Dr. Schenkein on AG-221 for the Treatment of AML

David Schenkein, MD
Published: Tuesday, Apr 08, 2014

David Schenkein, MD, Chief Executive Officer, Agios Pharmaceuticals, discusses AG-221 for the treatment of acute myeloid leukemia (AML).

AG-221 is a small molecule that inhibits a mutated form of the metabolic enzyme isocitrate dehydrogenase 2 (IDH2). This molecule can bind to the mutant form of the protein, turn off production of the metabolite, and hopefully benefit patients. Preclinical data were presented at the 2013 ASH Meeting.

Initial clinical results presented at the 2014 AACR Annual Meeting showed that AG-221 demonstrated promising clinical and pharmacodynamic activity in patients with relapsed/refractory IDH2-mutant hematologic malignancies, particularly AML. In the analysis, 5 of 7 evaluable patients achieved complete remission or complete remission with incomplete platelet count recovery.

David Schenkein, MD, Chief Executive Officer, Agios Pharmaceuticals, discusses AG-221 for the treatment of acute myeloid leukemia (AML).

AG-221 is a small molecule that inhibits a mutated form of the metabolic enzyme isocitrate dehydrogenase 2 (IDH2). This molecule can bind to the mutant form of the protein, turn off production of the metabolite, and hopefully benefit patients. Preclinical data were presented at the 2013 ASH Meeting.

Initial clinical results presented at the 2014 AACR Annual Meeting showed that AG-221 demonstrated promising clinical and pharmacodynamic activity in patients with relapsed/refractory IDH2-mutant hematologic malignancies, particularly AML. In the analysis, 5 of 7 evaluable patients achieved complete remission or complete remission with incomplete platelet count recovery.


View Conference Coverage
Online CME Activities
TitleExpiration DateCME Credits
Hematology Briefings™: Advancing Care and Improving Outcomes for Patients With Pyruvate Kinase DeficiencyOct 31, 20181.0
Rapid Reviews in Oncology®: Practice-Changing Data in Acute Myeloid Leukemia: A Rapid Update From Atlanta OnlineDec 21, 20182.0
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