VIP
clinical trialsAlso known as: Vasoactive Intestinal Peptide, Aviptadil
**Mechanism of Action** Vasoactive Intestinal Peptide (VIP; 28 amino acids) exerts its effects primarily through G-protein-coupled VPAC1 and VPAC2 receptors, which are widely expressed in the respiratory, cardiovascular, gastrointestinal, and immune systems. Activation of these receptors stimulates adenylate cyclase, increasing intracellular cAMP, leading to smooth muscle relaxation (vasodilation, bronchodilation), inhibition of pro-inflammatory cytokine release, and modulation of T-cell responses. VIP also suppresses NF-κB signaling and promotes regulatory T-cell differentiation, contributing to its anti-inflammatory profile. **Key Research Findings** Clinical trials have investigated synthetic VIP (aviptadil) for acute respiratory distress syndrome (ARDS), pulmonary hypertension, and inflammatory bowel disease. In phase II/III trials for COVID-19-related ARDS, intravenous aviptadil improved oxygenation and reduced mortality in severe cases, though results varied by subgroup. Preclinical studies demonstrate VIP’s neuroprotective effects in models of Parkinson’s and Alzheimer’s disease, mediated by reduced microglial activation and enhanced neuronal survival. Pharmacokinetic challenges (short half-life, ~2–3 minutes) have driven development of sustained-release formulations and analogs. **Clinical Relevance** VIP is approved in some regions for erectile dysfunction (intracavernosal) and pulmonary hypertension (inhalation). Ongoing trials target sarcoidosis, pulmonary fibrosis, and autoimmune uveitis. Its dual vasodilatory and anti-inflammatory actions position it as a candidate for conditions involving ischemia-reperfusion injury and chronic inflammation. However, rapid degradation and systemic side effects (hypotension, flushing) limit widespread use. For research purposes only — not medical advice.
Key data
C147H237N43O43SResearch & studies
VIP and VPAC1 gene expression were present in both WAT and BAT under normal conditions, while VPAC2 was absent.; Cold exposure upregulated VIP gene expression in both WAT and BAT, and induced VPAC2 gene expression, while VPAC1 showed no significant change in BAT and a slight reduction in WAT.; VIP, VPAC1, and VPAC2 proteins were detected in white and brown adipocytes, with significant increases in all three protein levels after cold exposure.
A 17-month-old child presented with MS-stage neuroblastoma and chronic diarrhea due to elevated VIP levels.; The combination of a VIP-secreting tumor with MS neuroblastoma is rare and not previously reported.; Exploratory laparotomy and tumor excision resulted in a significant decline in VIP levels and symptom resolution.
VIP is an abundant neurotransmitter in the lungs with diverse biological impacts.; VIP is involved in multiple pulmonary diseases such as asthma, cystic fibrosis, and lung tumors.; Two main limitations of VIP as a medication are outlined.; Extended-release formulations and VIP analogues are being developed to address these limitations.
On-VIP and On-VIPR1 genes were identified in Nile tilapia, with high expression in the intestine and induction by S. agalatiae.; On-VIP reduced expression of P65, P38, MyD88, STAT3, and AP1 while upregulating CREB and CBP.; In vivo, On-VIP protected tilapia from bacterial infection and promoted apoptosis and pyroptosis.
VIP stimulates glucose-dependent insulin secretion primarily via VPAC2 receptors.; VIP promotes islet β-cell proliferation through the forkhead box M1 pathway.; Clinical application of VIP is limited due to its short half-life and wide distribution.; VPAC2-selective agonists are being developed as potential novel hypoglycemic drugs.
Cylindrical VIPAMs with aspect ratios of 1.5-150 and moderate positive surface charge potentiate VIP bioactivity.; PalmK-(EK)4-VIP showed comparable or enhanced anti-inflammatory effects relative to unmodified VIP at all dosages.; VIPA formulation influences micelle shape, size, surface charge, cytotoxicity, and immunomodulatory effects.; Block arrangement and lipid block size provide insights into chemical structure-function relationships of PA micelles for peptide delivery.
Sympathectomy impaired femoral micro-architecture, bone density, and mechanical properties.; VIP expression at the fracture site was significantly decreased in sympathectomized mice.; VIP treatment rescued the repressive effects of sympathectomy on bone remodeling and increased osteogenic markers OCN and OPN.; VIP promoted fracture healing by inhibiting bone resorption.
Frequently asked questions
What is VIP?
**Mechanism of Action** Vasoactive Intestinal Peptide (VIP; 28 amino acids) exerts its effects primarily through G-protein-coupled VPAC1 and VPAC2 receptors, which are widely expressed in the respiratory, cardiovascular, gastrointestinal, and immune systems. Activation of these receptors stimulates adenylate cyclase, i
How does VIP work?
28-aa neuropeptide acting on VPAC1/2 receptors; vasodilatory, bronchodilatory, and anti-inflammatory.
What is the research status of VIP?
VIP is currently classified as clinical trials, with 27,642 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of VIP?
VIP has a molecular weight of approximately 3326.8 g/mol (formula C147H237N43O43S).
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