Faricimab: A New Bispecific Antibody with Promising Durability in AMD


Results of recent phase III clinical trials with respect to efficacy and safety of faricimab, an investigational bispecific antibody which inhibits both VEGF-A and angiopoietin-2.   

Carl Regillo, MD: There have been other exciting developments in our field in the past year, and going on that theme of more durable anti-VEGF effect, now we’re back to simple intravitreal injections, but there is a novel biologic called faricimab. Can you tell me a little about what faricimab is and about the phase 3 experience we just heard about?

Diana Do, MD: Recently the phase 3 global studies of faricimab, which is a novel bispecific antibody that inhibits both VEGF and angiopoietin-2, were released. These trials met the primary end point in that people who received faricimab injections at fixed intervals of up to every 16 weeks had similar visual acuity outcomes that were noninferior to fixed dosing of aflibercept. More importantly, nearly half, about 45% of patients who were treated with faricimab, could go 16 weeks between treatments. This is very promising because this would be the first office-based intravitreal medicine that could provide up to 16 weeks of durability in nearly half of the patients. This is a very exciting development, and hopefully this will be available for retina specialists to use in the near future. In addition, thankfully there have been no significant safety signals with faricimab, so it appears to be both effective and safe. Carl, what do you think of this new bispecific antibody? Will you be using it for your patients?

Carl Regillo, MD: Yes, I agree, this is looking really promising. It’s a very successful phase 3 trial program. It works as well as the drugs we’re using now and definitely looks to be more durable. I think we’re on to the next generation of anti-VEGF therapy, something that can break us beyond 3 months in our patients. The median durability of what we’ve been using is about 2 months. This is looking like 3 months and maybe pushing the envelope to 4 months or so to get good anti-VEGF effect. We’re talking about burden, it’s not just coming to the office and getting the injection, it’s also about maintaining those gains because this is an unforgiving disease. You can miss visits, there are lapses in time required to get the drug on board, and we’ll start to lose vision and that can be permanent. That accounts for why in the real world our vision outcomes are not as good as the clinical trials where the patients are coming in on a fixed, frequent basis. Here, the patients miss visits. A drug that is more long-acting is more forgiving, and we’re less likely to lose vision over time. I think that is going to help with long-term outcomes.

I am very excited with the prospect in the next couple of years to have both PDS [Port Delivery System] and faricimab, and pick and choose. I can already think of at least 30% to 40% of my patients who are getting drug frequently who want to switch right over to faricimab to see how that works. If we’re not getting great durability in some patients, we can think about PDS. It will be wonderful to have them both. I think they complement each other very well. What about you with faricimab? I am glad you also mentioned the safety because it’s great to say it works as well and lasts longer, but it’s got to be as safe or else we’re back to the brolucizumab issue where we don’t want to use it because we’re afraid of vision problem, even if it’s only 1% or 2%. Fortunately, like you said, in the clinical trials we’re not seeing that. We’re getting even more durability, but the safety profile looks to be comparable to what we’ve been using. That’s best of both worlds. Your impressions?

Diana Do, MD: I agree. I think the combination of efficacy, durability, and safety is very promising for faricimab, and it’s advantageous because it can be delivered in the office as an intravitreal injection. I think that’s going to be great for treatment-naïve patients who have new onset wet AMD [age-related macular degeneration], and I’ll be eager to use that in that patient population. Certainly, I’ll also use it in my prior treated patients who as you mentioned we want to see if we can extend the durability of VEGF suppression over time. I think it’s unique because it’s a bispecific that inhibits both VEGF-A and angiopoietin-2, which has also been implicated in the angiogenic pathway. It might provide a little more benefit over time. That remains to be seen, but trying to get at the pathophysiology of angiogenesis can only help in this chronic disease.

Carl Regillo, MD: That added mechanism of action of blocking, you mentioned it blocks all VEGF-A, which is what our current drugs do. It also blocks angiopoietin-2, and that’s at least getting us the durability part of the benefits. As you said, it may also enhance the drying, which could help some of our patients who don’t have a complete or ideal response to some of the drugs we have been using now. There is a hint of that in the DME [diabetic macular edema] studies, which are looking just as promising, where better drying definitely correlates to better vision. This is really a big step forward to have both the PDS and faricimab potentially in our hands in the near future. But there are other exciting things coming.

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Transcript Edited for Clarity

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