Advances in the Clinical Management of Diabetic Macular Edema and Age-Related Macular Degeneration - Episode 8
Carl D. Regillo, MD, FACS; and David R. Lally, MD, discuss the recent FDA approval of faricimab and the potential impact of having a molecule that inhibits 2 pathways that play a role in diabetic macular edema and neovascularization in the treatment armamentarium.
Carl D. Regillo, MD, FACS: Can you tell us about this novel or new mechanism of action and clinical profile or what makes faricimab unique?
David R. Lally, MD: Having faricimab now FDA approved is exciting because for the first time we have a single molecule that can inhibit 2 pathways that we think play a role in the disease of diabetic macular edema [DME] and neovascularization. Faricimab blocks not only the VEGF pathway…but also the angiopoietin pathway. The angiopoietin pathway is important in maintaining vascular stability. It’s a pathway that is ongoing in normal physiological conditions and there is a balance to that pathway. We know now that in disease states such as [DME] or neovascular age-related macular degeneration that there can be dysregulation of this pathway where the eye can start making increased levels of angiopoietin-2 [Ang2]. When there are higher levels of Ang2 being developed, that leads to loosening of endothelial-type junctions and vascular leakage. It promotes inflammation and leukocytes or white blood cell migration out of the vessels and into the tissues. Faricimab is…considered the first bispecific antibody, and…it’s a full size antibody where on one of the short arms that blocks VEGF-A similar to ranibizumab but on the other arm it blocks Ang2. We have the ability with 1 molecule to inhibit both pathways and by blocking Ang2 we hope that we’re going to be promoting more vascular stability and keeping those vessels from leaking more than by just blocking the VEGF pathway.
Carl D. Regillo, MD, FACS: It is exciting to have a new therapeutic medicine as a new mechanism of action above and beyond what we have been using, which we know works well. Blocking VEGF-A has been validated and works great; blocking Ang2 is officially now validated; strong preclinical evidence plays a role in both these disease states, so it’s an ideal way to target both pathways with 1 drug.
Transcript Edited for Clarity