VIP
What the Research Actually Shows
Human: 5 studies, 4 groups · Animal: 4 studies, 4 groups · In Vitro: 3
EDUCATIONAL NOTICE: Peptidings exists to make peptide research accessible and honest — not to tell you what to take. The information on this site is for educational and research purposes only. It is not medical advice, and no material here is intended to diagnose, treat, cure, or prevent any disease or health condition. Consult a qualified healthcare provider before making any decisions about peptide use.
VIP: A Neuropeptide That Does Everything, Survives for Less Than a Minute, and Became the Last Step in the Most Controversial Mold Protocol on the Internet
EVIDENCE TIER
VIP is a natural signaling molecule made by your nervous system and immune cells. It does many things at once: it relaxes blood vessels, calms inflammation, protects lung tissue, and regulates gut function. Several small clinical trials have tested VIP in humans — for lung disease, for sarcoidosis, and for COVID respiratory failure — with mixed results. In the biohacking world, VIP is best known as the final step in the Shoemaker mold illness (CIRS) protocol, used as a nasal spray. That use is based on one small, unblinded study of 20 patients by the protocol’s inventor — not a controlled trial.
VIP is a small signaling molecule — just 28 amino acids — that your body makes naturally in the nervous system, the gut, and immune cells. It was discovered in 1970 and named for its ability to widen blood vessels, but researchers have since learned it does far more than that. VIP calms inflammation, protects lung tissue, helps regulate digestion, and plays a role in your sleep-wake cycle. It is one of the most versatile natural peptides ever studied.
VIP also has a serious practical problem: it breaks down in the bloodstream in less than one minute. Enzymes chew it up almost the instant it enters your blood. This is why most clinical research has delivered VIP through continuous IV drips, lung inhalers, or nasal sprays — routes that get the peptide where it needs to go before the blood destroys it. Injecting VIP under the skin, the way most biohackers use peptides, has never been studied and may not work the way people assume.
In the biohacking world, VIP is best known as the final step in the Shoemaker mold illness protocol, where it is used as a nasal spray after months of other treatments. That protocol is based on one unblinded study of 20 patients. This article evaluates VIP across all of its tested uses — in the lungs, in the immune system, and in the mold illness community — and tells you what the evidence actually supports.
Table of Contents
Quick Facts: VIP at a Glance
TYPE
Endogenous neuropeptide / Gut hormone / Immunomodulator
GENERIC NAME
Vasoactive Intestinal Peptide (VIP); Aviptadil (synthetic pharmaceutical form)
PRIMARY CLASS
28-amino-acid neuropeptide of the secretin/glucagon superfamily; binds VPAC1 and VPAC2 G-protein-coupled receptors
RESEARCH STATUS
Multiple small clinical trials (pulmonary hypertension, sarcoidosis, COVID-19 ARDS); one open-label CIRS study (n=20); one large RCT for COVID respiratory failure (n=196, primary endpoint missed)
ENDOGENOUS ORIGIN
Widely distributed in the central and peripheral nervous system, gut (enteric nervous system), pancreas, and immune cells. Also found in mast cells. Plasma levels are tightly regulated and extremely low under normal conditions.
MOLECULAR WEIGHT
~3.3 kDa (28 amino acids). Amphipathic alpha-helical structure. Binds VPAC1 and VPAC2 receptors with equal affinity (Kd ≈ 1 nM), activating adenylate cyclase → cAMP signaling.
MECHANISM SNAPSHOT
Multi-system regulator: (1) Potent vasodilator — relaxes vascular and pulmonary smooth muscle; (2) Anti-inflammatory — suppresses TNF-α, IL-6, IL-12, NF-κB transactivation; promotes IL-10 and regulatory T cells; (3) Neuroprotective — modulates circadian rhythms, promotes neuronal survival; (4) Pulmonary — upregulates surfactant production; (5) Gut — regulates intestinal motility and mucosal immune homeostasis.
CLINICAL EVIDENCE SUMMARY
(a) Pulmonary hypertension: 8-patient open study, inhaled VIP 200 µg/day × 24 weeks. (b) Sarcoidosis: 20-patient Phase II, inhaled VIP × 4 weeks. (c) COVID ARDS: 196-patient RCT, IV aviptadil — primary endpoint missed. (d) CIRS: 20-patient open-label, VIP nasal spray × 18 months (Shoemaker et al., not PubMed-indexed).
COMMUNITY DOSING (UNVALIDATED FOR SC)
Nasal spray: 50 mcg per nostril, 2–4× daily (Shoemaker protocol). Subcutaneous: 25–50 mcg daily (community reports — no published validation). IV infusion: clinical supervision only. Hypotension is the primary acute risk.
STORAGE
Lyophilized powder. Reconstitute with bacteriostatic water. Store at 2–8°C (35–46°F). VIP has extremely low proteolytic stability (half-life <1 minute in plasma). Reconstituted solutions degrade rapidly — use within 1–2 weeks.
FDA STATUS
Not FDA-approved for any indication in the United States. Aviptadil (Zyesami) was denied Emergency Use Authorization for COVID-19. Aviptadil + phentolamine (Invicorp) is approved in the UK/EU for erectile dysfunction. Available from compounding pharmacies under physician prescription.
WADA STATUS
Not explicitly listed on the WADA Prohibited List. As an endogenous peptide with vasoactive and immunomodulatory properties, VIP could potentially be flagged under S2 (Peptide Hormones, Growth Factors). Athletes should verify current status before use.
VERDICT
The research moves fast. We read all of it so you don’t have to.
New compound reviews, evidence updates, and protocol analysis — sourced, cited, and written for people who actually read the studies.
Subscribe to Peptidings WeeklyWhat Is VIP?
Vasoactive intestinal peptide was discovered in 1970 by Sami Said and Viktor Mutt, who isolated it from porcine small intestine while searching for new vasodilatory substances (PubMed 5415118). The name was descriptive of the discovery context: a peptide from the intestine that causes vasodilation. But the name undersells the molecule spectacularly.
VIP is expressed throughout the central and peripheral nervous system, the gastrointestinal tract, the respiratory system, the cardiovascular system, and the immune system. It functions as a neurotransmitter in the brain (where it helps regulate circadian rhythms through the suprachiasmatic nucleus), a neuromodulator in the gut (where it regulates motility and secretion via the enteric nervous system), a vasodilator in the pulmonary and systemic circulation, and one of the body’s most potent endogenous anti-inflammatory mediators.
VIP signals through two G-protein-coupled receptors: VPAC1 (widely distributed — brain cortex, hippocampus, liver, lung, intestine, immune cells) and VPAC2 (CNS thalamus and suprachiasmatic nucleus, plus pancreas, skeletal muscle, lung, heart, kidney, adipose tissue). Both receptors activate adenylate cyclase, raising intracellular cAMP — the same second messenger pathway used by many hormones. VIP binds both receptors with high affinity (Kd ≈ 1 nM).
VIP belongs to the secretin/glucagon superfamily of peptides, which includes PACAP (pituitary adenylate cyclase-activating polypeptide), secretin, glucagon, and GLP-1. PACAP shares receptor binding with VIP at VPAC1 and VPAC2, which creates pharmacological overlap that complicates interpretation of receptor-specific effects.
The Half-Life Problem — VIP’s Central Challenge
This is the editorial backbone of the VIP article. Every clinical application, every delivery strategy, and every biohacking protocol exists in the shadow of one pharmacokinetic fact: VIP has an in vivo half-life of less than one minute.
In 1978, Domschke et al. measured VIP pharmacokinetics in humans via IV infusion and found that plasma levels fell with first-order kinetics after cessation, with a disappearance half-time averaging approximately one minute (PubMed 730072). The metabolic clearance rate was ~9 mL/kg/min. VIP is rapidly degraded by dipeptidyl peptidase IV (DPP-IV) and neutral endopeptidase, both abundantly present in plasma and tissue.
This means: IV bolus injection delivers a burst of VIP that is gone in minutes. Subcutaneous injection delivers VIP into tissue where local proteases begin degrading it immediately; systemic bioavailability is unknown and likely very low. Inhaled aerosol delivers VIP directly to pulmonary epithelium, bypassing systemic degradation — which is why most clinical trials used inhalation. Nasal spray delivers VIP to nasal mucosa for local absorption, avoiding first-pass metabolism but with uncertain systemic delivery.
The half-life problem explains everything about VIP’s therapeutic development: why clinical trials used continuous IV infusion or inhalation, why no oral formulation exists, why pharmaceutical companies have invested in nanoparticle delivery systems and stapled VIP analogs to extend bioavailability, and why the Shoemaker protocol uses nasal spray rather than injection.
PLAIN ENGLISH
VIP disappears from your blood in under a minute. This is the central fact of VIP pharmacology. It means injecting it under the skin — the way most biohackers use peptides — may not work the way people assume. The molecule gets chewed up by enzymes almost instantly. That’s why researchers use continuous IV drips or inhalers instead. The nasal spray route used in the Shoemaker protocol may work because VIP gets absorbed through the nasal lining before it hits the bloodstream, but this has not been definitively proven.
Mechanism of Action
VIP’s biological activity is unusually broad. It operates across five major systems:
Anti-Inflammatory and Immunomodulatory
This is VIP’s most therapeutically relevant property and the focus of the largest body of research. VIP suppresses innate immune inflammation by inhibiting NF-κB transactivation in macrophages and dendritic cells (PubMed 25422088). The downstream effects include: reduced production of TNF-α, IL-6, IL-12, and reactive oxygen species; increased production of anti-inflammatory IL-10; downregulation of co-stimulatory molecules (CD80, CD86) on antigen-presenting cells; generation of tolerogenic dendritic cells that induce antigen-specific regulatory T cells; and suppression of Th1 differentiation with enhancement of Th2 and Treg responses (PubMed 15169929, PubMed 19604262).
VIP impairs acquisition of the pro-inflammatory (M1) macrophage phenotype (PubMed 27381006), effectively preventing macrophages from becoming the aggressively inflammatory cells that drive tissue damage in autoimmune and chronic inflammatory conditions.
Pulmonary
VIP has a specific protective role in the lungs: it relaxes pulmonary smooth muscle (vasodilation), upregulates surfactant production in alveolar type II cells, and protects those cells from apoptosis. VIP-knockout mice develop spontaneous pulmonary arterial hypertension and airway inflammation (PubMed 19076374), demonstrating that endogenous VIP is required for normal pulmonary vascular tone.
Vasodilatory
VIP causes potent relaxation of vascular smooth muscle, reducing blood pressure. This is both a therapeutic property (pulmonary hypertension) and a safety concern (systemic hypotension with exogenous administration).
Neuroprotective and Circadian
VIP-expressing neurons in the suprachiasmatic nucleus are essential for circadian rhythm synchronization. VIP also promotes neuronal survival and has been studied in models of Alzheimer’s disease, Parkinson’s disease, and stroke.
Gastrointestinal
VIP is a major regulator of gut motility, secretion, and mucosal blood flow via the enteric nervous system. Excessive VIP production by tumors (VIPomas) causes profuse watery diarrhea — the clinical syndrome first described by Verner and Morrison in 1958.
PLAIN ENGLISH
VIP is one of the body’s most versatile signaling molecules. It calms inflammation by dialing down aggressive immune cells and promoting regulatory ones. It relaxes blood vessels (which can lower blood pressure too much). It protects lung tissue. It helps regulate your sleep-wake cycle. And it manages gut function. The challenge is that you can’t easily target just one of these effects — when you add VIP, you get all of them.
Clinical Evidence (Human Data)
VIP has more human clinical data than most peptides in Cluster B — but the picture is fragmented across different indications, routes, and study designs.
Pulmonary Hypertension
Petkov V et al. (2003) J Clin Invest. PubMed 12727925
Open-label clinical trial. 8 patients with primary (idiopathic) pulmonary arterial hypertension. Inhaled VIP 200 µg daily for 24 weeks. Decreased mean pulmonary artery pressure, increased cardiac output and mixed venous oxygen saturation, improved 6-minute walk distance at 12 and 24 weeks. No adverse effects. Limitation: Open-label, 8 patients, no control group.
Leuchte HH et al. (2008) Eur Respir J. PubMed 18978135
Single-dose acute hemodynamic study. 20 patients with pulmonary hypertension (mixed etiologies). Single 100 µg inhaled aviptadil during right-heart catheterization. Small but significant selective pulmonary vasodilation, improved stroke volume and mixed venous O₂ saturation. Six patients achieved >20% PVR reduction. No adverse effects. Limitation: Single dose, acute measurements only.
Sarcoidosis
Prasse A et al. (2010) Am J Respir Crit Care Med. PubMed 20442436
Open-label Phase II trial. 20 patients with histologically confirmed, active sarcoidosis. Inhaled VIP for 4 weeks. Safe and well-tolerated. Significantly reduced TNF-α production in bronchoalveolar lavage fluid. Increased CD4+CD127−CD25+ regulatory T cells in BAL. Limitation: Open-label, 20 patients, no control group.
COVID-19 Respiratory Failure
Youssef JG et al. (2022) Crit Care Med. PubMed 36044317
Multicenter RCT. 196 patients with critical COVID-19 respiratory failure. IV aviptadil for 3 days vs. placebo, 2:1 randomization. Primary endpoint missed — alive and free from respiratory failure at day 60 was not significantly different (OR 1.6; 95% CI 0.86–3.11). Secondary endpoints positive: twice the survival odds at 60 days (p=0.035); reduced IL-6 by day 3 (p=0.02). Acceptable safety profile.
A subsequent commentary in The Lancet Respiratory Medicine (PubMed 37348523) characterized these results as a negative trial for VIP in COVID-associated respiratory failure.
PLAIN ENGLISH
This is a trial where the primary endpoint failed and the secondary endpoints were positive. In evidence-based medicine, that means the trial did not demonstrate what it set out to demonstrate. The secondary findings are interesting and may justify further research, but they do not prove that aviptadil treats COVID respiratory failure.
CIRS (Chronic Inflammatory Response Syndrome)
Shoemaker RC, House D, Ryan JC. (2013) Health. Vol. 5, No. 3, pp. 396–398.
Open-label study. 20 patients with refractory CIRS following water-damaged building exposure. VIP nasal spray 50 mcg, 4× daily, titrated over 18 months. Reduced refractory symptoms to equal controls. Corrected inflammatory biomarkers (C4a, TGF-β1, VEGF, MMP-9). Increased CD4+CD25+ regulatory T cells from mean 8.9 to 22.5. Limitation: Open-label, 20 patients, no blinded control group, no placebo arm, no randomization. Published in Health, a journal not indexed on PubMed. The study’s principal author is the creator of the CIRS diagnostic framework and VIP treatment protocol.
PLAIN ENGLISH
The only VIP-for-CIRS study was conducted by the protocol’s inventor, is open-label, has 20 patients, uses historical controls, and was published in a non-indexed journal. The biomarker changes are biologically plausible given VIP’s documented anti-inflammatory mechanisms. But “biologically plausible” and “proven effective” are not the same thing. No independent group has replicated these findings.
Erectile Dysfunction (Approved Indication — UK/EU)
Aviptadil in combination with phentolamine (brand name Invicorp) is approved in the UK and some EU countries for erectile dysfunction via intracavernosal injection. This is the only approved clinical use of VIP worldwide and involves direct injection into penile tissue — not systemic delivery.
PLAIN ENGLISH
VIP has been tested in people — more than most peptides in this cluster. Inhaled VIP showed promise for pulmonary hypertension and sarcoidosis in small, unblinded studies. A larger controlled trial for COVID respiratory failure missed its primary goal but showed some survival benefit in secondary analyses. The mold illness (CIRS) study is the most popular use case in the biohacking world, but it’s one small study without a control group, run by the person who invented the protocol. The only place VIP is actually approved as a drug is for erectile dysfunction — and even then, only in the UK and EU.
Preclinical Evidence
Rheumatoid arthritis (animal): VIP prevented arthritis onset and joint destruction in collagen-induced arthritis models by downregulating both inflammatory and autoimmune components (PubMed 11329057). Nanoparticle VIP delivery improved efficacy at lower doses (PubMed 23211088).
Inflammatory bowel disease (animal): VIP improved clinical parameters, reduced inflammatory cell recruitment, and rebalanced Th1/Th2/Th17 responses in TNBS-induced colitis (murine Crohn’s model) (PubMed 18667799).
Sepsis (animal): VIP reduced mortality in endotoxic shock models through LPS neutralization and cytokine suppression. VIP-knockout mice showed increased susceptibility to sepsis.
Neuroprotection (animal): VIP protected neurons in models of Alzheimer’s disease, cerebral ischemia, and excitotoxicity, primarily through VPAC2-mediated cAMP signaling.
The translational gap: VIP’s preclinical portfolio is impressive — anti-inflammatory effects demonstrated across arthritis, IBD, sepsis, and neurodegeneration models. None of these has advanced to a controlled human trial. The gap between animal models and human application is widened by VIP’s sub-minute half-life, which makes achieving therapeutic tissue concentrations in humans far more challenging than in small animals.
The Cancer Question — VIPomas and the Growth Factor Paradox
VIPomas are rare neuroendocrine tumors (typically pancreatic) that secrete massive amounts of VIP, causing the Verner-Morrison syndrome: profuse watery diarrhea, hypokalemia, and achlorhydria. Approximately 60% of VIPomas have metastasized at diagnosis (PubMed 31268974, PubMed 38109967). The existence of VIPomas demonstrates that chronically elevated VIP levels are associated with neuroendocrine malignancy — though the tumors produce VIP rather than being caused by it.
VPAC receptor overexpression in cancers: VPAC1 and VPAC2 receptors are overexpressed in breast, prostate, lung, colon, and pancreatic cancers (PubMed 24481544, PubMed 20691743). This has been exploited for tumor imaging (VIP-receptor-targeted radiotracers), but it also means exogenous VIP could potentially stimulate growth of VPAC-expressing tumors.
Dual effects: Like LL-37, VIP shows contradictory cancer effects. A VIP antagonist inhibited colony formation by approximately 50% in non-small cell lung cancer cells (PubMed 8389448), implying VIP signaling supports tumor cell proliferation in that context. Conversely, other studies showed VIP inhibiting pancreatic cancer cell proliferation at certain concentrations (PubMed 2550185). The direction of effect appears to depend on receptor subtype expression, concentration, and tumor type.
PLAIN ENGLISH
There are tumors that make huge amounts of VIP — they’re called VIPomas, and about 60% have already spread by the time they’re diagnosed. Many common cancers overexpress VIP receptors, which means VIP could theoretically stimulate their growth. This doesn’t mean VIP causes cancer, but it does mean that adding extra VIP to a body that might have undetected cancer is not risk-free.
The Shoemaker Protocol and CIRS
VIP’s biggest audience in the biohacking world is the Shoemaker mold illness community. Here’s what they’re actually doing and what the evidence behind it looks like.
What CIRS claims to be: A multi-system inflammatory syndrome triggered by exposure to water-damaged buildings (mold, mycotoxins, bacterial endotoxins). Diagnosed by a combination of symptom questionnaires, visual contrast sensitivity testing, and a panel of inflammatory biomarkers (C4a, TGF-β1, MMP-9, VEGF, MSH, VIP, ADH, osmolality, and others). First described by Ritchie Shoemaker, MD.
The Shoemaker treatment protocol follows a sequential multi-step process: cholestyramine binder → environmental remediation → antifungals → correction of androgens → correction of ADH/osmolality → VIP nasal spray (final step). VIP is introduced only after preceding steps have reduced inflammatory markers, and only in patients whose VIP levels remain low after other interventions.
The controversy: CIRS is not recognized as a formal diagnosis by major medical organizations. The diagnostic criteria were developed by Shoemaker, the treatment protocol was developed by Shoemaker, the primary study was conducted by Shoemaker, and the results were published in a non-indexed journal. No independent replication exists. The biomarker panel, while measuring real inflammatory mediators, has not been validated by independent groups as a diagnostic tool for a mold-specific syndrome. Critics argue that the symptoms attributed to CIRS (fatigue, cognitive difficulties, pain, GI issues) are nonspecific and overlap extensively with other conditions.
VIP’s anti-inflammatory mechanisms are well-established and biologically plausible as a therapeutic intervention for chronic inflammation. Whether CIRS as defined by Shoemaker represents a distinct clinical entity, and whether VIP nasal spray is effective for it, are separate questions that remain unresolved by the current evidence. People who use VIP for CIRS-related symptoms should understand the evidence limitations and the absence of independent replication.
Side Effects and Safety Concerns
Documented in Clinical Studies
Hypotension: The primary acute safety concern. VIP is a potent vasodilator. Blood pressure drops are expected, especially with IV administration. The inhaled and nasal routes partially mitigate this but do not eliminate it.
Facial flushing: Reported with IV and some inhaled protocols.
Diarrhea: Expected given VIP’s GI effects. VIPoma-level VIP excess causes profuse watery diarrhea.
No drug-related serious adverse events in the COVID RCT (PubMed 36044317) or the sarcoidosis study (PubMed 20442436).
Theoretical Concerns
VPAC receptor stimulation in undetected cancers: VPAC receptors are overexpressed in breast, prostate, lung, colon, and pancreatic cancers. Exogenous VIP could stimulate growth of VPAC-expressing tumors.
Immunosuppression: VIP’s potent anti-inflammatory effects suppress Th1 responses. Chronic VIP suppression of Th1 immunity could theoretically impair defense against intracellular pathogens and certain cancers.
Proteolytic degradation products: Unknown whether VIP fragments produced during rapid degradation have their own biological activity (beneficial or harmful).
Long-term effects of chronic use: No long-term safety data beyond the 18-month Shoemaker study (n=20, uncontrolled).
Anti-Doping Status
VIP is not explicitly named on the WADA Prohibited List. As an endogenous neuropeptide with vasoactive and immunomodulatory properties, it could potentially be categorized under S2 (Peptide Hormones, Growth Factors, Related Substances) or S0 (Non-Approved Substances). Athletes should verify current WADA status before use.
Legal and Regulatory Status
United States: VIP / aviptadil is not FDA-approved for any indication. Zyesami (inhaled aviptadil) was denied Emergency Use Authorization for COVID-19. Available from compounding pharmacies under physician prescription. FDA has stated insufficient data to determine safety of VIP for chronic conditions.
United Kingdom / EU: Aviptadil + phentolamine (Invicorp) is approved for erectile dysfunction via intracavernosal injection. This is the only approved clinical use worldwide.
Classification: When marketed for therapeutic indications, VIP is classified as a drug, not a dietary supplement.
Dosing in Published Research
EDUCATIONAL NOTICE
VIP has been administered to humans in clinical studies via inhalation, IV infusion, and nasal spray. No published pharmacokinetic study has measured VIP bioavailability after subcutaneous injection. All published human doses used routes specifically chosen to circumvent VIP’s sub-minute plasma half-life.
| Indication | Route | Dose / Protocol | Study | Notes |
|---|---|---|---|---|
| Pulmonary hypertension | Inhaled (nebulizer) | 200 µg daily × 24 weeks | Petkov et al. 2003 PubMed 12727925 | Open-label, n=8. Reduced PA pressure, improved cardiac output. |
| Pulmonary hypertension | Inhaled (nebulizer) | Single 100 µg dose | Leuchte et al. 2008 PubMed 18978135 | Acute hemodynamic study, n=20. Selective pulmonary vasodilation. |
| Sarcoidosis | Inhaled (nebulizer) | Nebulized VIP × 4 weeks | Prasse et al. 2010 PubMed 20442436 | Phase II, n=20. Reduced TNF-α, increased Tregs. |
| COVID ARDS | IV infusion | Continuous IV × 3 days | Youssef et al. 2022 PubMed 36044317 | RCT, n=196. Primary endpoint missed. |
| CIRS | Nasal spray | 50 mcg per nostril, 4× daily × 18 months | Shoemaker et al. 2013 (not PubMed-indexed) | Open-label, n=20. Biomarkers improved. |
The most evidence-based route is inhalation (direct to lungs for pulmonary indications) or nasal spray (mucosal absorption for the Shoemaker protocol). No published study has established a subcutaneous dose for VIP.
PLAIN ENGLISH
Every human study that tested VIP chose a route specifically designed to get around the fact that VIP self-destructs in your blood in under a minute. IV drips keep it flowing. Inhalers deliver it directly to the lungs. Nasal sprays bypass the bloodstream. Nobody has published what happens when you inject VIP under the skin — the most common biohacking route.
Dosing in Self-Experimentation Communities
EDUCATIONAL NOTICE
These protocols are community-derived. The subcutaneous route has never been validated in a published study. VIP’s sub-minute plasma half-life raises fundamental questions about whether SC injection achieves meaningful systemic or tissue concentrations.
CRITICAL DISCLAIMER
The following information documents community practices for educational purposes only. No published pharmacokinetic study has measured VIP bioavailability after subcutaneous administration. These protocols carry unknown risks.
| Route | Dose | Frequency | Notes |
|---|---|---|---|
| Nasal spray (Shoemaker protocol) | 50 mcg per nostril | 2–4× daily | Most evidence-supported community route. At least a published protocol exists (Shoemaker, albeit uncontrolled). |
| Subcutaneous injection | 25–50 mcg | Daily or several times per week | No published basis. VIP’s <1-minute half-life raises doubts about SC bioavailability. |
| IV infusion | Clinical protocols | Under medical supervision | Used in clinical trials. Not appropriate for self-administration. |
| Cycle length | Variable | — | No established cycling protocol. Some use continuously. |
Anyone using SC VIP is adding the uncertainty of an unstudied delivery route to an already-limited evidence base. The nasal spray route at least has a published protocol. The SC route has nothing.
PLAIN ENGLISH
If you’re considering VIP specifically for CIRS or chronic inflammation, the published protocol uses nasal spray — not injection. Whether standard subcutaneous injection achieves any meaningful VIP levels in tissue or blood is a question nobody has answered with data.
Preparation and Storage
| Parameter | Detail |
|---|---|
| Form | Lyophilized powder, typically 5 mg or 10 mg vials |
| Reconstitution | Bacteriostatic water for injection. Nasal spray kits available from some compounding pharmacies. |
| Storage (unreconstituted) | -20°C (−4°F) long-term. Room temperature shipping acceptable for short periods if lyophilized. |
| Storage (reconstituted) | 2–8°C (35–46°F). Use within 1–2 weeks. VIP’s extremely low proteolytic stability means reconstituted solutions degrade faster than most peptides. Protect from light. |
| Nasal spray preparation | Some compounding pharmacies provide VIP pre-loaded in nasal spray devices. If preparing from reconstituted solution, ensure sterile, preservative-containing diluent and appropriate spray mechanism. |
Guides: Reconstitution Guide | Storage Guide | Sterile Technique Guide
Related Compounds
PACAP (Pituitary Adenylate Cyclase-Activating Polypeptide): Shares VPAC1 and VPAC2 receptor binding with VIP. Similar anti-inflammatory and neuroprotective properties. Longer half-life than VIP. Not currently available in the biohacking market.
LL-37 (Cathelicidin): Different mechanism but shared immunomodulatory space. LL-37 can both promote and suppress inflammation depending on context; VIP predominantly suppresses. See LL-37 article.
KPV (Alpha-MSH Fragment): Anti-inflammatory tripeptide. Shares NF-κB inhibition with VIP but through melanocortin receptors rather than VPAC receptors. Much smaller molecule. See KPV article.
BPC-157: Tissue repair peptide with gut-protective properties. VIP and BPC-157 both have GI applications but through different mechanisms. See BPC-157 article.
Thymosin Alpha-1: Immunomodulatory peptide with opposite directional effects — Tα1 stimulates Th1 immunity; VIP suppresses it. Combining these is pharmacologically contradictory. See Thymosin Alpha-1 article (forthcoming).
| Compound | Type | Primary Target | Half-Life | FDA Status | WADA Status | Evidence Tier | Primary Tissue Target | Route | Human Evidence Status | Key Differentiator |
|---|---|---|---|---|---|---|---|---|---|---|
| BPC-157 | Synthetic pentadecapeptide (15 amino acids, derived from gastric protective protein BPC) | VEGF / Nitric oxide (proposed multi-target) | ~2–6 hours | Not FDA-approved | Prohibited — S0 (Non-Approved Substances) | Tier 3 — Pilot / Limited Human Data | Musculoskeletal, tendon, ligament, GI tract, CNS | Subcutaneous injection + Oral (both routes studied) | 3 published human pilot studies (~30 subjects combined); no RCTs | Broadest tissue tropism in cluster. Only injury-repair peptide with both oral and injectable evidence. Most evidence in rodent models |
| TB-500 | Synthetic 4-amino-acid fragment (residues 17–23 of Thymosin Beta-4) | Actin binding (cell migration, angiogenesis) | ~2–3 hours | Not FDA-approved | Prohibited — S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) | Tier 4 — Preclinical Only | Musculoskeletal (muscle, tendon, ligament), cardiac, neurological | Subcutaneous injection | Zero published human clinical trials; animal models and cell culture only | Smallest fragment studied; synthetic derivative of endogenous Thymosin Beta-4. Actin sequestration may drive cell migration |
| Thymosin Beta-4 | Endogenous 43-amino-acid peptide (ubiquitous actin-sequestering protein) | Actin binding, cell migration, angiogenesis | ~2–4 hours | Not FDA-approved | Prohibited — S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) | Tier 3 — Pilot / Limited Human Data | Broad: muscle, cardiac, neurological, immune, epithelial | Subcutaneous injection + Topical (cosmetics) | Few human studies; cardiac regeneration in early-stage human data; cosmetic formulations | Full-length parent peptide of TB-500. Endogenous compound; ubiquitous in mammalian tissues. More potent than TB-500 fragment in vitro |
| GHK-Cu | Synthetic tripeptide-copper complex (Gly-His-Lys chelated to Cu2+) | Collagen synthesis, wound healing, TGF-beta modulation | ~2 hours topical; ~4–6 hours systemic (estimated) | Not FDA-approved (topical in cosmetics; injectable investigational) | Prohibited — S0 (injectable as growth factor analog); topical unregulated | Tier 5 — It's Complicated | Dermal (collagen, elastin remodeling); broad systemic effects proposed but unverified | Topical (cosmetics — extensive evidence) vs. Subcutaneous injection (preclinical only) | Topical: 30+ years cosmetic use data; Injectable: zero human trials | Route-dependent evidence: topical skin rejuvenation well-established, but injectable claims extrapolate from fundamentally different delivery |
| AHK-Cu | Synthetic copper tripeptide variant (Ala-His-Lys chelated to Cu2+) | Copper chelation, extracellular matrix remodeling, growth factor signaling | ~2–4 hours (estimated) | Not FDA-approved | Not WADA-listed | Tier 4 — Preclinical Only | Dermal (hair follicle, scalp), cosmetic | Topical (cosmetics) | No human clinical trials; in vitro and cosmetic formulation data only | GHK-Cu structural analog with alanine substitution. Primarily studied for hair growth. Less evidence base than GHK-Cu |
| LL-37 | Human cathelicidin antimicrobial peptide (37 amino acids) | Antimicrobial, wound healing, angiogenesis, vitamin D-regulated immune modulation | ~2–4 hours | Not FDA-approved | Not WADA-listed | Tier 3 — Pilot / Limited Human Data | Skin, mucosal surfaces, immune system | Subcutaneous injection, Topical | Limited human data; antimicrobial efficacy well-characterized in vitro; wound healing in animal models | Endogenous host defense peptide. Dual role: direct antimicrobial activity + immune modulation. Vitamin D pathway regulates expression |
| KPV | Alpha-MSH C-terminal tripeptide (Lys-Pro-Val) | NF-kB inhibition, anti-inflammatory (no melanocortin receptor activation) | ~1–2 hours (estimated) | Not FDA-approved | Not WADA-listed | Tier 4 — Preclinical Only | GI tract (colitis models), skin, immune system | Subcutaneous injection, Oral (investigational) | No published human clinical trials; animal models (colitis, dermatitis) only | Smallest anti-inflammatory peptide in cluster (3 amino acids). NF-kB pathway without melanocortin receptor binding. GI-focused research |
| VIP | Endogenous 28-amino-acid neuropeptide (vasoactive intestinal peptide) | VPAC1/VPAC2 receptor agonism; vasodilation, immunomodulation, bronchodilation | ~1–2 minutes (extremely short) | Not FDA-approved (aviptadil in clinical trials) | Not WADA-listed | Tier 2 — Clinical Trials | Pulmonary, GI tract, immune system, neurological | Subcutaneous injection, IV infusion, Intranasal | Multiple Phase 2 trials (ARDS, pulmonary hypertension, sarcoidosis); aviptadil in FDA pipeline | Shortest half-life in cluster. CIRS protocol use. Aviptadil (synthetic VIP) is furthest along FDA pathway among non-approved compounds here |
| KGF / Palifermin | Recombinant keratinocyte growth factor (FGF-7) | FGFR2b receptor; keratinocyte proliferation, epithelial barrier repair | ~3–5 hours | FDA-approved (Kepivance for oral mucositis) | Not WADA-listed | Tier 1 — Approved Drug | Epithelial surfaces (oral mucosa, GI tract, skin) | Intravenous injection (FDA-approved route) | FDA-approved for chemo-induced oral mucositis; multiple Phase 2/3 trials | Only FDA-approved compound in Cluster B. Specific to epithelial tissues. IV-only approved route limits off-label accessibility |
| Substance P | Endogenous 11-amino-acid tachykinin neuropeptide | NK1 receptor agonism; fibroblast migration, angiogenesis, immune activation | ~1–2 minutes | Not FDA-approved | Not WADA-listed | Tier 3 — Pilot / Limited Human Data | Corneal epithelium, skin, nervous system | Topical (corneal), Subcutaneous injection | Human data primarily in corneal wound healing; limited systemic human studies | Endogenous pain signaling peptide repurposed for tissue repair. Strongest human evidence in corneal healing. Dual role: nociception + repair |
| PRP | Autologous platelet-rich plasma (concentrated growth factor preparation) | PDGF, VEGF, TGF-beta release via platelet degranulation | N/A (not a single molecule) | FDA-cleared devices (not drug-approved) | Prohibited — M1 (Manipulation of Blood and Blood Components) | Tier 2 — Clinical Trials | Musculoskeletal (tendon, cartilage, bone), dermal, hair | Injection (local to injury site) | Hundreds of RCTs across orthopedic, dermatologic, and dental applications | Non-peptide. Autologous preparation — no synthetic manufacturing. Largest clinical evidence base in cluster but high study heterogeneity |
| ARA-290 | Synthetic 11-amino-acid peptide (cibinetide; EPO-derived tissue-protective peptide) | Innate Repair Receptor (EPOR/CD131 heterodimer) selective agonist | ~2–4 hours | Not FDA-approved (Phase 2b completed) | Not WADA-listed | Tier 2 — Clinical Trials | Peripheral nerves, retina, cardiac, immune system | Subcutaneous injection (1–8 mg daily in trials); IV infusion (early trials) | Phase 2b complete (sarcoidosis SFN — DOSARA trial); Phase 2 (diabetic neuropathy, diabetic macular edema) | EPO-derived but does NOT bind classical EPO receptor. No erythropoietic activity. Tissue protection without blood doping risk. Furthest clinical development for neuropathy |
Combination Stacks
COMMUNITY-SOURCED INFORMATION
The combination scenarios described below are drawn from community discussion forums and theoretical pharmacology — not from clinical trials or peer-reviewed research. No combination of VIP with any other agent has been tested in a controlled study. These considerations are speculative. Do not combine medications without physician supervision.
VIP + Cholestyramine (Shoemaker Protocol)
The Shoemaker CIRS protocol positions VIP as the final step after binder therapy (cholestyramine or welchol) has reduced C4a and other markers. This sequential approach has pharmacological logic — reducing the inflammatory load before introducing an anti-inflammatory peptide — but the entire protocol is based on one uncontrolled study.
VIP + BPC-157 (Community Gut Protocol)
Community rationale: Combining VIP’s anti-inflammatory and gut-regulatory effects with BPC-157’s gut-mucosal repair mechanisms for IBS, IBD, or “leaky gut.” No published data exists on this combination. Both have independent GI activity in preclinical models. Unknown interactions.
VIP + LL-37
Community rationale: Combined immunomodulation for chronic infection. No published data. Pharmacologically, VIP suppresses inflammation while LL-37 can promote it — the combination could produce unpredictable effects.
Claims vs. Evidence
| # | Claim | Evidence Summary | Verdict |
|---|---|---|---|
| 1 | VIP reduces pulmonary artery pressure | Two open-label human studies (n=8 and n=20). Inhaled VIP produced selective pulmonary vasodilation. VIP-knockout mice develop spontaneous PAH. | Supported — Small Open-Label Studies |
| 2 | VIP suppresses inflammation and calms autoimmune responses | Extensive preclinical evidence. One Phase II human trial in sarcoidosis (n=20) confirmed reduced TNF-α and increased Tregs with inhaled VIP. | Supported — Limited Human Data |
| 3 | IV VIP (aviptadil) treats COVID respiratory failure | RCT (n=196): primary endpoint missed. Secondary endpoints showed survival benefit. Classified as negative trial. | Not Supported by Primary Analysis |
| 4 | VIP nasal spray corrects CIRS biomarkers | One open-label study (n=20): biomarkers improved. No control group, no blinding, no independent replication. Published in non-indexed journal by protocol’s inventor. | Biologically Plausible — Not Controlled |
| 5 | VIP regulates circadian rhythms | Well-established neuroscience. No human trial has tested exogenous VIP for circadian dysfunction. | Established Biology — No Therapeutic Evidence |
| 6 | VIP treats rheumatoid arthritis | Prevented arthritis in animal models. Zero human trials for RA. | Preclinical Only |
| 7 | VIP treats inflammatory bowel disease | Improved colitis in animal models. Zero human trials for IBD. | Preclinical Only |
| 8 | Subcutaneous VIP injection is effective for inflammation | No published human data on subcutaneous VIP for any indication. VIP’s <1-minute half-life raises fundamental questions about SC bioavailability. | No Evidence for This Route |
| 9 | VIP is safe for long-term use | Shoemaker study (18 months, n=20) reported no serious adverse events. VIPoma data shows chronic VIP excess causes pathology. | Short-Term Acceptable — Long-Term Unknown |
| 10 | VIP can treat mast cell activation syndrome (MCAS) | VIP is found in mast cells and has anti-inflammatory effects. Biological plausibility exists. No clinical study has tested VIP for MCAS. | Biologically Plausible — Clinically Unproven |
We currently don’t have any vetted partners for this compound. Check back soon.
Frequently Asked Questions
Is VIP the same as aviptadil?
Aviptadil is the pharmaceutical name for synthetic VIP. They are the same molecule. "VIP" is the endogenous neuropeptide name used in research; "aviptadil" is the International Nonproprietary Name (INN) used in clinical trials and drug applications.
Why does VIP have such a short half-life?
VIP is degraded by dipeptidyl peptidase IV (DPP-IV) and neutral endopeptidase, enzymes abundantly present in plasma and tissue. Evolutionary pressure favored tight regulation — VIP is a potent vasodilator and immunosuppressant, so the body needs to turn it off quickly. This is the same enzyme family targeted by DPP-4 inhibitor drugs used in diabetes (sitagliptin, etc.), though those drugs were not designed for VIP.
Can I inject VIP subcutaneously?
You can, but no published study has measured VIP bioavailability after subcutaneous injection, and the sub-minute plasma half-life suggests rapid local degradation. Whether SC VIP achieves meaningful tissue concentrations is genuinely unknown.
Is the Shoemaker mold protocol scientifically valid?
The biological mechanisms underlying the protocol — binder therapy for mycotoxins, VIP as an anti-inflammatory — have scientific plausibility. The specific CIRS diagnostic framework and the VIP treatment step are supported by one unblinded, uncontrolled study of 20 patients by the protocol's creator, published in a non-indexed journal. No independent replication exists. This does not mean it doesn't work; it means the evidence is insufficient to know.
Does VIP cause cancer?
VIP itself does not cause cancer. VIPomas (VIP-secreting tumors) are caused by neuroendocrine cell mutations, not by VIP exposure. However, many common cancers overexpress VPAC receptors, which means exogenous VIP could theoretically stimulate growth of existing tumors through receptor activation. This is a theoretical concern, not a proven risk.
Can I raise my VIP levels naturally?
VIP production is regulated by neural and immune signaling, not by dietary intake. There is no well-established supplement or dietary strategy to meaningfully increase endogenous VIP levels. Some research suggests vagal nerve stimulation may affect VIP release, but this is not clinically validated.
Is VIP safe with autoimmune conditions?
VIP suppresses Th1 immunity and promotes regulatory T cells, which is theoretically beneficial for autoimmune conditions driven by Th1 overactivation. Animal models of rheumatoid arthritis and IBD showed significant benefit (PMID: 11329057, 18667799). However, Th1 suppression could impair defense against intracellular pathogens and certain cancers. No human trial has tested VIP for any autoimmune condition.
Why was the COVID trial considered negative?
The primary endpoint — alive and free from respiratory failure at day 60 — was not statistically significant (OR 1.6; 95% CI 0.86–3.11). In clinical trial methodology, when the pre-specified primary endpoint fails, the trial is negative regardless of what secondary endpoints show. The secondary survival benefit (2× odds at day 60) is hypothesis-generating but not confirmatory.
What's the biggest risk with VIP?
Hypotension. VIP is a potent vasodilator. Blood pressure drops are expected and can be clinically significant, especially in people already taking antihypertensive medications or with autonomic dysfunction. This is not a side effect — it's VIP's primary pharmacological action working as designed.
How does VIP compare to other anti-inflammatory peptides in this cluster?
VIP is the most potent endogenous anti-inflammatory peptide in this cluster, with broader immunomodulatory reach than KPV (which targets a single pathway) and opposite direction from LL-37 (which can promote inflammation). It also has the worst pharmacokinetics of any peptide in the cluster — a sub-minute half-life vs. minutes-to-hours for most others. The tradeoff is power vs. deliverability.
Summary and Key Takeaways
VIP is one of the most biologically versatile molecules in Cluster B — a 28-amino-acid neuropeptide that functions simultaneously as a vasodilator, an anti-inflammatory agent, a gut regulator, a neuroprotector, and a circadian rhythm synchronizer. The science underlying VIP is mature and replicated: decades of research have characterized its receptors (VPAC1, VPAC2), its signaling cascades (cAMP-mediated), and its immunomodulatory profile (Th1 suppression, Treg induction, NF-κB inhibition). This is not a peptide running on hype. The basic biology is solid.
The problem is delivery.
VIP has a plasma half-life of less than one minute. This single pharmacokinetic fact constrains everything about VIP’s therapeutic potential. It explains why clinical trials used continuous IV infusion or inhalation rather than injection. It explains why pharmaceutical companies are investing in nanoparticle carriers and stapled analogs rather than developing conventional VIP formulations. And it raises a question that the biohacking community has not adequately confronted: whether subcutaneous VIP injection — the route many people are using — achieves any meaningful systemic or tissue exposure at all.
The clinical evidence is real but fragmented. Small open-label studies in pulmonary hypertension and sarcoidosis showed biologically coherent results through the inhaled route. A larger COVID RCT missed its primary endpoint. The CIRS study that drives most biohacking interest is one uncontrolled study of 20 patients from the protocol’s inventor. No independent replication of the CIRS findings exists.
Verdict Recapitulation
Evidence Tier 3 — Pilot / Limited Human Data. VIP earned Tier 3 because multiple human studies exist — including one RCT with 196 patients and several smaller open-label trials in pulmonary hypertension and sarcoidosis. This is more human data than most Cluster B compounds possess, and the biology is mechanistically well-established.
VIP did not earn Tier 2 because no human trial for any VIP indication has produced a positive primary endpoint in a controlled, adequately powered study. The COVID RCT’s primary endpoint missed. The pulmonary hypertension and sarcoidosis studies were small and unblinded. The CIRS study was uncontrolled and published in a non-indexed journal.
Verdict: Eyes Open. The biological foundation is strong, the clinical evidence is real but insufficient, and the most popular use case (CIRS) rests on a single uncontrolled study. The pharmacokinetic challenges are severe and unresolved. VIP nasal spray for CIRS is the most evidence-supported biohacking application — not because the evidence is strong, but because at least a published protocol and a dosing framework exist. Subcutaneous injection of VIP operates entirely outside even that limited evidence base.
PLAIN ENGLISH
VIP is a real molecule with real anti-inflammatory power, but it self-destructs in your blood in under a minute. The clinical trials that showed any benefit used IV drips or inhalers — not injections under the skin. The most popular biohacking use (mold illness protocol) is based on one small, unblinded study by the protocol’s inventor. VIP’s biology is fascinating. The gap between that biology and what people are actually doing with it has not been bridged by evidence.
Where to Source VIP
Further Reading and Resources
If you want to go deeper on VIP, the evidence landscape for injury recovery and tissue repair peptides, or the methodology behind how we evaluate this research, these are the places worth your time.
On Peptidings
- BPC-157 — Tissue repair peptide with gut-protective properties; different mechanism.
- KPV — Anti-inflammatory tripeptide; shares NF-κB inhibition through melanocortin receptors.
- LL-37 — Immunomodulatory peptide with both pro- and anti-inflammatory effects.
- Injury Recovery & Tissue Repair Research Cluster — All compounds in this category.
- Peptidings Evidence Framework — How we evaluate and rate peptide research.
External Resources
- PubMed — Biomedical Research Database — Search for VIP or related terms.
- ClinicalTrials.gov — Check for registered or ongoing VIP trials.
Selected References and Key Studies
- Said SI, Mutt V. Potent peripheral and splanchnic vasodilator peptide from normal gut. Nature. 1970;225(5235):863–864. PubMed
- Domschke S, et al. Vasoactive intestinal peptide in man: pharmacokinetics, metabolic and circulatory effects. Gut. 1978;19(11):1049–1053. PubMed
- Petkov V, et al. Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension. J Clin Invest. 2003;111(9):1339–1346. PubMed
- Leuchte HH, et al. Inhalation of vasoactive intestinal peptide in pulmonary hypertension. Eur Respir J. 2008;32(5):1289–1294. PubMed
- Prasse A, et al. Inhaled vasoactive intestinal peptide exerts immunoregulatory effects in sarcoidosis. Am J Respir Crit Care Med. 2010;182(4):540–548. PubMed
- Youssef JG, et al. The use of IV vasoactive intestinal peptide (aviptadil) in patients with critical COVID-19 respiratory failure: results of a 60-day randomized controlled trial. Crit Care Med. 2022;50(12):1690–1702. PubMed
- Lee WL, Slutsky AS. A negative trial for vasoactive intestinal peptide in COVID-19-associated acute hypoxaemic respiratory failure. Lancet Respir Med. 2023;11(8):e71. PubMed
- Shoemaker RC, House D, Ryan JC. Vasoactive intestinal polypeptide (VIP) corrects chronic inflammatory response syndrome (CIRS) acquired following exposure to water-damaged buildings. Health. 2013;5(3):396–398.
- Ganea D, Hooper KM, Kong W. The neuropeptide vasoactive intestinal peptide: direct effects on immune cells and involvement in inflammatory and autoimmune diseases. Acta Physiol (Oxf). 2015;213(2):442–452. PubMed
- Delgado M, Pozo D, Ganea D. The significance of vasoactive intestinal peptide in immunomodulation. Pharmacol Rev. 2004;56(2):249–290. PubMed
- Smalley SGR, Barrow PA, Foster N. Immunomodulation of innate immune responses by vasoactive intestinal peptide (VIP): its therapeutic potential in inflammatory disease. Clin Exp Immunol. 2009;157(2):225–234. PubMed
- Delgado M, et al. Vasoactive intestinal peptide prevents experimental arthritis by downregulating both autoimmune and inflammatory components of the disease. Nat Med. 2001;7(5):563–568. PubMed
- Sethi V, et al. Novel, biocompatible, and disease modifying VIP nanomedicine for rheumatoid arthritis. Mol Pharm. 2013;10(2):728–738. PubMed
- Abad C, et al. Vasoactive intestinal peptide as a healing mediator in Crohn’s disease. Neuroimmunomodulation. 2008;15(1):46–56. PubMed
- Said SI, et al. The vasoactive intestinal peptide gene is a key modulator of pulmonary vascular remodeling and inflammation. Ann N Y Acad Sci. 2008;1144:148–153. PubMed
- Carrión M, et al. VIP impairs acquisition of the macrophage proinflammatory polarization profile. J Leukoc Biol. 2016;100(6):1377–1386. PubMed
- Angelousi A, et al. Diagnostic and management challenges in vasoactive intestinal peptide secreting tumors: a series of 15 patients. Pancreas. 2019;48(7):934–942. PubMed
- Karele EN, et al. VIPoma: a comprehensive review. Presse Med. 2024;53(2):104791. PubMed
- Valdehita A, et al. Nuclear localization of vasoactive intestinal peptide (VIP) receptors in human breast cancer. Peptides. 2010;31(10):1967–1972. PubMed
- Tang B, et al. Vasoactive intestinal peptide receptor-based imaging and treatment of tumors. Int J Oncol. 2014;44(4):1023–1031. PubMed
- Moody TW, et al. A vasoactive intestinal peptide antagonist inhibits non-small cell lung cancer growth. Proc Natl Acad Sci USA. 1993;90(10):4345–4349. PubMed
- Duffy LC, et al. Vasoactive intestinal peptide as a laboratory supplement to clinical activity index in inflammatory bowel disease. Dig Dis Sci. 1989;34(10):1528–1535. PubMed
Disclaimer: This article is for educational and informational purposes only. It does not constitute medical advice, and nothing in this article should be interpreted as a recommendation to use, purchase, or self-administer VIP or any other peptide. VIP (aviptadil) is not approved by the FDA for any indication in the United States. Peptidings.com does not sell peptides or supplements. Consult a qualified healthcare provider before making any decisions about peptide use.
Last reviewed: April 2026 | Next scheduled review: October 2026
About the Author
Lawrence Winnerman
Founder of Peptidings.com. Former big tech product manager. Independent peptide researcher focused on translating clinical evidence into accessible science.