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The demonstration that VEGF-A is a critical stimulus in retinal/choroidal vascular diseases and the development of intravitreous injections of potent VEGF-A antagonists as a therapy have greatly benefited millions of patients (1, 2). However, compared with outcomes in clinical trials, those in clinical practice have been substantially worse because of difficulties maintaining sufficient frequency of injections (3). This unmet medical need has motivated development of a variety of new approaches to providing sustained suppression of VEGF. However, some clinicians and investigators are concerned that sustained suppression of VEGF may cause retinal damage and loss of vision. One reason for this concern is that conditional deletion of murine Vegfa in retinal pigmented epithelium (RPE) or retina results in retinal damage (4, 5). Complete elimination of a gene product is a valuable experimental technique that can demonstrate autocrine and paracrine activities of the gene product, but it is difficult to mimic by delivery of an antagonist of that gene product. Transgenic expression of a potent VEGF-A– and -B–binding protein using the strong, retina-specific rhodopsin promoter for up to seven months caused no reduction in electroretinographic (ERG) retinal function and no retinal damage in mice (6). In nonhuman primates, intravitreous adenoassociated virus delivery of the VEGF-neutralizing protein sFLT01 (a modified version of soluble Flt1) resulted in aqueous humor levels of sFLT01 of 59 [...] Viewpoint

Low risk to retina from sustained suppression of VEGF