15-keto-Prostaglandin E2

15-keto-Prostaglandin E2 (15-keto-PGE2) is an endogenous PGE₂ metabolite. 15-keto-Prostaglandin E2 inhibits STAT3 activation by binding to the Cys259 residue of STAT3. 15-keto-Prostaglandin E2 binds to and stabilizes EP2 and EP4 receptors. 15-keto-Prostaglandin E2 inhibits the growth and progression of breast cancer cells. 15-keto-Prostaglandin E2 activates PPAR-γ and promotes fungal growth. 15-keto-Prostaglandin E2 disrupts glomerular vascularization during zebrafish development and reduces the surface area of the glomerular filtration barrier^[1][2][3]. In Vitro:15-keto-PGE2 (1 μM; 20 min) binds to and stabilizes HiBiT-tagged hEP2 receptors on the cytoplasmic membrane of MMY28 yeast^[1].
15-keto-PGE₂ (10-20 μM; 24 h) dose-dependently inhibits the clonogenic capacity of MDA-MB-231 cells^[3]. In Vivo:15-keto-Prostaglandin E2 (500 μM; immersion) impairs pronephric development and glomerular filtration barrier formation in zebrafish via the EP2/EP4 receptor signaling pathway, resulting in pronephric abnormalities combined with yolk sac edema in embryos, late insertion defects in glomeruli, and a significant reduction in glomerular surface area^[1].
15-keto-Prostaglandin E2 (10 μM; immersion) significantly increases the fungal load of Cryptococcus neoformans Δplb1-GFP in zebrafish larvae, reaching 1.56 times that of the control group^[2].
15-keto-Prostaglandin E2 (70-140 μg/kg; subcutaneous injection; administered daily for 4 consecutive weeks) dose-dependently inhibits the growth of MDA-MB-231 breast cancer xenografts in BALB/c nude mice^[3].