Frontline Treatment Options for Patients With IDH2-Mutated AML

EP: 1.Overview of Acute Myeloid Leukemia

EP: 2.Current Classifications of Acute Myeloid Leukemia

EP: 3.Molecular Biomarker Testing in Acute Myeloid Leukemia

EP: 4.Acute Myeloid Leukemia: Optimizing Risk Stratification

EP: 5.Role of Intensive Chemotherapy in Young, Fit Patients With AML

EP: 6.Frontline Therapy for Patients With AML and FLT3 Alterations

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EP: 7.Frontline Treatment Options for Patients With IDH2-Mutated AML

EP: 8.Acute Myeloid Leukemia: Frontline Treatment With CPX-351

EP: 9.Optimizing Management of TP53-Mutated Acute Myeloid Leukemia

EP: 10.Acute Myeloid Leukemia: VEN + AZA Treatment in Patients Unfit for Intensive Chemotherapy

EP: 11.Frontline Treatment in Patients With IDH-Mutated AML Unfit for Intensive Chemotherapy

EP: 12.Novel Venetoclax-Based Regimens in Patients With AML Unfit for Intensive Chemotherapy

EP: 13.Role of Stem Cell Transplant in Acute Myeloid Leukemia

EP: 14.Treatment Strategies in Patients With Relapsed/Refractory AML

EP: 15.A Potential Role for IDH-1 Inhibitor Olutasidenib in Relapsed/Refractory AML?

EP: 16.Sequencing Therapies in Patients With Relapsed/Refractory AML

EP: 17.Emerging Treatment Strategies in Acute Myeloid Leukemia

EP: 18.Future Directions in the Management of Acute Myeloid Leukemia

Transcript:

Jorge E. Cortes, MD: Let me move to another category, and I’ll go back to Brian. What about patients with IDH mutations? We have IDH inhibitors, but in the frontline, we have some combinations approved and some therapy, but mostly with low-intensity therapy. What do you do for a fit patient with an IDH mutation where you would usually use a 3+7 [chemotherapy regimen]? Do you change your therapy in that setting for the front line in the fit patient?

Brian Andrew Jonas, MD, PhD: I’m not sure yet. I always want to call myself a dinosaur, meaning that I have been practicing long enough to earn that title. But perhaps I want to say in our general practice, we’re still using 7+3 for the IDH patients who are fit for induction, and not necessarily changing from that at this point. I will point out that [Eytan] Stein, [MD,] led a multicenter study that was published in Blood about a year ago that showed some interesting outcomes when you combined IDH inhibitors with 7+3 therapy in terms of promising response rates. I would like to see a randomized trial to change my practice there. In general, I would say 7+3 is still the way to go for the clear induction-eligible patients. We may have a separate discussion later for induction-ineligible patients, where I think there are some interesting debates can be had at this point with recent data. But I’d be curious to see if any of my other colleagues on the call here might have a different opinion.

Margaret T. Kasner, MD: I’ll jump in because I have a different practice. The truth is, and I already said it, I have a bias and it’s very anti-7+3, and I’m not sure where it came from to be perfectly honest. We have incorporated using FLAG-IDA [fludarabine, cytarabine, granulocyte colony-stimulating factor, idarubicin] and venetoclax for fit IDH-mutated patients, with the idea that exposing them to venetoclax, based on the preponderance of data that we feel are available, is a better option for them. I have not adopted azacitidine, venetoclax for the patient who is fit for induction because I feel that’s an area that needs head-to-head comparison before I’m willing to change my practice. Maybe I’m a dinosaur in the idea that curing patients without chemotherapy currently seems impossible to me. Even if they’ve gotten azacitidine, venetoclax and then gone to transplant, they get chemotherapy in that setting. For those patients who can get it and who are fit, and who I’m going to move aggressively toward transplant, I use that combination up front until there are data to support a less aggressive approach even for the subset of patients. I’ll wait for the phase 3 data.

Transcript edited for clarity.