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EHA 2025 | Combining targeted agents with existing backbones to improve outcomes in AML
Gail Roboz, MD, University of Florence, Florence, Italy, comments on the potential of combining targeted agents with existing backbones to improve outcomes for patients with acute myeloid leukemia (AML). Dr Roboz discusses combining IDH or FLT3 inhibitors with venetoclax and hypomethylating agents, with upcoming trials investigating the potential benefits. This interview took place at the 30th Congress of the European Hematology Association (EHA) in Milan, Italy.
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Transcript
A hot topic at the meeting was how to do better in AML. So how do you get deeper remissions faster and how do we cure more patients? So I would say an emerging discussion both for patients who don’t currently have curative options, so older patients who aren’t going on to transplant, but also for younger patients who are on a curative path is what about triplet therapy or what about adding in agents to existing backbones? So this is a very hot topic...
A hot topic at the meeting was how to do better in AML. So how do you get deeper remissions faster and how do we cure more patients? So I would say an emerging discussion both for patients who don’t currently have curative options, so older patients who aren’t going on to transplant, but also for younger patients who are on a curative path is what about triplet therapy or what about adding in agents to existing backbones? So this is a very hot topic. And the question is that, for example, if you have a combination therapy, let’s say of a hypomethylating agent and venetoclax, but you have an IDH mutation, should we be adding an IDH inhibitor on top of that? This is not standard of care. These are in clinical trials, but the MD Anderson Cancer Center, for example, has led efforts in IDH1 mutated patients to have a combination of a hypomethylating agent, an IDH1 inhibitor, and venetoclax. In FLT3 mutated patients, also led by MD Anderson, preliminary data looking very promising for a hypomethylating agent plus venetoclax plus gilteritinib for FLT3 mutated patients. And these are moving into the randomized trial setting so that we can finally actually learn who do we need to do this for? And from a survival perspective, are we actually prolonging survival? Are we getting closer to curing those patients? Or are we just layering in additional medications?
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