AG-221, a First-in-Class Therapy Targeting Acute Myeloid Leukemia Harboring Oncogenic IDH2 Mutations.

نویسندگان

  • Katharine Yen
  • Jeremy Travins
  • Fang Wang
  • Muriel D David
  • Erin Artin
  • Kimberly Straley
  • Anil Padyana
  • Stefan Gross
  • Byron DeLaBarre
  • Erica Tobin
  • Yue Chen
  • Raj Nagaraja
  • Sung Choe
  • Lei Jin
  • Zenon Konteatis
  • Giovanni Cianchetta
  • Jeffrey O Saunders
  • Francesco G Salituro
  • Cyril Quivoron
  • Paule Opolon
  • Olivia Bawa
  • Véronique Saada
  • Angelo Paci
  • Sophie Broutin
  • Olivier A Bernard
  • Stéphane de Botton
  • Benoît S Marteyn
  • Monika Pilichowska
  • YingXia Xu
  • Cheng Fang
  • Fan Jiang
  • Wentao Wei
  • Shengfang Jin
  • Lee Silverman
  • Wei Liu
  • Hua Yang
  • Lenny Dang
  • Marion Dorsch
  • Virginie Penard-Lacronique
  • Scott A Biller
  • Shin-San Michael Su
چکیده

Somatic gain-of-function mutations in isocitrate dehydrogenases (IDH) 1 and 2 are found in multiple hematologic and solid tumors, leading to accumulation of the oncometabolite (R)-2-hydroxyglutarate (2HG). 2HG competitively inhibits α-ketoglutarate-dependent dioxygenases, including histone demethylases and methylcytosine dioxygenases of the TET family, causing epigenetic dysregulation and a block in cellular differentiation. In vitro studies have provided proof of concept for mutant IDH inhibition as a therapeutic approach. We report the discovery and characterization of AG-221, an orally available, selective, potent inhibitor of the mutant IDH2 enzyme. AG-221 suppressed 2HG production and induced cellular differentiation in primary human IDH2 mutation-positive acute myeloid leukemia (AML) cells ex vivo and in xenograft mouse models. AG-221 also provided a statistically significant survival benefit in an aggressive IDH2R140Q-mutant AML xenograft mouse model. These findings supported initiation of the ongoing clinical trials of AG-221 in patients with IDH2 mutation-positive advanced hematologic malignancies.Significance: Mutations in IDH1/2 are identified in approximately 20% of patients with AML and contribute to leukemia via a block in hematopoietic cell differentiation. We have shown that the targeted inhibitor AG-221 suppresses the mutant IDH2 enzyme in multiple preclinical models and induces differentiation of malignant blasts, supporting its clinical development. Cancer Discov; 7(5); 478-93. ©2017 AACR.See related commentary by Thomas and Majeti, p. 459See related article by Shih et al., p. 494This article is highlighted in the In This Issue feature, p. 443.

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عنوان ژورنال:
  • Cancer discovery

دوره 7 5  شماره 

صفحات  -

تاریخ انتشار 2017