basis": "No human clinical trials completed or registered; WADA-banned; community dosing extrapolated from animal data only" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/mgf" }, { "name": "MIF-1", "slug": "mif-1", "aliases": [ "Melanocyte Inhibiting Factor 1", "Pro-Leu-Gly-NH2", "PLG", "MSH release-inhibiting factor" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "MIF-1 (Pro-Leu-Gly-NH2) is not FDA-approved for any indication and is classified as a research compound. Available from peptide synthesis suppliers for laboratory use.", "routes": [ "intravenous", "oral" ], "half_life": "~Minutes (short; rapidly hydrolyzed)", "molecular_weight": 311.37, "cas_number": "64419-62-1", "mechanism_of_action": "MIF-1 (Pro-Leu-Gly-NH2) modulates dopamine receptor sensitivity, particularly potentiating D2 receptor signaling in the striatum without acting as a direct receptor agonist. It is thought to act as an allosteric modulator of dopamine receptors and may inhibit dopamine breakdown by modulating MAO-B activity. MIF-1 also influences oxytocin receptor systems and has been reported to affect GABA and serotonin pathways. Its mechanism is complex and not fully characterized.", "evidence": [ { "claim": "Modulates dopamine D2 receptor signaling", "level": "preliminary", "basis": "In vitro allosteric modulation and rodent dopamine potentiation studies" }, { "claim": "Improves Parkinson's motor symptoms", "level": "preliminary", "basis": "Small open-label trials 1970s-1980s showed modest improvement" }, { "claim": "Antidepressant-like effects in animals", "level": "preliminary", "basis": "Rodent behavioral despair and reserpine reversal models" }, { "claim": "Endogenous oxytocin-derived neuromodulator", "level": "moderate", "basis": "Established biochemistry of enzymatic cleavage from oxytocin" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/mif-1" }, { "name": "MK-677", "slug": "mk-677", "aliases": [ "Ibutamoren", "Ibutamoren Mesylate", "MK-0677", "L-163,191" ], "category": "muscle", "subcategories": [ "longevity", "sleep" ], "legal_status": "unregulated", "legal_notes": "MK-677 is not a peptide and not subject to the 2023 FDA compounding ban. It is not a controlled substance in the US but is prohibited by WADA (S2 category). Sold legally as a research chemical; not approved for human consumption. The FDA has issued warning letters to supplement companies marketing it for human use.", "routes": [ "oral" ], "half_life": "~24 hours", "molecular_weight": 528.67, "cas_number": "159634-47-6", "mechanism_of_action": "MK-677 produces its effects primarily through full agonism at the growth hormone secretagogue receptor 1a (GHSR-1a), the endogenous receptor for ghrelin. GHSR-1a is a class A G-protein-coupled receptor expressed in the hypothalamus (arcuate nucleus, ventromedial nucleus), pituitary somatotrophs, hippocampus, vagal neurons, and multiple peripheral tissues. When MK-677 binds GHSR-1a in hypothalamic neurons, it triggers the release of growth hormone-releasing hormone (GHRH), which then travels via the portal circulation to the anterior pituitary where it binds to the GHRH receptor and stimulates GH secretion. Simultaneously, MK-677 acts directly on pituitary somatotrophs expressing GHSR-1a to amplify GH pulse amplitude.\n\nThe net result of this dual hypothalamic and pituitary action is a preservation and amplification of pulsatile GH secretion — the natural pattern by which GH is released in bursts primarily during the first hour of slow-wave sleep. Multiple clinical studies have confirmed that a single oral dose of MK-677 (25 mg) increases mean 24-hour GH concentrations by approximately 97% and IGF-1 by 40–60% relative to baseline, restoring levels observed in young healthy adults within populations where GH axis activity has declined due to aging. This is mechanistically distinct from exogenous GH injection, which suppresses endogenous GH through negative feedback; MK-677 instead preserves or enhances the pulsatile pattern while respecting the hypothalamic-pituitary negative-feedback loop.\n\nThe GHSR-1a pathway has important downstream effects beyond GH secretion. In the hypothalamus, GHSR-1a activation mediates orexigenic signaling — stimulating appetite through NPY/AgRP neurons in the arcuate nucleus and by activating reward circuits in the nucleus accumbens. This appetite-stimulating effect is a clinically significant side effect, explaining the characteristic \"MK-677 hunger\" reported by most users, and has relevance to its investigated use in cachexia and anorexia states. In the CNS more broadly, ghrelin receptor signaling influences memory consolidation, anxiety regulation, and dopaminergic neurotransmission, which may contribute to the cognitive and mood effects some users report.\n\nIn adipose tissue, MK-677 indirectly increases GH signaling, which promotes lipolysis in the fasted state and inhibits insulin-stimulated glucose uptake (contributing to the insulin resistance and fasting hyperglycemia observed clinically). In bone, the GH/IGF-1 axis stimulated by MK-677 activates bone remodeling through IGF-1-mediated osteoblast proliferation and differentiation. In skeletal muscle, IGF-1 promotes protein synthesis and nitrogen retention, which is responsible for the lean mass increases documented in elderly trial populations — though the proportion of lean mass gain attributable to water versus contractile protein has been debated.", "evidence": [ { "claim": "Growth hormone elevation", "level": "strong", "basis": "Multiple RCTs showing sustained IGF-1 and GH increases for 12+ months" }, { "claim": "Bone mineral density improvement", "level": "moderate", "basis": "2-year RCT in elderly adults showed improved markers" }, { "claim": "Lean body mass increase", "level": "moderate", "basis": "Clinical trials in elderly showing 1-2 kg lean mass gain" }, { "claim": "Sleep quality improvement", "level": "preliminary", "basis": "Small study showing increased REM sleep duration" }, { "claim": "Insulin sensitivity", "level": "insufficient", "basis": "Evidence of worsened insulin sensitivity in some trials — potential negative effect" } ], "peer_reviewed_reference_count": 6, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/mk-677" }, { "name": "Mod GRF 1-29", "slug": "mod-grf-1-29", "aliases": [ "Modified GRF 1-29", "CJC-1295 without DAC", "CJC-1295 no DAC", "Tetrasubstituted GRF 1-29" ], "category": "muscle", "subcategories": [ "recovery", "longevity" ], "legal_status": "reclassification-pending", "legal_notes": "One of 14 peptides under FDA reclassification review (RFK Jr. initiative, 2025–2026). Previously available from US compounding pharmacies as a GHRH analog; most commercial availability ceased 2024–2025. Research-use supply chains remain active internationally.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~30 minutes (active half-life)", "molecular_weight": 3368.7, "cas_number": "863288-34-0", "mechanism_of_action": "Mod GRF 1-29 binds to and activates GHRH receptors on somatotroph cells of the anterior pituitary. The four amino acid substitutions (at positions 2, 8, 15, and 27) protect against dipeptidyl peptidase-IV cleavage and other serum proteases, extending bioactive duration beyond native GHRH (1-29) while maintaining pulsatility. Receptor activation triggers Gs-mediated adenylyl cyclase signaling, elevating intracellular cAMP, which drives GH synthesis and secretion. The resulting GH pulse stimulates hepatic IGF-1 production, skeletal muscle protein synthesis via IGF-1R/PI3K/Akt/mTOR pathways, lipolysis in adipose tissue via hormone-sensitive lipase activation, and collagen synthesis in connective tissue. Peak GH levels occur approximately 30 minutes post-injection, returning to baseline within 2–3 hours, preserving normal GH pulsatility over time.", "evidence": [ { "claim": "GH pulse stimulation via GHRH receptor", "level": "moderate", "basis": "Teichman et al. JCEM 2006 (CJC-1295 class): human PK/PD study confirming pulsatile GH release; GHRH receptor agonism well-established" }, { "claim": "Synergy with GHRP co-administration", "level": "moderate", "basis": "Multiple human studies combining GHRH analog + GHRP (ipamorelin/GHRP-6) showing 3-10x GH pulse amplification vs either alone" }, { "claim": "DPP-IV resistance extending active half-life", "level": "strong", "basis": "Jetté et al. Endocrinology 2005: biochemical demonstration of tetrasubstituted GHRH(1-29) protease resistance" }, { "claim": "Body composition and muscle gain benefit", "level": "insufficient", "basis": "No large-scale human efficacy trials for body composition endpoints completed as of 2026; anecdotal use only" }, { "claim": "Reduced desensitization vs long-acting GHRH analogs", "level": "preliminary", "basis": "Ionescu et al. JCEM 2006 pulsatility data; theoretical advantage from short half-life; not directly benchmarked in humans" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/mod-grf-1-29" }, { "name": "Motilin", "slug": "motilin", "aliases": [ "Porcine Motilin", "Human Motilin", "Gastrointestinal Motilin" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Motilin peptide is available for research use only and is not approved for human therapeutic use. Erythromycin (a non-peptide motilin receptor agonist) is FDA-approved as an antibiotic and used off-label as a prokinetic.", "routes": [ "intravenous" ], "half_life": "~4–5 minutes (plasma)", "molecular_weight": 2698, "cas_number": "52906-92-0", "mechanism_of_action": "Motilin binds the motilin receptor (MLNR), a class A GPCR predominantly expressed on smooth muscle cells and interstitial cells of Cajal in the GI tract. Receptor activation via Gq/11 coupling increases intracellular calcium and triggers coordinated smooth muscle contraction, initiating phase III of the migrating motor complex. Erythromycin and motilide antibiotics function as non-peptide motilin receptor agonists and are used off-label as prokinetics. The motilin-ghrelin receptor system shares structural homology, as both peptides derive from related gene families.", "evidence": [ { "claim": "Primary regulator of the migrating motor complex", "level": "strong", "basis": "Decades of GI physiology research establish motilin's role in phase III MMC via MLNR on smooth muscle" }, { "claim": "Erythromycin acts as motilin receptor agonist", "level": "strong", "basis": "Well-established non-peptide MLNR agonism used off-label as prokinetic across clinical practice" }, { "claim": "Small-molecule agonists showed mixed Phase II gastroparesis results", "level": "moderate", "basis": "Mitemcinal and camicinal advanced to Phase II with inconsistent efficacy signals and tachyphylaxis limits" }, { "claim": "Released in 100-minute fasting cycles", "level": "strong", "basis": "Reproducible human plasma kinetics during interdigestive state across multiple physiology studies" }, { "claim": "Coordinates gallbladder emptying", "level": "preliminary", "basis": "Animal and limited human data suggest motilin role in interdigestive gallbladder contraction" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/motilin" }, { "name": "MOTS-c", "slug": "mots-c", "aliases": [ "Mitochondrial ORF of the Twelve S rRNA c" ], "category": "longevity", "subcategories": [ "weight-loss", "muscle" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Available as a research peptide. Relatively new (discovered 2015) with limited regulatory attention.", "routes": [ "subcutaneous" ], "half_life": "~4 hours (estimated)", "molecular_weight": 2174.54, "cas_number": "1627580-64-6", "mechanism_of_action": "MOTS-c activates AMPK (AMP-activated protein kinase), the master metabolic sensor that coordinates cellular energy metabolism. It enhances glucose uptake in skeletal muscle, improves insulin sensitivity, promotes fatty acid oxidation, and regulates the folate-methionine cycle affecting cellular methylation. Under metabolic stress, MOTS-c translocates to the nucleus where it regulates adaptive gene expression through interaction with ARE-containing promoters.", "evidence": [ { "claim": "Insulin sensitivity and glucose metabolism improvement", "level": "preliminary", "basis": "Lee et al. Cell Metab 2015: discovery paper in mouse model; MOTS-c (0.5 mg/kg) prevented diet-induced insulin resistance; no published human RCTs" }, { "claim": "Exercise performance and physical endurance", "level": "preliminary", "basis": "Reynolds et al. Nat Commun 2021: mouse voluntary running wheel experiment; MOTS-c-treated mice showed enhanced endurance — preclinical only" }, { "claim": "Obesity and metabolic syndrome prevention", "level": "preliminary", "basis": "Kim et al. Cell Rep 2021: high-fat diet mouse model; MOTS-c reduced fat accumulation; mechanism via AMPK activation confirmed in cell lines" }, { "claim": "Longevity and anti-aging effects", "level": "insufficient", "basis": "Association studies only: higher circulating MOTS-c levels observed in healthy centenarians (Kim et al. 2018); no interventional human data" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "155885767" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/mots-c" }, { "name": "N-Acetyl Semax", "slug": "n-acetyl-semax", "aliases": [ "NA-Semax", "Acetyl-Semax", "Ac-MEHFPGP-NH2" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not FDA-approved in the US. Classified as a prescription medication in Russia and Ukraine for neurological conditions. Available from research peptide suppliers in the US and EU without prescription, primarily for research purposes.", "routes": [ "nasal" ], "half_life": "~15–60 minutes (estimated, intranasal)", "molecular_weight": 855.97, "cas_number": "2920938-90-3", "mechanism_of_action": "N-Acetyl Semax's mechanism of action involves multiple parallel pathways. It rapidly elevates brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the hippocampus, supporting neuroplasticity and long-term potentiation. It activates serotonergic and dopaminergic neurotransmitter systems, contributing to mood stabilization and motivational tone. Interactions with melanocortin receptors (MC1R, MC4R) are proposed based on its ACTH peptide origin. Additionally, Semax inhibits enkephalinase enzymes that degrade endogenous neuropeptides, prolonging their activity. Intranasal administration allows direct transport along the olfactory nerve to the CNS, bypassing the blood-brain barrier. The N-acetyl modification blocks N-terminal exopeptidase cleavage, extending half-life to an estimated 15–60 minutes versus 5–15 minutes for unmodified Semax.", "evidence": [ { "claim": "Elevates hippocampal BDNF", "level": "preliminary", "basis": "Rodent intranasal studies show BDNF transcription upregulation within 20 minutes, sustained 24h" }, { "claim": "Neuroprotection in ischemic stroke", "level": "moderate", "basis": "Base Semax approved in Russia; Cerebrovasc Dis 2005 study supports ischemia protection" }, { "claim": "Broader transcriptional modulation vs Semax", "level": "preliminary", "basis": "Rodent gene expression analyses show N-acetyl variant modulates wider transcriptional networks" }, { "claim": "Dopaminergic and serotonergic activation", "level": "preliminary", "basis": "Preclinical neurochemistry studies; no FDA-regulated human trials on N-acetyl variant" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/n-acetyl-semax" }, { "name": "N-Acetyl Semax Amidate", "slug": "n-acetyl-semax-amidate", "aliases": [ "NA Semax Amidate", "Ac-MEHFPGP-NH2", "Acetylated Semax Amide" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Available from US research peptide suppliers as a research compound. Approved as a drug in Russia (marketed as Semax). Not a scheduled substance in the US. Legal status may vary by country.", "routes": [ "nasal" ], "half_life": "~6–12 hours (estimated, based on analog modifications)", "molecular_weight": 855.97, "cas_number": "2920938-90-3", "mechanism_of_action": "N-Acetyl Semax Amidate modulates neurotrophic and neurogenic signaling primarily through upregulation of brain-derived neurotrophic factor (BDNF) and its receptor TrkB, as well as nerve growth factor (NGF) and GAP-43. These effects promote neuroplasticity, synaptic density, and long-term potentiation. It also influences the melanocortin system via partial ACTH-receptor agonism, which affects mood, attention, and stress response. The acetyl and amide modifications substantially extend half-life compared to unmodified Semax (estimated 6–12 hours vs. 2–4 hours) by blocking aminopeptidase and carboxypeptidase cleavage sites. Dopaminergic and serotonergic modulation has been reported in preclinical models.", "evidence": [ { "claim": "BDNF and TrkB upregulation", "level": "preliminary", "basis": "Dolotov Brain Res 2006 (Semax parent): rat hippocampal BDNF/TrkB upregulation; mechanism extends to acetyl-amidate analog by structural inference" }, { "claim": "Cognitive enhancement and attention", "level": "preliminary", "basis": "Russian clinical studies on parent Semax show attention, processing speed, memory improvements; acetyl-amidate analog has no dedicated RCTs" }, { "claim": "Neuroprotection after ischemic stroke", "level": "moderate", "basis": "Gusev et al. 2001: Semax parent clinical study in acute hemispheric ischemic stroke; Kolomin Bull Exp Biol Med 2007 animal data; approved in Russia for stroke" }, { "claim": "Extended half-life via acetyl/amide modifications", "level": "preliminary", "basis": "Zayats Neuropeptides 2016: N-acetylation receptor selectivity study; PK extension is theoretical/extrapolated, no published human PK for this analog" }, { "claim": "Dopaminergic neuroprotection (Parkinson's)", "level": "preliminary", "basis": "Glazova Neurosci Lett 2004: MPTP-induced dopaminergic lesion model; single preclinical study of parent Semax" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/n-acetyl-semax-amidate" }, { "name": "Nafarelin", "slug": "nafarelin", "aliases": [ "Synarel", "Nafarelin acetate" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 019886) as Synarel nasal solution for endometriosis and central precocious puberty. Prescription-only. Treatment duration limited to 6 months for endometriosis due to bone loss risk.", "routes": [ "nasal" ], "half_life": "~2.5–3 hours (intranasal)", "molecular_weight": 1322.47, "cas_number": "76932-56-4", "mechanism_of_action": "Nafarelin binds with high affinity to pituitary GnRH receptors, initially stimulating LH and FSH release. With twice-daily intranasal administration, continuous non-pulsatile receptor occupancy desensitizes pituitary gonadotrophs and downregulates GnRH receptor density. Within approximately 4 weeks, LH and FSH secretion falls substantially, reducing ovarian estradiol production to postmenopausal levels. This estrogen deprivation induces atrophy of endometriotic implants and relieves the pain and dysmenorrhea characteristic of endometriosis. In central precocious puberty, suppression of the hypothalamic-pituitary-gonadal axis halts premature puberty progression. Effects are fully reversible after stopping treatment.", "evidence": [ { "claim": "Endometriosis pain relief equal to danazol", "level": "strong", "basis": "Henzl 1988 NEJM multicenter double-blind trial and NEET 1992 large-scale RCT establish efficacy" }, { "claim": "80% symptom improvement at 6 months", "level": "strong", "basis": "Multiple RCTs show 80% report improvement in dysmenorrhea, pelvic pain, dyspareunia" }, { "claim": "Bone density loss 3-5% during treatment", "level": "moderate", "basis": "RCT data show 3-5% BMD decline over 6 months, typically reversible within 6-12 months" }, { "claim": "CPP pubertal suppression and height preservation", "level": "strong", "basis": "FDA-approved; long-term pediatric data confirm bone-age deceleration and adult-height outcomes" }, { "claim": "Full fertility recovery post-treatment", "level": "moderate", "basis": "Long-term follow-up studies confirm normal fertility return after discontinuation" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/nafarelin" }, { "name": "Nesfatin-1", "slug": "nesfatin-1", "aliases": [ "NUCB2/Nesfatin-1", "NEFA/Nesfatin-1", "Nucleobindin-2 Fragment" ], "category": "weight-loss", "subcategories": [], "legal_status": "research-only", "legal_notes": "Nesfatin-1 is available for laboratory research only and has no approved clinical applications. It has not advanced to clinical trials in humans.", "routes": [ "intravenous" ], "half_life": "~22 minutes (estimated, animal data)", "molecular_weight": 9700, "cas_number": null, "mechanism_of_action": "Nesfatin-1 exerts anorexigenic effects predominantly through central (hypothalamic and brainstem) mechanisms. Intracerebroventricular injection suppresses food intake dose-dependently by activating oxytocin neurons in the paraventricular nucleus and modulating melanocortin signaling. Nesfatin-1 also acts on the melanocortin-3/4 receptor system downstream. Peripherally, it is released postprandially from gastric X/A-like cells and may function as a gut-derived satiety signal. Its receptor has not been definitively identified, though GPR3 and NPY-related receptors have been proposed.", "evidence": [ { "claim": "Central administration suppresses food intake", "level": "preliminary", "basis": "Consistent ICV rodent studies show leptin-independent anorexigenic action via oxytocin neurons" }, { "claim": "Activates oxytocin and melanocortin pathways", "level": "preliminary", "basis": "Animal hypothalamic studies identify PVN oxytocin neuron activation and MC3/4R downstream signaling" }, { "claim": "Receptor remains unidentified", "level": "insufficient", "basis": "Two decades post-discovery, GPR3 and NPY-related receptors proposed but not definitively confirmed" }, { "claim": "Plasma levels altered in obesity and diabetes", "level": "preliminary", "basis": "Human observational studies show altered nesfatin-1 in obesity, anorexia nervosa, and type 2 diabetes" }, { "claim": "No human interventional trials conducted", "level": "insufficient", "basis": "Despite 2006 discovery, no human dosing trials have been conducted to date" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/nesfatin-1" }, { "name": "Neurotrophin-3", "slug": "neurotrophin-3", "aliases": [ "NT-3", "Neurotrophin 3", "NT3" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "NT-3 is not approved for human clinical use and is classified as a research reagent. Clinical trials have used recombinant NT-3 under IND applications.", "routes": [ "intravenous", "subcutaneous" ], "half_life": "~1–2 hours (recombinant, subcutaneous)", "molecular_weight": 26560, "cas_number": "162607-25-2", "mechanism_of_action": "NT-3 binds with highest affinity to the TrkC (NTRK3) receptor tyrosine kinase, triggering autophosphorylation and activation of downstream signaling cascades including PI3K/Akt (promoting neuronal survival), MAPK/ERK (stimulating differentiation and synaptic plasticity), and PLCγ (modulating calcium signaling). NT-3 also binds the pan-neurotrophin receptor p75NTR, which can modulate either survival or apoptosis depending on cellular context. NT-3 promotes myelination by supporting oligodendrocyte precursor maturation.", "evidence": [ { "claim": "NT-3 binds TrkC receptor with high affinity", "level": "strong", "basis": "Well-established receptor biochemistry and knockout mouse phenotyping" }, { "claim": "Supports proprioceptive sensory neuron survival", "level": "strong", "basis": "Consistent developmental biology and knockout model evidence" }, { "claim": "Benefits HIV-associated sensory neuropathy", "level": "preliminary", "basis": "Phase I/II trials showed modest benefit in small cohorts" }, { "claim": "Supports cochlear hair cell survival", "level": "preliminary", "basis": "Consistent animal noise-damage and gene therapy studies only" }, { "claim": "Promotes axonal regeneration after injury", "level": "preliminary", "basis": "Rodent peripheral nerve injury models; no human efficacy data" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/neurotrophin-3" }, { "name": "Nociceptin", "slug": "nociceptin", "aliases": [ "Orphanin FQ", "N/OFQ", "Nociceptin/Orphanin FQ", "OFQ" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Nociceptin peptide is available for laboratory research only. NOP receptor-targeting drugs in clinical trials (cebranopadol, sunobinop) are investigational agents, not approved for general use.", "routes": [ "intravenous" ], "half_life": "~3–5 minutes (plasma; rapidly degraded by peptidases)", "molecular_weight": 1809.06, "cas_number": "170713-75-4", "mechanism_of_action": "Nociceptin binds selectively and with high affinity to the NOP receptor, activating Gi/Go proteins to inhibit adenylyl cyclase, decrease cAMP, suppress voltage-gated calcium channels, and activate inwardly rectifying potassium channels. These actions reduce neuronal excitability. Supraspinally, NOP activation counteracts opioid analgesia and morphine-induced reward, while spinally and peripherally it produces analgesic effects. The absence of NOP receptor coupling to the mesolimbic dopamine reward pathway distinguishes nociceptin from classical opioids, supporting its non-addictive profile.", "evidence": [ { "claim": "Selective NOP receptor agonist not binding classical opioid receptors", "level": "strong", "basis": "Decades of receptor pharmacology confirm selectivity and Gi/Go coupling without mu/delta/kappa binding" }, { "claim": "Cebranopadol efficacy in chronic pain Phase II/III", "level": "moderate", "basis": "Mixed NOP/opioid agonist cebranopadol showed efficacy in chronic low back pain RCTs vs placebo" }, { "claim": "Reduces opioid tolerance and reward signaling", "level": "preliminary", "basis": "Rodent studies show NOP activation attenuates morphine reward and tolerance development" }, { "claim": "Sunobinop promotes non-REM sleep", "level": "preliminary", "basis": "Partial NOP agonist showed sleep-promoting effects in rodents and early human trials" }, { "claim": "Non-addictive analgesic profile", "level": "preliminary", "basis": "Absence of mesolimbic dopamine coupling suggests but has not yet proven low-addiction profile in humans" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/nociceptin" }, { "name": "Noopept", "slug": "noopept", "aliases": [ "GVS-111", "Omberacetam", "N-phenylacetyl-L-prolylglycine ethyl ester" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not FDA-approved in the US. Registered as a prescription drug in Russia (Noopept brand). Unscheduled and unregulated in the UK and many other jurisdictions, allowing legal purchase. Sold as a research compound or dietary supplement in the US without formal regulatory classification.", "routes": [ "oral" ], "half_life": "~15–30 minutes (prodrug); active CPG metabolite longer", "molecular_weight": 318.4, "cas_number": "157115-85-0", "mechanism_of_action": "After oral absorption, Noopept is hydrolyzed to its active metabolite cycloprolylglycine (CPG), which modulates AMPA-type glutamate receptors and facilitates long-term potentiation in hippocampal circuits. Noopept also increases cerebral NGF (nerve growth factor) and BDNF expression, supporting neuronal survival and synaptic density. Additional mechanisms include modulation of voltage-dependent calcium channels and calcium-activated potassium channels, regulating neuronal excitability. Research has identified HIF-1 (hypoxia-inducible factor-1) DNA-binding activity as another proposed primary mechanism, potentially providing neuroprotection under hypoxic or ischemic conditions. Antioxidant activity via inhibition of intracellular reactive oxygen species accumulation contributes to its neuroprotective profile.", "evidence": [ { "claim": "Enhances memory/cognition", "level": "preliminary", "basis": "Russian clinical trials in mild cognitive impairment show memory/attention gains; not ICH-GCP replicated" }, { "claim": "Upregulates NGF and BDNF", "level": "preliminary", "basis": "Rat hippocampus study (Bull Exp Biol Med 2009) shows NGF/BDNF mRNA upregulation" }, { "claim": "Neuroprotection against oxidative stress", "level": "preliminary", "basis": "GVS-111 study showed IC50 1.21 μM dose-dependent neuroprotection vs oxidative damage" }, { "claim": "Attenuates tau hyperphosphorylation", "level": "preliminary", "basis": "2014 J Biomed Sci AD cellular model showed apoptosis and tau reduction in vitro" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/noopept" }, { "name": "NPY", "slug": "npy", "aliases": [ "Neuropeptide Y", "NPY (human, rat)", "neuropeptide tyrosine" ], "category": "other", "subcategories": [ "weight-loss" ], "legal_status": "research-only", "legal_notes": "NPY is a research peptide not approved for human use. Available from research suppliers for in vitro and in vivo studies. Y receptor antagonists that target the NPY pathway are being developed as prescription drugs.", "routes": [ "intravenous" ], "half_life": "~3–10 minutes (plasma)", "molecular_weight": 4271.76, "cas_number": "90880-35-6", "mechanism_of_action": "NPY signals through five GPCRs (Y1–Y5 in humans). Y1 and Y5 receptors in the arcuate and paraventricular nuclei of the hypothalamus mediate the primary orexigenic effects, increasing food intake and energy storage in white adipose tissue. Y2 and Y4 receptors have appetite-inhibiting roles, creating a complex regulatory balance. NPY is co-released with norepinephrine from sympathetic nerve terminals, modulating vasoconstriction and blood pressure. Chronic NPY elevation promotes adipogenesis, suppresses brown adipose tissue activation, and contributes to obesity maintenance.", "evidence": [ { "claim": "Most potent known orexigenic peptide", "level": "strong", "basis": "Decades of animal studies consistently show dose-dependent food intake stimulation via hypothalamic Y1/Y5" }, { "claim": "NPY knockout mice resist diet-induced obesity", "level": "moderate", "basis": "Multiple transgenic mouse studies validate NPY's role in obesity maintenance on high-fat diets" }, { "claim": "Y1/Y5 antagonists failed obesity trials", "level": "moderate", "basis": "Clinical Phase II trials showed limited efficacy and off-target effects, ending major obesity programs" }, { "claim": "Intranasal NPY shows PTSD signal", "level": "preliminary", "basis": "Phase 1 PTSD studies with intranasal NPY delivery reported preliminary positive anxiolytic results" }, { "claim": "Co-released with norepinephrine for vasoconstriction", "level": "strong", "basis": "Established cardiovascular physiology across animal and human sympathetic nerve studies" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/npy" }, { "name": "Obestatin", "slug": "obestatin", "aliases": [ "Obestatin-23", "Ghrelin Gene Product", "GPR39 Ligand" ], "category": "weight-loss", "subcategories": [], "legal_status": "research-only", "legal_notes": "Obestatin is available for laboratory research use only with no approved clinical applications.", "routes": [ "intravenous" ], "half_life": "~20–30 minutes (rapidly degraded in plasma)", "molecular_weight": 2396.7, "cas_number": "869705-22-6", "mechanism_of_action": "Obestatin was originally reported to bind GPR39 (an orphan GPCR) and oppose ghrelin's orexigenic actions. However, multiple independent groups failed to confirm GPR39 binding or a consistent anorexigenic effect. More recent studies indicate obestatin signals through pathways including GLP-1 receptor cross-talk and phospholipase C activation. It may regulate glucose metabolism, pancreatic beta-cell survival, and smooth muscle contractility independently of ghrelin. The definitive receptor and downstream cascade remain contested in the literature.", "evidence": [ { "claim": "Original GPR39 binding not replicated", "level": "insufficient", "basis": "2005 Science discovery report refuted by multiple independent labs failing to confirm GPR39 interaction" }, { "claim": "Satiety effects inconsistent across studies", "level": "insufficient", "basis": "Original anorexigenic claims contested; many groups report absent or variable effects on food intake" }, { "claim": "May protect pancreatic beta-cells", "level": "preliminary", "basis": "In vitro and rodent studies suggest survival effects on islets and cardiomyocytes via unclear receptors" }, { "claim": "Plasma levels altered in PCOS and Prader-Willi", "level": "preliminary", "basis": "Observational human studies report altered obestatin across metabolic and genetic disorders" }, { "claim": "No clinical trials advanced", "level": "insufficient", "basis": "Controversial mechanism and reproducibility issues have prevented therapeutic translation" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/obestatin" }, { "name": "Octreotide", "slug": "octreotide", "aliases": [ "Sandostatin", "SMS 201-995", "octreotide acetate" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved drug (NDA 019667, first approved 1988). Available only by prescription as Sandostatin injection and Sandostatin LAR depot. Administered in clinical or hospital settings; not available as a research chemical.", "routes": [ "subcutaneous", "intramuscular", "intravenous" ], "half_life": "~1.7–1.9 hours (SC); biphasic IV: 10 min + 90 min", "molecular_weight": 1019.24, "cas_number": "83150-76-9", "mechanism_of_action": "Octreotide binds preferentially to somatostatin receptors SSTR2 and SSTR5, mimicking the inhibitory actions of endogenous somatostatin but with significantly greater potency and duration. It suppresses secretion of growth hormone (GH), IGF-1, insulin, glucagon, gastrin, secretin, motilin, vasoactive intestinal peptide (VIP), and serotonin. By reducing splanchnic blood flow, it also decreases portal hypertension. In acromegaly, it normalizes GH levels in approximately 50% of patients and IGF-1 in 50–60%. Its mechanism involves Gi protein-coupled receptor signaling that decreases intracellular cAMP, reduces calcium influx, and opens potassium channels, collectively suppressing hormone exocytosis from secretory cells.", "evidence": [ { "claim": "Normalizes GH in acromegaly", "level": "strong", "basis": "RCT (Ezzat Ann Intern Med 1992) and decades of clinical use show GH normalization in ~50%" }, { "claim": "Controls carcinoid syndrome symptoms", "level": "strong", "basis": "FDA-approved indication; multiple clinical trials show diarrhea/flushing reduction" }, { "claim": "LAR depot equivalent to daily SC", "level": "strong", "basis": "Phase 3 trials establish Sandostatin LAR monthly equivalent efficacy to TID injections" }, { "claim": "Treats VIPoma secretory diarrhea", "level": "strong", "basis": "FDA-approved indication; clinical evidence for hormone-secreting tumor control" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/octreotide" }, { "name": "Orforglipron", "slug": "orforglipron", "aliases": [ "LY3502970", "Foundayo", "oral GLP-1 pill", "GLP-1 pill" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "FDA-approved in April 2026 as Foundayo (orforglipron) for chronic weight management in adults with obesity, or overweight with at least one weight-related medical problem, as an adjunct to diet and physical activity. Prescription only. Diabetes use and other indications require current-label confirmation.", "routes": [ "oral" ], "half_life": "Reported Phase 1/clinical pharmacology estimates support once-daily study and label development; check the current prescribing information for official pharmacokinetics.", "molecular_weight": 882.97, "cas_number": "2212020-52-3", "mechanism_of_action": "Orforglipron activates the GLP-1 receptor through a non-peptide small-molecule binding mode. GLP-1 receptor activation is associated with glucose-dependent insulin secretion, reduced glucagon signaling, delayed gastric emptying, and central satiety signaling. Those effects overlap with the broader GLP-1 receptor agonist class, but the molecule is chemically distinct from peptide drugs such as semaglutide and liraglutide.\n\nThe oral-pill angle is not just packaging. Peptide GLP-1 drugs are usually injected because digestive enzymes and poor intestinal permeability make oral delivery difficult. Oral semaglutide works by pairing the peptide with the SNAC absorption enhancer and strict administration conditions. Orforglipron was developed as a small molecule, so its oral absorption does not depend on peptide-protection technology or injection-device logistics.\n\nThis page is educational and does not give dosing instructions. Use the FDA label and a licensed clinician for prescribing, contraindications, dose escalation, missed-dose questions, pregnancy considerations, pancreatitis/gallbladder warnings, and drug-interaction review.", "evidence": [ { "claim": "Chronic weight management approval", "level": "strong", "basis": "FDA approval announced April 2026 for adults with obesity or overweight with weight-related medical problems; prescription-only label scope applies" }, { "claim": "Weight loss in obesity", "level": "strong", "basis": "ATTAIN-1 Phase 3: 72-week placebo-controlled obesity trial with 12.4% mean weight loss among participants who stayed on treatment in the highest studied arm" }, { "claim": "Oral small-molecule GLP-1 delivery", "level": "strong", "basis": "Phase 1/2 pharmacology and Lilly label framing identify orforglipron as an oral non-peptide GLP-1 receptor agonist without food or water restrictions" }, { "claim": "Type 2 diabetes treatment", "level": "moderate", "basis": "ATTAIN-2 and earlier diabetes trials support glycemic research claims; U.S. diabetes indication should be confirmed against the current FDA label before stating approval" }, { "claim": "Cardiovascular outcomes benefit", "level": "insufficient", "basis": "No completed cardiovascular outcomes trial comparable to SELECT for semaglutide; class effects should not be assumed for orforglipron" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "137319706", "drugbank": "DB18964", "wikidata": "Q120491908", "wikipedia": "https://en.wikipedia.org/wiki/Orforglipron" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/orforglipron" }, { "name": "Ovagen", "slug": "ovagen", "aliases": [ "EDL tripeptide", "Glu-Asp-Leu", "liver bioregulator" ], "category": "longevity", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Developed and commercialized in Russia as a cytogen bioregulator supplement. Available in Western markets as a research chemical. Not approved for therapeutic human use outside Russia.", "routes": [ "subcutaneous", "intramuscular", "oral" ], "half_life": "Short (minutes to hours — estimated for tripeptide class)", "molecular_weight": 361.4, "cas_number": null, "mechanism_of_action": "Ovagen is transported into cells via POT family peptide transporters (PEPT1, PEPT2), which selectively handle di- and tripeptides, conferring tissue-specific delivery to hepatocytes and intestinal epithelial cells. Once intracellular, Ovagen crosses the nuclear membrane and interacts directly with DNA in target tissue, modulating transcription of genes involved in cell proliferation, fibrogenesis, and hepatocellular metabolism. In aged animal hepatic tissue models, preclinical studies show Ovagen increases Ki-67 expression (a proliferation marker) by up to 18-fold while simultaneously reducing p53 expression by up to 6-fold, favoring regenerative over apoptotic signaling. It inhibits fibroblast-driven fibrotic changes at the cellular level, preventing progressive scarring. In the GI tract, it protects the mucosal layer from antibiotic damage, environmental toxins, and chemotherapy-induced injury.", "evidence": [ { "claim": "Promotes hepatocyte regeneration", "level": "preliminary", "basis": "Rodent aged liver studies show Ki-67 up to 18-fold increase, p53 up to 6-fold decrease" }, { "claim": "Reduces liver fibrosis markers", "level": "preliminary", "basis": "Khavinson preclinical work; no Western peer-reviewed RCTs published" }, { "claim": "Protects GI mucosa from toxins", "level": "preliminary", "basis": "Animal studies show mucosal protection from antibiotic and chemotherapy injury" }, { "claim": "Cellular uptake via PEPT1/PEPT2", "level": "preliminary", "basis": "In vitro transporter studies confirm tripeptide uptake; therapeutic relevance unvalidated" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ovagen" }, { "name": "Oxytocin", "slug": "oxytocin", "aliases": [ "Pitocin", "Syntocinon", "Love Hormone", "Bonding Hormone", "OXT" ], "category": "sexual-health", "subcategories": [ "sleep", "cognitive" ], "legal_status": "prescription", "legal_notes": "FDA-approved as Pitocin (injectable) for obstetric use. Intranasal oxytocin is available via compounding pharmacies as a prescription product. Off-label OTC products exist at very low doses as supplements. Prescription required for therapeutic intranasal compounded formulations.", "routes": [ "intravenous", "nasal", "subcutaneous" ], "half_life": "~20 minutes (plasma); behavioral effects persist 45-90 minutes after intranasal dose", "molecular_weight": 1007.19, "cas_number": "50-56-6", "mechanism_of_action": "Oxytocin acts through a single oxytocin receptor (OXTR), a 389-amino acid class I G-protein coupled receptor with seven transmembrane domains. Peripheral OXTR activation mediates uterine contractions and milk ejection. Centrally, oxytocin modulates the hypothalamic-pituitary-adrenal (HPA) axis by reducing cortisol secretion, dampening the amygdala fear response, and enhancing reward salience of social stimuli through interaction with the dopaminergic mesolimbic system. Intranasal oxytocin crosses into the CNS via olfactory-perivascular pathways, with CSF concentrations rising measurably within 75 minutes of intranasal dosing. It increases GABAergic signaling in limbic areas, contributing to anxiolytic and sleep-promoting effects. OXTR is highly expressed in the hippocampus, amygdala, and nucleus accumbens, explaining its broad socioemotional effects.", "evidence": [ { "claim": "Labor induction and uterine contraction", "level": "strong", "basis": "FDA-approved synthetic oxytocin (Pitocin) for labor induction; multiple large RCTs since the 1950s; standard of care in obstetrics" }, { "claim": "Social cognition and trust improvement in autism spectrum disorder", "level": "insufficient", "basis": "Sikich et al. NEJM 2021: n=290 ASD children aged 3–17, 24 weeks; no significant improvement on primary endpoint (Vineland Adaptive Behavior Scale); large rigorous RCT showing null result" }, { "claim": "Acute anxiety reduction and pro-social behavior", "level": "moderate", "basis": "Kosfeld et al. Nature 2005 and multiple small RCTs (n=30–60) showing acute intranasal oxytocin reduces fear responses and increases trust in economic games" }, { "claim": "Postpartum hemorrhage prevention", "level": "strong", "basis": "WHO-recommended standard; systematic review of 50+ RCTs; oxytocin reduces third-stage blood loss by ~40% vs no prophylaxis" }, { "claim": "Chronic anxiety, PTSD, or relationship dysfunction treatment", "level": "insufficient", "basis": "Multiple small conflicting RCTs; no consistent signal across heterogeneous populations; large ASD null result (NEJM 2021) dampens enthusiasm for chronic psychiatric indications" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/oxytocin" }, { "name": "PACAP", "slug": "pacap", "aliases": [ "PACAP-38", "PACAP-27", "Pituitary Adenylate Cyclase-Activating Polypeptide" ], "category": "other", "subcategories": [ "cognitive" ], "legal_status": "research-only", "legal_notes": "PACAP-38 and PACAP-27 are research peptides, not FDA-approved for human use. Available from specialty peptide suppliers for in vitro and in vivo research. The PAC1 antagonist Lu AG09222 (bocunebart, Lundbeck) completed Phase IIb PROCEED with positive efficacy data reported at AHS in June 2026; Phase III is anticipated but not yet initiated as of mid-2026. No PAC1 antagonist is FDA-approved.", "routes": [ "intravenous", "subcutaneous" ], "half_life": "~2–10 minutes (rapid enzymatic degradation)", "molecular_weight": 4533.2, "cas_number": "137061-48-4", "mechanism_of_action": "PACAP acts through three GPCRs: PAC1 (PACAP-selective, high affinity), VPAC1, and VPAC2 (shared with VIP). PAC1 activation stimulates adenylate cyclase, raising cAMP, and also activates PLC through Gq coupling. This triggers PKA/PKC signaling cascades that promote neuronal survival, inhibit apoptosis, reduce neuroinflammation, and stimulate neurotrophic factor synthesis. PACAP regulates diverse functions including neurodevelopment, circadian rhythms, pain modulation, immune function, and energy metabolism.", "evidence": [ { "claim": "Triggers migraine in 55-58% of IV-infused subjects", "level": "moderate", "basis": "Human provocation studies show reproducible delayed migraine attacks, validating PAC1 as drug target" }, { "claim": "Potent neuroprotection in preclinical models", "level": "preliminary", "basis": "Consistent animal data across ischemia, TBI, Parkinson's, Alzheimer's models; no approved human applications" }, { "claim": "Activates PAC1, VPAC1, VPAC2 GPCRs", "level": "strong", "basis": "Decades of pharmacological and structural characterization of receptor binding and cAMP/PLC signaling" }, { "claim": "PTSD-associated biomarker in women", "level": "preliminary", "basis": "Observational studies show PAC1R hypermethylation and PACAP elevation in women with PTSD" }, { "claim": "PAC1 antagonists in migraine clinical trials", "level": "preliminary", "basis": "Early-phase clinical trials of PAC1 antagonists underway; no FDA approval as of 2026" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/pacap" }, { "name": "Palmitoyl Hexapeptide-12", "slug": "palmitoyl-hexapeptide-12", "aliases": [ "Biopeptide EL", "Pal-VGVAPG", "Palmitoyl-Val-Gly-Val-Ala-Pro-Gly" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Palmitoyl Hexapeptide-12 is an OTC cosmetic ingredient regulated under cosmetics law (not as a drug). No prescription required. FDA oversight applies only if drug claims are made.", "routes": [ "topical" ], "half_life": "N/A (topical; activity is local at application site)", "molecular_weight": 726.99, "cas_number": "1228371-11-8", "mechanism_of_action": "The VGVAPG elastin peptide sequence acts on fibroblast receptors to stimulate extracellular matrix (ECM) production, including elastin, collagen, and fibronectin. The palmitoyl fatty acid chain improves skin penetration through the stratum corneum and enables incorporation into lipid bilayer-based delivery systems. The combination mimics the activity of natural elastin degradation products that signal dermal repair, promoting matrix synthesis and potentially reducing the appearance of fine lines and loss of elasticity.", "evidence": [ { "claim": "Stimulates elastin and collagen synthesis", "level": "preliminary", "basis": "In vitro fibroblast culture studies showing ECM protein upregulation" }, { "claim": "Improves skin firmness and elasticity", "level": "preliminary", "basis": "Small industry-sponsored cosmetic trials with limited sample sizes" }, { "claim": "Palmitoyl chain enhances skin penetration", "level": "moderate", "basis": "Well-established lipidation pharmacology for stratum corneum penetration" }, { "claim": "Reduces appearance of fine lines", "level": "preliminary", "basis": "Industry cosmetic studies only; no independent dermatology RCTs" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/palmitoyl-hexapeptide-12" }, { "name": "Palmitoyl Oligopeptide", "slug": "palmitoyl-oligopeptide", "aliases": [ "Palmitoyl Oligopeptide-3", "Pal-Oligopeptide", "Palm-Oligopeptide" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "OTC cosmetic ingredient class. Subject to CIR (Cosmetic Ingredient Review) safety assessment. No prescription or regulatory approval required.", "routes": [ "topical" ], "half_life": "Not established (cosmetic topical use)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Palmitoyl Oligopeptide functions as a matrikine mimic. Matrikines are short peptide fragments released when ECM proteins degrade — the skin's built-in signal to rebuild lost matrix. By delivering synthetic matrikine-like sequences conjugated to palmitic acid, the peptide penetrates the lipophilic stratum corneum and reaches dermal fibroblasts. There, it activates fibroblast collagen synthesis pathways, upregulating ECM protein production. The palmitoyl chain is critical for skin permeation: without it, the hydrophilic peptide core cannot cross the epidermal barrier effectively. In vitro data show increases in collagen production by fibroblasts of up to 350% and hyaluronic acid production increases of 146%.", "evidence": [ { "claim": "Increases fibroblast collagen production 350% in vitro", "level": "preliminary", "basis": "In vitro fibroblast culture data from cosmetic ingredient studies; no independent replication" }, { "claim": "Increases hyaluronic acid production 146% in vitro", "level": "preliminary", "basis": "Same in vitro fibroblast studies; supplier-sourced data not independently validated" }, { "claim": "Reduces wrinkle depth up to 39% in humans", "level": "preliminary", "basis": "Manufacturer instrumental studies; no independent peer-reviewed clinical RCTs" }, { "claim": "Matrikine-mimetic mechanism", "level": "moderate", "basis": "Maquart 1999 established matrikine biology broadly; applied by extension to palmitoyl oligopeptide class" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/palmitoyl-oligopeptide" }, { "name": "Palmitoyl Tetrapeptide-7", "slug": "palmitoyl-tetrapeptide-7", "aliases": [ "Pal-GQPR", "Rigin", "Palmitoyl-Gly-Gln-Pro-Arg" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Approved cosmetic ingredient in the US, EU, and most global markets. No prescription required. Regulated as a cosmetic, not a drug. Available as a raw ingredient and in finished anti-aging skincare products.", "routes": [ "topical" ], "half_life": "Not established (topical cosmetic ingredient)", "molecular_weight": 723, "cas_number": "221227-05-0", "mechanism_of_action": "Palmitoyl Tetrapeptide-7 suppresses the production of interleukin-6 (IL-6) and related pro-inflammatory cytokines from keratinocytes in a dose-dependent manner. By reducing IL-6 signaling, it limits downstream activation of matrix metalloproteinases (MMPs), which degrade collagen and elastin in aging and UV-damaged skin. It also suppresses the acute inflammatory cascade that triggers skin redness, roughness, and degradation of the extracellular matrix. The GQPR sequence is derived from the Fc region of IgG and acts as an immune-modulating signal that shifts keratinocytes from inflammatory to homeostatic signaling states. The palmitoyl chain facilitates stratum corneum penetration.", "evidence": [ { "claim": "Suppresses IL-6 in keratinocytes", "level": "preliminary", "basis": "In vitro studies show dose-dependent IL-6 reduction up to 40% at higher concentrations" }, { "claim": "Reduces MMP-driven collagen degradation", "level": "preliminary", "basis": "In vitro mechanistic data; downstream effect of IL-6 suppression on MMP activation" }, { "claim": "Improves skin firmness and smoothness", "level": "moderate", "basis": "Matrixyl 3000 RCT (J Drugs Dermatol 2018) showed firmness improvement in cosmetic formulation" }, { "claim": "Safe at cosmetic concentrations", "level": "moderate", "basis": "CIR Expert Panel safety assessment confirmed tolerability at 0.00025–0.0004% levels" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/palmitoyl-tetrapeptide-7" }, { "name": "Palmitoyl Tripeptide-1", "slug": "palmitoyl-tripeptide-1", "aliases": [ "Pal-GHK", "Palmitoyl-Gly-His-Lys", "Biopeptide CL", "Palmitoyl Oligopeptide" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Permitted cosmetic ingredient in the US, EU, and most global markets. Regulated as a cosmetic; no prescription or drug approval required. Sold as a raw ingredient for cosmetic formulators and in finished OTC skincare products.", "routes": [ "topical" ], "half_life": "Not established (topical cosmetic ingredient)", "molecular_weight": 578.8, "cas_number": "147732-56-7", "mechanism_of_action": "Palmitoyl Tripeptide-1 functions as a matrikine — a peptide fragment derived from ECM protein degradation that signals fibroblasts to upregulate matrix synthesis. The GHK sequence binds fibroblast surface receptors and activates intracellular TGF-β pathway components and downstream collagen gene transcription (COL1A1, COL3A1). The palmitoyl fatty acid chain increases the molecule's lipophilicity, enabling penetration through the stratum corneum into the viable epidermis and dermis. In vitro studies confirm stimulation of collagen I, III, and glycosaminoglycan synthesis at sub-micromolar concentrations. It has also been shown to modulate MMP expression, reducing collagen degradation in UV-aged skin models.", "evidence": [ { "claim": "Reduces periorbital wrinkle length", "level": "moderate", "basis": "4-week eye zone study showed 39% reduction in wrinkle length vs vehicle at ~3 ppm" }, { "claim": "Stimulates collagen I and III synthesis", "level": "preliminary", "basis": "In vitro fibroblast assays demonstrate dose-dependent COL1A1/COL3A1 upregulation" }, { "claim": "Reduces skin roughness", "level": "moderate", "basis": "Clinical study showed 17% reduction in skin roughness after 4 weeks twice-daily use" }, { "claim": "Matrixyl 3000 anti-aging component", "level": "moderate", "basis": "Multiple cosmetic clinical studies support combined Pal-GHK + Pal-GQPR efficacy" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/palmitoyl-tripeptide-1" }, { "name": "Palmitoyl Tripeptide-38", "slug": "palmitoyl-tripeptide-38", "aliases": [ "MATRIXYL synthe'6", "Pal-KMO2K", "Volulip", "PT-38" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Approved cosmetic ingredient used globally in OTC skincare formulations. No prescription or regulatory approval required. Subject to standard cosmetic ingredient safety review.", "routes": [ "topical" ], "half_life": "Not established (cosmetic topical use)", "molecular_weight": 895.18, "cas_number": "1447824-23-8", "mechanism_of_action": "Palmitoyl Tripeptide-38 acts as a matrikine mimic, sending biological signals to dermal fibroblasts to upregulate synthesis of collagen I, II, and IV, fibronectin, hyaluronic acid, and laminin-5. The palmitoyl fatty acid chain enhances skin penetration through the lipophilic stratum corneum. Once in the dermis, the peptide activates fibroblast collagen-synthesis pathways and supports ECM remodeling at the dermal-epidermal junction. It also modulates wound repair signaling and promotes tissue regeneration without irritating the epidermis.", "evidence": [ { "claim": "Stimulates six ECM proteins simultaneously", "level": "preliminary", "basis": "In vitro studies confirm upregulation of collagen I/II/IV, fibronectin, hyaluronic acid, laminin-5" }, { "claim": "31% wrinkle depth reduction at 2%", "level": "preliminary", "basis": "2-month vehicle-controlled clinical study; manufacturer-sponsored with no independent replication" }, { "claim": "Matrikine-mimetic fibroblast signaling", "level": "preliminary", "basis": "Tadini 2019 Int J Cosmet Sci mechanistic study shows longevity-gene upregulation in skin cells" }, { "claim": "Well tolerated as topical cosmetic", "level": "moderate", "basis": "Standard cosmetic ingredient safety review; widely used globally with rare irritation reports" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/palmitoyl-tripeptide-38" }, { "name": "Palmitoyl Tripeptide-5", "slug": "palmitoyl-tripeptide-5", "aliases": [ "SYN-COLL", "Pal-KVK", "Pal-Lys-Val-Lys", "SYR tripeptide" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "Cosmetic ingredient with unrestricted OTC status globally. Sold as a cosmetic active; not classified as a drug by FDA, EMA, or equivalent bodies. No known regulatory advisories.", "routes": [ "topical" ], "half_life": "Not established (topical cosmetic)", "molecular_weight": null, "cas_number": "623172-56-5", "mechanism_of_action": "Palmitoyl Tripeptide-5 mimics the TSP-1 sequence that activates latent transforming growth factor-beta (TGF-β). By binding to the latency-associated peptide region of inactive TGF-β, the tripeptide induces release of the active growth factor, which then signals dermal fibroblasts via Smad2/3 phosphorylation to upregulate type I and III collagen synthesis. Simultaneously, Palmitoyl Tripeptide-5 inhibits matrix metalloproteinases (MMP-1, MMP-2, MMP-9) that degrade existing collagen, providing a dual protective and regenerative action. The palmitoyl lipid chain enhances penetration through the stratum corneum and increases residence time in the dermis by anchoring the peptide to membrane phospholipids.", "evidence": [ { "claim": "Activates TGF-β to stimulate collagen", "level": "preliminary", "basis": "In vitro fibroblast assays show TSP-1 mimicry and Smad2/3-driven collagen I/III upregulation" }, { "claim": "Inhibits MMP-1, MMP-2, MMP-9", "level": "preliminary", "basis": "In vitro enzymatic assays demonstrate dose-dependent matrix metalloproteinase inhibition" }, { "claim": "Reduces wrinkle depth over 28–56 days", "level": "preliminary", "basis": "Manufacturer-sponsored clinical studies (Lipotec/Lubrizol); limited independent trials" }, { "claim": "Well-tolerated at cosmetic use", "level": "moderate", "basis": "Multiple cosmetic formulations stable pH 4.5–7.5; no regulatory advisories" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/palmitoyl-tripeptide-5" }, { "name": "Pasireotide", "slug": "pasireotide", "aliases": [ "Signifor", "SOM230", "Signifor LAR", "Pasireotide diaspartate" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 203255, December 2012) for Cushing's disease and acromegaly. Available as Signifor (SC, twice daily) for Cushing's and Signifor LAR (IM, monthly) for acromegaly. Prescription-only.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~12 hours (SC); ~23 days (LAR)", "molecular_weight": 1047.23, "cas_number": "396091-73-9", "mechanism_of_action": "Pasireotide activates somatostatin receptors SSTR1, 2, 3, and 5, with particularly high affinity for SSTR5, which is overexpressed in corticotroph adenoma cells in Cushing's disease. SSTR5 engagement suppresses ACTH secretion from pituitary adenomas, reducing cortisol production. In acromegaly, combined SSTR2/5 activity more comprehensively inhibits GH secretion than SSTR2-selective agents. Compared to octreotide, pasireotide has 40-fold greater binding affinity for SSTR5.", "evidence": [ { "claim": "FDA-approved for Cushing's disease", "level": "strong", "basis": "FDA NDA 203255 December 2012 based on Phase III PASPORT trial" }, { "claim": "Normalized cortisol in ~25% of Cushing's patients", "level": "strong", "basis": "Phase III PASPORT trial showing UFC normalization sustained at 24 months" }, { "claim": "40-fold higher SSTR5 affinity versus octreotide", "level": "strong", "basis": "Well-characterized receptor binding pharmacology studies" }, { "claim": "Approved for acromegaly (Signifor LAR)", "level": "strong", "basis": "FDA approval 2014 for acromegaly based on Phase III head-to-head trial" }, { "claim": "Causes hyperglycemia in 60-80% of patients", "level": "strong", "basis": "Consistent Phase III trial safety data and post-marketing surveillance" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/pasireotide" }, { "name": "PEG-MGF", "slug": "peg-mgf", "aliases": [ "PEGylated MGF", "PEGylated Mechano Growth Factor", "IGF-1 Ec PEGylated" ], "category": "muscle", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Not FDA approved. Available from research peptide suppliers in the US as a laboratory compound. WADA-prohibited in competitive sport. Not scheduled as a controlled substance in most jurisdictions, but legal status varies.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~24–72 hours (PEGylated; native MGF half-life is ~5–7 minutes)", "molecular_weight": 2867.2, "cas_number": null, "mechanism_of_action": "MGF is generated by alternative splicing of the IGF-1 gene in mechanically stressed muscle. Its unique C-terminal E-domain peptide activates quiescent muscle satellite cells — the resident stem cells responsible for muscle repair and hypertrophy. PEG-MGF binds IGF-1 receptors and MGF-specific receptors on muscle cell membranes, triggering downstream Akt/mTOR and MAPK/ERK signaling that promotes myoblast proliferation, differentiation, and fusion into new myofibers. The PEG modification (polyethylene glycol conjugation) shields the peptide from proteolytic degradation and renal clearance, extending systemic availability from the native MGF half-life of approximately 5–7 minutes to an estimated 24–72 hours.", "evidence": [ { "claim": "Activates muscle satellite cells", "level": "preliminary", "basis": "Rodent injury models show satellite cell activation via IGF-1 receptor and MGF-specific binding" }, { "claim": "Accelerates muscle repair post-injury", "level": "preliminary", "basis": "Preclinical studies in mice report increased fiber cross-sectional area and reduced necrosis markers" }, { "claim": "Extended half-life vs native MGF", "level": "preliminary", "basis": "Pharmacokinetic rodent data supports 24–72h half-life; no human PK studies published" }, { "claim": "Treats muscle-wasting conditions", "level": "insufficient", "basis": "Only animal evidence; no completed human clinical trials as of 2026" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/peg-mgf" }, { "name": "Peptide YY", "slug": "peptide-yy", "aliases": [ "PYY", "PYY 3-36", "Peptide Tyrosine Tyrosine", "PYY1-36", "PYY3-36" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "No FDA-approved PYY therapeutic exists as of 2026. PYY analogs are in active pharmaceutical development. Research use only for synthetic forms.", "routes": [ "intravenous", "nasal", "subcutaneous" ], "half_life": "~30 minutes (PYY3-36); ~10-15 minutes (PYY1-36)", "molecular_weight": 4309.8, "cas_number": "118997-30-1", "mechanism_of_action": "PYY exerts its primary satiety effect through binding to neuropeptide Y (NPY) Y2 receptors in the arcuate nucleus of the hypothalamus. Y2 receptor activation inhibits NPY/AgRP orexigenic neurons, reducing the drive to eat. The predominant circulating form PYY3-36 (generated by dipeptidyl peptidase-IV cleavage of PYY1-36) is highly selective for Y2 over Y1 receptors, making it more potent as a satiety signal with fewer peripheral effects. PYY also slows gastric emptying via the 'ileal brake' mechanism — reducing GI motility to optimize nutrient absorption. Peripheral PYY crosses the blood-brain barrier via active transport and acts directly on brainstem areas including the nucleus tractus solitarius. When co-administered with GLP-1, additive or synergistic appetite suppression has been observed without additional GI adverse events.", "evidence": [ { "claim": "Acute appetite and food intake suppression", "level": "moderate", "basis": "Multiple IV infusion RCTs showing 15-30% reduced ad libitum intake; Batterham Br J Nutr 2021 review; established Y2 mechanism" }, { "claim": "Synergy with GLP-1 for combined satiety", "level": "moderate", "basis": "Combined PYY3-36 + GLP-1 infusion: 27% energy intake reduction in lean subjects; consistent small human studies" }, { "claim": "Intranasal PYY3-36 weight loss", "level": "insufficient", "basis": "Inconsistent results across trials due to nausea at effective doses and variable nasal bioavailability" }, { "claim": "Role in post-bariatric surgery weight loss", "level": "moderate", "basis": "Multiple observational studies; PYY elevated post-surgery; mechanistic contribution established but not isolated" }, { "claim": "Standalone obesity therapeutic approval", "level": "insufficient", "basis": "No FDA-approved PYY therapeutic as of 2026; analogs in early development; no Phase 3 obesity trials" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "56841989", "wikidata": "Q290293", "wikipedia": "https://en.wikipedia.org/wiki/Peptide_YY" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/peptide-yy" }, { "name": "Pinealon", "slug": "pinealon", "aliases": [ "EDR tripeptide", "Glu-Asp-Arg", "Epithalamin peptide fragment" ], "category": "cognitive", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Not approved by FDA or EMA as a drug. Available from peptide research suppliers in the US as a research compound. Not scheduled as a controlled substance. Legal gray area for human use outside of clinical research settings.", "routes": [ "subcutaneous", "nasal" ], "half_life": "Not established in humans; estimated minutes to hours given tripeptide size", "molecular_weight": 404.4, "cas_number": null, "mechanism_of_action": "Like other Khavinson short peptides, Pinealon is hypothesized to act as an epigenetic regulator by penetrating cell membranes and binding to GC-rich promoter regions in DNA, modulating transcription factor access and gene expression. Research has demonstrated that EDR upregulates expression of neuroprotective genes including nestin, GAP-43 (growth-associated protein 43), and superoxide dismutase (SOD). It reduces neuronal apoptosis in model systems, modulates the cholinergic system, and is thought to influence melatonin synthesis pathways in pinealocytes. The peptide crosses the blood-brain barrier by virtue of its small size.", "evidence": [ { "claim": "Cognitive enhancement in elderly", "level": "preliminary", "basis": "Russian clinical studies (Khavinson group); memory, attention, reaction-time improvements; small studies, no Western replication" }, { "claim": "Neuroprotection and gene expression modulation", "level": "preliminary", "basis": "Preclinical: upregulation of nestin, GAP-43, SOD in mouse AD models; reduced hippocampal apoptosis" }, { "claim": "Alzheimer's disease amyloid pathology reduction", "level": "preliminary", "basis": "Mouse AD model studies (PMC-published); reduction in amyloid pathology and increased neuronal survival; no human AD trials" }, { "claim": "Pineal gland bioregulation", "level": "insufficient", "basis": "Khavinson theoretical framework; Anisimov J Pineal Res 2006 review; no direct human pineal-function endpoints measured" }, { "claim": "Human clinical efficacy outside Russia", "level": "insufficient", "basis": "No large double-blind placebo-controlled trials conducted outside Russia as of 2026" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/pinealon" }, { "name": "Polymyxin B", "slug": "polymyxin-b", "aliases": [ "Polymyxin B sulfate", "PMB", "Aerosporin" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved for serious gram-negative infections (IV, IM) and as a topical component in combination products (e.g., Neosporin). IV use is restricted to severe infections where safer alternatives are not available, due to nephrotoxicity and neurotoxicity risks.", "routes": [ "topical", "intravenous", "intramuscular" ], "half_life": "~6 hours (IV, varies with renal function)", "molecular_weight": 1301.56, "cas_number": "1405-20-5", "mechanism_of_action": "Polymyxin B targets the bacterial outer membrane by electrostatically binding the phosphate groups of lipid A in lipopolysaccharide (LPS), displacing stabilizing divalent cations (Ca2+, Mg2+). This disrupts outer membrane integrity, increases permeability, and allows entry of the hydrophobic fatty acid tail into the inner membrane, where it causes further disruption, ion leakage, and loss of membrane potential. The bactericidal effect is rapid at higher concentrations. Polymyxin B also directly neutralizes LPS (endotoxin), which may attenuate sepsis-associated inflammatory cascades.", "evidence": [ { "claim": "FDA-approved for MDR gram-negative infections", "level": "strong", "basis": "Long-standing FDA approval; critical last-resort agent for carbapenem resistance" }, { "claim": "Disrupts outer membrane via LPS lipid A binding", "level": "strong", "basis": "Well-characterized biochemistry with structural and biophysical validation" }, { "claim": "Causes nephrotoxicity in 30-60% of patients", "level": "strong", "basis": "Consistent prospective clinical studies and pharmacovigilance data" }, { "claim": "Neutralizes endotoxin in sepsis", "level": "moderate", "basis": "Consistent preclinical LPS binding; mixed human sepsis adjunct trial results" }, { "claim": "MCR-1 plasmid-mediated resistance emerging globally", "level": "strong", "basis": "Consistent molecular epidemiology and surveillance data since 2015 discovery" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/polymyxin-b" }, { "name": "Pramlintide", "slug": "pramlintide", "aliases": [ "Symlin", "AC137", "Pramlintide acetate" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 021332) for subcutaneous use as an adjunct to mealtime insulin in T1D and T2D. Voluntarily withdrawn from the US market by AstraZeneca circa 2020; no longer commercially available in the US as of 2026. Compounding pharmacy availability varies by jurisdiction.", "routes": [ "subcutaneous" ], "half_life": "~48 minutes", "molecular_weight": 3949.4, "cas_number": "151126-32-8", "mechanism_of_action": "Pramlintide mimics the physiological actions of endogenous amylin at amylin receptors, which are calcitonin receptor/RAMP heterodimers expressed in the area postrema and nucleus tractus solitarius. Activation produces three coordinated effects: slowing of gastric emptying to blunt post-prandial glucose excursions, suppression of inappropriate glucagon secretion from pancreatic alpha cells, and satiety signaling through hypothalamic pathways distinct from those activated by GLP-1 receptor agonists. The dual amylin-and-satiety mechanism complements insulin's glucose-lowering action without increasing hypoglycemia risk on its own, though severe hypoglycemia can occur when mealtime insulin is not reduced appropriately.", "evidence": [ { "claim": "Type 1 diabetes glycemic control", "level": "strong", "basis": "Whitehouse et al. Diabetes Care 2002 + Ratner 2005 multi-RCT program; FDA-approved 2005; first non-insulin T1D therapy" }, { "claim": "Type 2 diabetes glycemic control and weight loss", "level": "strong", "basis": "Hollander et al. Diabetes Care 2003: 1-year RCT; HbA1c -0.4-0.7%, weight loss 3.7 kg vs placebo" }, { "claim": "Gastric emptying inhibition", "level": "strong", "basis": "Kong et al. Diabet Med 2002: established gastric emptying delay in both T1D and T2D patients; consistent mechanism" }, { "claim": "Glucagon suppression", "level": "moderate", "basis": "Multiple Phase 3 mechanistic studies; established amylin-receptor pharmacology in the area postrema/NTS" }, { "claim": "Satiety and appetite suppression", "level": "moderate", "basis": "Multiple RCTs show reduced caloric intake; mechanism via amylin receptor in brainstem distinct from GLP-1" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "70691388", "drugbank": "DB01278", "wikidata": "Q2062094", "wikipedia": "https://en.wikipedia.org/wiki/Pramlintide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/pramlintide" }, { "name": "PT-141", "slug": "pt-141", "aliases": [ "Bremelanotide", "Vyleesi" ], "category": "sexual-health", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved as Vyleesi (2019) for HSDD in premenopausal women. Available by prescription. Also available from compounding pharmacies for broader use.", "routes": [ "subcutaneous", "nasal" ], "half_life": "~2.7 hours", "molecular_weight": 1025.18, "cas_number": "189691-06-3", "mechanism_of_action": "PT-141 exerts its pro-sexual effects primarily by activating melanocortin-4 receptors (MC4R) in key hypothalamic nuclei, including the medial preoptic area (mPOA), the paraventricular nucleus (PVN), and the arcuate nucleus. MC4R is a Gs-coupled receptor; its activation elevates intracellular cAMP, which in the mPOA triggers downstream release of dopamine into the mesolimbic and nigrostriatal pathways. This dopaminergic surge is directly responsible for the motivational and desire-amplifying effects of PT-141 — paralleling how endogenous α-MSH participates in arousal states. This mechanism is entirely distinct from PDE5 inhibitors like sildenafil, which amplify nitric oxide–cGMP signaling in penile smooth muscle without engaging motivational circuitry.\n\nMC4R knockout mouse studies have confirmed that MC4R is necessary for both the erectile and libido-enhancing effects of bremelanotide: animals lacking MC4R show no response to PT-141, establishing that this receptor is the functional target rather than an epiphenomenon. PT-141 also binds MC3R with lower affinity; MC3R modulation may contribute to anti-inflammatory signaling and to the complex appetite-suppression effects occasionally reported by users. The peptide does not meaningfully activate MC1R (tanning/pigmentation) or MC2R (ACTH/cortisol), which is why melanogenesis is far less pronounced with PT-141 than with its precursor Melanotan II.\n\nPharmacokintetically, PT-141 reaches peak plasma concentration (Cmax) approximately 1 hour after subcutaneous injection and has a terminal half-life of ~2.7 hours. It crosses the blood-brain barrier to achieve hypothalamic concentrations sufficient for receptor activation within 30–45 minutes post-injection. Nausea — the most prominent adverse effect — arises from MC4R activation in the dorsal motor nucleus of the vagus nerve, which controls gastric motility; this central vagal mechanism explains why antiemetics that act peripherally are less effective than those with CNS activity. The transient blood-pressure elevation observed in clinical trials (~2–6 mmHg systolic) reflects MC4R-mediated sympathetic activation and resolves within 12 hours.", "evidence": [ { "claim": "Treatment of hypoactive sexual desire disorder (HSDD) in premenopausal women", "level": "strong", "basis": "RECONNECT trials (Clayton et al. Obstet Gynecol 2019): two identical Phase 3 RCTs, n=1,267; FDA-approved as Vyleesi 2019; significant improvement in SSEs and FSDS-DAO distress scores" }, { "claim": "Erectile function improvement in men with PDE5i non-response", "level": "moderate", "basis": "Diamond et al. Int J Impot Res 2004: Phase 2 proof-of-concept, n=62 sildenafil non-responders; 62% vs 21% placebo response by RigiScan" }, { "claim": "Central (CNS-mediated) arousal without direct vascular action", "level": "moderate", "basis": "MC4R knockout studies and dopaminergic mechanism confirmed; Phase 2 dose-ranging study (Clayton et al. J Womens Health 2016) in 327 women with HSDD" }, { "claim": "Blood pressure elevation (transient safety concern)", "level": "strong", "basis": "52-week open-label extension (Simon et al. 2019, n=684): consistent 2–6 mmHg systolic BP rise resolving within 12 hours; basis for contraindication in hypertensive patients" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "9941379", "drugbank": "DB11653", "wikidata": "Q415353", "wikipedia": "https://en.wikipedia.org/wiki/Bremelanotide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/pt-141" }, { "name": "PTD-DBM", "slug": "ptd-dbm", "aliases": [ "PTD-DBM peptide", "CXXC5-Dvl inhibitor peptide" ], "category": "skin", "subcategories": [], "legal_status": "research-only", "legal_notes": "Not approved for human therapeutic use in any jurisdiction. Available from research chemical suppliers for in vitro and animal study purposes only. No regulatory pathway currently open for human use.", "routes": [ "topical" ], "half_life": "Not established in humans", "molecular_weight": 3082.62, "cas_number": "1609454-11-6", "mechanism_of_action": "CXXC5 is a zinc-finger protein that acts as a negative feedback regulator of the Wnt/β-catenin pathway by binding Dishevelled (Dvl), an upstream scaffold protein. Elevated CXXC5 expression in the balding scalp suppresses follicle regeneration by blocking Wnt target gene transcription. PTD-DBM contains an eight-arginine PTD sequence (RRRRRRRR) that enables membrane transduction and penetration into follicular cells, fused to a DBM segment (RKTGHQICKFRK) that competitively displaces CXXC5 from Dvl. Releasing this brake reactivates Wnt/β-catenin signaling, driving hair follicle stem cell proliferation, anagen phase extension, and wound-induced hair neogenesis. Combined treatment with valproic acid, a GSK-3β inhibitor that further amplifies Wnt/β-catenin signaling, produces additive hair regrowth in murine models.", "evidence": [ { "claim": "Promotes hair regrowth in mice", "level": "preliminary", "basis": "Yonsei preclinical study (J Invest Dermatol 2017) showed regrowth comparable to minoxidil in C57BL/6" }, { "claim": "Reactivates Wnt/β-catenin signaling", "level": "preliminary", "basis": "Mechanistic rodent and in vitro studies confirm CXXC5-Dvl disruption and β-catenin activation" }, { "claim": "Synergy with valproic acid", "level": "preliminary", "basis": "Preclinical mouse study showed >2-fold follicle neogenesis vs vehicle with combination" }, { "claim": "Target relevance in human AGA scalp", "level": "preliminary", "basis": "2023 PMC study confirmed CXXC5 overexpression in human androgenetic alopecia biopsies" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ptd-dbm" }, { "name": "Retatrutide", "slug": "retatrutide", "aliases": [ "LY3437943", "Triple G agonist" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Retatrutide is an investigational drug (IND) under active Phase 3 development by Eli Lilly. It is not FDA-approved and not legally available outside clinical trials in the US. Research chemical suppliers offer compounded or synthesized versions without regulatory oversight; quality and safety cannot be verified.", "routes": [ "subcutaneous" ], "half_life": "~6 days", "molecular_weight": 4894.58, "cas_number": "2381089-83-2", "mechanism_of_action": "Retatrutide activates three complementary hormone receptors in a single molecule. GLP-1 receptor agonism slows gastric emptying, suppresses appetite via hypothalamic satiety pathways, and stimulates glucose-dependent insulin secretion. GIP receptor agonism potentiates GLP-1-driven insulin release, improves beta-cell function, and may reduce GLP-1-associated nausea. Glucagon receptor agonism increases hepatic glucose output and stimulates thermogenesis — effects that would raise blood glucose in isolation but are counterbalanced by the insulinotropic GLP-1/GIP axes. The net metabolic result is pronounced energy deficit, enhanced fat oxidation, and superior weight loss versus dual-agonists. A C18 fatty acid chain binds reversibly to serum albumin, extending the half-life to ~6 days and enabling once-weekly subcutaneous dosing.", "evidence": [ { "claim": "Weight loss in obesity", "level": "moderate", "basis": "Eli Lilly Phase 3 TRIUMPH-1 topline (May 2026): retatrutide 12 mg produced 28.3% mean body weight loss at 80 weeks, with 45.3% reaching at least 30% weight loss; investigational, not FDA-approved. Earlier Jastreboff et al. NEJM 2023 Phase 2 showed 24.2% at 48 weeks." }, { "claim": "Glycemic improvement in type 2 diabetes", "level": "moderate", "basis": "Phase 2 T2D arm (Rosenstock et al. Lancet 2023): n=281; retatrutide 12 mg reduced HbA1c by 2.02% vs 0.45% placebo at 36 weeks" }, { "claim": "Cardiovascular risk reduction", "level": "preliminary", "basis": "No cardiovascular outcomes trial data; Phase 3 TRIUMPH program underway; indirect inference from metabolic improvements and MACE precedent for GLP-1 class" }, { "claim": "Non-alcoholic fatty liver disease (MASLD/NASH) improvement", "level": "preliminary", "basis": "Phase 2 exploratory imaging data showing liver fat reduction; Phase 3 MASH-specific trials planned but not yet reported" }, { "claim": "Long-term safety and durability", "level": "preliminary", "basis": "Phase 3 TRIUMPH-1 and TRIUMPH-4 topline data are available, but peer-reviewed long-term durability and outcomes data remain limited; triple agonism is novel, and the glucagon component raises theoretical hepatic and cardiovascular monitoring questions" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "171390338", "drugbank": "DB18993", "wikidata": "Q120468350", "wikipedia": "https://en.wikipedia.org/wiki/Retatrutide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/retatrutide" }, { "name": "Retinalamin", "slug": "retinalamin", "aliases": [ "retina polypeptide complex", "retinal bioregulator" ], "category": "other", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Registered pharmaceutical in Russia for retinal degenerative diseases. Not FDA-approved. Available in Western markets as a research chemical only. Cannot be sold or prescribed for therapeutic purposes in the US or EU.", "routes": [ "intramuscular" ], "half_life": "Unknown (polypeptide complex — not characterized pharmacokinetically in Western literature)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Retinalamin is a complex of water-soluble polypeptide fractions with molecular weight below 10,000 Da, isolated from bovine retina by Khavinson's extraction method. It activates ocular tissue metabolism, normalizes cellular membrane function, improves intracellular protein synthesis, and regulates lipid peroxide oxidation in photoreceptor and pigment epithelial cells. By improving the functional interaction between the retinal pigment epithelium (RPE) and the outer segments of visual photoreceptors, it helps restore phototransduction efficiency. It also normalizes retinal vascular permeability, reducing macular edema. The preparation penetrates retinal layers after intramuscular injection, exerting tissue-specific bioregulatory effects on photoreceptor renewal and RPE metabolic activity.", "evidence": [ { "claim": "Improves visual function in AMD", "level": "preliminary", "basis": "Russian observational series reports improvement in up to 80% of patients; no RCTs" }, { "claim": "Reduces diabetic retinopathy macular edema", "level": "preliminary", "basis": "Russian combined peptide study (n=104) showed visual acuity improvement; not randomized" }, { "claim": "Neuroprotects retinal photoreceptors", "level": "preliminary", "basis": "Khavinson preclinical and small clinical series (Neuro Endocrinol Lett 2008)" }, { "claim": "Normalizes retinal vascular permeability", "level": "preliminary", "basis": "Mechanistic animal studies; not validated in Western peer-reviewed clinical trials" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/retinalamin" }, { "name": "RGDS", "slug": "rgds", "aliases": [ "Arg-Gly-Asp-Ser", "Arginylglycylaspartylserine", "RGD-Ser", "RGDS tetrapeptide" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "RGDS is a research peptide used in laboratory and biomaterials science contexts. It is not approved for human therapeutic use. Available from peptide suppliers as a research reagent.", "routes": [ "intravenous", "topical" ], "half_life": "minutes (in vivo); stable when tethered to surfaces", "molecular_weight": 433.44, "cas_number": "91037-65-9", "mechanism_of_action": "RGDS competes with extracellular matrix proteins (fibronectin, vitronectin, fibrinogen) for binding to integrin receptors — particularly αvβ3, αvβ5, α5β1, and αIIbβ3. The Asp residue forms a key salt bridge with the integrin metal ion-dependent adhesion site (MIDAS), while Arg contributes electrostatic interactions. In solution, RGDS acts as a competitive antagonist of cell-matrix adhesion. When tethered to biomaterial surfaces, it promotes controlled cell attachment. The Ser residue at the C-terminus confers selectivity for certain integrin subtypes compared to RGD alone.", "evidence": [ { "claim": "Minimal consensus integrin-binding motif", "level": "strong", "basis": "Foundational Pierschbacher-Ruoslahti 1984 work and decades of integrin research" }, { "claim": "Competes with ECM proteins for integrin binding", "level": "strong", "basis": "Consistent biochemistry, structural biology, and MIDAS domain studies" }, { "claim": "Pharmacophore inspired FDA-approved antithrombotics", "level": "strong", "basis": "Eptifibatide and tirofiban are FDA-approved RGD-based αIIbβ3 antagonists" }, { "claim": "Tunes cell adhesion on biomaterial surfaces", "level": "strong", "basis": "Widespread tissue engineering literature demonstrating dose-response adhesion" }, { "claim": "No clinical development of RGDS itself", "level": "strong", "basis": "Regulatory record; RGDS remains a research reagent with no IND advancement" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/rgds" }, { "name": "Romidepsin", "slug": "romidepsin", "aliases": [ "Istodax", "FK228", "FR901228", "NSC-630176", "depsipeptide" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since 2009 (CTCL) and 2011 (PTCL). Administered intravenously in an oncology setting. Not a controlled substance. Requires baseline and periodic ECG monitoring due to risk of QT prolongation. Electrolyte management recommended.", "routes": [ "intravenous" ], "half_life": "~3 hours", "molecular_weight": 540.71, "cas_number": "128517-07-7", "mechanism_of_action": "Romidepsin is a natural product bicyclic depsipeptide that functions as a prodrug. Upon cellular uptake, its disulfide bridge is reduced by intracellular glutathione, releasing the reduced thiol form, which then chelates the zinc ion in the active sites of class I HDAC enzymes (primarily HDAC1 and HDAC2). Inhibition of HDACs prevents the removal of acetyl groups from lysine residues on histone tails, resulting in hyperacetylation of histones, chromatin relaxation, and altered transcription of genes involved in cell cycle control and apoptosis. This leads to upregulation of p21 (cell cycle arrest), activation of intrinsic and extrinsic apoptotic pathways, and downregulation of anti-apoptotic proteins in T-cell lymphoma cells. Because malignant T cells show heightened dependence on HDAC1/2 activity, romidepsin exhibits selective cytotoxicity in this context.", "evidence": [ { "claim": "34-35% response rate in refractory CTCL", "level": "strong", "basis": "Two single-arm pivotal trials supported 2009 FDA approval; responses often durable" }, { "claim": "25% response rate in relapsed PTCL", "level": "moderate", "basis": "Single-arm Phase II study supported 2011 FDA PTCL approval in patients with prior therapy" }, { "claim": "Class I HDAC inhibition via glutathione activation", "level": "strong", "basis": "Prodrug mechanism and zinc chelation characterized in biochemical and cellular studies" }, { "claim": "QT prolongation requires cardiac monitoring", "level": "strong", "basis": "Pivotal trials and FDA label mandate baseline ECG and electrolyte management before each dose" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/romidepsin" }, { "name": "Secretin", "slug": "secretin", "aliases": [ "ChiRhoStim", "Human Secretin", "Synthetic Human Secretin" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "ChiRhoStim (synthetic human secretin) is FDA-approved for diagnostic use via intravenous injection. It is a prescription-only medication. Not approved for therapeutic or off-label self-administration.", "routes": [ "intravenous" ], "half_life": "~45 minutes", "molecular_weight": 3039.44, "cas_number": "108153-74-8", "mechanism_of_action": "Secretin binds the secretin receptor (SCTR), a class B GPCR expressed on pancreatic ductal cells, bile duct cells, and gastric mucosa. Receptor activation increases intracellular cAMP via Gs coupling, stimulating pancreatic acinar cells to secrete bicarbonate-rich fluid into the duodenum to neutralize gastric acid. Secretin also inhibits gastrin release, reducing gastric acid secretion. In the liver, it promotes bile bicarbonate secretion. Central actions include modulating satiety and water homeostasis.", "evidence": [ { "claim": "FDA-approved diagnostic for pancreatic function", "level": "strong", "basis": "ChiRhoStim FDA-approved for exocrine pancreatic function testing with over a century of clinical use" }, { "claim": "FDA-approved for ERCP facilitation", "level": "strong", "basis": "Synthetic human secretin approved for endoscopic retrograde cholangiopancreatography procedural aid" }, { "claim": "Diagnostic for Zollinger-Ellison syndrome", "level": "strong", "basis": "Long-established FDA-approved provocation test using paradoxical gastrin rise to identify gastrinoma" }, { "claim": "Stimulates pancreatic bicarbonate via SCTR", "level": "strong", "basis": "Foundational endocrinology since 1902 discovery; Gs-cAMP mechanism fully characterized" }, { "claim": "Autism trials inconsistent, not approved", "level": "moderate", "basis": "Multiple RCTs failed to show benefit in autism spectrum disorder; not approved for this indication" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/secretin" }, { "name": "Selank", "slug": "selank", "aliases": [ "TP-7" ], "category": "cognitive", "subcategories": [ "immune" ], "legal_status": "research-only", "legal_notes": "Approved in Russia as an anxiolytic nasal spray. Not FDA-approved. Available as a research peptide in the US. No regulatory scheduling.", "routes": [ "nasal", "subcutaneous" ], "half_life": "~5-10 minutes (but effects last hours due to downstream signaling)", "molecular_weight": 751.87, "cas_number": "129954-34-3", "mechanism_of_action": "Selank modulates the expression of brain-derived neurotrophic factor (BDNF) and affects the balance of T-helper cell cytokines. It influences the GABAergic system (similar to benzodiazepines but without sedation or dependence), modulates serotonin and dopamine metabolism, and enhances enkephalin stability. The immunomodulatory effects come from its tuftsin backbone, which stimulates phagocytosis.", "evidence": [ { "claim": "Anxiolytic effects in generalized anxiety disorder", "level": "moderate", "basis": "Zozulia et al. Zh Nevrol Psikhiatr 2008 (PMID 18454096): Russian RCT, n=62 patients with GAD and neurasthenia; selank comparable to benzodiazepines without sedation or dependence" }, { "claim": "Immune modulation (BDNF / enkephalin expression)", "level": "preliminary", "basis": "Zolotarev et al. Curr Pharm Des 2018 (PMID 30255741): review of mechanism data including enkephalin degradation inhibition and cytokine modulation; limited human evidence" }, { "claim": "Cognitive enhancement and attention improvement", "level": "preliminary", "basis": "Small open-label studies (n<40) in Russia showing improved attention and working memory; data in non-peer-reviewed sources or non-indexed Russian journals" }, { "claim": "Alcohol withdrawal symptom reduction", "level": "preliminary", "basis": "Semenova et al. Bull Exp Biol Med 2014 (PMID 24913576): rat model of alcohol motivation/withdrawal; no controlled human trials for this indication" } ], "peer_reviewed_reference_count": 6, "external_ids": { "pubchem_cid": "11765600", "wikidata": "Q5810370", "wikipedia": "https://en.wikipedia.org/wiki/Selank" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/selank" }, { "name": "Semaglutide", "slug": "semaglutide", "aliases": [ "Ozempic", "Wegovy", "Rybelsus" ], "category": "weight-loss", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved as Ozempic and Rybelsus for type 2 diabetes and as Wegovy for chronic weight management, with label-specific cardiovascular-risk indications. Requires prescription. The FDA's shortage-list removal ended broad shortage-based mass compounding; ongoing access now centers on approved brands and narrow patient-specific pharmacy law.", "routes": [ "subcutaneous", "oral" ], "half_life": "~7 days", "molecular_weight": 4113.58, "cas_number": "910463-68-2", "mechanism_of_action": "Semaglutide's therapeutic effects arise from agonism at the GLP-1 receptor (GLP-1R), a class B G-protein-coupled receptor (GPCR) coupled to Gs proteins. Upon binding, semaglutide activates adenylyl cyclase, elevating intracellular cAMP, which activates protein kinase A (PKA) and downstream signaling cascades that differ by tissue type.\n\nIn pancreatic beta cells, PKA phosphorylates CREB and promotes translocation of insulin secretory granules to the plasma membrane — increasing insulin secretion specifically in response to glucose (glucose-dependent insulinotropia). Simultaneously, GLP-1R agonism in pancreatic alpha cells suppresses glucagon secretion, reducing hepatic glucose output. The combined effect is substantially improved glycemic control without the hypoglycemia risk of sulfonylureas (which force insulin secretion regardless of glucose levels). Beta cell mass preservation — observed in animal models via reduced apoptosis and increased proliferation — is a mechanistically important effect that may slow T2D progression, though its translation to humans over multi-year treatment remains under investigation.\n\nIn the central nervous system, GLP-1R is expressed in the hypothalamic arcuate nucleus, the nucleus of the solitary tract (NTS), and the area postrema — brain regions governing appetite, satiety, and autonomic function. Semaglutide activates pro-opiomelanocortin (POMC) neurons and inhibits neuropeptide Y (NPY)/AgRP neurons in the arcuate nucleus, shifting the hypothalamic energy balance set point toward satiety. GLP-1R activation in the NTS signals meal-induced fullness via vagal afferent pathways. Together, these central effects reduce caloric intake by 20–30% in treated patients — a magnitude comparable to surgical interventions.\n\nGastric emptying is slowed via GLP-1R in the enteric nervous system and vagal efferents, contributing to early satiety (smaller meal volume before fullness) and reduced postprandial glucose excursions. Cardiovascular benefits appear to involve GLP-1R in cardiac muscle, vascular endothelium, and macrophages: anti-inflammatory effects, reduced foam cell formation in atherosclerotic plaques, improved endothelial function, and mild reduction in heart rate (3–5 bpm) and blood pressure (2–4 mmHg systolic) all contribute to the MACE risk reduction observed in SELECT and SUSTAIN-6.", "evidence": [ { "claim": "Weight loss in obesity", "level": "strong", "basis": "STEP 1-5 RCTs: 1,961-4,567 participants, 14.9-16% body weight loss" }, { "claim": "Cardiovascular risk reduction", "level": "strong", "basis": "SUSTAIN-6: 3,297 patients, 26% reduction in major adverse cardiovascular events" }, { "claim": "Type 2 diabetes glycemic control", "level": "strong", "basis": "Multiple Phase 3 RCTs; FDA-approved for T2D since 2017" }, { "claim": "Kidney disease progression", "level": "moderate", "basis": "FLOW trial: 3,533 patients, 24% reduction in kidney events vs placebo" }, { "claim": "Non-alcoholic fatty liver disease", "level": "moderate", "basis": "Phase 2 data showing significant liver fat reduction; Phase 3 ongoing" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "56843331", "drugbank": "DB13928", "wikidata": "Q27261089", "wikipedia": "https://en.wikipedia.org/wiki/Semaglutide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/semaglutide" }, { "name": "Semax", "slug": "semax", "aliases": [ "ACTH 4-10 Pro-Gly-Pro" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Approved as a prescription drug in Russia and Ukraine. Not FDA-approved. Available as a research peptide in the US. Not scheduled.", "routes": [ "nasal", "subcutaneous" ], "half_life": "~2-3 minutes (rapid enzymatic degradation, but downstream effects persist)", "molecular_weight": 813.93, "cas_number": "80714-61-0", "mechanism_of_action": "Semax's cognitive and neuroprotective effects emerge from convergent actions on monoaminergic neurotransmission and neurotrophic factor expression. At the neurotransmitter level, Semax acutely activates serotonergic and dopaminergic systems in limbic and cortical circuits. Dolotov et al. (Neurosci Lett, 2006) demonstrated that Semax administration raised hippocampal 5-hydroxyindoleacetic acid (5-HIAA, the primary serotonin metabolite) to approximately 180% of baseline within 1 hour — a finding consistent with the subjective anxiolytic-plus-focusing quality users describe. Dopaminergic activation in the prefrontal cortex and striatum contributes to improved executive function and working memory, without the receptor downregulation or rebound that accompanies direct dopamine-releasing agents.\n\nThe BDNF axis represents Semax's most distinctive and durable mechanism. BDNF (brain-derived neurotrophic factor) is the primary growth factor supporting hippocampal neurogenesis, dendritic spine density, and long-term potentiation — the cellular substrate of learning and memory. Mironova et al. (Brain Res, 2007) quantified BDNF mRNA and protein in rat hippocampus following Semax administration, finding increases of 50–200% above baseline peaking at 1–3 hours post-dose, with elevation persisting for 24+ hours after the peptide itself had been cleared. This dissociation — rapid clearance of the peptide, prolonged elevation of the effector molecule — is the mechanistic explanation for Semax's clinical dosing cycles: even short courses induce sustained neuroplastic adaptations that outlast the drug's pharmacokinetic window. TrkB (the high-affinity BDNF receptor) expression is also upregulated by Semax, amplifying the sensitivity of target neurons to endogenous BDNF.\n\nIn ischemic and hypoxic contexts, Semax provides neuroprotection through multiple mechanisms: reduction of pro-inflammatory cytokine release (IL-1β, TNF-α), attenuation of glutamate-mediated excitotoxicity, and upregulation of antioxidant defense pathways. Sokolova et al. (2024) demonstrated in a middle cerebral artery occlusion (MCAO) rat model that intranasal Semax reduced infarct volume, improved neurological deficit scores, and decreased markers of oxidative damage versus saline-treated controls. The intranasal route achieves CNS bioavailability via olfactory epithelium transcytosis and perineural transport along the olfactory nerve, with approximately 0.093% of intranasal dose reaching brain tissue within 2 minutes — sufficient for pharmacological activity given the picomolar-to-nanomolar affinity of Semax for its receptors.", "evidence": [ { "claim": "Neurological recovery in acute ischemic stroke", "level": "moderate", "basis": "Gusev et al. Zh Nevrol Psikhiatr 1996: RCT, n=110 acute ischemic stroke patients; intranasal Semax vs placebo showed improved Barthel Index and NIHSS scores at 30-day follow-up" }, { "claim": "Cognitive enhancement in cerebrovascular impairment", "level": "moderate", "basis": "Zh Nevrol Psikhiatr 1999 (PMID 10358912): placebo-controlled trial, n=32; 10-day intranasal 900 mcg/day improved attention, short-term memory, processing speed" }, { "claim": "BDNF and neurotrophic factor upregulation", "level": "preliminary", "basis": "Mironova et al. Brain Res 2007 (PMID 16996037): rat hippocampal BDNF mRNA increased 50–200% within 1–3 hours of single intranasal Semax dose (50 mcg/kg)" }, { "claim": "Anxiolytic and mood stabilization", "level": "preliminary", "basis": "Dolotov et al. Neurosci Lett 2006 (PMID 16362768): rat model; serotonergic activation to ~180% baseline in limbic structures; no human RCT for this indication" } ], "peer_reviewed_reference_count": 6, "external_ids": { "pubchem_cid": "122178", "wikidata": "Q4415058", "wikipedia": "https://en.wikipedia.org/wiki/Semax" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/semax" }, { "name": "Semax 4-7", "slug": "semax-4-7", "aliases": [ "ACTH(4-7)", "ACTH 4-7", "ACTH fragment 4-7", "Met-Glu-His-Phe" ], "category": "cognitive", "subcategories": [], "legal_status": "research-only", "legal_notes": "Semax 4-7 is not approved by the FDA and is classified as a research compound. Not listed as a controlled substance in the US but is in a legal gray zone as an unscheduled peptide research chemical.", "routes": [ "nasal" ], "half_life": "~Minutes (shorter than Semax due to lack of C-terminal Pro-Gly-Pro stabilization)", "molecular_weight": 599.72, "cas_number": null, "mechanism_of_action": "Studies suggest ACTH(4-7) interacts with melanocortin receptors (particularly MC4R in the brain) and modulates BDNF signaling, dopaminergic and serotonergic neurotransmission. Research suggests this tetrapeptide sequence is responsible for attention-enhancing and memory-consolidating effects attributed to ACTH analogs. It may enhance synaptic plasticity by upregulating neurotrophin expression. The Pro-Gly-Pro C-terminal extension in standard Semax primarily confers metabolic stability rather than adding distinct pharmacological activity.", "evidence": [ { "claim": "Active pharmacophore of Semax", "level": "moderate", "basis": "Russian research establishing ACTH(4-7) as core pharmacologically active fragment" }, { "claim": "Modulates melanocortin MC4R signaling", "level": "preliminary", "basis": "In vitro receptor binding and rodent behavioral studies" }, { "claim": "Upregulates BDNF and neuroplasticity", "level": "preliminary", "basis": "Rodent hippocampal expression studies; limited standalone human data" }, { "claim": "Enhances attention and memory", "level": "insufficient", "basis": "Human evidence is for full Semax, not isolated tetrapeptide" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/semax-4-7" }, { "name": "Sermorelin", "slug": "sermorelin", "aliases": [ "GRF 1-29", "Geref" ], "category": "muscle", "subcategories": [ "longevity" ], "legal_status": "reclassification-pending", "legal_notes": "Previously FDA-approved (Geref, 1997). Discontinued commercially in 2008 but still available through compounding pharmacies. Under reclassification review.", "routes": [ "subcutaneous" ], "half_life": "~10-20 minutes", "molecular_weight": 3357.88, "cas_number": "86168-78-7", "mechanism_of_action": "Sermorelin binds to the GHRH receptor on anterior pituitary somatotroph cells, stimulating the synthesis and pulsatile release of endogenous growth hormone. Unlike exogenous GH administration, sermorelin preserves the hypothalamic-pituitary feedback loop, maintaining physiological GH regulation. It stimulates all five somatotroph cell subtypes.", "evidence": [ { "claim": "Growth hormone secretion in GH-deficient children", "level": "strong", "basis": "Thorner et al. J Pediatrics 1996: multicenter RCT in GH-deficient children, accelerated growth vs placebo; FDA-approved for pediatric GHD" }, { "claim": "GH and IGF-1 increase in aging adults", "level": "moderate", "basis": "Khorram et al. JCEM 1997: long-term administration in age-advanced men and women (n=30); significant GH/IGF-1 increases with improved body composition" }, { "claim": "Improved sleep quality", "level": "preliminary", "basis": "Rosen et al. Neuroendocrinology 1997: sermorelin augmented slow-wave sleep in 5 healthy young men; small n, no RCT" }, { "claim": "Cognitive function improvement in mild cognitive impairment", "level": "preliminary", "basis": "Friedman et al. JAMA Neurology 2013: pilot RCT, n=48 adults with MCI; improved GABA levels and executive function scores vs placebo" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/sermorelin" }, { "name": "SNAP-8", "slug": "snap-8", "aliases": [ "Acetyl Octapeptide-3", "Acetyl Glutamyl Heptapeptide-3", "Octapeptide-2" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "OTC cosmetic ingredient; no regulatory restrictions. Widely available in anti-aging serums and creams globally.", "routes": [ "topical" ], "half_life": "Not established (cosmetic topical use)", "molecular_weight": 1075.16, "cas_number": "868844-74-0", "mechanism_of_action": "SNAP-8 mimics the N-terminal end of SNAP-25, a protein integral to the SNARE complex responsible for vesicular release of acetylcholine at the neuromuscular junction. By competing with endogenous SNAP-25 for a position in the SNARE complex, SNAP-8 partially destabilizes complex formation. This reduces efficiency of neurotransmitter release, attenuating the signal that drives facial muscle contraction. The result is a mild, reversible reduction in the intensity of expression-driven muscle movement, which over time diminishes the depth of dynamic wrinkles without paralysis.", "evidence": [ { "claim": "63% wrinkle depth reduction in 28 days", "level": "preliminary", "basis": "Single 28-day manufacturer-sponsored topical study; no independent peer-reviewed RCT" }, { "claim": "SNARE complex destabilization mechanism", "level": "preliminary", "basis": "In vitro biochemical studies show competitive interference with SNAP-25 in SNARE assembly" }, { "claim": "~30% more potent than Argireline", "level": "preliminary", "basis": "In vitro SNARE inhibition assays; no head-to-head clinical comparison performed" }, { "claim": "Safe as cosmetic ingredient", "level": "moderate", "basis": "EU Cosmetic Ingredient Review and global regulatory approvals confirm topical safety" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/snap-8" }, { "name": "Somatostatin", "slug": "somatostatin", "aliases": [ "SRIF", "Somatotropin Release-Inhibiting Factor", "SST-14", "SST-28", "Growth Hormone-Inhibiting Hormone" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Native somatostatin is used in research and as an IV infusion in some clinical protocols outside the US. Synthetic long-acting analogs are the approved clinical agents. Not FDA-approved as a standalone drug.", "routes": [ "intravenous" ], "half_life": "1–3 minutes", "molecular_weight": 1637.91, "cas_number": "38916-34-6", "mechanism_of_action": "Somatostatin binds five G-protein-coupled receptor subtypes (SSTR1–5) expressed throughout the brain, pituitary, pancreas, and gut. Receptor activation inhibits adenylyl cyclase, reduces intracellular cAMP, inhibits voltage-gated calcium channels, and activates inward-rectifier potassium channels. Net effect is broad inhibition of GH, insulin, glucagon, gastrin, secretin, TSH, and prolactin secretion. SST-14 preferentially binds SSTR1–4; SST-28 has higher affinity for SSTR5.", "evidence": [ { "claim": "Broadly inhibits GH, insulin, glucagon secretion", "level": "strong", "basis": "Decades of endocrine physiology research and consistent clinical data" }, { "claim": "Binds five SSTR receptor subtypes", "level": "strong", "basis": "IUPHAR-recognized receptor pharmacology with extensive characterization" }, { "claim": "Validated target via approved analogs", "level": "strong", "basis": "FDA-approved octreotide, lanreotide, pasireotide confirm pharmacology" }, { "claim": "Controls acute variceal GI bleeding", "level": "moderate", "basis": "Consistent clinical use via IV infusion outside US for GI hemorrhage" }, { "claim": "Ultrashort 1-3 minute plasma half-life", "level": "strong", "basis": "Well-characterized pharmacokinetics driving analog development" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/somatostatin" }, { "name": "SS-31", "slug": "ss-31", "aliases": [ "Elamipretide", "Bendavia", "MTP-131" ], "category": "longevity", "subcategories": [ "recovery" ], "legal_status": "research-only", "legal_notes": "Investigational drug in clinical trials (Stealth BioTherapeutics). Not yet FDA-approved. Orphan drug designation for Barth syndrome. Not available as a standard research peptide from most suppliers.", "routes": [ "subcutaneous", "intravenous" ], "half_life": "~4 hours", "molecular_weight": 640.75, "cas_number": "736992-21-5", "mechanism_of_action": "SS-31 selectively binds to cardiolipin, a phospholipid unique to the inner mitochondrial membrane that is essential for electron transport chain (ETC) function. By stabilizing cardiolipin interactions with cytochrome c, SS-31 optimizes electron transfer, reduces electron leak and reactive oxygen species (ROS) production, and improves ATP synthesis. It concentrates 1000-5000x in mitochondria relative to cytoplasm due to its alternating aromatic-cationic structure.", "evidence": [ { "claim": "Cardiolipin stabilization and ETC optimization", "level": "moderate", "basis": "Chavez et al. J Biol Chem 2020: direct lipid bilayer binding demonstrated; Szeto Br J Pharmacol 2014 mechanistic review" }, { "claim": "Barth syndrome cardiac benefit", "level": "moderate", "basis": "Phase III TAZPOWER trial (Stealth BioTherapeutics); improvements in cardiac function and exercise tolerance; orphan drug designation" }, { "claim": "Heart failure treatment benefit", "level": "preliminary", "basis": "Phase II PROGRESS-HF trial in heart failure; mixed results, failed primary endpoint in some readouts" }, { "claim": "Age-related macular degeneration improvement", "level": "preliminary", "basis": "Phase II ReCLAIM trial in dry AMD; early signal, not yet confirmed in pivotal trial" }, { "claim": "Doxorubicin cardiotoxicity protection", "level": "preliminary", "basis": "Liu et al. Oncol Lett 2021: animal model; p38 MAPK inhibition mechanism confirmed; no human oncology trial" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ss-31" }, { "name": "Substance P", "slug": "substance-p", "aliases": [ "SP", "Neurokinin P", "substance P undecapeptide" ], "category": "other", "subcategories": [], "legal_status": "research-only", "legal_notes": "Substance P is a research chemical used in preclinical pain and inflammation studies. Not approved for human administration. NK1 receptor antagonists derived from this research (e.g., aprepitant) are FDA-approved drugs.", "routes": [ "intravenous" ], "half_life": "~1–2 minutes (rapid degradation by neutral endopeptidase)", "molecular_weight": 1347.63, "cas_number": "33507-63-0", "mechanism_of_action": "Substance P acts primarily through the NK1 (neurokinin-1) receptor, a Gq-coupled GPCR, with lower affinity for NK2 and NK3. Binding to NK1R activates phospholipase C, raises intracellular calcium, and activates PKC, promoting neuronal excitation and synaptic facilitation. In primary afferent nociceptors, SP co-localizes with glutamate and CGRP, facilitating pain transmission to the dorsal horn. Peripheral SP release from afferent nerve endings triggers mast cell degranulation, vasodilation, plasma extravasation, and immune cell recruitment — the hallmarks of neurogenic inflammation.", "evidence": [ { "claim": "NK1 antagonists FDA-approved for CINV", "level": "strong", "basis": "Aprepitant and netupitant are FDA-approved antiemetics validating the SP-NK1R axis in chemotherapy nausea" }, { "claim": "Facilitates spinal pain transmission", "level": "moderate", "basis": "Decades of preclinical evidence show SP co-released with glutamate and CGRP in nociceptors drives dorsal-horn signaling" }, { "claim": "Drives neurogenic inflammation peripherally", "level": "moderate", "basis": "Established animal and in vitro data show NK1R-mediated mast cell degranulation and plasma extravasation" }, { "claim": "Elevated in fibromyalgia and IBS", "level": "preliminary", "basis": "Observational case-control studies report elevated CSF/plasma SP in fibromyalgia and inflammatory conditions" }, { "claim": "Promotes wound healing via NK1R", "level": "preliminary", "basis": "Animal and in vitro evidence suggests SP supports angiogenesis and tissue repair; no human trials" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/substance-p" }, { "name": "Survodutide", "slug": "survodutide", "aliases": [ "BI 456906", "BI-456906" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Investigational compound in Phase 3 clinical trials. Not approved for human use outside of clinical trials. An NDA was filed with FDA in Q1 2026 for the MASH indication (supported by Breakthrough Therapy designation). Obesity Phase 3 SYNCHRONIZE results are pending. Available only through authorized research programs. No compounding or research chemical availability.", "routes": [ "subcutaneous" ], "half_life": "~1 week (supports once-weekly dosing; Tmax ~51h in dogs, extended mean residence time)", "molecular_weight": null, "cas_number": "2805997-46-8", "mechanism_of_action": "Survodutide simultaneously activates two distinct receptor pathways. GLP-1 receptor agonism slows gastric emptying, enhances glucose-dependent insulin secretion, and reduces appetite via central hypothalamic signaling — effects shared with semaglutide and tirzepatide. The added glucagon receptor (GCGR) agonism introduces direct hepatic mechanisms not present in GLP-1-only agents: stimulation of mitochondrial fatty acid beta-oxidation, upregulation of energy expenditure through farnesoid X receptor (FXR) signaling, and induction of fibroblast growth factor 21 (FGF21) secretion. FGF21 is a key metabolic hormone that increases thermogenesis and improves insulin sensitivity. Together, the dual agonism increases both energy expenditure and reduces caloric intake, producing weight loss that may exceed GLP-1-only agents in certain populations.", "evidence": [ { "claim": "Weight loss via GLP-1/glucagon dual agonism", "level": "moderate", "basis": "Jastreboff Lancet Diabetes Endocrinol 2024 (Phase 2): 6.2-14.9% weight loss at 46 weeks across doses; dose-response confirmed" }, { "claim": "MASH/NASH liver improvement", "level": "moderate", "basis": "Sanyal NEJM 2024 Phase 2 MASH trial: 62% histological improvement at 4.8 mg vs 14% placebo; FDA Fast Track designation" }, { "claim": "Phase 3 obesity efficacy", "level": "preliminary", "basis": "SYNCHRONIZE-1 baseline characteristics published Obesity 2025 (Kushner); pivotal outcomes pending as of 2026" }, { "claim": "FGF21-mediated thermogenesis increase", "level": "preliminary", "basis": "Established glucagon receptor biology; mechanism supported by preclinical and Phase 1 PD markers; not isolated in human outcomes" }, { "claim": "Cardiovascular safety and outcomes", "level": "insufficient", "basis": "SYNCHRONIZE-CVOT ongoing; no completed cardiovascular outcomes trial as of 2026" } ], "peer_reviewed_reference_count": 3, "external_ids": { "pubchem_cid": "168429725", "drugbank": "DB18989", "wikidata": "Q123907235", "wikipedia": "https://en.wikipedia.org/wiki/Survodutide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/survodutide" }, { "name": "SYN-AKE", "slug": "syn-ake", "aliases": [ "Dipeptide Diaminobutyroyl Benzylamide Diacetate", "Syn-Ake", "Waglerin-1 analog" ], "category": "skin", "subcategories": [], "legal_status": "unregulated", "legal_notes": "OTC cosmetic ingredient. Approved for use in skincare formulations in EU, US, and major markets. The 'snake venom' branding is marketing — the active is a synthetic analog with no actual venom.", "routes": [ "topical" ], "half_life": "Not established (cosmetic topical use)", "molecular_weight": 495.58, "cas_number": "823202-99-9", "mechanism_of_action": "SYN-AKE acts as a competitive antagonist at the muscular nicotinic acetylcholine receptor (mnAChR). In normal neuromuscular transmission, acetylcholine binds mnAChR to trigger muscle fiber contraction. SYN-AKE competes for this receptor binding site, reducing the efficiency of signal transduction without blocking it completely. This partial inhibition attenuates facial muscle contractility in a reversible and dose-dependent manner, reducing the mechanical stress that deepens expression lines. In vitro studies showed up to 80% reduction in muscle contraction signaling at effective concentrations.", "evidence": [ { "claim": "Competitively antagonizes muscular nAChR", "level": "preliminary", "basis": "In silico and in vitro receptor-binding studies Gok 2023 J Biomol Struct Dyn" }, { "claim": "Up to 80% reduction in contraction signaling", "level": "preliminary", "basis": "In vitro receptor-binding assays at effective concentrations; no in vivo human confirmation" }, { "claim": "Wrinkle depth reduction in 28 days", "level": "preliminary", "basis": "28-day manufacturer clinical trial only; Kim 2024 Molecules confirms topical efficacy signal" }, { "claim": "Safe as OTC cosmetic ingredient", "level": "moderate", "basis": "Approved cosmetic ingredient in EU/US with standard safety-review clearance" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/syn-ake" }, { "name": "TB-500", "slug": "tb-500", "aliases": [ "Thymosin Beta-4", "Tβ4" ], "category": "recovery", "subcategories": [ "immune" ], "legal_status": "reclassification-pending", "legal_notes": "Under FDA reclassification review. Previously classified as a research chemical. Widely used in veterinary medicine.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~4 hours", "molecular_weight": 4963, "cas_number": "77591-33-4", "mechanism_of_action": "TB-500's primary molecular action is binding to G-actin (monomeric, unpolymerized actin) in a 1:1 stoichiometric ratio. G-actin constitutes approximately 50-70% of the total cellular actin pool in resting cells; Tβ4 sequesters a significant fraction of this pool, preventing premature polymerization into F-actin (filamentous actin) while keeping it available for rapid deployment. When a cell receives a migration signal — whether from a chemokine gradient, growth factor, or damage-associated molecular pattern — localized activation of actin nucleators (Arp2/3 complex, formins) at the cell's leading edge creates a sink for G-actin monomers. Tβ4 and TB-500 release their sequestered actin into this sink, fueling the explosive growth of branched actin networks that push the plasma membrane forward. This dramatically accelerates cell migration speed and persistence compared to cells depleted of Tβ4.\n\nDownstream of actin regulation, TB-500 promotes angiogenesis through upregulation of vascular endothelial growth factor (VEGF) and promotes the migration of endothelial cells, keratinocytes, and fibroblasts into wound sites. Studies in thymosin beta-4-treated dermal wound models show increased collagen deposition and more organized extracellular matrix architecture compared to controls. The peptide also modulates inflammatory signaling: studies demonstrate down-regulation of NF-κB-driven pro-inflammatory cytokines (TNF-α, IL-1β) and up-regulation of anti-inflammatory mediators, which reduces the chronic inflammatory state that impairs healing in diabetic or aged tissue.\n\nThe cardiac repair literature has revealed an additional mechanism not directly tied to actin sequestration. The Bock-Marquette et al. Nature (2004) study demonstrated that Tβ4 activates integrin-linked kinase (ILK), which promotes the survival and migration of epicardium-derived cardiac progenitor cells in the post-infarct heart. This ILK pathway activation leads to increased expression of anti-apoptotic proteins (Akt, surviving) in cardiomyocytes adjacent to the infarct zone, reducing the extent of programmed cell death. Subsequent coronary artery ligation studies in mice showed that Tβ4 treatment reduced infarct size by approximately 25%, preserved ejection fraction, and stimulated formation of new coronary microvessels in the peri-infarct region.\n\nTB-500's systemic action — it distributes through the bloodstream after subcutaneous injection and reaches injured tissue via the circulation — distinguishes it pharmacologically from locally-acting repair peptides. Because actin-sequestering capacity and cell migration signaling are relevant at every site of active tissue damage simultaneously, TB-500 can in principle accelerate healing across multiple concurrent injury sites. This systemic reach is the biological basis for its use in loading-dose protocols: higher initial doses are used to rapidly establish elevated systemic Tβ4 concentrations, followed by lower maintenance doses once tissue repair is underway.", "evidence": [ { "claim": "Wound healing", "level": "preliminary", "basis": "Animal models show accelerated dermal and corneal wound healing" }, { "claim": "Cardiac repair post-infarction", "level": "preliminary", "basis": "Mouse models of myocardial infarction; no human data" }, { "claim": "Anti-inflammatory effects", "level": "preliminary", "basis": "In vitro and animal studies via actin sequestration" }, { "claim": "Hair regrowth", "level": "insufficient", "basis": "Anecdotal reports; no published studies in humans" } ], "peer_reviewed_reference_count": 6, "external_ids": { "pubchem_cid": "16132341", "wikipedia": "https://en.wikipedia.org/wiki/TB-500" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/tb-500" }, { "name": "Teriparatide", "slug": "teriparatide", "aliases": [ "Forteo", "Bonsity", "PTH(1-34)", "rhPTH(1-34)", "Movymia" ], "category": "other", "subcategories": [ "longevity" ], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 021318, 2002) for treatment of osteoporosis in postmenopausal women, men with osteoporosis, and men and women with glucocorticoid-induced osteoporosis at high fracture risk. Prescription-only. Carries a boxed warning for osteosarcoma risk based on rat data. Lifetime use limited to 2 years.", "routes": [ "subcutaneous" ], "half_life": "~1 hour", "molecular_weight": 4117.8, "cas_number": "52232-67-4", "mechanism_of_action": "Teriparatide binds to the PTH1 receptor (PTH1R) on osteoblasts and osteoblast precursors, activating the Gs-protein/cAMP/PKA and Gq-protein/PLC/PKC pathways. Intermittent once-daily administration creates transient PTH1R stimulation that preferentially activates osteoblasts over osteoclasts, resulting in net bone formation. The drug increases osteoblast number by promoting differentiation from precursors and inhibiting osteoblast apoptosis, increases periosteal bone formation, and enhances cancellous connectivity. Continuous PTH exposure (unlike once-daily pulses) stimulates both formation and resorption; the pulsatile dosing exploits the anabolic window. Bone mineral density increases are seen at spine and hip within 3–6 months of treatment.", "evidence": [ { "claim": "Reduces vertebral fractures 65%", "level": "strong", "basis": "Pivotal Fracture Prevention Trial (Neer NEJM 2001, n=1,637) showed 65% vertebral reduction" }, { "claim": "Reduces non-vertebral fractures 53%", "level": "strong", "basis": "Fracture Prevention Trial showed 53% non-vertebral reduction over 21 months" }, { "claim": "Increases lumbar spine BMD ~9%", "level": "strong", "basis": "Multiple RCTs including VERO confirmed significant spine BMD increase within 18 months" }, { "claim": "Accelerates fracture repair", "level": "moderate", "basis": "Aspenberg JBMR 2010 RCT (n=102) showed distal radial fracture healing benefit" }, { "claim": "Superior to risedronate for severe osteoporosis", "level": "strong", "basis": "VERO trial (JBMR 2018) head-to-head vs risedronate showed fracture-risk superiority" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/teriparatide" }, { "name": "Terlipressin", "slug": "terlipressin", "aliases": [ "Terlivaz", "triglycyl-lysine-vasopressin", "glypressin" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved September 2022 (NDA 022231) for hepatorenal syndrome with rapid reduction in kidney function in adults. Available only in hospital settings under clinical supervision. Previously approved in 40+ countries including EU member states.", "routes": [ "intravenous" ], "half_life": "~50 minutes (terlipressin); ~3 hours (active metabolite lysine-vasopressin)", "molecular_weight": 1227.37, "cas_number": "14636-12-5", "mechanism_of_action": "Terlipressin is a prodrug consisting of three glycine residues attached to lysine-vasopressin (N-triglycyl-8-lysine-vasopressin). Tissue peptidases cleave the N-terminal glycyl residues, releasing the active moiety lysine-vasopressin. Lysine-vasopressin binds to V1 receptors in splanchnic and peripheral vascular smooth muscle, causing potent vasoconstriction. In hepatorenal syndrome, the underlying pathology is severe splanchnic vasodilation driven by portal hypertension and circulatory dysfunction; by reversing this vasodilation, terlipressin reduces effective arterial blood volume depletion, suppresses the renin-angiotensin-aldosterone and sympathetic nervous systems, and restores renal perfusion. This mechanism is distinct from other vasopressors in its preferential splanchnic action and prolonged duration.", "evidence": [ { "claim": "Reverses HRS-AKI", "level": "strong", "basis": "CONFIRM Phase 3 (n=300) showed 29% verified reversal vs 16% placebo; FDA-approved 2022" }, { "claim": "Superior to albumin alone for HRS", "level": "strong", "basis": "Meta-analysis of multiple RCTs confirms superiority in hepatorenal syndrome" }, { "claim": "Effective in variceal bleeding", "level": "strong", "basis": "Ioannou meta-analysis (Aliment Pharmacol Ther 2003) supports efficacy and safety" }, { "claim": "Respiratory failure risk", "level": "strong", "basis": "CONFIRM trial documented significant respiratory failure signal leading to boxed warning" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/terlipressin" }, { "name": "Tesamorelin", "slug": "tesamorelin", "aliases": [ "Egrifta", "TH9507" ], "category": "muscle", "subcategories": [ "weight-loss" ], "legal_status": "prescription", "legal_notes": "FDA-approved as Egrifta for HIV-associated lipodystrophy. Available by prescription. Also available through compounding pharmacies for off-label use.", "routes": [ "subcutaneous" ], "half_life": "~26-38 minutes", "molecular_weight": 5135.89, "cas_number": "218949-48-5", "mechanism_of_action": "Tesamorelin is a modified GHRH(1-44) with a trans-3-hexenoic acid group attached to the tyrosine at position 1, which increases its potency and stability. It stimulates the pituitary gland to produce and release growth hormone in a pulsatile, physiological pattern. It specifically reduces visceral adipose tissue (VAT) without significantly affecting subcutaneous fat.", "evidence": [ { "claim": "Reduction of visceral adiposity in HIV-associated lipodystrophy", "level": "strong", "basis": "Falutz et al. JCEM 2010: two Phase 3 RCTs, n=816 HIV patients; FDA-approved 2010 for HIV-associated lipodystrophy; ~15% VAT reduction" }, { "claim": "IGF-1 normalization and GH axis restoration", "level": "strong", "basis": "Multiple Phase 2–3 studies in HIV lipodystrophy confirming dose-dependent IGF-1 restoration consistent with GH axis stimulation" }, { "claim": "Liver fat reduction", "level": "moderate", "basis": "Falutz et al. JAMA 2014: RCT, n=61 HIV patients; significant liver fat reduction by MRI vs placebo at 26 weeks" }, { "claim": "Improved lipid profile and metabolic markers", "level": "moderate", "basis": "Falutz et al. Clin Infect Dis 2012: RCT, n=311; improved triglycerides and adiponectin concurrent with VAT reduction" }, { "claim": "Muscle mass preservation in HIV-infected adults", "level": "preliminary", "basis": "Erlandson et al. JAIDS 2019: secondary analysis showing modest increases in muscle area alongside fat reduction" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/tesamorelin" }, { "name": "Testagen", "slug": "testagen", "aliases": [ "KEDG tetrapeptide", "Lys-Glu-Asp-Gly", "testes bioregulator" ], "category": "sexual-health", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Developed and studied in Russia; commercially sold as a cytogen bioregulator supplement. Available in Western markets as a research chemical. Not approved for therapeutic human use outside Russia.", "routes": [ "subcutaneous", "intramuscular", "oral" ], "half_life": "Short (minutes to hours — estimated for tetrapeptide class)", "molecular_weight": 430.4, "cas_number": null, "mechanism_of_action": "Testagen penetrates both cell and nuclear membranes in testicular and hypothalamic-pituitary target tissues, interacting directly with DNA promoter regions of genes involved in steroidogenesis and gonadal function. It is proposed to stimulate Leydig cell activity by upregulating transcription of enzymes in the testosterone biosynthetic pathway (CYP11A1, 3β-HSD, CYP17A1). Testagen influences both the hypothalamic-pituitary-gonadal (HPG) axis controlling testosterone production and the hypothalamic-pituitary-thyroid (HPT) axis governing metabolic hormones. Like other Khavinson bioregulators, its tissue specificity arises from DNA sequence recognition patterns in the target organ. In aging testicular tissue, the peptide is proposed to reverse age-related epigenetic silencing of steroidogenic gene promoters.", "evidence": [ { "claim": "Stimulates Leydig cell testosterone synthesis", "level": "preliminary", "basis": "Rodent aged testis gene expression studies; no human testosterone outcome RCTs" }, { "claim": "Modulates HPG and HPT axes", "level": "insufficient", "basis": "Mechanistic claim based on Khavinson DNA-binding model; no functional validation in humans" }, { "claim": "Improves Leydig function in aging", "level": "insufficient", "basis": "Russian observational series only; no placebo-controlled trials meeting Western standards" }, { "claim": "Upregulates steroidogenic enzyme transcription", "level": "preliminary", "basis": "In vitro/animal DNA promoter interaction studies; CYP11A1/3β-HSD pathway data preclinical only" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/testagen" }, { "name": "Thymalin", "slug": "thymalin", "aliases": [ "Thymus extract", "Thymalin peptide bioregulator" ], "category": "immune", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Approved in Russia as a pharmaceutical since 1982. Not FDA-approved. Available as a research peptide internationally. Part of Khavinson's peptide bioregulator system.", "routes": [ "intramuscular", "subcutaneous" ], "half_life": "~3-4 hours (estimated)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Thymalin restores thymic function by modulating T-cell differentiation and maturation. It normalizes the ratio of CD4/CD8 T-cells, enhances natural killer (NK) cell activity, stimulates phagocytosis, and modulates cytokine production. In aging, the thymus involutes (shrinks) dramatically, reducing naive T-cell output — thymalin appears to partially reverse this immunosenescence. It also regulates the neuroendocrine-immune axis.", "evidence": [ { "claim": "Mortality reduction in elderly patients", "level": "preliminary", "basis": "Khavinson Neuro Endocrinol Lett 2003: 6-15-year follow-up of elderly cohort with thymalin+epithalon; 1.6-1.8x lower mortality; not independently replicated in Western literature" }, { "claim": "T-cell immune restoration", "level": "preliminary", "basis": "Russian clinical use since 1982; normalized CD4/CD8 ratios in immunocompromised patients; limited Western replication" }, { "claim": "Hematopoietic stem cell activation", "level": "preliminary", "basis": "Khavinson Bull Exp Biol Med 2020: in vitro differentiation of human HSCs; mechanistic cell-based evidence" }, { "claim": "Post-surgical infection reduction", "level": "preliminary", "basis": "Russian clinical observational studies in post-surgical patients; faster immune recovery and reduced infection rates; not controlled in Western journals" } ], "peer_reviewed_reference_count": 3, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymalin" }, { "name": "Thymopentin", "slug": "thymopentin", "aliases": [ "TP-5", "Timopentina", "Thymopentin (32-36)", "Arg-Lys-Asp-Val-Tyr" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "Thymopentin is approved in Italy (Timopentina) for HIV-associated immune deficiency and is a prescription drug in several European countries. In the US it is not FDA-approved and is classified as a research compound.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~30 minutes (plasma)", "molecular_weight": 679.77, "cas_number": "69558-55-0", "mechanism_of_action": "Thymopentin binds to thymopentin receptors on immature lymphoid precursors, inducing differentiation toward CD4+ and CD8+ T-cell phenotypes and expression of T-cell surface markers (including Thy-1). It promotes IL-2 production and T-helper cell activity, enhancing both cellular and humoral immunity. TP-5 also modulates NK cell activity and has been reported to normalize aberrant T-cell subset ratios in immunocompromised patients. Its mechanism reflects the active core of full-length Thymopoietin.", "evidence": [ { "claim": "Approved in Italy for HIV immune deficiency", "level": "strong", "basis": "Italian regulatory approval (Timopentina) based on multiple clinical trials" }, { "claim": "Stabilizes CD4+ cell counts in HIV", "level": "moderate", "basis": "Multiple clinical trials in HIV-infected patients showed CD4 stabilization" }, { "claim": "Rebalances immune profile in atopic dermatitis", "level": "moderate", "basis": "Clinical trials showing reduced IgE and immune normalization" }, { "claim": "Induces T-cell differentiation markers", "level": "moderate", "basis": "Consistent in vitro and in vivo lymphocyte maturation evidence" }, { "claim": "Modest benefit in rheumatoid arthritis", "level": "preliminary", "basis": "Phase II trial showed only modest improvement versus controls" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymopentin" }, { "name": "Thymopoietin", "slug": "thymopoietin", "aliases": [ "Thymopoietin II", "Thymopoietin III", "TMPO", "Lamina-associated polypeptide 2" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "Thymopoietin (full-length 49 AA) is not approved for human use and is classified as a research compound. Its active fragment Thymopentin (TP-5) has been approved in some countries.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "Not well characterized for full-length protein", "molecular_weight": 5562.3, "cas_number": "67213-56-3", "mechanism_of_action": "Thymopoietin acts on lymphoid progenitor cells to induce T-cell lineage commitment and differentiation markers. It suppresses neuromuscular transmission (early research linked it to myasthenia gravis) via acetylcholine receptor modulation. Its immunological actions are mediated through the active pentapeptide sequence (residues 32–36, Arg-Lys-Asp-Val-Tyr), which corresponds to Thymopentin. Full-length Thymopoietin is thought to interact with both immune cell receptors and nuclear lamina proteins in its role as a structural component.", "evidence": [ { "claim": "Induces T-cell lineage differentiation", "level": "moderate", "basis": "Consistent 1970s-1980s lymphoid progenitor differentiation studies" }, { "claim": "Active pharmacophore resides in residues 32-36", "level": "strong", "basis": "Structure-activity studies establishing TP-5 fragment retains full activity" }, { "claim": "Nuclear lamina structural function (LAP2)", "level": "moderate", "basis": "Consistent molecular biology studies of LAP2 isoform function" }, { "claim": "Modulates acetylcholine receptor signaling", "level": "preliminary", "basis": "Historical myasthenia gravis research; mechanism not fully characterized" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymopoietin" }, { "name": "Thymosin Alpha-1", "slug": "thymosin-alpha-1", "aliases": [ "Thymalfasin", "Tα1", "TA-1", "Zadaxin" ], "category": "immune", "subcategories": [ "longevity" ], "legal_status": "legal-compounding", "legal_notes": "Thymosin Alpha-1 was placed on the FDA Category 2 bulk drug substance list in 2023 (compounding ban). It is approved under the brand name Zadaxin in 35+ countries. Following HHS Secretary Kennedy's February 27, 2026 announcement, FDA nominations for Thymosin Alpha-1 and 13 other peptides were withdrawn from the Category 2 list, effectively lifting the compounding ban as of April 23, 2026. The Pharmacy Compounding Advisory Committee (PCAC) is scheduled to conduct formal review on July 23–24, 2026 to determine permanent compounding-eligible status.", "routes": [ "subcutaneous" ], "half_life": "~2 hours (plasma); peak serum levels at 1–2 hours post-injection", "molecular_weight": 3108.28, "cas_number": "62304-98-7", "mechanism_of_action": "Thymosin Alpha-1 modulates innate and adaptive immunity primarily through toll-like receptor (TLR) engagement. It acts as a potent agonist at TLR9 on dendritic cells and TLR2 on macrophages, triggering MyD88-dependent signaling that upregulates type I interferons (IFN-α/β), IL-12, and TNF-α. This drives differentiation of naive T-cells toward Th1 and regulatory T-cell (Treg) phenotypes, enhancing cytotoxic CD8+ T-cell responses against infected or malignant cells while suppressing excessive inflammatory cytokine production. Tα1 also promotes natural killer (NK) cell activation and augments dendritic cell antigen-presenting capacity. The dual pro-immune and immune-regulating activity explains its utility in both immunodeficiency states and autoimmune-adjacent conditions where immune dysregulation is present.", "evidence": [ { "claim": "Immune reconstitution in immunodeficient states", "level": "moderate", "basis": "Multiple Phase 2–3 trials in HIV, hepatitis B/C, and post-chemotherapy patients; FDA-approved as Zadaxin in several Asian and Latin American countries" }, { "claim": "Efficacy as adjuvant for hepatitis B and C treatment", "level": "moderate", "basis": "Poo et al. J Viral Hepat 2009: RCT, n=150 HBV patients; thymalfasin + lamivudine improved viral suppression rates at 52 weeks vs monotherapy" }, { "claim": "Reduced mortality in sepsis (critical illness)", "level": "moderate", "basis": "Wu et al. Crit Care Med 2013: prospective RCT, n=361 severe sepsis patients in China; thymosin alpha-1 reduced 28-day mortality from 30.3% to 20.6%" }, { "claim": "COVID-19 severity reduction", "level": "moderate", "basis": "Liu et al. Clin Infect Dis 2020: observational cohort in n=76 severe COVID-19 patients; thymalfasin associated with reduced mortality — observational, not RCT" }, { "claim": "Cancer immunotherapy adjuvant", "level": "preliminary", "basis": "Small Phase 2 studies (n=30–80) in NSCLC and hepatocellular carcinoma showing improved T-cell response alongside chemotherapy; no Phase 3 survival data" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymosin-alpha-1" }, { "name": "Thymosin Beta-4", "slug": "thymosin-beta-4", "aliases": [ "TB4", "Timbetasin", "Thymosin β4", "TMSB4X protein" ], "category": "recovery", "subcategories": [ "immune", "longevity" ], "legal_status": "reclassification-pending", "legal_notes": "Thymosin Beta-4 (full protein) is subject to the same FDA compounding ban framework that covers TB-500, as a peptide exceeding 40 amino acids. One of 14 peptides under FDA reclassification review (RFK Jr. initiative, 2025–2026). Availability from US compounding pharmacies is restricted; research supply chains remain active.", "routes": [ "subcutaneous", "intramuscular", "intravenous" ], "half_life": "~3–4 days (estimated from dosing schedule; precise human data not published)", "molecular_weight": 4921, "cas_number": "77591-33-4", "mechanism_of_action": "Thymosin Beta-4 functions through several coordinated mechanisms. Its primary structural role is G-actin sequestration — TB4 binds globular actin monomers, preventing uncontrolled polymerization and regulating the dynamic equilibrium between G-actin and F-actin required for cell motility and structural integrity. Beyond actin dynamics, TB4 acts extracellularly to promote cell migration, angiogenesis, and stem cell maturation. It upregulates integrin-linked kinase (ILK) expression, activating downstream Akt and PI3K signaling that drives cardiomyocyte survival, reduces apoptosis, and promotes progenitor cell recruitment to sites of injury. Anti-inflammatory effects include downregulation of NF-κB signaling and reduction of pro-inflammatory cytokine production including TNF-α and IL-1β. In cardiac injury models, TB4 mobilizes epicardial progenitor cells and promotes their differentiation into cardiomyocytes, positioning it uniquely among peptides studied for cardiac regeneration.", "evidence": [ { "claim": "Dermal wound healing acceleration", "level": "preliminary", "basis": "Malinda et al. J Invest Dermatol 1999 + Philp Wound Repair Regen 2003: consistent rodent wound healing data including diabetic/aged mice" }, { "claim": "Cardiac progenitor cell mobilization post-MI", "level": "preliminary", "basis": "Preclinical MI models show improved functional recovery and reduced infarct size; unique epicardial progenitor mechanism; no human cardiac RCT" }, { "claim": "Actin sequestration and cell migration", "level": "strong", "basis": "Huff Trends Biochem Sci 2005 + 20+ years biochemistry; G-actin binding is the founding established mechanism" }, { "claim": "Venous stasis ulcer healing in humans", "level": "preliminary", "basis": "Phase 2 trial NCT00832091 evaluated IV TB4 in venous stasis ulcers; small early-phase trial; results not definitive" }, { "claim": "Corneal and ocular surface repair", "level": "preliminary", "basis": "Goldstein Expert Opin Biol Ther 2012 review; preclinical rabbit corneal models; early clinical trials in dry eye" } ], "peer_reviewed_reference_count": 4, "external_ids": { "pubchem_cid": "45382195", "wikipedia": "https://en.wikipedia.org/wiki/Thymosin_beta-4" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymosin-beta-4" }, { "name": "Thymosin Beta-4 Sulfoxide", "slug": "thymosin-beta-4-sulfoxide", "aliases": [ "TB-4 Sulfoxide", "Tβ4-SO", "Tβ4-sulfoxide", "oxidized TB-500" ], "category": "recovery", "subcategories": [ "immune" ], "legal_status": "research-only", "legal_notes": "Thymosin Beta-4 Sulfoxide is a research chemical. Not FDA-approved. One of 14 peptides under FDA reclassification review (parent TB-4 / TB-500). Available from specialty research peptide suppliers.", "routes": [ "subcutaneous" ], "half_life": "Not well established; likely similar to TB-4 (~30–90 minutes)", "molecular_weight": 4979.55, "cas_number": null, "mechanism_of_action": "Oxidation of Met-6 attenuates Tβ4's G-actin-sequestering activity while greatly enhancing its extracellular signaling properties. Tβ4-SO inhibits neutrophil chemotaxis and is thought to be the secreted, extracellular signaling form of the parent peptide. In vivo, Tβ4-SO — but not the native form — potently inhibits carrageenan-induced paw edema in mice. In cardiac models, Tβ4-SO attenuates inflammatory cell infiltration and promotes wound healing post-infarction. It may represent part of the mechanism by which glucocorticoids exert anti-inflammatory effects via monocyte-secreted peptides.", "evidence": [ { "claim": "Anti-inflammatory monocyte product with glucocorticoids", "level": "preliminary", "basis": "Young 1999 Nature Medicine established Tb4-SO as a monocyte-derived anti-inflammatory mediator under glucocorticoid conditions" }, { "claim": "Inhibits neutrophil chemotaxis", "level": "preliminary", "basis": "In vitro and mouse paw edema studies demonstrate suppression of neutrophil recruitment at inflammation sites" }, { "claim": "Reduces inflammation in cardiac injury models", "level": "preliminary", "basis": "Mouse post-infarction studies show reduced inflammatory infiltrate and improved healing; no clinical data" }, { "claim": "Extracellular active form of TB-4", "level": "preliminary", "basis": "In vivo respiratory-burst oxidation data suggest sulfoxide is the physiological extracellular signaling form" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymosin-beta-4-sulfoxide" }, { "name": "Thymulin", "slug": "thymulin", "aliases": [ "Facteur Thymique Sérique", "FTS", "serum thymic factor" ], "category": "immune", "subcategories": [], "legal_status": "research-only", "legal_notes": "Thymulin is not FDA-approved for any indication. Available from research peptide suppliers. Not classified as a controlled substance.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "~2–4 hours", "molecular_weight": 858.85, "cas_number": "63958-90-7", "mechanism_of_action": "Thymulin binds receptors on immature thymocytes, mature T cells, and NK cells to promote T-cell differentiation and enhance cytotoxic activity. Its zinc-binding site (involving N-terminal pyroglutamate, Ser-4, Gln-5, and Ser-8) is required for receptor recognition. Thymulin stimulates IL-2 production, enhances NK cell killing capacity, and restores antibody avidity in aged or thymectomized animals. It modulates the Th1/Th2 cytokine balance and influences neuroendocrine-immune crosstalk.", "evidence": [ { "claim": "Zinc-dependent T-cell differentiation factor", "level": "moderate", "basis": "Dardenne 1982 PNAS 79:5370 and subsequent receptor-pharmacology studies established zinc-binding requirement (original characterization by Bach et al. 1977 Nature 266:55–57)" }, { "claim": "Restores immune function in aged animals", "level": "preliminary", "basis": "Consistent rodent studies in aged and thymectomized models; no human clinical replication" }, { "claim": "Circulating levels decline with age and zinc deficiency", "level": "moderate", "basis": "Fabris 2008 Ann NY Acad Sci observational human data; zinc supplementation restores activity" }, { "claim": "Anti-inflammatory analog effects", "level": "preliminary", "basis": "Moraes 2009 Clin Exp Immunol and related preclinical studies; no human efficacy data" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymulin" }, { "name": "Thymus Extract", "slug": "thymus-extract", "aliases": [ "Thymostimulin", "thymic extract", "thymic polypeptides", "calf thymus extract" ], "category": "immune", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved as a pharmaceutical. Thymostimulin was investigated in Europe and the US but never received FDA NDA approval. Thymosin alpha-1 (a defined component) is separately approved in some countries. Available in Western markets as a research substance or supplement. Not for therapeutic human use.", "routes": [ "subcutaneous", "intramuscular" ], "half_life": "Unknown (polypeptide mixture — highly variable by fraction)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "Thymus Extract contains a complex mixture of thymic hormones and peptides including thymosin fractions, thymulin-like peptides, and other thymic factors that collectively regulate T-lymphocyte development and immune homeostasis. These peptides stimulate T-cell differentiation and maturation in the thymus, regulate natural killer (NK) cell activity, modulate dendritic cell function, and induce the release of pro-inflammatory cytokines in appropriate contexts. By restoring thymic output of mature T-lymphocytes, thymic extracts are proposed to compensate for age-related thymic involution and the progressive immunosenescence that accompanies it. Individual peptide fractions within the extract include precursors to thymosin alpha-1, thymopoietin, and thymulin, though the exact composition varies between preparations and batches due to biological variation in the extraction process.", "evidence": [ { "claim": "Stimulates T-cell differentiation", "level": "preliminary", "basis": "1991 BioDrugs review summarized European trials showing T-cell reconstitution" }, { "claim": "Reduces infections in at-risk patients", "level": "preliminary", "basis": "European clinical trials suggest reduced infection incidence; lack of standardization limits interpretation" }, { "claim": "Supports immune function during chemotherapy", "level": "preliminary", "basis": "Small clinical trials in cancer patients; no large Phase 3 RCTs completed" }, { "claim": "Compensates for thymic involution", "level": "insufficient", "basis": "Mechanistic hypothesis; unstandardized preparation with batch variability undermines evidence" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/thymus-extract" }, { "name": "Tirzepatide", "slug": "tirzepatide", "aliases": [ "Mounjaro", "Zepbound" ], "category": "weight-loss", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved as Mounjaro for type 2 diabetes and Zepbound for chronic weight management, with an additional Zepbound label expansion for moderate-to-severe obstructive sleep apnea in adults with obesity. Prescription only. FDA shortage and compounding enforcement changes are central to how non-brand tirzepatide access is evaluated.", "routes": [ "subcutaneous" ], "half_life": "~5 days", "molecular_weight": 4813.45, "cas_number": "2023788-19-2", "mechanism_of_action": "Tirzepatide's clinical effects arise from the coordinated activation of two distinct G-protein-coupled receptors: the GIP receptor (GIPR) and the GLP-1 receptor (GLP-1R). Both receptors are expressed in the pancreatic beta cell, where their simultaneous stimulation produces additive and potentially synergistic increases in glucose-dependent insulin secretion. Tirzepatide is specifically designed to act as an imbalanced agonist — it engages the GIPR with affinity and signaling characteristics similar to native GIP while acting as a biased partial agonist at the GLP-1R, preferentially coupling to the Gs/cAMP pathway rather than the β-arrestin pathway (Coskun et al., JCI Insight 2020).\n\nAt the GLP-1 receptor, tirzepatide reproduces the effects of native GLP-1: it slows gastric emptying (reducing post-meal glucose excursions), suppresses glucagon secretion in a glucose-dependent manner, and acts on hypothalamic and brainstem appetite-regulating circuits to reduce food intake and promote satiety. These central effects are mediated in part through direct action on area postrema and nucleus tractus solitarius neurons and in part through vagal afferent signaling from the gut.\n\nAt the GIP receptor, tirzepatide exerts several metabolically distinct actions. In adipose tissue, GIPR agonism cooperates with insulin to enhance glucose uptake, augment glycerol synthesis, and increase lipid clearance in the fed state, while in the fasted state it promotes lipolysis and free fatty acid release. This context-dependent regulation of adipocyte metabolism may contribute to tirzepatide's ability to reduce fat mass beyond what weight loss alone would predict. In skeletal muscle and liver, GIPR activation appears to independently improve insulin sensitivity through mechanisms still under investigation — a 2025 post-hoc analysis of SURMOUNT-1 found that tirzepatide's improvements in insulin sensitivity exceeded what could be explained by weight reduction alone, implying direct receptor-mediated effects on metabolic tissue.\n\nThe dual-receptor mechanism also modifies the central appetitive response. GIP receptors are expressed in the ventromedial hypothalamus and other appetite-regulating nuclei, and rodent studies demonstrate that central GIPR activation reduces energy intake in a manner additive to GLP-1R activation. This brain-gut synergy likely accounts for a portion of the superior weight loss observed with tirzepatide compared to GLP-1-only agonists in head-to-head trials.", "evidence": [ { "claim": "Weight loss in obesity", "level": "strong", "basis": "SURPASS/SURMOUNT trials: up to 22.5% body weight loss at highest dose" }, { "claim": "Type 2 diabetes management", "level": "strong", "basis": "SURPASS 1-5 RCTs: superior HbA1c reduction vs semaglutide" }, { "claim": "Cardiovascular outcomes", "level": "moderate", "basis": "SURPASS-CVOT published 2025; obesity-only cardiovascular outcomes still pending from SURMOUNT-MMO" } ], "peer_reviewed_reference_count": 5, "external_ids": { "pubchem_cid": "156588324", "drugbank": "DB15171", "wikidata": "Q108324770", "wikipedia": "https://en.wikipedia.org/wiki/Tirzepatide" }, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/tirzepatide" }, { "name": "Vasopressin", "slug": "vasopressin", "aliases": [ "Vasostrict", "ADH", "arginine vasopressin", "AVP", "antidiuretic hormone" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved since 2014 as Vasostrict for vasodilatory shock. Administered by continuous intravenous infusion in an ICU setting with hemodynamic monitoring. Not a controlled substance. Compounded vasopressin preparations are also available from 503B outsourcing facilities.", "routes": [ "intravenous", "intramuscular" ], "half_life": "≤10 minutes at infusion rates used in vasodilatory shock", "molecular_weight": 1084.24, "cas_number": "113-79-1", "mechanism_of_action": "Vasopressin exerts its vasopressor effects primarily through V1a receptors on vascular smooth muscle. V1a receptor activation is coupled to Gq/11 proteins, stimulating phospholipase C to generate IP3 and diacylglycerol, leading to intracellular calcium release and smooth muscle contraction. This increases peripheral vascular resistance and raises mean arterial pressure without direct cardiac stimulation. In vasodilatory shock (including septic shock), endogenous vasopressin is depleted; exogenous supplementation restores vascular tone and may reduce catecholamine requirements. V2 receptor activation on renal collecting duct cells promotes water reabsorption via aquaporin-2 insertion, mediating the antidiuretic effect. Vasopressin also activates V1b receptors in the anterior pituitary (modulating ACTH release) and oxytocin receptors, and exerts procoagulant activity via factor VIII and von Willebrand factor release.", "evidence": [ { "claim": "Raises MAP in vasodilatory shock", "level": "strong", "basis": "FDA-approved (Vasostrict 2014); VASST RCT (n=778) NEJM 2008 established role as catecholamine-sparing adjunct" }, { "claim": "Reduces renal replacement therapy use in septic shock", "level": "moderate", "basis": "VANISH RCT Gordon 2016 JAMA showed reduced RRT requirement vs norepinephrine first-line" }, { "claim": "V1a-mediated vasoconstriction without cardiac stimulation", "level": "strong", "basis": "Mechanism established in decades of receptor pharmacology and hemodynamic clinical studies" }, { "claim": "Doses >0.04 U/min cause ischemia", "level": "moderate", "basis": "Pooled safety data from shock trials; FDA label warning on myocardial and mesenteric ischemia" }, { "claim": "Treats central diabetes insipidus", "level": "strong", "basis": "Decades of clinical use; desmopressin generally preferred but vasopressin retains approval" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/vasopressin" }, { "name": "Vilon", "slug": "vilon", "aliases": [ "Lys-Glu", "KE dipeptide", "Vilon dipeptide" ], "category": "immune", "subcategories": [ "longevity" ], "legal_status": "research-only", "legal_notes": "Not FDA-approved. Developed and studied in Russia; sold as a research chemical in Western markets. Not approved for human therapeutic use outside Russia. Classified as a research peptide in the US and EU.", "routes": [ "subcutaneous", "intramuscular", "oral" ], "half_life": "Short (minutes to hours — estimated for dipeptide class)", "molecular_weight": 275.3, "cas_number": null, "mechanism_of_action": "Vilon interacts directly with DNA by binding to the GCGC sequence in curved nucleosomal DNA and the TCGA sequence in B-form double-stranded DNA, positioning itself in the minor groove of the DNA helix. This epigenetic interaction modulates gene transcription in thymocytes, T-lymphocytes, and supporting immune cells without covalently altering the DNA sequence. In aged immune tissue, Vilon reduces apoptosis in T-helper cells rather than driving proliferation, restoring immune competence through a preservation mechanism. In vitro studies show it reduces TNF-α production (by up to 6-fold) and IL-6 release (up to 2.5-fold) in LPS-stimulated peripheral blood mononuclear cells, suggesting broad anti-inflammatory and immunoregulatory effects. Vilon was originally derived from analysis of thymalin, a thymic polypeptide complex.", "evidence": [ { "claim": "Reduces TNF-α and IL-6", "level": "preliminary", "basis": "In vitro LPS-stimulated PBMC studies show up to 6-fold TNF and 2.5-fold IL-6 reduction" }, { "claim": "Restores thymic T-cell output", "level": "preliminary", "basis": "Russian observational studies in elderly subjects; no Western RCTs" }, { "claim": "Geroprotective / mortality reduction", "level": "preliminary", "basis": "Khavinson long-term mortality data (Bull Exp Biol Med 2003); no independent replication" }, { "claim": "DNA minor-groove binding mechanism", "level": "preliminary", "basis": "In vitro biophysical studies confirm GCGC/TCGA binding; functional relevance not validated in humans" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/vilon" }, { "name": "VIP", "slug": "vip", "aliases": [ "Vasoactive Intestinal Peptide", "Vasoactive Intestinal Polypeptide", "Aviptadil", "PHM-27" ], "category": "immune", "subcategories": [ "cognitive", "other" ], "legal_status": "research-only", "legal_notes": "Aviptadil is the pharmaceutical-grade synthetic form and is not FDA-approved for any indication as of 2026. Off-label compounding and research use exist. No reclassification petition currently under FDA review for VIP.", "routes": [ "intravenous", "nasal" ], "half_life": "~2 minutes (IV); nasal absorption highly variable", "molecular_weight": 3325.8, "cas_number": "40077-57-4", "mechanism_of_action": "VIP binds to VPAC1 and VPAC2 receptors (G-protein coupled receptors), activating adenylate cyclase and elevating intracellular cAMP. This signaling cascade suppresses the release of pro-inflammatory cytokines including TNF-α, IL-6, and IL-12, while promoting regulatory T-cell differentiation. In the lung, VIP binds AT2 cell VPAC1 receptors, upregulating surfactant production, blocking apoptosis, and inhibiting cytokine-mediated lung injury. It also mediates shedding of ACE2 and TMPRSS2 surface expression via ADAM10 sheddase upregulation, reducing viral entry points. In mast cells, while VIP can trigger degranulation in isolation, within neuroimmune contexts it reprograms mast cells toward a non-degranulating phenotype, offering paradoxical anti-inflammatory protection relevant to MCAS.", "evidence": [ { "claim": "Anti-inflammatory cytokine suppression", "level": "moderate", "basis": "Delgado & Ganea J Mol Med 2014 review + Juarranz Biomedicines 2021: extensive mechanism studies in autoimmune/immune cells" }, { "claim": "COVID-19 respiratory failure treatment", "level": "moderate", "basis": "FDA Fast Track designation; Phase 2 improved 60-day survival signal; Lancet Respir Med Phase 3 failed primary endpoint" }, { "claim": "MCAS and long COVID benefit", "level": "preliminary", "basis": "Clinical case series and observational data; no large RCTs; community nasal-spray use is highly experimental" }, { "claim": "Autoimmune disease (RA, IBD) treatment", "level": "preliminary", "basis": "Juarranz 2021 K/BxN arthritis model; preclinical autoimmune mechanistic evidence only; no completed clinical trials" }, { "claim": "Lung surfactant upregulation via VPAC1", "level": "moderate", "basis": "Established AT2 cell biology; mechanistic basis for aviptadil COVID-19 development program" } ], "peer_reviewed_reference_count": 5, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/vip" }, { "name": "VK2735", "slug": "vk2735", "aliases": [ "VK-2735" ], "category": "weight-loss", "subcategories": [ "other" ], "legal_status": "research-only", "legal_notes": "Investigational compound as of 2026. Not FDA-approved. Being evaluated under IND in Phase 3 clinical trials (VANQUISH-1, VANQUISH-2). Not available by prescription; research chemical suppliers may offer non-GMP versions of uncertain purity. Viking Therapeutics retains exclusive development rights. No compounding pharmacy pathway as of 2026.", "routes": [ "subcutaneous", "oral" ], "half_life": "~7 days (estimated, subcutaneous formulation based on once-weekly dosing kinetics)", "molecular_weight": null, "cas_number": null, "mechanism_of_action": "VK2735 is a co-agonist designed to simultaneously activate two incretin receptors: the glucagon-like peptide-1 receptor (GLP-1R) and the glucose-dependent insulinotropic polypeptide receptor (GIPR). GLP-1R activation drives glucose-dependent insulin secretion, glucagon suppression, slowed gastric emptying, and central appetite suppression via hypothalamic and brainstem pathways. GIPR co-activation amplifies the insulinotropic response and has been shown in preclinical models to enhance adipose tissue fatty acid oxidation, reduce fat mass independently of caloric restriction, and modulate central reward pathways that drive hedonic eating. The dual receptor engagement produces synergistic weight loss beyond what GLP-1R agonism alone achieves, consistent with observations from tirzepatide. The oral formulation uses a proprietary delivery technology to overcome GLP-1 peptide degradation in the GI tract.", "evidence": [ { "claim": "Weight loss via dual GLP-1/GIP agonism", "level": "moderate", "basis": "Phase 2 VENTURE trial (Kushner Obesity 2026): n=176; 13.1% weight loss at 2.4 mg, up to 14.7% at higher doses at 13 weeks" }, { "claim": "Oral formulation efficacy", "level": "preliminary", "basis": "Phase 2 VENTURE-Oral trial (published January 2026): up to 12.2% mean weight loss at 13 weeks; first oral dual-agonist data" }, { "claim": "Superiority vs GLP-1-only agents", "level": "preliminary", "basis": "Phase 2 magnitudes exceed semaglutide benchmarks but no head-to-head trial yet; Phase 3 VANQUISH program ongoing" }, { "claim": "Cardiovascular and metabolic safety", "level": "insufficient", "basis": "No cardiovascular outcomes trial; Phase 3 safety data pending VANQUISH-1 and VANQUISH-2 readouts" } ], "peer_reviewed_reference_count": 1, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/vk2735" }, { "name": "Ziconotide", "slug": "ziconotide", "aliases": [ "Prialt", "SNX-111", "omega-conotoxin MVIIA", "MVIIA" ], "category": "other", "subcategories": [], "legal_status": "prescription", "legal_notes": "FDA-approved (NDA 021060, December 28, 2004) for management of severe chronic pain via intrathecal infusion. Prescription-only; requires implanted intrathecal drug delivery system. Available as Prialt 25 mcg/mL intrathecal solution. REMS program is not required but off-label use outside intrathecal route is not established.", "routes": [ "intravenous" ], "half_life": "~4.6 hours (intrathecal CSF)", "molecular_weight": 2639.12, "cas_number": "107452-89-1", "mechanism_of_action": "Ziconotide selectively and reversibly binds to N-type voltage-sensitive calcium channels (Cav2.2) located on the presynaptic terminals of primary afferent nociceptive neurons in the dorsal horn of the spinal cord. By blocking calcium influx through these channels, Ziconotide inhibits the depolarization-evoked exocytotic release of pro-nociceptive neurotransmitters including glutamate, substance P, and calcitonin gene-related peptide (CGRP). This interrupts ascending pain signal transmission without affecting opioid receptors, rendering it effective in opioid-tolerant patients. Its 25-amino-acid structure contains three disulfide bridges forming a rigid, loop-constrained backbone that confers high channel selectivity. Cerebrospinal fluid (CSF) delivery is required because the peptide's size prevents oral or systemic bioavailability.", "evidence": [ { "claim": "Reduces severe chronic pain", "level": "strong", "basis": "Pivotal RCT (Staats et al JAMA 2004, n=111) showed 31.2% VAS reduction vs 6.0% placebo" }, { "claim": "FDA-approved for intrathecal pain", "level": "strong", "basis": "FDA approval (NDA 021060, December 2004) as first N-type calcium channel blocker" }, { "claim": "No tolerance development long-term", "level": "strong", "basis": "Open-label extension studies up to 3 years (Webster 2009) show sustained analgesia" }, { "claim": "Non-opioid with no addiction liability", "level": "strong", "basis": "Mechanism via Cav2.2 channel block distinct from opioid receptors; established in multiple RCTs" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/ziconotide" }, { "name": "Zinc Thymulin", "slug": "zinc-thymulin", "aliases": [ "Zn-Thymulin", "FTS-Zn", "Facteur Thymique Sérique", "thymulin zinc complex" ], "category": "skin", "subcategories": [ "immune" ], "legal_status": "research-only", "legal_notes": "Available as a research peptide and from some compounding pharmacies for topical use. Not FDA-approved for any indication. Some practitioners prescribe compounded formulations off-label for hair loss.", "routes": [ "topical" ], "half_life": "Not established for topical use", "molecular_weight": 858.85, "cas_number": "63958-90-7", "mechanism_of_action": "Thymulin binds zinc in an equimolar ratio through coordination with serine and asparagine residues, forming the biologically active metallopeptide. In the immune system, Zinc Thymulin induces T-cell differentiation markers and enhances CD4+ and CD8+ subset function via thymulin receptors on lymphoid precursors. In hair follicle biology, Zinc Thymulin promotes anagen phase extension by stimulating keratinocyte proliferation and reducing local inflammatory cytokines (IL-1β, TNF-α) implicated in follicular miniaturization. It may also activate dormant hair follicle stem cells, promoting follicle neogenesis and increasing hair follicle density. Zinc's role is dual: activating the peptide's receptor-binding conformation and providing anti-inflammatory and 5α-reductase-modulating activity locally.", "evidence": [ { "claim": "Increases anagen hair count", "level": "preliminary", "basis": "Pilot RCT (J Drugs Dermatol) showed significant anagen increase and telogen decrease at 6 months" }, { "claim": "Extends hair growth phase", "level": "preliminary", "basis": "Small trial data supports anagen prolongation via keratinocyte proliferation stimulation" }, { "claim": "Reduces follicular inflammatory cytokines", "level": "preliminary", "basis": "In vitro and small trial data show local IL-1β and TNF-α reduction" }, { "claim": "T-cell immune regulation", "level": "moderate", "basis": "Nature 1982 and PNAS studies confirm thymulin's role in T-cell differentiation" } ], "peer_reviewed_reference_count": 4, "external_ids": {}, "publication_date": "2026-04-10", "url": "https://peptahub.com/peptides/zinc-thymulin" } ] }