About DME

DME is an important cause of vision loss in diabetes and is due to leakage from the blood vessels in the retina. The leakage of fluid from damaged blood vessels results in swelling and a buildup of pressure in the eye, which leads to disorganization of the retinal layers and ultimately results in vision loss.¹ While current treatments focus on vascular endothelial growth factor (VEGF) inhibition, DME can develop from other mechanisms, such as the kallikrein-bradykinin pathway, a system at the cellular level that plays a vital role in human physiology. This is supported by observations that many patients with DME have an incomplete response to intravitreal anti-VEGF therapies that are administered every 4 to 8 weeks.^2,3

We are developing avoralstat, a plasma kallikrein inhibitor that is designed to target the kallikrein-bradykinin system on the retinal vascular endothelial cells and may result in less vascular leakage and less edema. Using a different mechanism of action from current anti-VEGF therapies and delivered to the suprachoroidal space as a depot formulation, avoralstat is designed to provide high dose levels to the retinal vessels with long-lasting exposure. This could result in less-frequent injections and a reduced burden on patients and the healthcare system. We plan to advance avoralstat into a clinical trial in patients with DME in 2025.