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Isocitrate dehydrogenase (IDH) mutations occur in approximately 20% of acute myeloid leukemia (AML) patients and the prevalence increases with patient age. IDH enzymes catalyze the conversion of isocitrate to α-ketoglutarate (αKG). However, mutations in IDH1/2 lead to a reverse reaction of αKG to the oncometabolite D-2-hydroxyglutarate (D-2HG). The accumulation of 2HG competitively inhibits αKG, thus leading to alterations in TET2-dependent hydroxymethylation, chromatin modification, activation of the hypoxic response, and increased dependence on BCL2. Ivosidenib and enasidenib are oral inhibitors of mutant IDH1 (mIDH1) and mutant IDH2 (mIDH2), respectively, approved for the treatment of relapsed/refractory IDH-mutant AML.
At the 60th American Society of Hematology Annual Meeting & Exposition, Eytan Stein from the Memorial Sloan Kettering Cancer Center, New York, US, presented data from a phase I multicenter study (NCT02632708), which is evaluating the safety of enasidenib or ivosidenib in combination with standard induction and consolidation therapy in newly diagnosed patients with mIDH1 or mIDH2 AML.
A total of 154 patients with mIDH1 or mIDH2 newly diagnosed AML were treated with induction therapy (daunorubicin 60 mg/m2/day or idarubicin 12 mg/m2/day for 3 days with cytarabine 200 mg/m2/day for 7 days) in combination with either ivosidenib (500mg daily; n = 60) for mIDH1 or enasidenib (100 mg once daily; n = 93). After induction, patients may receive ≤ 4 cycles of consolidation therapy while continuing the mIDH inhibitor.
Eytan Stein concluded by stating that the “combination of ivosidenib or enasidenib with induction and consolidation therapy is safe and well tolerated in patients with newly diagnosed AML with IDH mutation. In subsets of patients who achieved CR, ivosidenib, and enasidenib led to an MRD-negative CR and mutation clearance in a population of older, high-risk patients with mIDH AML.”
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