VIP (6-28)


  • Description

  • Application Data


VIP (6-28) is a vasoactive intestinal peptide (VIP) receptor antagonist that functions as a neuropeptide modulator.

See full description

Application Data

Catalogue number crb1000506
Molecular Weight 898.5
Sequence (one letter code)


Sequence (three letter code)


Purity >95%
Storage -20°C

Henning and Sawmiller, (2001). Vasoactive intestinal peptide: cardiovascular effects. Cardiovasc. Res., 49(1): 27. PMID: 11121793.

Schuelert and McDougall (2006). Electrophysiological evidence that the vasoactive intestinal peptide receptor antagonist VIP6-28 reduces nociception in an animal model of osteoarthritis. Osteoarthritis Cartilage, 14(11): 1155. PMID: 16740398.

Manufactured in: United Kingdom
Data Sheet Material Safety Data Sheet (MSDS)

Vasoactive intestinal peptide (VIP) is a neuropeptide found throughout the body and the central nervous system (CNS). VIP is located within cell bodies and nerve endings of the enteric nervous system, brain and pancreas. VIP neurons in the peripheral system fire to regulate blood vessels, and the  CNS innervate cerebral vasculature. VIP  binds to G protein-coupled receptors VPAC1 and VPAC2. VIP and VPAC2 are detected in circular smooth muscle cells of cerebral arterioles. VIP and VPAC1 are also found in lymphatic tissue. VIP can block inflammation, modify the Th response favouring Th2 and induce regulatory T cells. Overexpression of each receptor has been linked to various cancers.

VIP administration leads to pancreatic bicarbonate-rich fluid secretion but not to the same degree stimulated by secretin. VIP stimulates insulin secretion in a glucose-dependent manner and also stimulates glucagon secretion. Studies have found that in morbidly obese patients, VIP levels are lowered and work to slow gastric and duodenal motility but increase gastric emptying. Therefore, decreasing VIP levels in obese patients may increase weight gain by accelerating gastric emptying.

VIP has been well studied in pancreatic acini. VIP is a full agonist of amylase secretion and increases cyclic AMP synchronised with an increase in intracellular Ca2+ triggered by stimuli that act through cholecystokinin (CCK) or cholinergic agonists. Most cAMP increases, and amylase secretion appear to be mediated via VPAC1.

The discovery of VPAC antagonists can help to understand VIPs roles and may also provide new therapies in VIP dysregulated systems such as cancers. VIP (6-28) is a specific competitive inhibitor of the VIP receptor derived from VIP. VIP-induced vasodilatation was blocked by co-administration of the VIP receptor antagonist VIP (6-28). Using a VIP receptor antagonist has made VIP function easier to study during neuronal injury, inflammation, and heart innervation. The VIP receptor antagonist is being considered for osteoarthritis treatment, an area with no current treatments other than analgesics.

VIP (6-28)

Cat No.Pack SizePriceQty.
Bulk Quote

You may also like…