VIP
Vasoactive Intestinal Peptide · Neuropeptide
Neuropeptide of 28 amino acids in the glucagon/secretin superfamily. Production occurs in many tissues, the gut, pancreas, and brain among them. Its vasodilatory, anti-inflammatory, and immunomodulatory effects are potent. Binding at the VPAC1 and VPAC2 receptors triggers cAMP-mediated signaling cascades. Research points to therapeutic potential for pulmonary hypertension, diabetes, neurological disorders, and autoimmune conditions.
Overview
Neuropeptide of 28 amino acids in the glucagon/secretin superfamily. Production occurs in many tissues, the gut, pancreas, and brain among them. Its vasodilatory, anti-inflammatory, and immunomodulatory effects are potent. Binding at the VPAC1 and VPAC2 receptors triggers cAMP-mediated signaling cascades. Research points to therapeutic potential for pulmonary hypertension, diabetes, neurological disorders, and autoimmune conditions.
Binding occurs at the VPAC1 and VPAC2 G protein-coupled receptors, which activates adenylyl cyclase and raises intracellular cAMP together with PKA activity. CREB and other transcription factors are phosphorylated in turn. Vasodilation follows by mechanisms both dependent on and independent of NO; intestinal secretion is stimulated, smooth muscle relaxes, gastric acid secretion is inhibited, and the cardiac effects are positive inotropic and chronotropic.
Research indications
What the compound has been studied for, grouped by body system. Effect size is the reported magnitude where it was measured — not a recommendation.
Inhaled VIP is strikingly efficacious, raising mixed venous oxygen saturation along with exercise capacity.
Above doses of 100 pmol, peripheral blood vessels dilate through NO-dependent mechanisms.
Coronary vessels dilate, and the heart shows positive inotropic and chronotropic effects.
A promising therapeutic target across Alzheimer's, Parkinson's, and further neurological disorders.
Under research in ASD as a potential therapeutic target.
Production occurs in the suprachiasmatic nuclei, with a part in circadian regulation.
Insulin secretion is promoted via VPAC2 in a glucose-dependent manner; hypoglycemia risk is low.
Anti-inflammatory effects are potent and useful in IBD and in autoimmune conditions.
Therapeutic potential in sarcoidosis, pulmonary and systemic.
- Class
- Neuropeptide
- Research status
- Extensively studied
- Chain length
- 28 residues
- Molecular weight
- 3326 Da
- Half-life
- ~2 min
- Typical dose
- 50–100 µg per dose (up to 200 µg in research protocols)
- Frequency
- 1–2 times daily
- Cycle length
- As prescribed for specific condition
- Storage
- Lyophilized powder: 2-8°C refrigerated; Reconstituted: use immediately (very short stability, ~2 minute half-life)
Molecular data
- Type
- Neuropeptide
- Molecular weight
- 3326 Da
- Chain length
- 28 residues
- Half-life
- 2 min
Levels in single-dose multiples. A shape, not a pharmacokinetic prediction.
Dosing reference
Doses reported in the literature and by suppliers. These are a record of what has been used in research — reference, never instruction.
| Context | Route | Amount | Frequency |
|---|---|---|---|
| General use | SubQ or IV | 50-100 mcg | 1-2x daily |
| Research protocols | SubQ or IV | 100-200 mcg | As directed |
| Pulmonary hypertension | Inhalation | 100-200 mcg/day | Daily (inhaled) |
Interactions
Distinct mechanisms; no negative interactions on record.
Immunomodulatory effects on both sides, which may complement.
Anti-inflammatory properties are shared.
What to expect
Safety
Mechanistic flags — properties of the pathway, not observed adverse events.
- Vasodilation (flushing, warmth)
- Hypotension
- Increased heart rate
- Headache
- Gastrointestinal effects, with diarrhea possible
- Severe hypotension
- Allergic reaction symptoms
- Severe diarrhea
- Cardiac arrhythmias
- Severe hypotension
- VIPoma or related tumors
- Pregnancy or breastfeeding
- Severe cardiac conditions
Quality checklist
What to confirm before trusting a batch of research material. A verification aid — not an endorsement of any supplier.
- Third-party Certificate of AnalysisIndependent lab · dated · lot-matched.
- HPLC purity ≥ 98%Reverse-phase trace included.
- Mass-spec confirms 3326 g/molMALDI-TOF or ESI-MS.
- Counterion stated (acetate ≫ TFA)TFA salts can confound bioassays.
- Endotoxin / sterility statementRelevant once reconstituted.
- Lyophilised · cold-chain shippedStored −20 °C, shipped on ice.
- Labelled “research use only”No therapeutic or dosing claims.
Recorded signals for this compound · 7
- ✓White lyophilized powder
- ✓Solution clear once reconstituted
- ✓Vacuum seal intact
- !Instability means prompt use after reconstitution
- ×Cloudy solution
- ×Powder discolored
- ×Visible particulates
FAQ
In pulmonary hypertension, how far does VIP go — is conventional therapy replaceable?
Inhaled VIP showed striking efficacy in pulmonary hypertension patients, raising mixed venous oxygen saturation and exercise capacity. It complements conventional therapy rather than replacing it: the very short 2-minute half-life demands frequent dosing, which makes long-term use challenging without newer stabilized analogs.
Does VIP cause dangerous hypotension, or is it safe in most patients?
Hypotension and flushing can follow from the vasodilation, higher doses especially. Careful titration of the dose, together with monitoring of the patient, is essential. Baseline hypotension or a severe cardiac condition rules out use; elsewhere the vasodilation is mild and transient, manageable across most populations where medical supervision is proper.
Why does VIP see so little clinical use when the research looks promising?
An extremely short half-life of 1–2 minutes makes routine clinical use impractical, since constant infusions or several daily injections are required. Analogs that have been stabilized — stearyl-Nle17-VIP among them — reach 100-fold greater potency, but outside research settings they are seldom obtainable. Clinical availability stays restricted by limited commercial development, the strong research foundation notwithstanding.
Can VIP improve insulin secretion in diabetes without causing hypoglycemia?
Yes. Insulin secretion is promoted via VPAC2 receptors in a glucose-dependent way, meaning insulin is stimulated only when blood glucose is elevated. That glucose dependence makes hypoglycemia risk very low next to other insulin secretagogues, and VIP theoretically safer for diabetes support.