VIP - Vasoactive Intestinal Peptide

VIP Clinical Summary

Vasoactive Intestinal Peptide (VIP) is a 28–amino acid neuropeptide widely distributed in the CNS and periphery. VIP is released by neurons and immune cells, and acts via VPAC1/VPAC2 receptors expressed on neurons, glia, macrophages, dendritic cells, and lymphocytes.^[1–5]

Immunomodulatory & Anti-inflammatory Actions

• Suppresses pro-inflammatory cytokines (e.g., TNF-α, IFN-γ), chemokines, and APC costimulators (CD80/CD86), dampening T-cell activation.^[3,6,7]
• Shifts immunity from Th1/Th17 toward Th2, promotes Tregs, and limits macrophage pro-inflammatory polarization, reducing autoimmune/inflammatory responses (RA, MS, IBD models).^{[1,3,4,6–12]}

Neuroprotective & CNS Effects

• Upregulated after CNS injury/inflammation; protects neurons and modulates microglia/astrocyte responses.^[1,5,9,12]
• Relevant across neurodegenerative and injury models (Alzheimer’s, Parkinson’s, Huntington’s, stroke, trauma, ALS).^[1,5,9,12]

Cardiovascular & Vascular Effects

Attenuates myocarditis and atherosclerosis by reducing Th1/Th17-driven inflammation, enhancing Treg activity, and modulating lipid handling (cholesterol efflux, foam cell formation).^[10]

Therapeutic Implications

Exogenous VIP shows benefit in preclinical models of autoimmune/inflammatory diseases (RA, MS, Crohn’s), myocarditis, and atherosclerosis. VIP analogs/VPAC-targeted agents are in development for precision multitarget therapy.^[3,4,8–12]

Clinical Considerations

• Pleiotropic actions (anti-inflammatory, immunoregulatory, neuroprotective, vascular) support adjunctive use across immune-mediated and neurodegenerative conditions.^[4,9,11]
• Optimization of stability, selectivity, delivery, and biomarkers is ongoing; standardized dosing has not been established in guidelines.

References

1. Waschek JA. Br J Pharmacol. 2013;169(3):512-23.
2. Delgado M, Ganea D. Amino Acids. 2013;45(1):25-39.
3. Gonzalez-Rey E, Varela N, Chorny A, Delgado M. Curr Pharm Des. 2007;13(11):1113-39.
4. Martínez C, Juarranz Y, Gutiérrez-Cañas I, et al. Int J Mol Sci. 2019;21(1):E65.
5. Ganea D, Hooper KM, Kong W. Acta Physiol. 2015;213(2):442-52.
6. Delgado M, Abad C, Martinez C, et al. J Mol Med. 2002;80(1):16-24.
7. Carrión M, Pérez-García S, Martínez C, et al. J Leukoc Biol. 2016;100(6):1385-93.
8. Leceta J, Garin MI, Conde C. Front Immunol. 2021;12:701862.
9. Moody TW, Jensen RT. Curr Opin Endocrinol Diabetes Obes. 2021;28(2):206-13.
10. Benitez R, Delgado-Maroto V, Caro M, et al. J Immunol. 2018;200(11):3697-3710.
11. Gomariz RP, Juarranz Y, Abad C, et al. Ann N Y Acad Sci. 2006;1070:51-74.
12. Abad C, Tan YV, Lopez R, et al. PNAS. 2010;107(45):19555-60.

All COA’s avail upon request by email info@truformlabs.com.

Storage & Handling (Research Use)

• Lyophilized (dry) vials: Store sealed at −20 °C to −80 °C (long-term), desiccated and protected from light. Short-term (≤2–3 weeks) at 2–8 °C is acceptable.
• After reconstitution: Store at 2–8 °C and use within 7 days, or aliquot immediately and freeze at −20 °C to −80 °C for up to 3 months.
• Avoid degradation: Minimize air/light exposure; keep solutions on ice during handling; prepare small aliquots to avoid repeat freeze–thaw.
• Solvent & pH: Reconstitute per protocol (e.g., sterile saline/bacteriostatic water) at neutral pH (~7.0–7.4); avoid reactive metals/oxidizers.
• Labeling: Mark concentration, solvent, and prep date on all aliquots; follow lab SOPs and any product-specific stability data.