Choroidal neovascularization and associated subretinal scarring (e.g. age-related macular degeneration) as well as the growth of abnormal blood vessels in the clear cornea and corneal scarring are serious conditions that can lead to a profound decline in vision or vision loss. There currently are no Food and Drug Administration–approved drugs that selectively reduce scar formation. Recent studies have demonstrated that a carbohydrate-binding protein, galectin-3 (Gal-3), promotes angiogenesis as well as fibrosis, and that it does so by independent mechanisms. Therefore, Gal-3 is an ideal candidate to target for developing dual-benefit drugs to control both neovascularization and fibrosis of ocular tissues. Our lab has already characterized the mechanism by which Gal-3 promotes angiogenesis. Currently, I am characterizing the mechanism by which Gal-3 modulates development of scar tissue, and am also conducting studies to identify the most potent galectin-3 inhibitor to develop novel strategies for reduction of corneal and sub-retinal fibrosis.