Current and Emerging Therapies for Wet Age-Related Macular Degeneration (AMD) - Episode 11
Expert panelists provide an overview of current unmet needs in wet AMD care and discuss the potential for improving clinical outcomes and treatment burden.
Charles C. Wykoff, MD, PhD: What is the largest unmet need that you see on a day-to-day basis? I’ll make it a 2-pronged question. The biggest unmet need, and then how do you think that need is going to be filled over the years to come as our field continues to evolve? Mark, I’ll start with you.
Mark P. Breazzano, MD: All these treatments are exciting on the horizon, I think we’re hitting that unmet need, which is trying to increase the efficiency of our treatment, to decrease the burden of the treatment but also increase the efficacy at the same time. COVID-19, looping back a little, has showed us that patients are scared to come in, but they’re also scared to lose their vision. It’s not only going to be a huge success for treating our patients during this pandemic, but even beyond that, and the future is bright for a lot of these new treatments that will transform the way we give them.
Charles C. Wykoff, MD, PhD: Great comments. Sophie?
Sophie J. Bakri, MD: I agree, treatment burden, obviously. In efficacy, we have reached very high efficacy, but then we have to think, what limits vision? It’s atrophy and fibrosis. And yes, those are other things that need to be worked on with regenerative therapies. There’s a lot of potential there as well.
Charles C. Wykoff, MD, PhD: I’ll unpack that for a second. You bring up the gorilla in the room in many ways, which is this concept of atrophy. We have the final common pathway for many of these eyes, which is where they become atrophic, whether you call it GA [geographic atrophy] or MA [macular atrophy], now we’ve got cRORA [complete retinal pigment epithelium and outer retinal atrophy]. We’ve got all these terms for this issue where the retina basically becomes atrophic. There is a lot of activity there, too much research to unpack in this short period. But it is exciting. We’re going to have phase 3 data from an inhibitor of C3 cleavage coming out in the second half of this year. And let’s say theoretically, that does become approved, and we have a molecule now that’s on label to slow geographic atrophy progression. How do you see incorporating that into your practice? Diana, I’ll refer that to you.
Diana V. Do, MD: It would be great to actually preserve vision before it’s lost. Of course, a lot of these clinical trials involve patients who already have center-involved geographic atrophy, so there’s really no chance of improving their vision. We’re just trying to limit the growth of the atrophy. You almost want to try the agent in people who have geographic atrophy that has not moved to the center, that might be juxtafoveal or extrafoveal, to try to preserve their central vision. I would be inclined to perhaps try it in that subset of patients who can benefit from stopping atrophy.
Charles C. Wykoff, MD, PhD: Very insightful. Mark, what’s your thought on how these inhibitors of GA progression will unfold clinically?
Mark P. Breazzano, MD: Diana brings up a good point, the exact location of the atrophy. And as Sophie was saying, it’s trying to understand the atrophy process itself in terms of increasing our efficacy for treating these patients with wet AMD [age-related macular degeneration]. I do think there will have to be something in the pipeline later on that address’s other parts downstream or upstream that are leading to these unfavorable aspects of the disease in these patients. As soon as we can target those in addition to VEGF, we’ll be going in the right direction, and giving the most preservation of vision for these patients. If we continue to keep our eye on the prize in the research realm, we’ll be headed in the right direction.
Charles C. Wykoff, MD, PhD: Super comments. Diana, I’ll bring it back to you then. The largest unmet need and how we’re going to fill that need over time.
Diana V. Do, MD: For me, the unmet need in most of my patients is durability of action. We’re seeing with a lot of these new agents in clinical trial development, that companies are trying to address that. When we look at real-world data, we see that a lot of patients in clinical practice receive on average 5 injections of VEGF inhibitors over a 1-year period. That’s why we’re not seeing the terrific visual acuity outcomes we would expect in patients who participate in clinical trials. If we can develop new agents that need to be injected 5 or fewer times a year in the office, that would be a game changer.
Charles C. Wykoff, MD, PhD: Thanks again to all of you, and thanks to our viewing audience. We hope you found this Ophthalmology Times® Viewpoints discussion to be useful and informative. Thank you.
Transcript edited for clarity.