Diminishing oncometabolic havoc: Approved IDH1 and IDH2 inhibitors in relapsed or refractory acute myeloid leukemia

Author Info

Jun Gong

Corresponding Author

Jun Gong
Department of Medicine, Division of Hematology/Oncology, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Los Angeles, CA 90048, USA

A B S T R A C T

Activating somatic mutations in isocitrate dehydrogenase (IDH) isoforms 1 and 2 in acute myeloid leukemia (AML) have been shown to contribute in wreaking intracellular oncometabolic havoc that adversely affects cellular growth and differentiation. Novel developments in IDH1 and IDH2 inhibitors have led to the recent U.S. Food and Drug Administration (FDA) approvals of these targeted agents in relapsed or refractory AML harboring these respective driver mutations. Their promising efficacy and well-tolerated toxicity profiles render them welcomed additions in the treatment landscape of AML. However, the IDH1 and IDH2 inhibitors ivosidenib and enasidenib, respectively, have unique class-effect toxicities that warrant early recognition in order for prompt management and re-institution of an otherwise effective class of agents.

Article Info

Article Type

Research Article

Publication history

Received: Mon 26, Nov 2018
Accepted: Tue 18, Dec 2018
Published: Fri 28, Dec 2018

Copyright

© 2023 Jun Gong. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.
DOI: 10.31487/j.ACO.2018.01.004