Unmet Needs and Future Perspectives in AML

EP: 1.Secondary Acute Myeloid Leukemia (AML): Overview

EP: 2.Patient Profile 1: Patient with Secondary Acute Myeloid Leukemia

EP: 3.CPX-351 in Treatment of AML and Clinical Considerations

EP: 4.Selecting the Right Patients for CPX-351 or Venetoclax + Azacitidine in AML

EP: 5.Considerations for Venetoclax + Azacitidine Administration and AE Management

EP: 6.Role of MRD in Treatment Decision Making in AML

EP: 7.Patient Profile 2: Patient with de novo AML and IDH2 Mutation

EP: 8.Importance of Molecular Testing in Acute Myeloid Leukemia to Guide Treatment

EP: 9.Targeted Therapy in Patients with AML and IDH1/IDH2 Mutations

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EP: 10.Unmet Needs and Future Perspectives in AML

Richard Stone, MD: Eunice, do you have any last thoughts?

Eunice Wang, MD: There are some newer IDH inhibitors in development. Some of them are pan-IDH1/IDH2. Primarily, there are data presented on some newer IDH1 inhibitors. Up until now, the data I’ve seen, which are obviously in very refractory/relapsed patients, suggest similar response rates. It’s still a question of whether some of these newer IDH1/IDH2 inhibitors—similar to a second-generation FLT3 inhibitor—are going to supersede the ivosidenib and enasidenib that we have right now.

We have a myriad of therapies. The discussion of these 2 cases is important because it suggests that all of these treatment approaches need to be highly personalized. Even with the retrospective data that we talked about with venetoclax-azacitidine vs CPX-351, one could argue that retrospective data support venetoclax-azacitidine for some of our younger patients, or it could also support the use of CPX-351 in our younger patients. The treatment approach is to test, look for these mutations, and personalize at every time point. It seems like there’s no 1 answer anymore. We keep having more of these discussions. Do you agree?

Richard Stone, MD: I agree with everything you said. I’ll just make a couple of remarks about these cases. The first case highlights the importance of thinking about the heterogeneity of secondary AML [acute myeloid leukemia], that not all patients with secondary AML are created equally. Although they’re obviously more likely to have adverse prognostic features because of their exposure to chemotherapy, perhaps in part due to selection of adverse clones when they’ve been exposed to the chemotherapy.

As you pointed out, the second case shows the importance of repetitive assessment of disease biology, which can change with time, and brings up the question of how to use targeted therapy, whether everybody should get it up front or wait until they relapse. That’s a big question in the IDH field. It also brings up the issue of when to use venetoclax: up front or at relapse. Certainly, I view venetoclax as a chemotherapy enhancer. Patients who are going to respond to chemotherapy are likely to benefit from the addition of venetoclax. People who aren’t likely to respond to chemotherapy, like those with TP53 mutations, might not. We have a lot of work to do with this.

It has been a great pleasure, as it always is, discussing leukemia cases with you because you’re so insightful. I want to thank our viewing audience for joining us. We hope you found this OncLive® My Treatment Approach program to be useful and valuable to the treatment of your patients with AML. Eunice and I would be happy to take questions by email from anybody in the audience. Thank you very much for joining us.

Eunice Wang, MD: Thank you very much. I hope you enjoyed this.

Transcript edited for clarity.