Suppression of pathological ocular neovascularization by a small molecule, SU1498.

• SU1498 has no obvious cytotoxicity and tissue toxicity. • SU1498 administration suppresses ocular angiogenesis in vivo. • SU1498 administration inhibits endothelial angiogenic function in vitro. • SU1498 regulates endothelial function through p38-MAPK signaling. Selective inhibition of vascular endothelial growth factor receptor (VEGFR), particularly VEGFR-2, is an efficient method for the treatment of ocular neovascularization. SU1498 is a specific inhibitor of VEGFR-2. In this study, we investigated the role of SU1498 in ocular neovascularization. Administration of SU1498 did not show any cytotoxicity and tissue toxicity at the tested concentrations. Administration of SU1498 reduced the size and thickness of choroidal neovascularization and decreased the mean length and mean number of corneal neovascular vessels induced by alkali burn. Pretreatment of SU1498 significantly reduced the proliferation, migration, and tube formation ability of HUVECs. SU1498 played the anti-angiogenic role through the regulation of p38-MAPK signaling. Taken together, inhibition of VEGFR-2 by SU1498 provides a novel therapeutic approach for ocular neovascularization. [ABSTRACT FROM AUTHOR]