Diabetic retinopathy (DR) is the most prominent complication of diabetes and the leading cause of blindness in working age individuals. DR affects over 7 million individuals in North America alone. While there are several manifestations of DR, diabetic macular edema (DME) is the most common cause of central vision loss in diabetics affecting over 25% of patients suffering from diabetes.
All currently approved therapeutic approaches for DME present several side-effects ranging from photoreceptor degeneration to retinal tissue destruction. Both human patients and animal models of diabetes reveal that ocular semaphorin 3A (SEMA 3A) is robustly induced in the early stages of diabetes and mediates the breakdown of the inner blood retinal barrier. SEMA 3A presents itself as an attractive candidate for therapeutic neutralization in ocular vasculopathies characterized by edema. We have recently identified this classical neuron guidance cue as a potent inducer of ocular vascular permeability in diabetic retinas. Neutralizing SEMA 3A thus represents an attractive alternative therapeutic strategy to counter pathologic vascular permeability.
The technology being developed neutralizes SEMA 3A locally in the vitreous via a biologic trap. The SEMA 3A trap limits retinal edema in diabetes and will be applicable to prevent macular edema in age-related macular degeneration.