Clinical Considerations for Retreatment in Failed Anti-VEGF Therapy

EP: 1.Overview of Wet Age-Related Macular Degeneration (AMD) and Diabetic Macular Edema (DME)

EP: 2.How Do the Patient Populations Differ for Wet AMD vs DME?

EP: 3.Important Considerations Regarding Treatment Selection for Wet AMD and DME Patient Populations

EP: 4.Anti-VEGF and Gene Therapy Impacting Wet AMD and DME Treatment Landscapes

EP: 5.Variability of Frequency Dosing for Anti-VEGF Agents in the Treatment of Wet AMD

EP: 6.Faricimab: Mechanism of Action, Payers’ Perspective, and Real-World Experience

EP: 7.Faricimab Approved Label Dosing Interval

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EP: 8.Clinical Considerations for Retreatment in Failed Anti-VEGF Therapy

EP: 9.Novel Treatment Mechanisms for Patients with DME and Wet AMD

EP: 10.Diagnostic Imaging Impacting DME and Wet AMD Treatment Landscape

EP: 11.Treatment Barriers Facing Patients With DME and Wet AMD

EP: 12.Utilization Management Strategies in Treatment of Wet AMD and DME

EP: 13.Wet AMD Resource Utilization Impacted by Medication Duration of Action

EP: 14.Evolution of Access to Treatment for Wet AMD/DME Therapies

EP: 15.Payer Engagement With the Retina Community

EP: 16.Trajectory of Treatment Landscape for Wet AMD and DME

Jim Kenney, RPh, MBA: Dr Sheth, when we talk about re-treating patients who have wet AMD [age-related macular degeneration] and didn’t respond to anti-VEGF, they essentially failed that. In what patient population is re-treatment appropriate or effective if there is 1?

Veeral Sheth, MD, MBA, FACS, FASRS: It depends on how you’re describing treatment failure. Caesar [Luo] mentioned under-responders and nonresponders. The way I’ll define it for the answer to this question is that patients who are being suboptimally treated—in other words, they have residual fluid, and we’re just not able to get them dry despite frequent therapy—are patients who I consider failures in my clinic because we’re not getting to that end point that we need to get them to. In those patients, before faricimab, we had only 1 option: to switch between anti-VEGF agents, which is what all of us would do in those patients. Today it’s different because we have a different type of agent with a different mechanism of action. If a patient isn’t responding well on anti-VEGF alone, it’s very easy to switch this patient to this dual mechanism of action with faricimab, for example.

Jim Kenney, RPh, MBA: If you have a patient who fails 1 anti-VEGF, what’s the likelihood they would respond to another? In a lot of disease areas—the autoimmune space, for example—we see a lot of this. If you’ve failed 1 anti–TNF [tumor necrosis factor], then it doesn’t make sense to start another 1. You should move to a different mechanism. Do you have a chance of getting a response from a second anti-VEGF agent?

Veeral Sheth, MD, MBA, FACS, FASRS: That’s a great question. We’re treating our own anxiety when we switch them, to be honest. You’re right: when we switch those patients, we don’t see many of them do significantly well. Do we see some patients dry out who weren’t dry on 1 agent and do dry on another agent? Sure, we see that. But to your point, the vast majority are going to do about the same because you’re not changing much other than the label on the actual syringe that you’re using.

Jim Kenney, RPh, MBA: That makes sense.

Transcript edited for clarity.