VIP: Mechanism, Handling & Research Guide
Also known as: VIP, Vasoactive Intestinal Peptide, Vasoactive intestinal polypeptide, Aviptadil, VIP 1-28
What is VIP?
VIP (Vasoactive Intestinal Peptide) is a 28-amino acid neuropeptide belonging to the secretin/glucagon superfamily, originally isolated from porcine duodenum by Said and Mutt in 1970. VIP signals through two G-protein coupled receptors, VPAC1 and VPAC2, both of which activate adenylyl cyclase to elevate intracellular cAMP. Widely distributed throughout the central and peripheral nervous systems, VIP functions as a neurotransmitter and neuromodulator with roles in vasodilation, smooth muscle relaxation, exocrine secretion, circadian rhythm regulation, and neuroprotection. Research by Delgado et al. (2004) in Pharmacological Reviews comprehensively characterized VIP's anti-inflammatory properties, demonstrating suppression of TNF-alpha, IL-6, and IL-12 in activated macrophages while upregulating the anti-inflammatory cytokine IL-10. Studies published in the Journal of Neuroscience by Bhatt et al. showed that VIP protected hippocampal neurons from excitotoxic and oxidative damage through VPAC2-mediated cAMP/PKA signaling. Abad et al. in Annals of the New York Academy of Sciences reported that VIP use ameliorated experimental autoimmune encephalomyelitis in murine models, suggesting therapeutic potential in neuroinflammatory conditions. Additional research has shown VIP regulates the suprachiasmatic nucleus master clock, influencing circadian output. Compared to PACAP (Pituitary Adenylate Cyclase-Activating Polypeptide), which shares significant structural homology and receptor overlap, VIP has higher selectivity for VPAC receptors and lower affinity for PAC1 receptors. This makes VIP preferred for research specifically targeting VPAC-mediated pathways rather than the broader PAC1-dependent neuroprotective signaling. VIP is sensitive to degradation. Store lyophilized at -20°C. Reconstitute with bacteriostatic water and store at 2-8°C, using within 2-3 weeks. Studied by neuroscientists, immunologists, chronobiologists, and pulmonary researchers investigating airway smooth muscle regulation.
VIP Research Applications
In published and preclinical research, VIP has been studied across the following areas:
- Cognition and neuroprotection research
- Vasodilation and blood flow
- Immunomodulation research
- Circadian rhythm regulation
VIP in Research: Study Context
VIP is a 28-amino-acid neuropeptide of the secretin/glucagon superfamily that signals through the G-protein-coupled receptors VPAC1 and VPAC2 to raise intracellular cAMP, and the literature characterizes broad roles in vasodilation, smooth-muscle relaxation, circadian (suprachiasmatic) regulation, neuroprotection, and potent anti-inflammatory immunomodulation - including suppression of TNF-alpha, IL-6, and IL-12 and promotion of regulatory/Th2 profiles (Delgado et al., 2004; Delgado & Ganea, 2013). For in-vitro and laboratory research use only - not FDA-approved and no human concentration is provided here. Reconstitute the lyophilized 10mg peptide with bacteriostatic water to a defined concentration of 10.0 mg/mL for laboratory handling, and confirm identity and purity against the primary literature and the lot-specific Certificate of Analysis (COA).
How VIP Compares
Researchers frequently evaluate VIP alongside related compounds:
- VIP vs Semax — Semax is an ACTH(4-10)-derived peptide studied for BDNF-mediated neurotrophic/cognitive effects; VIP is a VPAC-receptor neuropeptide with broader vasodilatory, circadian, and anti-inflammatory signaling, so the two address different research mechanisms.
- VIP vs Selank — Selank is a tuftsin-derived anxiolytic-studied peptide acting largely on GABA/monoamine and immune-modulatory pathways; VIP acts through cAMP-coupled VPAC1/VPAC2 receptors with distinct anti-inflammatory and neuroprotective profiles.