VIP (2mg) / BPC-157 (500mcg) x 30 Tablets
A naturally occurring 28-amino-acid neuropeptide with potent immunomodulatory, vasodilatory, and neuroprotective properties—expressed throughout the nervous and immune systems—studied in research models of autoimmune disease, neurodegeneration, pulmonary hypertension, and inflammatory bowel disease.
The Science
What is VIP (Vasoactive Intestinal Peptide)?
Vasoactive Intestinal Peptide (VIP) is a 28-amino-acid neuropeptide first isolated from porcine intestine in 1970. It belongs to the glucagon/secretin peptide superfamily and is expressed throughout the central and peripheral nervous systems, the gastrointestinal tract, and immune cells. VIP acts via two primary G-protein-coupled receptors—VPAC1 (expressed broadly on immune and epithelial cells) and VPAC2 (expressed in smooth muscle, brain, and lymphoid tissue)—activating adenylate cyclase and downstream cAMP-PKA signaling.
VIP is one of the most pleiotropic neuropeptides known, simultaneously modulating smooth muscle tone (vasodilation, bronchodilation), gastrointestinal motility and secretion, circadian rhythm regulation (acting as the primary output signal of the suprachiasmatic nucleus), immune tolerance, and neuronal survival. Its anti-inflammatory properties are particularly well-characterized: VIP suppresses Th1-type immune responses, promotes regulatory T cell induction, and inhibits the production of pro-inflammatory cytokines by activated macrophages and dendritic cells.
Research interest in exogenous VIP spans conditions including pulmonary arterial hypertension (PAH), rheumatoid arthritis, inflammatory bowel disease, Crohn's disease, sepsis, COVID-19-associated lung injury, autism spectrum disorder, and neurodegenerative diseases. VIP's short plasma half-life (approximately 2 minutes, due to rapid enzymatic cleavage) is a major pharmacological limitation, driving research into stable analogs and specialized delivery systems.
Laboratory Observations
Research-Observed Areas of Interest
Pulmonary Arterial Hypertension
Clinical pilot studies of inhaled VIP in PAH research subjects demonstrated acute reductions in pulmonary vascular resistance and improved exercise capacity. A VIP deficiency state has been detected in PAH research subjects, providing pathophysiological rationale for supplementation research.
Inflammatory Bowel Disease
VIP is highly expressed in enteric neurons and modulates gut motility, secretion, and mucosal immunity. Research suggests reduced VIP signaling contributes to IBD pathophysiology, and exogenous VIP or VPAC agonists have shown protective effects in colitis animal models.
Neurodegeneration Research
VIP and the closely related peptide PACAP have been studied as neuroprotective agents in Alzheimer's disease, Parkinson's disease, and traumatic brain injury models, where they reduce neuroinflammation and support neurotrophic factor expression.
Circadian Rhythm and Sleep Research
VIP is the primary neurotransmitter coordinating circadian clock output from the suprachiasmatic nucleus (SCN). Research suggests VIP signaling is critical for maintaining robust circadian synchrony, and its disruption is implicated in circadian-rhythm-related pathologies.
Mechanism of Action
How VIP Works
VIP exerts its broad biological effects through three functionally distinct mechanistic axes:
Immune Tolerance and Anti-inflammatory Signaling
VIP binding to VPAC1 and VPAC2 on immune cells activates cAMP/PKA signaling that suppresses NF-κB activation and the production of pro-inflammatory cytokines (TNF-α, IL-6, IL-12, IFN-γ) by macrophages, dendritic cells, and T cells. Simultaneously, VIP promotes the differentiation of regulatory T cells (Tregs) and induces tolerogenic dendritic cell phenotypes—shifting the immune balance from pro-inflammatory toward tolerance.
Smooth Muscle Relaxation and Vasodilation
VIP is a potent vasodilator and bronchodilator acting through VPAC2 receptors on vascular and airway smooth muscle. cAMP elevation reduces intracellular calcium and promotes smooth muscle relaxation. In the pulmonary vasculature, VIP deficiency has been identified in pulmonary arterial hypertension research subjects, and inhaled VIP was evaluated in clinical trials for PAH with evidence of acute hemodynamic improvement.
Neuroprotection and Neurotrophic Support
VIP is constitutively expressed by neurons and astrocytes and promotes neuronal survival through multiple mechanisms: induction of neurotrophic factors (BDNF, NGF), activation of anti-apoptotic Bcl-2 family proteins, inhibition of glutamate excitotoxicity, and suppression of microglial-mediated neuroinflammation. Research in Alzheimer's, Parkinson's, and ALS models suggests VIP and its analogs (e.g., PACAP) attenuate neurodegeneration in preclinical settings.
FAQ
Frequently Asked Questions
What is the relationship between VIP and PACAP?+
PACAP (Pituitary Adenylate Cyclase-Activating Polypeptide) is a structurally related neuropeptide sharing approximately 68% sequence homology with VIP in their receptor-binding domains. Both peptides activate VPAC1 and VPAC2 receptors; PACAP also activates a high-affinity PAC1 receptor, giving it distinct CNS and endocrine actions. The two are often studied together as neuroprotective agents.
Has VIP been studied in COVID-19 or acute lung injury?+
Yes. Given VIP's anti-inflammatory and bronchodilatory properties, researchers investigated inhaled and systemic VIP in ARDS and COVID-19-associated cytokine storm models. Early case reports and pilot studies reported improvements in oxygenation and inflammatory markers, though large controlled trials have not been completed.
Research-Only Notice
VIP (2mg) / BPC-157 (500mcg) x 30 Tablets is categorized by the FDA as for research-purposes-only. It is not intended for human consumption, diagnosis, treatment, cure, or prevention of any disease. The information above summarizes effects observed in laboratory studies to date and is provided strictly for scientific and educational reference.