Overview
VIP is an endogenous 28-residue neuropeptide first isolated from intestinal tissue and later found throughout the nervous, cardiovascular, gastrointestinal, and immune systems. It functions as a signaling molecule with vasodilatory and immunomodulatory roles. VIP is the subject of broad physiological and pharmacological research and is studied in numerous experimental contexts, though it is not broadly approved as a therapeutic peptide.
Mechanism of action
VIP acts primarily through the G-protein-coupled receptors VPAC1 and VPAC2, which couple to adenylate cyclase and raise intracellular cyclic AMP. Through these receptors it is reported to promote smooth-muscle relaxation and vasodilation, modulate immune cell activity toward an anti-inflammatory profile, and influence neuronal signaling. It belongs to the secretin/glucagon peptide superfamily and shares receptor biology with related peptides.
Research findings
Reported potent vasodilatory effects on vascular and other smooth muscle.,Studied as an immunomodulator that can shift responses toward an anti-inflammatory profile.,Research describes neuroprotective and signaling roles in the nervous system.,Examined in models of inflammatory and respiratory conditions.,Rapid plasma degradation limits its window of activity in studies.
Research context
VIP has a notably short plasma half-life due to rapid enzymatic degradation, which is a central feature of its pharmacology and has motivated research into analogs and delivery approaches. Human pharmacokinetics beyond this are not fully characterized, and reported experimental ranges vary by route and model. This is a research reference only. Not approved for human use outside regulated settings; consult the primary literature.
Handling & storage
Lyophilized powder is typically stored frozen, protected from light and moisture, in a laboratory setting. As a labile peptide it is generally handled cold and protected from degradation; reconstituted material is used within a limited window per laboratory protocol. Follow institutional handling guidance.
Reported safety signals
Because of its vasodilatory activity, the literature notes effects such as flushing and changes in blood pressure in experimental settings. Human safety as a research agent is not well characterized outside of specific clinical study contexts.
Studied alongside
In research discussion VIP is sometimes considered alongside KPV and LL-37 in immune-modulation contexts, and with tissue-repair peptides such as BPC-157 in broader signaling research.
At a glance
Research strengths
- Endogenous, well-characterized human neuropeptide
- Defined receptor biology (VPAC1/VPAC2)
- Broad physiological research across multiple systems
- Clear mechanistic rationale for vasodilation and immune modulation
Limitations & cautions
- Very short plasma half-life due to rapid degradation
- Not broadly approved as a therapeutic peptide
- Vasodilatory effects can complicate interpretation
- Human pharmacokinetics incompletely characterized
