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Compound guide

VIP

A pathway-focused guide to molecular mechanisms, published evidence, and the limits of interpretation.

Overview

A Summary:VIP

VIP, or vasoactive intestinal peptide, is an endogenous 28-amino-acid neuropeptide that signals mainly through the VPAC1 and VPAC2 receptors.

VPAC1 and VPAC2 are G-protein-coupled receptors that commonly activate adenylyl cyclase and cyclic-AMP signaling. Their distribution makes VIP useful for studying neural, vascular, intestinal, and immune signaling.

Cell, tissue, animal, and small human physiology studies describe VIP signaling, but they do not establish broad therapeutic benefits for a research material. Human infusion findings are exposure-specific and are not instructions for personal use.

Research model

Cellular & MolecularHow VIP Is Studied

These receptors, enzymes, and signaling networks define the primary laboratory questions associated with this research material.

01Cyclic-AMP signaling

VPAC1 receptor

At the cellular or molecular level

VIP binding to VPAC1 commonly activates Gs proteins, adenylyl cyclase, and cyclic AMP. Structure–activity studies show that multiple residues across the 28-amino-acid peptide contribute to receptor binding and activation.

02Subtype-dependent response

VPAC2 receptor

At the cellular or molecular level

VPAC2 shares VIP sensitivity with VPAC1 but differs in tissue distribution and selected structure–activity relationships. Experiments use subtype-selective analogues to separate the two pathways.

03Controlled human exposure

Neurovascular physiology

At the cellular or molecular level

Small infusion studies measured rapid clearance, vascular changes, parasympathetic activity, and headache-related endpoints after controlled VIP exposure.

Research interpretation

How to read the pathway.

01

Cyclic-AMP signaling

VIP binding to VPAC1 commonly activates Gs proteins, adenylyl cyclase, and cyclic AMP.

02

Subtype-dependent response

VPAC2 shares VIP sensitivity with VPAC1 but differs in tissue distribution and selected structure–activity relationships.

03

Controlled human exposure

Small infusion studies measured rapid clearance, vascular changes, parasympathetic activity, and headache-related endpoints after controlled VIP exposure.

Evidence boundary

Cell, tissue, animal, and small human physiology studies describe VIP signaling, but they do not establish broad therapeutic benefits for a research material. Human infusion findings are exposure-specific and are not instructions for personal use.

Read the evidence

Sources BehindThis Guide

Human VPAC1 and VPAC2 receptor structure–activity study (opens in a new tab)VIP pharmacokinetics and physiology in four volunteers (opens in a new tab)Placebo-controlled VIP infusion study (opens in a new tab)Vasoactive intestinal peptide identity record (opens in a new tab)

One important note

Educational Notice

Human research consists of small, controlled physiology studies and does not establish a general therapeutic benefit for a research vial or support personal use.

This guide summarizes molecular mechanisms, published evidence, and evidence limits in everyday language. It is educational information, not medical advice or instructions for personal use. Products offered on this site are intended exclusively for laboratory research and are not for human or veterinary use.