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IMMUNEPEPTIDE PROFILE

VIP

Also known as Vasoactive Intestinal Peptide, Vasoactive Intestinal Polypeptide, Aviptadil, PHM-27

Vasoactive Intestinal Peptide (VIP) is a 28-amino acid endogenous neuropeptide found throughout the central and peripheral nervous systems and gut. Its synthetic pharmaceutical form, aviptadil, has been investigated for COVID-19 respiratory failure, MCAS, and autoimmune conditions. VIP suppresses inflammatory cytokine cascades and modulates mast cell behavior, making it a candidate for chronic inflammatory and post-viral syndromes including long COVID.

Last updated June 25, 2026

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VIP: quick citable summary

VIP is listed by PeptaHub as a immune peptide with a research only 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. “VIP: Mechanism, Research Context, Safety.” peptahub.com, 2026. https://peptahub.com/peptides/vip. Licensed CC BY 4.0.

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

SAMEAS / EXTERNAL IDS
VIP CAS: 37221-79-7
QUICK ANSWER

What is VIP?

VIP is a 28-amino acid endogenous neuropeptide that suppresses inflammatory cytokine cascades and modulates mast cell behavior. Its synthetic form aviptadil received FDA Fast Track designation for COVID-19 respiratory failure and is investigated for MCAS and long COVID.

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Overview

Vasoactive Intestinal Peptide (VIP) is a 28-amino acid endogenous neuropeptide found throughout the central and peripheral nervous systems and gut. Its synthetic pharmaceutical form, aviptadil, has been investigated for COVID-19 respiratory failure, MCAS, and autoimmune conditions. VIP suppresses inflammatory cytokine cascades and modulates mast cell behavior, making it a candidate for chronic inflammatory and post-viral syndromes including long COVID.

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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.

§ 03

Reported study ranges

PurposeRouteReported rangeFrequency
COVID-19 respiratory failure (clinical trial protocol)intravenous0.1660.498 mcg/kg/hrescalating over 3 days
MCAS / long COVID (off-label nasal, community use)nasal50100 mcgonce to twice daily

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

Convert VIP research-range units

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

§ 04

Research summary

Aviptadil, the synthetic form, received FDA Fast Track designation for critical COVID-19 with respiratory failure, and the clinical programme has now largely reported out negative. A 196-patient placebo-controlled trial missed its primary endpoint of being alive and free from respiratory failure at day 60 (odds ratio 1.6, 95 percent CI 0.86-3.11), though a secondary survival analysis favoured aviptadil (Youssef, Crit Care Med 2022). The larger TESICO trial (461 patients, Lancet Respir Med 2023) was stopped for futility: no significant difference on the primary day-90 outcome (odds ratio 1.11, p=0.54) and 90-day mortality of 38 percent with aviptadil versus 36 percent with placebo. For MCAS and long COVID there is no controlled trial evidence at all; community use is based on practitioner reports. Autoimmune work (IBD, rheumatoid arthritis) remains in animal models.[1][2][3][4][5]

📄This section cites 5 peer-reviewed sources. View all references →
§ 04b

Evidence grading

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

moderate
Anti-inflammatory cytokine suppressionGanea Acta Physiol 2015 review and Leceta Front Immunol 2021: cytokine suppression via VPAC receptors, demonstrated in immune cell culture and mouse autoimmune models. Mechanism is well characterised; clinical benefit is a separate question
insufficient
COVID-19 respiratory failure treatmentBoth controlled trials missed their primary endpoint. Youssef Crit Care Med 2022 (n=196): primary endpoint not met, secondary survival analysis favoured aviptadil. TESICO (Lancet Respir Med 2023, n=461) was stopped for futility with 90-day mortality of 38 versus 36 percent. FDA Fast Track is a review-speed designation, not evidence of efficacy
preliminary
MCAS and long COVID benefitClinical case series and observational data; no large RCTs; community nasal-spray use is highly experimental
preliminary
Autoimmune disease (RA, IBD) treatmentLeceta Front Immunol 2021: K/BxN mouse arthritis model. Preclinical mechanistic evidence only; no completed clinical trials
preliminary
Lung surfactant upregulation via VPAC1Alveolar type II cell biology described in the aviptadil development rationale. No study is cited here measuring surfactant output after VIP dosing in humans, and the clinical programme built on this rationale did not show benefit

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

§ 05

Side effects

Facial flushing
Hypotension
Nausea
Diarrhea
Tachycardia
Transient anxiety or restlessness

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

§ 06

Common stacks

Peptides commonly paired with VIP for synergistic effects.

§ 08

Sourcing & access

Research compound

VIP is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).

§ 09

Frequently asked questions

VIP (Vasoactive Intestinal Peptide) is a 28-amino acid neuropeptide found throughout the central and peripheral nervous systems and gut. Its pharmaceutical form, aviptadil, has been investigated for COVID-19 respiratory failure, MCAS, and autoimmune conditions.

VIP binds VPAC1 and VPAC2 receptors, elevating intracellular cAMP. This suppresses pro-inflammatory cytokines (TNF-alpha, IL-6, IL-12), promotes regulatory T-cell differentiation, and in the lung upregulates surfactant production while blocking apoptosis.

Side effects include facial flushing, hypotension, nausea, diarrhea, tachycardia, and transient anxiety. VIP has a very short half-life (~2 minutes IV). Aviptadil is not FDA-approved for any indication as of 2026.

There is no controlled trial evidence for VIP in either condition. The rationale is mechanistic, drawn from VIP's cytokine-suppressing effects in cell and animal work, plus practitioner reports. Community protocols use compounded nasal spray at 50-100 mcg, a route and dose no published study has evaluated.

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Research references

  1. The neuropeptide vasoactive intestinal peptide: direct effects on immune cells and involvement in inflammatory and autoimmune diseasesGanea D, Hooper KM, Kong WActa Physiologica (Oxford), 2015PubMed
  2. Mechanism of Immunoregulatory Properties of Vasoactive Intestinal Peptide in the K/BxN Mice Model of Autoimmune ArthritisLeceta J, Garin MI, Conde CFrontiers in Immunology, 2021PubMed
  3. Therapeutic potential of vasoactive intestinal peptide and its receptor VPAC2 in type 2 diabetesHou X, Yang D, Yang G, Li M, et al.Frontiers in Endocrinology, 2022PubMed
  4. Understanding VPAC receptor family peptide binding and selectivityPiper SJ, Deganutti G, Lu J, Zhao P, et al.Nature Communications, 2022PubMed
  5. Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal systemIwasaki M, Akiba Y, et al.F1000Research, 2019Review
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