VIP

Also known as: Vasoactive Intestinal Peptide, Aviptadil

**Mechanism of Action** Vasoactive Intestinal Peptide (VIP) is a 28-amino-acid neuropeptide that exerts its effects primarily through binding to VPAC1 and VPAC2 receptors, which are G-protein-coupled receptors widely expressed in the respiratory, cardiovascular, gastrointestinal, and immune systems. Activation of these receptors stimulates adenylate cyclase, increasing intracellular cAMP levels, leading to smooth muscle relaxation (vasodilation and bronchodilation), inhibition of pro-inflammatory cytokine release, and modulation of immune cell activity. VIP also promotes epithelial barrier integrity and reduces vascular permeability, contributing to its anti-inflammatory profile. **Key Research Findings** Clinical trials have investigated VIP (aviptadil) for acute respiratory distress syndrome (ARDS), pulmonary hypertension, and inflammatory bowel disease. In ARDS, intravenous VIP improved oxygenation and reduced lung inflammation in phase II/III trials, though results were mixed. Studies in pulmonary arterial hypertension showed enhanced pulmonary vasodilation and exercise capacity. Preclinical models demonstrate VIP’s neuroprotective effects in neurodegenerative diseases, but human data remain limited. Over 27,000 PubMed references support its pleiotropic roles, including cardioprotection and immunomodulation. **Clinical Relevance** VIP is under investigation as a therapeutic for conditions involving vasoconstriction, bronchoconstriction, or excessive inflammation. Aviptadil received emergency use authorization for COVID-19-related ARDS in some regions, though broader approval is pending. Its short half-life and need for parenteral administration limit clinical translation, though synthetic analogs with improved stability are in development. Current evidence supports potential utility in respiratory and inflammatory disorders, but larger confirmatory trials are needed. For research purposes only — not medical advice.

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