KPV — Anti-inflammatory tripeptide — C-terminal fragment of alpha-MSH / melanocortin receptor ligand
KPV is the C-terminal tripeptide (Lys-Pro-Val) of alpha-MSH (alpha-melanocyte-stimulating hormone). Alpha-MSH's full-length anti-inflammatory activity is concentrated in its C-terminal KPV sequence, allowing oral or topical delivery without melanotropic (tanning) effects of the full peptide. Mechanisms: (1) MC1R and MC3R agonism — activates melanocortin receptors expressed on macrophages, monocytes, and dendritic cells, suppressing NF-κB signaling and reducing TNF-α, IL-1β, IL-6, and IL-8; (2) Intestinal epithelial NF-κB inhibition — maintains tight junction integrity and reduces intestinal permeability; (3) Crosses intestinal epithelium intact via oral route (intact tripeptide absorption confirmed in animal studies); (4) Activates anti-apoptotic pathways in enterocytes. CRITICAL LIMITATION: all human-relevant mechanistic data is from rodent colitis models (DSS-colitis, TNBS-colitis). No published human clinical trials as of 2024.
نظرة عامة
هذه الصفحة جزء من مكتبة المركّبات المُصنَّفة بالأدلة في Hormonaly. جميع الادعاءات السريرية مرتبطة بمصادر علمية مُحكَّمة عبر خط أنابيب التحقق المزدوج للاستشهادات.
فئة المركّب
Anti-inflammatory tripeptide — C-terminal fragment of alpha-MSH / melanocortin receptor ligand
آلية العمل
KPV is the C-terminal tripeptide (Lys-Pro-Val) of alpha-MSH (alpha-melanocyte-stimulating hormone). Alpha-MSH's full-length anti-inflammatory activity is concentrated in its C-terminal KPV sequence, allowing oral or topical delivery without melanotropic (tanning) effects of the full peptide. Mechanisms: (1) MC1R and MC3R agonism — activates melanocortin receptors expressed on macrophages, monocytes, and dendritic cells, suppressing NF-κB signaling and reducing TNF-α, IL-1β, IL-6, and IL-8; (2) Intestinal epithelial NF-κB inhibition — maintains tight junction integrity and reduces intestinal permeability; (3) Crosses intestinal epithelium intact via oral route (intact tripeptide absorption confirmed in animal studies); (4) Activates anti-apoptotic pathways in enterocytes. CRITICAL LIMITATION: all human-relevant mechanistic data is from rodent colitis models (DSS-colitis, TNBS-colitis). No published human clinical trials as of 2024.
الوضع التنظيمي
NOT FDA approved. No IND application on file. Research chemical only. Do not use in clinical practice without IRB-approved protocol.
مستوى الأدلة
D — PRECLINICAL ONLY. All evidence from DSS-colitis and TNBS-colitis mouse/rat models. No published Phase 1 human safety trial as of 2024. Cannot be applied clinically without human data.