VIP (Vasoactive Intestinal Peptide)
28-residue vasoactive / immune neuropeptide
Overview
VIP (Vasoactive Intestinal Peptide) is a 28-amino-acid neuropeptide and member of the secretin/glucagon peptide superfamily, originally isolated from porcine duodenum but later found to be widely distributed in the central and peripheral nervous systems. The molecule signals through two G-protein-coupled receptors (VPAC1 and VPAC2) and produces a remarkably broad pharmacological profile: vasodilation, bronchodilation, suppression of pro-inflammatory cytokine production by macrophages and T-cells, modulation of circadian rhythms in the suprachiasmatic nucleus, and effects on gut motility and exocrine secretion. The breadth of VIP's biology makes it both a fundamental research tool and a difficult target for selective therapeutic development. Lyochem supplies VIP as a lyophilized powder at ≥99.0% HPLC purity. The 28-residue sequence is reliably synthesized but the C-terminal amidation must be confirmed at +1 Da relative to the free-acid form, VIP requires the C-terminal amide for full receptor binding, and unamidated material has substantially reduced activity. The analytical packet covers peak-integration HPLC, mass spec confirming the amidated form, water content, and counter-ion. VIP has a short plasma half-life (1-2 minutes) due to rapid DPP-4 cleavage, which is a feature for acute-pharmacology research and a limitation for chronic-elevation research; engineered VIP analogs with extended half-life (Aviptadil and related modifications) are available on request through OEM service.
Who buys this, and why
Cognitive and neuropeptide buyers are predominantly research labs running in vivo rodent studies. The dominant administration route in the published literature is intranasal — Semax, Selank, DSIP, Pinealon — because these peptides are not meaningfully blood-brain-barrier permeable when delivered systemically. For in vivo workflows, endotoxin and microbial-limit testing is recommended at the CoA stage so the bioassay readout is not confounded by contamination unrelated to the test article.
Primary buyer fit: academic and contract research laboratories.
Specifications
- CAS
- 40077-57-4
- Purity (HPLC)
- ≥ 99.0%
- Common vial sizes
- 10 mg
- MOQ
- On request
- Lead time
- 14–21 days
- Storage
- -20°C, protect from light
Documentation available on request
- Lot-specific Certificate of Analysis (CoA)
- RP-HPLC chromatogram with peak integration
- ESI-MS identity confirmation (±0.5 Da)
- Sequence verification by LC-MS/MS
- Water content by Karl Fischer
- SDS / MSDS
- Bacterial endotoxin (LAL) on request — in vivo workflows
- Intranasal-formulation reconstitution guidance
- Sequence ladder (full b/y-ion) on request
Regulatory note
Sold for Research Use Only under the receiving laboratory's institutional and jurisdictional regulations. Not a finished dosage form and not labelled for human administration. In vivo research workflows should request endotoxin and microbial-limit testing on the specific lot so the bioassay readout is not confounded by contamination.
Frequently asked questions
Why does the C-terminal amidation of VIP matter?▾
VIP's C-terminal Asn28 is amidated in the native molecule (giving an Asn-NH₂ rather than a free Asn-COOH), and this amidation is essential for full binding affinity at the VPAC1 and VPAC2 receptors. Unamidated VIP has roughly 10-100-fold lower receptor affinity in published binding studies, which translates to dramatically reduced biological activity in cell-based and in vivo readouts. The analytical confirmation that Lyochem's VIP is the amidated form (rather than the free-acid contaminant from incomplete amidation during synthesis) is the mass-spec check at the theoretical amidated mass, at the +1 Da position relative to the free-acid form.
What's the difference between VPAC1 and VPAC2 receptors, and does VIP distinguish them?▾
VIP binds both VPAC1 and VPAC2 receptors with comparable affinity, it does not pharmacologically distinguish between them. The two receptors are encoded by separate genes (VIPR1 and VIPR2) and have distinct tissue-distribution patterns: VPAC1 is more concentrated in CNS, liver, and lung; VPAC2 is more concentrated in vascular smooth muscle, immune cells, and pancreatic β-cells. Engineered VIP analogs with selective VPAC1 or VPAC2 activity exist as research tools (Bay 55-9837 for VPAC2 selectivity, for example), but native VIP itself is non-selective. Research workflows requiring receptor-selective probing should use the engineered analogs rather than VIP.
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