Vasoactive intestinal peptide (VIP)

**Vasoactive intestinal peptide (VIP)** is a 28-amino-acid neuropeptide and peptide hormone originally characterized as a potent vasodilator[2][3][6]. It is widely distributed in central and peripheral nervous systems and acts mainly through its receptors—VPAC1, VPAC2, and also PAC1—all of which are class B G protein-coupled receptors (GPCRs)[1][5][7][10]. VIP regulates a range of physiological processes including modulation of vascular tone, neurotransmission, stimulation of exocrine and endocrine secretions, immune homeostasis, fetal development, glycemic control, and cell proliferation[1][5][2][9]. VIP has been identified as a potential therapeutic agent and drug target in cardiovascular diseases (especially pulmonary hypertension), diabetes (particularly via the VPAC2 receptor for insulin secretion), neurodegenerative and inflammatory disorders, and some cancers[6][2][5][3]. Direct pharmacological use of VIP is limited by its rapid inactivation and broad tissue distribution, which pose challenges for effective and safe drug development[2][6]. Most drug development focuses on more stable analogs or targeted delivery systems to exploit the beneficial properties of VIP receptor activation while minimizing systemic side effects[2][6]. **Important note:** The **correct therapeutic targets** related to VIP are not VIP itself, but its receptors—**VPAC1 receptor**, **VPAC2 receptor**, and **PAC1 receptor**—which are class B GPCRs[1][7][10]. VIP is a ligand, not a target. Thus, VIP *by itself* should not be classified as a canonical "therapeutic target"; rather, its major biological effects are mediated through binding to these specific receptor molecules[1][10]. The user’s entry of "Vasoactive intestinal polypeptide" as a therapeutic target is **incorrect**—the full, specific receptor names (e.g., "Vasoactive intestinal peptide receptor 1 (VPAC1)") are the appropriate drug targets.

Other names

VIPvasoactive intestinal polypeptide

Binds to VPAC1, VPAC2, and PAC1 G protein-coupled receptors, triggering downstream cAMP or cGMP signaling and secondary systemic effects (e.g., vasodilation, immune modulation, stimulation of insulin secretion) Indirectly modulates nitric oxide release and smooth muscle relaxation