Identity
a 28-amino-acid endogenous neuropeptide of the secretin/glucagon family, first isolated (Said & Mutt, ~1970) from intestine — hence the name — but in fact distributed body-wide: brain, gut, lungs, pancreas, immune system, vasculature. It signals through VPAC1/VPAC2 receptors (GPCRs, cAMP). Unlike most register entries (synthetic or gray-market-only), VIP is a genuine human hormone with broad, textbook physiology — which is exactly what makes its narrow gray-market positioning notable.
Mechanism (as proposed)
VIP signals through VPAC1 and VPAC2 receptors (G-protein-coupled, raising cAMP). Its natural actions are wide: relaxing vascular and airway smooth muscle (vasodilation/bronchodilation), down-regulating innate immune/inflammatory responses (shifting cytokine balance, calming over-active innate immunity), providing neuroprotection, and — in the suprachiasmatic nucleus — synchronising the cellular circadian oscillators (the CLOCK/BMAL1–PER/CRY feedback loop) to environmental light via ERK1/2 signalling. In the CIRS framework, the proposed therapeutic logic is replacement: if regulatory neuropeptides are depleted by biotoxin illness, restoring VIP provides the "capstone" regulatory signal that lets the inflammatory cascade resolve — but note this framework's clinical validation is exactly what's limited. The biology is robust; the niche-therapeutic claim is not (yet) independently substantiated.