Optimizing next-generation AML therapy: Activity of mutant IDH2 inhibitor AG-221 in preclinical models

Daniel Thomas; Ravindra Majeti

doi:10.1158/2159-8290.CD-17-0270

Optimizing next-generation AML therapy: Activity of mutant IDH2 inhibitor AG-221 in preclinical models

Daniel Thomas, Ravindra Majeti

Research output: Contribution to journal › Article › peer-review

15 Citations (Scopus)

Abstract

AG-221 or enasidenib is a first-in-class selective inhibitor of mutated isocitrate dehydrogenase 2 (IDH2) with early demonstrated clinical efficacy in acute myeloid leukemia as a single agent, yet with persistence of mutant IDH2 clones. Two articles in this issue of Cancer Discovery provide further insight into the biological activity of AG-221 in promoting differentiation of IDH2-mutant cells and reversing aberrant DNA methylation over time, and demonstrating preclinical activity in combination with a targeted FLT3 kinase inhibitor to eliminate IDH2-mutant clones.

Original language	English
Pages (from-to)	459-461
Number of pages	3
Journal	Cancer Discovery
Volume	7
Issue number	5
DOIs	https://doi.org/10.1158/2159-8290.CD-17-0270
Publication status	Published or Issued - May 2017
Externally published	Yes

ASJC Scopus subject areas

Oncology

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abstract = "AG-221 or enasidenib is a first-in-class selective inhibitor of mutated isocitrate dehydrogenase 2 (IDH2) with early demonstrated clinical efficacy in acute myeloid leukemia as a single agent, yet with persistence of mutant IDH2 clones. Two articles in this issue of Cancer Discovery provide further insight into the biological activity of AG-221 in promoting differentiation of IDH2-mutant cells and reversing aberrant DNA methylation over time, and demonstrating preclinical activity in combination with a targeted FLT3 kinase inhibitor to eliminate IDH2-mutant clones.",

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Optimizing next-generation AML therapy: Activity of mutant IDH2 inhibitor AG-221 in preclinical models

Abstract

ASJC Scopus subject areas

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