VIP

VIP is reported to act through VPAC1 and VPAC2 receptors. The supplied mechanism evidence links receptor activation to increased cyclic AMP, relaxation of smooth muscle, dilation in vascular and airway tissues, and dampening of inflammatory pathways. The same evidence connects immune effects with reduced NF-kB activity and lower TNF-alpha signaling. Because VPAC receptors are distributed across immune cells, the gut, blood vessels, and the brain, the source characterizes VIP as a broad signaling hormone rather than a narrowly targeted agent.

The source describes most human evidence for VIP as coming from aviptadil, a synthetic analog. It cites a randomized trial in about 196 critically ill COVID-19 patients with respiratory failure, published in Critical Care Medicine in 2022, where intravenous aviptadil did not meet the 60-day primary endpoint of survival without respiratory failure, although exploratory findings were noted. It also reports that larger and inhaled approaches were evaluated in the ACTIV-3b/TESICO program, with mixed overall results. Outside pulmonary disease, the source mentions rheumatoid arthritis, pulmonary arterial hypertension, and other inflammatory conditions as areas of mechanistic or early-stage study. The supplied evidence explicitly does not support anti-aging, longevity, or general wellness claims.