Fibulin-7 C-terminal fragment and its active synthetic peptide suppress choroidal and retinal neovascularization

Wet age-related macular degeneration (AMD) and diabetic retinopathy are the leading causes of blindness through increased angiogenesis. Although VEGF-neutralizing proteins provide benefit, inconsistent responses indicate a need for new therapies. We previously identified the Fibulin-7 C-terminal fragment (Fbln7-C) as an angiogenesis inhibitor in vitro. Here we show that Fbln7-C inhibits neovascularization in vivo, in both a model of wet AMD involving choroidal neovascularization (CNV) and diabetic retinopathy involving oxygen-induced ischemic retinopathy. Furthermore, a short peptide sequence from Fbln7-C is responsible for the anti-angiogenic properties of Fbln7-C. Our work suggests Fbln7-C as a therapeutic candidate for wet AMD and ischemic retinopathy. •Wet AMD and diabetic retinopathy are prevalent angiogenesis-mediated causes of blindness.•Neovascularization was inhibited by Fbln7-C in wet AMD and diabetic retinopathy mouse models.•A short peptide sequence of Fbln7-C suppressed choroidal neovascularization in the wet AMD model.•Fbln7-C is a potential therapy for targeting wet AMD and diabetic retinopathy.