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IMMUNEPEPTIDE PROFILE

KPV

Also known as Lys-Pro-Val, α-MSH C-terminal tripeptide

KPV is a naturally occurring tripeptide derived from the C-terminal end of alpha-melanocyte stimulating hormone (α-MSH). Despite being only three amino acids long, KPV retains the potent anti-inflammatory properties of the full α-MSH molecule without the melanogenic (tanning) or steroidogenic effects. It has shown promise in inflammatory bowel disease and general inflammation management.

Last updated June 25, 2026

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KPV: quick citable summary

KPV is listed by PeptaHub as a immune peptide with a reclassification pending legal-status classification. The page summarizes mechanism, research context, common routes, safety notes, and references for writers and AI answer engines.

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PeptaHub. “KPV: Mechanism, Research Context, Safety.” peptahub.com, 2026. https://peptahub.com/peptides/kpv. Licensed CC BY 4.0.

License: Creative Commons Attribution 4.0 International. Link back to https://peptahub.com/peptides/kpv.

SAMEAS / EXTERNAL IDS
KPV CAS: 67727-97-3
QUICK ANSWER

What is KPV?

KPV is a naturally occurring anti-inflammatory tripeptide from alpha-MSH that inhibits NF-kB signaling at nanomolar concentrations in cell culture. It is taken up by the intestinal PepT1 transporter, and oral dosing reduced colitis in mouse models. There is no human clinical trial evidence.

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Overview

KPV is a naturally occurring tripeptide derived from the C-terminal end of alpha-melanocyte stimulating hormone (α-MSH). Despite being only three amino acids long, KPV retains the potent anti-inflammatory properties of the full α-MSH molecule without the melanogenic (tanning) or steroidogenic effects. It has shown promise in inflammatory bowel disease and general inflammation management.

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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.

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Reported study ranges

PurposeRouteReported rangeFrequency
anti-inflammatory / gut healthoral200500 mcg1-2x daily
systemic inflammationsubcutaneous200500 mcgdaily

Reported ranges are for research context only. Consult a qualified healthcare professional before using any peptide.

Convert KPV research-range units

Need to convert mg to mcg, dose volume, or U-100 syringe units? The KPV dose calculator is preloaded with these ranges, or use the general dose unit converter.

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Research summary

Oral KPV reduced the incidence of DSS- and TNBS-induced colitis in mice and lowered pro-inflammatory cytokine expression (Dalmasso, Gastroenterology 2008). Uptake is mediated by the PepT1 di/tripeptide transporter, which is induced in inflamed colon. Hyaluronic-acid-functionalised nanoparticle delivery improved targeting to colonic epithelium and macrophages and accelerated mucosal healing in a mouse ulcerative colitis model (Xiao, Mol Ther 2017). In vitro, nanomolar KPV inhibited NF-κB and MAP kinase signalling in human intestinal epithelial and T-cell lines. No human clinical trials have been completed, and FDA staff noted the absence of human clinical data when reviewing KPV in 2026.[1][2][3][4][5]

📄This section cites 5 peer-reviewed sources. View all references →
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Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

preliminary
Anti-inflammatory action via NF-kB inhibitionDalmasso Gastroenterology 2008: nanomolar KPV inhibited NF-kB and MAP kinase signalling in human intestinal epithelial and Jurkat T-cell lines. Kannengiesser Inflamm Bowel Dis 2008 showed the same anti-inflammatory potential in murine IBD models. Cell-culture and animal evidence only
preliminary
Ulcerative colitis / IBD benefitDalmasso Gastroenterology 2008 (oral KPV reduced the incidence of DSS- and TNBS-induced colitis in mice) and Xiao Mol Ther 2017 (nanoparticle-delivered KPV accelerated mucosal healing and downregulated TNF-alpha in a mouse UC model); no human trials
preliminary
Oral bioavailability via PepT1 transportDalmasso 2008 and Viennois Cell Mol Gastroenterol Hepatol 2016: PepT1-mediated uptake demonstrated in cell lines and mice; not validated in humans
preliminary
Colitis-associated cancer preventionViennois Cell Mol Gastroenterol Hepatol 2016: KPV prevented AOM/DSS-induced carcinogenesis in wild-type mice but had no effect in PepT1-knockout mice, indicating a PepT1-dependent effect. Preclinical only

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

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Side effects

Minimal reported side effects
Mild GI discomfort (oral route)
Injection site reactions

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

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Common stacks

Peptides commonly paired with KPV for synergistic effects.

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Sourcing & access

Reclassification in progress

KPVis one of 12 peptides the FDA removed from its Category 2 “do not compound” list on April 15, 2026, after the original nominations were withdrawn. That removal did not place it on the 503A Bulks List or into Category 1, so it is not currently eligible for compounding. The Pharmacy Compounding Advisory Committee is reviewing these substances for the Bulks List; adding one requires formal rulemaking, which typically takes 12 to 24 months. See our regulatory status tracker and regulatory timeline for the current position.

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Frequently asked questions

KPV (Lys-Pro-Val) is a tripeptide derived from the C-terminal end of alpha-melanocyte stimulating hormone. Despite being only three amino acids, it retains the full anti-inflammatory properties of alpha-MSH without causing tanning or hormonal effects.

KPV enters cells and directly inhibits NF-kB activation by preventing the phosphorylation and degradation of IkBa. This reduces the transcription of pro-inflammatory genes and lowers production of TNF-alpha, IL-6, and IL-1beta.

Oral KPV reduced colitis in mouse models, which is unusual for a peptide. Uptake is mediated by the intestinal PepT1 di/tripeptide transporter rather than by general peptide absorption. Hyaluronic-acid-functionalised nanoparticle delivery further improved targeting to colonic cells in mice. None of this has been tested in humans.

In mice, oral KPV reduced the incidence of chemically induced colitis and lowered pro-inflammatory cytokine expression, and nanoparticle-delivered KPV accelerated mucosal healing. This is animal and cell-culture evidence; there are no human trials. KPV is often combined with BPC-157 in community gut protocols, a pairing that has not been studied.

Oral protocols typically use 200 to 500 mcg once or twice daily. For systemic inflammation, subcutaneous injection of 200 to 500 mcg daily is used. Cycles of 4 to 8 weeks are common.

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Research references

  1. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammationDalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, et al.Gastroenterology, 2008PubMed
  2. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel diseaseKannengiesser K, Maaser C, Heidemann J, Luegering A, et al.Inflammatory Bowel Diseases, 2008PubMed
  3. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptidesGetting SJ, Schiöth HB, Perretti MJournal of Pharmacology and Experimental Therapeutics, 2003PubMed
  4. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative ColitisXiao B, Xu Z, Viennois E, et al.Molecular Therapy, 2017PubMed
  5. Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine modelViennois E, Ingersoll SA, Ayyadurai S, Zhao Y, et al.Cellular and Molecular Gastroenterology and Hepatology, 2016PubMed
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