VIP is strictly for laboratory research and is commonly employed in the following investigational areas:

Immunomodulation and Autoimmunity

Research utilizes VIP to study the “VIP axis” in inflammatory models. Investigators measure the peptide’s ability to inhibit Th1-driven immune responses, suppress the production of pro-inflammatory cytokines (such as TNF-α and IL-6), and induce the differentiation of regulatory T cells (Tregs) in vitro.

Glucose Metabolism and Insulin Signaling

In metabolic research, VIP is applied to pancreatic islet models to characterize glucose-dependent insulin secretion. Studies focus on the activation of VPAC2 receptors on beta-cells, quantifying downstream cAMP accumulation and its correlation with improved glucose tolerance and insulin release under hyperglycemic conditions.

Cardiovascular and Hemodynamic Regulation

VIP is employed in ex vivo vascular models to assess its potent vasodilatory properties. Researchers evaluate its capacity to reduce vascular resistance and increase blood flow in coronary and pulmonary arteries, providing mechanistic insight into non-adrenergic, non-cholinergic vascular control.

Pathway / Mechanistic Context

The primary mechanistic context for VIP in research settings is the activation of Class B G-protein coupled receptors (VPAC1 and VPAC2).

• Adenylate Cyclase Activation: Binding of VIP to VPAC receptors triggers Gs-protein coupling, leading to the activation of adenylate cyclase and a rapid increase in intracellular cyclic AMP (cAMP).
• PKA Signaling: Elevated cAMP levels activate Protein Kinase A (PKA), which phosphorylates downstream targets involved in smooth muscle relaxation, inhibition of nuclear factor-kappa B (NF-κB) translocation, and modulation of cytokine gene expression.
• Potassium Channel Modulation: In vascular smooth muscle research, VIP signaling is linked to the opening of potassium channels, resulting in hyperpolarization and relaxation.

Preclinical Research Summary

Published preclinical literature documents investigations of VIP across experimental models for pathway characterization and endpoint measurement:

• Autoimmune Models: In models of collagen-induced arthritis and autoimmune encephalomyelitis, VIP administration is associated with a reduction in inflammatory scores and a shift in the cytokine profile from Th1 (pro-inflammatory) to Th2/Treg (anti-inflammatory) phenotypes.
• Diabetes Models: Transgenic mouse models overexpressing VIP in pancreatic beta-cells have demonstrated enhanced insulin secretion and improved glucose tolerance in response to glucose loading.
• Gastrointestinal Models: Studies in colitis models characterize VIP’s role in maintaining epithelial barrier integrity and regulating luminal secretion, acting as a crucial modulator of intestinal homeostasis.

Form & Analytical Testing

This material is produced via solid-phase peptide synthesis (SPPS) and supplied as a lyophilized (freeze-dried) powder.

• Lyophilization: Removes water content under vacuum to maintain compound integrity and extend shelf-life.
• Identity Verification: Each lot undergoes Mass Spectrometry (MS) to confirm the presence and molecular weight of the peptide.
• Purity Verification: High-Performance Liquid Chromatography (HPLC) is performed to ensure the product meets the ≥99% purity standard required for reproducible research data.

Storage & Handling

• Storage: Stable at -20C (-4F).
• Handling: Refer to the SDS and your institution’s SOPs for storage and handling.
• Note: Avoid repeated freeze-thaw cycles, as this degrades the peptide structure.

Referenced Citations

References are provided for informational purposes only and are not clinical claims.

[1] Henning, R. J. (2001). Vasoactive intestinal peptide: cardiovascular effects. Cardiovascular Research, 49(1), 27–37. https://doi.org/10.1016/s0008-6363(00)00229-7

[2] Iwasaki, M., Akiba, Y., & Kaunitz, J. D. (2019). Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system. F1000Research, 8, F1000 Faculty Rev-1629. https://doi.org/10.12688/f1000research.18039.1

[3] Martínez, C., Juarranz, Y., Gutiérrez-Cañas, I., Carrión, M., Pérez-García, S., Villanueva-Romero, R., … & Gomariz, R. P. (2019). A Clinical Approach for the Use of VIP Axis in Inflammatory and Autoimmune Diseases. International Journal of Molecular Sciences, 21(1), 65. https://doi.org/10.3390/ijms21010065

[4] Fahrenkrug, J. (1993). Transmitter Role of Vasoactive Intestinal Peptide. Pharmacology & Toxicology, 72(1), 353–369. https://doi.org/10.1111/j.1600-0773.1993.tb01344.x

[5] Langer, I. (2012). Mechanisms involved in VPAC receptors activation and regulation: lessons from pharmacological and mutagenesis studies. Frontiers in Endocrinology, 3, 129. https://doi.org/10.3389/fendo.2012.00129

[6] Kato, I., Suzuki, Y., Akabane, A., Yonekura, H., Tanaka, O., Kondo, H., … & Okamoto, H. (1994). Transgenic mice overexpressing human vasoactive intestinal peptide (VIP) gene in pancreatic beta cells. Evidence for improved glucose tolerance and enhanced insulin secretion by VIP and PHM-27 in vivo. Journal of Biological Chemistry, 269(33), 21223–21228.

• Stable at room temperature for up to 90 days. For long-term storage, keep at -20°C (-4°F) or colder.
• Once mixed with a solvent (e.g., bacteriostatic water), the solution must be stored at 4 °C (39°F) and utilized within 30 days. Avoid repeated freeze-thaw cycles, as this degrades the peptide structure.

RESEARCH USE ONLY

This product is intended strictly for laboratory research use only. It is not for human or veterinary use. It is not intended for diagnosis, treatment, cure, or prevention of any disease. All purchases are subject to our Terms of Service and Purity Guarantee.

No COAs available for this product.