VIP

The row below carries a price per mg figure: listed price divided by stated peptide content, excluding shipping and codes. It is the same calculation applied on every compound page, so a figure here is directly comparable to one anywhere else on the site.

We currently track a single listing for this compound. When a second vendor is added the rows are ordered by measured $/mg, and the flags for testing and shipping are computed from the data shown. Each row carries its own verification date.

Category : Cellular Peptide Product name : VIP Synonyms : Vasoactive Intestinal Peptide, VIP-28 CAS : 37221-79-7 Size : 10 mg Testing : 8x tested · ISO/IEC 17025

H-His-Ser-Asp-Ala-Val-Phe-Thr-Asp-Asn-Tyr-Thr-Arg-Leu-Arg-Lys- Gln-Met-Ala-Val-Lys-Lys-Tyr-Leu-Asn-Ser-Ile-Leu-Asn-NH2

37221-79-7 — the more widely quoted of the two 40077-57-4 — used by other suppliers for the same 28-mer Both appear against VIP in vendor and catalogue listings. Verify against the lot-specific COA rather than treating either as definitive.

This is the one specification detail that has to be right, and the supplier field splits cleanly on it. Native VIP is amidated at Asn28. The free acid is a different molecule.

C-terminus -Asn-NH2 Molecular formula C147H238N44O42S Molecular weight 3325.85 g/mol

C-terminus -Asn-OH Molecular formula C147H237N43O43S Molecular weight 3326.84 g/mol

The two differ by one nitrogen, one hydrogen and one oxygen — a net 0.98 Da. Converting an amide to an acid removes NH2 and adds OH.

C-terminal amidation is a post-translational modification of the native peptide, not a synthesis convenience. For peptides in this class the amide contributes to receptor recognition and to resistance against carboxypeptidase cleavage. A free-acid preparation is not equivalent material.

Check that the formula and the written sequence agree. If the sequence ends -NH2, the formula should be C147H238N44O42S. If it ends -OH, the formula should be C147H237N43O43S. Any page pairing an amidated sequence with the free-acid formula, or the reverse, has a spec-sheet error rather than a different product.

The VIP gene does not encode VIP alone. Prepro-VIP is processed into two distinct bioactive peptides, and the second one varies by species — which is why several similar-looking names appear in catalogues.

PHM-27 peptide histidine methioninamide, 27 residues (human) PHI-27 peptide histidine isoleucinamide, 27 residues (porcine, rat) PHV-42 peptide histidine valine, 42 residues — an extended form

PHM-27, PHI-27 and PHV-42 are separate products from the same precursor, not alternative names for VIP. Catalogue entries listing "Vasoactive Intestinal Peptide, PHI-27 (porcine)" are selling the sibling peptide, not VIP.

Fragments are also sold separately, for example VIP (1-12), used in structure-activity work rather than as a full agonist.

VPAC1 gene VIPR1 class B (secretin-family) GPCR VPAC2 gene VIPR2 class B GPCR

VIP binds both with high affinity. A third related receptor, PAC1, is selective for PACAP rather than VIP. VPAC2 is also known as the helodermin-preferring VIP receptor and as PACAP type III receptor.

Both receptors couple to Gs. Receptor occupancy activates adenylate cyclase, raising intracellular cAMP, which activates protein kinase A and the downstream phosphorylation events that mediate the peptide's effects.

This is the same class B GPCR / cAMP architecture used by secretin, glucagon and GHRH — which is what places VIP in that superfamily and why cross-reactivity within the family is a live concern in assay design.

VIPR2 sits at a locus (designated SCZD16) where copy-number duplications have been associated with schizophrenia, which is one reason the receptor rather than the ligand is a target of interest in neuropsychiatric work.

Originally isolated from intestine, VIP is now known to be widely distributed across the central and peripheral nervous systems and peripheral tissues, functioning as neurotransmitter, neuromodulator and hormone.

VIP is characterized as a potent vasodilator, reported at 50 to 100 times the potency of acetylcholine. Reported effects include increased coronary blood flow, reduced vascular resistance, improved cardiac contractility, and support of ventricular-vascular coupling with lowered arterial pressure.

(Henning & Sawmiller, Cardiovascular Research, 2001)

In innate immunity, reported inhibition of inflammatory cytokine and chemokine release from macrophages, microglia and dendritic cells, with reduced co-stimulatory molecule expression on antigen-presenting cells. In adaptive immunity, a reported shift of the Th1/Th2 balance toward Th2 with enhanced regulatory T cell activity. Rheumatoid arthritis models report reduced pathogenic antibody levels.

(Gonzalez-Rey & Delgado, 2005; Martínez et al., IJMS, 2019; Leceta et al., Front Immunol, 2021)

The most clinically advanced line. VIP acts as an airway neuromodulator with reported bronchodilation, surfactant support and alveolar cell protection; analogues such as IK312532 and inhaler delivery systems have been developed for asthma and COPD.

In critical COVID-19 respiratory failure, intravenous aviptadil — synthetic VIP — was evaluated in a 60-day randomized controlled trial, with reported doubling of survival odds at 60 days alongside reduced cytokine release and respiratory distress.

(Onoue et al., Peptides, 2007; Youssef et al., Critical Care Medicine, 2022)

Regulation of gut motility, ion secretion, nutrient absorption and mucosal immune response. In the TNBS-induced colitis model, VIP reduced inflammation, weight loss and intestinal damage with downregulation of TNF-α, IL-1 and IL-6 and of Th1-driven responses, and reduced recurrence when given after disease onset.

(Abad et al., Gastroenterology, 2003; Iwasaki et al., F1000 Research, 2019)

Reported glucose-dependent stimulation of insulin secretion through VPAC2, with support of islet β-cell growth — the basis for interest in type 2 diabetes. Separate work reports metabolic rewiring of cytotrophoblast cells, improving fatty acid uptake and glucose utilization. The short half-life is repeatedly cited as the limiting factor for translation.

(Hou et al., Frontiers in Endocrinology, 2022; Merech et al., BBA Molecular Cell Research, 2025)

Elevated serum VIP has been reported to correlate with low-voltage areas in the left atrium during atrial fibrillation, proposed as a noninvasive biomarker.

(Nishino et al., JAHA, 2025)

In lambs on a high-grain diet, exogenous VIP reduced pro-inflammatory cytokines and circulating LPS without changing tight junction mRNA expression.

(Mia et al., Journal of Animal Science, 2024)

VIP is an endogenous human peptide. As a pharmaceutical it carries the INN aviptadil and has been investigated clinically, most visibly in critical COVID-19 respiratory failure. It is not FDA-approved for any indication in the United States.

Material supplied for laboratory use is a research chemical, not a pharmaceutical preparation. It is not manufactured, tested or released to pharmacopoeial or GMP standards, is not a drug, food, cosmetic or dietary supplement, has not been evaluated by the FDA, and is not intended for human or veterinary use.

Reported effects in study settings include flushing, headache, dizziness, blood pressure changes and heart rate changes — consistent with the compound's vasodilatory and smooth-muscle actions.