BRN-103

BRN-103 is a nicotinamide derivative and an inhibitor of the VEGF/VEGFR2 angiogenesis signaling pathway. BRN-103 concentration-dependently inhibits VEGF-induced migration, proliferation and capillary-like tube formation of HUVECs, and suppresses microvascular sprouting of ex vivo aortic rings. BRN-103 inhibits VEGF-induced phosphorylation of VEGFR2 Tyr1175, as well as the downstream phosphorylation of AKT Ser473 and eNOS Ser1172, while exerting a weak inhibitory effect on ERK phosphorylation. BRN-103 can be used in studies related to VEGF/VEGFR2 signaling and angiogenesis^[1]. In Vitro:BRN-103 (0.1-10 μM; 24 h) inhibits VEGF-induced migration of human umbilical vein endothelial cells in Transwell assays in a dose-dependent manner^[1].
BRN-103 (0.1-1 μM; 1 h pre-incubation, 24 h incubation with VEGF) inhibits VEGF-induced scratch wound healing migration of human umbilical vein endothelial cells in a dose-dependent manner^[1].
BRN-103 (0.1-1 μM) inhibits VEGF-induced proliferation of human umbilical vein endothelial cells (HUVECs) in a dose-dependent manner^[1].
BRN-103 (0.1-1 μM) dose-dependently inhibits VEGF-induced capillary-like tube formation in human umbilical vein endothelial cells^[1].
BRN-103 (0.1-1 μM; 1 h pre-incubation, 5 min incubation with VEGFR2) dose-dependently inhibits VEGF-induced phosphorylation of VEGFR2 (Tyr-1175) in human umbilical vein endothelial cells^[1].
BRN-103 (0.1-1 μM; 1 h pre-incubation, followed by 5 min, 30 min, or 1 h of incubation with VEGF) dose-dependently inhibits VEGF-induced phosphorylation of AKT (Ser-473) and eNOS (Ser-1172), and slightly inhibits phosphorylation of ERK (Thr-202/Tyr-204) in human umbilical vein endothelial cells^[1].