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VIP peptides are Synthesized and Lyophilized in the USA.
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What is the Vasoactive Intestinal Peptide (VIP)?
Studies suggest the potential for Vasoactive Intestinal Peptide (VIP) in controlling inflammation, especially in neurodegenerative disease, pulmonary fibrosis, inflammatory bowel disease, and cardiac fibrosis. The peptide appears to be effective in the treatment of fibrosis as well. VIP has been suggested to be a potent immune system regulator and general anti-inflammatory peptide. It is of active scientific interest for its proposed ability to preserve cognitive function in the setting of neurodegenerative disease. Vasoactive intestinal peptide (VIP, vasoactive intestinal polypeptide, PHM27) is a short peptide hormone made in the gut, pancreas, and brain of most vertebrate animals, including humans. VIP appears to bind to class II G protein-coupled receptors and is suggested to:
· Trigger the breakdown of glycogen in liver and muscle
· Reduce blood pressure
· Relax smooth muscle throughout the GI tract
· Trigger contraction of cardiac muscle
· Stimulate the secretion of water in the GI tract
· Influence vaginal lubrication
· Regulate prolactin release
· Protect cartilage
· Protect neurons against ischemia and oxidative stress
· Affect autonomic nerve function
· Synchronize the central nervous system and regulates circadian rhythm.
AKA: PHM27, Vasoactive intestinal polypeptide
Molecular Formula: C147H237N43O43S
Molecular Weight: 3326.8 g/mol
CAS Number: 37221-79-7
Vasoactive Intestinal Peptide (VIP) and Bowel Inflammation
VIP is synthesized from the immune nerve fibers in blood vessels of the central and peripheral nervous systems and immune cells. It appears to reduce inflammation in inflammatory bowel diseases (IBDs) like Crohn’s and ulcerative colitis by suppressing the production of interleukin-10 and improving intestinal barrier function. Researchers report that “VIP and its analogs have been proposed as promising alternative candidates to existing therapies for the treatment of acute and chronic inflammatory and autoimmune diseases.” Compromised barrier function leads to increased antigenic material in the space between cells, which interacts with immune cells to trigger an inflammatory response. Studies have suggested that VIP may thus reduce the antigen presentation to immune cells by improving the barrier function.
Vasoactive Intestinal Peptide (VIP) and Lung Function
VIP appears to impact lung function through the following two pathways. The first mechanism alters pulmonary vascular remodeling in response to inflammation by suppressing a peptide called NFAT, which is suggested to activate T cells, leading to increased inflammation. The scientists note that “VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation.” In particular, NFAT suppression may play a very important role in preventing pulmonary fibrosis, the end stage of diverse inflammatory conditions such as COPD, sarcoidosis, etc. Smooth muscle cell proliferation is one of the long-term consequences of lung inflammation and is a challenge in bronchial asthma that has been uncontrolled for extended periods. VIP is a potential molecule that inhibits smooth muscle proliferation. Preliminary research also suggests that VIP may lower blood pressure in the pulmonary artery, leading to increased cardiac output and improved venous oxygen saturation.
Vasoactive Intestinal Peptide (VIP) and Transplants
Rejection by the body’s immune system is one of the primary challenges faced in organ transplants. Currently, it is addressed through the use of broad-spectrum anti-inflammatory medications. Unfortunately, these medications can lead to susceptibility to serious infections and have side effects, such as scarring and organ fibrosis. VIP appears to affect dendritic cells (DCs). By reducing DC proliferation and activation, VIP may help suppress immune responses. Hence, VIP has a potential to selectively inhibit the proliferation of DCs that might cause an autoimmune reaction. This could make VIP/VIP analogs potential foundations of transplant anti-rejection medicine in the future.
Vasoactive Intestinal Peptide (VIP) and Neuroprotection
Researchers propose that VIP may hold a three-fold role in the central nervous system: as neurotransmitter, neurotrophic/neurogenic, and anti-inflammatory/neuroprotectant. In research studies related to neuroprotection, the peptide may help maintain the very critical function of the blood-brain barrier (BBB). Compromise of the BBB has been implicated in multiple sclerosis, encephalomyelitis, and even stroke. VIP may offer neuroprotective functions in Alzheimer’s disease and Parkinson’s disease, and is being researched for its potential in this area. VIP appears to act as an important neuroprotectant in the developing brain, warding off excitotoxic white matter damage and improving neuron fatty acid myelination. The exact role of VIP in Alzheimer’s disease (AD) is less clear. Research suggests that the processing of VIP is inhibited in AD, with levels of the peptide and amino acid byproducts being lower in the brains of people affected by AD. The effect of VIP appears to be mediated through VPAC1 and VPAC2 receptors. In both cases, stimulation results in increased secretion of neurotrophic factors like ADNP (activity-dependent neurotrophic factor) and BDNF (brain-derived neurotrophic factor). The peptide may help to protect synapses and astrocytes in these cases.
Vasoactive Intestinal Peptide (VIP) and Cardiac Fibrosis
As with lung disease, fibrosis is the end stage of several cardiac conditions. Cardiac fibrosis leads to several serious problems, including valve dysfunction, decreases in contractility, changes in cardiac filling, and more. As in lung disease, cardiac fibrosis is the common end-stage of many heart conditions, thus requiring a transplant. Research on rat models suggests that VIP may not only slow fibrosis down but may also reverse scarring. This possible effect is apparently partly mediated by a massive reduction in the expression of angiotensinogen and angiotensin receptor type 1a. This hypothosis seems plausible as angiotensin receptor blockers and ACE inhibitors have long been studied for their potential to slow down cardiac modeling/fibrosis and researchers suggest they are first line of prevention for fibrosis.
Vasoactive Intestinal Peptide (VIP) and COVID 19
A synthetic version of VIP, called Aviptadil (RLF-100), may help to improve the lung complications in severe cases of Covid 19. Aviptadil, like VIP, appears to inhibit pro-inflammatory cytokine production. This translates into protecting type-2 alveolar cells, the cells responsible for the bulk of oxygen exchange in the lungs. In fact, Aviptadil may actually block the SARS-2 coronavirus entry into alveolar cells. Patients on ventilators and ECMO exhibited remarkable recovery rates just three days after treatment with RLF-100. General antiviral agents have not demonstrated as rapid a recovery from infection and inhibition of viral replication the way that Aviptadil did in this research study. VIP is a member of a much larger group of neuro and endocrine peptides. It has been suggests to affect the central nervous system, GI tract, pulmonary tissue, and immune system. It is also suggested to have the potential to help in embryonic growth and development. VIP has been suggested to regulate inflammation throughout the body, especially in neurodegenerative disease, pulmonary fibrosis, inflammatory bowel disease, and cardiac fibrosis. The peptide is appears to be a potential immune system regulator and general anti-inflammatory. This is due to its suggested ability to regulate the central nervous system and preserve cognitive function in the setting of neurodegenerative disease. Finally, synthetic variants of VIP have shown promise in treating COVID 19 and have been marked for stage 2 and 3 clinical trials. This may ultimately prove beneficial for other VIP-related treatments and help pharmaceutical companies to invest in therapeutics. Innovation and research on Vasoactive Intestinal Peptides may be one of the crucial focuses in the upcoming decade.
- Gonzalez-Rey E, Delgado M. Role of vasoactive intestinal peptide in inflammation and autoimmunity. Curr Opin Investig Drugs. 2005 Nov;6(11):1116-23. PMID: 16312132.
- Seo S, Miyake H, Alganabi M, Janssen Lok M, O’Connell JS, Lee C, Li B, Pierro A. Vasoactive intestinal peptide decreases inflammation and tight junction disruption in experimental necrotizing enterocolitis. J Pediatr Surg. 2019 Dec;54(12):2520-2523. doi: 10.1016/j.jpedsurg.2019.08.038. Epub 2019 Aug 30. PMID: 31668399.
- Said SI. The vasoactive intestinal peptide gene is a key modulator of pulmonary vascular remodeling and inflammation. Ann N Y Acad Sci. 2008 Nov;1144:148-53. doi: 10.1196/annals.1418.014. PMID: 19076374.
- Petkov V, Mosgoeller W, Ziesche R, Raderer M, Stiebellehner L, Vonbank K, Funk GC, Hamilton G, Novotny C, Burian B, Block LH. Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension. J Clin Invest. 2003 May;111(9):1339-46. doi: 10.1172/JCI17500. PMID: 12727925; PMCID: PMC154449.
- Chorny A, Gonzalez-Rey E, Delgado M. Regulation of dendritic cell differentiation by vasoactive intestinal peptide: therapeutic applications on autoimmunity and transplantation. Ann N Y Acad Sci. 2006 Nov;1088:187-94. doi: 10.1196/annals.1366.004. PMID: 17192565.
- de Souza FRO, Ribeiro FM, Lima PMD. Implications of VIP and PACAP in Parkinson’s Disease: What do we Know So Far? Curr Med Chem. 2021;28(9):1703-1715. doi: 10.2174/0929867327666200320162436. PMID: 32196442.
- Mosley RL, Lu Y, Olson KE, Machhi J, Yan W, Namminga KL, Smith JR, Shandler SJ, Gendelman HE. A Synthetic Agonist to Vasoactive Intestinal Peptide Receptor-2 Induces Regulatory T Cell Neuroprotective Activities in Models of Parkinson’s Disease. Front Cell Neurosci. 2019 Sep 18;13:421. doi: 10.3389/fncel.2019.00421. PMID: 31619964; PMCID: PMC6759633.
- Duggan KA, Hodge G, Chen J, Hunter T. Vasoactive intestinal peptide infusion reverses existing myocardial fibrosis in the rat. Eur J Pharmacol. 2019 Nov 5;862:172629. doi: 10.1016/j.ejphar.2019.172629. Epub 2019 Aug 23. PMID: 31449808.
Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.