Joseph M. Coney, MD, provides an overview of the drug faricimab for treating diabetic macular edema.
Nancy Holekamp, MD: We have had a great discussion about anti-VEGF [vascular endothelial growth factor] agents and the standard of care. We’ve discussed how effective it is to preserve and improve vision in patients with diabetic macular edema [DME]. We discussed how anti-VEGF injections can prevent future complications of anti-VEGF agents; the ones we currently have can also reverse the diabetic retinopathy score. That sounds great, but we’re still not satisfied because an underlying theme is the treatment burden, as it’s hard to translate what we see in clinical trials with highly motivated patients into the real world where there are real-world challenges. For the last 15 minutes, we’ll discuss emerging treatment options that may help us reduce the treatment burden. Dr Coney, can you to talk about one in particular? Which we have 2 FDA [Food and Drug Administration] phase 3 clinical trials that say it’s effective and it appears safe for treating diabetic macular edema. This molecule is a bispecific monoclonal antibody called faricimab. Can tell us about it?
Joseph M. Coney, MD: This is when good is not good enough. We have great therapies, but we still have an unmet need and unmet burden. We still have room to grow in this space. We discussed the multi-factorial pathophysiology of diabetes and diabetic retinopathy. Because we have this there is some potential for multi-targeted treatments that may affect different pathways to get better visual outcomes. There’s a molecule that we’ve been observing, it’s called faricimab, which is a single molecule with a dual mechanism of action, and it blocks this VEGFA [vascular endothelial growth factor A] that we’ve been discussing. We know that VEGF is elevated in individuals with both DME and diabetic retinopathy, but this antibody also has a different arm, which blocks Ang2 [angiopoietin-2], which has been shown to be regulated in the vitreous levels in individuals with diabetic retinopathy. Ang2 works through an inflammatory pathway called the Tie2 pathway. This is potentially important because it promotes vessels breakdown, which then leads to leakage and proliferation that we normally see in diabetes and elevated levels of Ang2. It’s also been associated with microvascular inflammation. For normal eyes there’s an Ang1 [angiopoietin-1] that promotes or activates the Ang2 pathway and this stabilizes vessels, but in disease or sick eyes, as we see in diabetes, diabetic macular edema, neovascular AMD [age-related macular degeneration], and even vein occlusions there’s this angiogenic switch where Ang2 levels in the eye cause an [INAUDIBLE] in the Tie2 receptor. This causes a lease to the destabilization, increased permeability, and increased inflammation in the eye. We have the ability now to block both VEGFA and Ang2. The goal is that this new molecule may provide more stability in the vessels, and more durability in terms of how long the drug lasts and the long-term outcome beyond using anti-VEGF.
Nancy Holekamp, MD: Thanks to all of you for this rich and informative discussion, and thank you for watching this HCPLive® Peer Exchange. If you enjoyed the content, please subscribe to our e-newsletters to receive upcoming Peer Exchanges and other great content right in your inbox.
Transcript edited for clarity.