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Related Experiment Videos

Enasidenib.

Alwin Krämer1,2, Tilmann Bochtler3,4

  • 1Clinical Cooperation Unit Molecular Hematology/Oncology, German Cancer Research Center (DKFZ), University of Heidelberg, Heidelberg, Germany. a.kraemer@dkfz.de.

Recent Results in Cancer Research. Fortschritte Der Krebsforschung. Progres Dans Les Recherches Sur Le Cancer
|August 3, 2018
PubMed
Summary

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Enasidenib, an inhibitor of mutant isocitrate dehydrogenase 2 (IDH2), shows promise in treating IDH2-mutant acute myeloid leukemia. Clinical trials indicate it is well-tolerated and induces durable remissions, with ongoing studies for solid tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Mutations in isocitrate dehydrogenase 2 (IDH2) drive tumorigenesis by producing the oncometabolite (R)-2-hydroxyglutarate.
  • Elevated (R)-2-hydroxyglutarate levels cause epigenetic alterations, blocking cell differentiation and promoting cancer development.
  • IDH2 mutations are prevalent in hematologic malignancies and solid tumors.

Purpose of the Study:

  • To evaluate the efficacy and safety of enasidenib, a selective IDH2 inhibitor.
  • To assess the impact of enasidenib on (R)-2-hydroxyglutarate levels and cancer cell differentiation.
  • To explore the potential of enasidenib in treating IDH2-mutant cancers.

Main Methods:

  • Enasidenib treatment in patient-derived xenograft (PDX) mice with IDH2-mutant acute myeloid leukemia.
Keywords:
2-hydroxyglutarateAG-221AMLAcute myeloid leukemiaGlioblastomaHypermethylationIDHIsocitrate dehydrogenaseKetoglutarate

Related Experiment Videos

  • Analysis of serum (R)-2-hydroxyglutarate levels, leukemic blast differentiation, and survival rates.
  • Review of early clinical data from patients with relapsed/refractory IDH2-mutant acute myeloid leukemia.

    • Main Results:

    • Enasidenib normalized (R)-2-hydroxyglutarate levels, induced differentiation, and improved survival in preclinical models.
    • Enasidenib demonstrated good tolerability and induced durable complete remissions in approximately 20% of patients as a single agent.
    • Differentiation syndrome was identified as a notable drug-related adverse effect.

    Conclusions:

    • Enasidenib is an effective treatment for relapsed/refractory IDH2-mutant acute myeloid leukemia, leading to durable remissions.
    • Enasidenib has received FDA approval for IDH2-mutant acute myeloid leukemia.
    • Clinical trials are underway to investigate enasidenib's efficacy in IDH2-mutant solid tumors, including gliomas, chondrosarcomas, and cholangiocarcinomas.