Sorafenib and omacetaxine mepesuccinate as a safe and effective treatment for acute myeloid leukemia carrying internal tandem duplication of Fms-like tyrosine kinase 3

Cancer. 2020 Jan 15;126(2):344-353. doi: 10.1002/cncr.32534. Epub 2019 Oct 3.

Abstract

Background: Omacetaxine mepesuccinate (OME) has antileukemic effects against acute myeloid leukemia (AML) carrying an internal tandem duplication of Fms-like tyrosine kinase 3 (FLT3-ITD). A phase 2 clinical trial was conducted to evaluate a combination treatment of sorafenib and omacetaxine mepesuccinate (SOME).

Methods: Relapsed or refractory (R/R) or newly diagnosed patients were treated with sorafenib (200-400 mg twice daily) and OME (2 mg daily) for 7 (first course) or 5 days (second course onward) every 21 days until disease progression or allogeneic hematopoietic stem cell transplantation (HSCT). The primary endpoint was composite complete remission, which was defined as complete remission (CR) plus complete remission with incomplete hematologic recovery (CRi). Secondary endpoints were leukemia-free survival (LFS) and overall survival (OS).

Results: Thirty-nine R/R patients and 5 newly diagnosed patients were recruited. Among the R/R patients, 28 achieved CR or CRi. Two patients showed partial remission, and 9 patients did not respond. Among the 5 newly diagnosed patients, 4 achieved CR, and 1 achieved CRi. The median LFS and OS were 5.6 and 10.9 months, respectively. Prior Fms-like tyrosine kinase 3 (FLT3) inhibitor exposure (P = .007), 2 or more inductions (P = .001), and coexisting IDH2 (P = .008) and RUNX1 mutations (P = .003) were associated with lower CR/CRi rates. HSCT consolidation and deep molecular responses (defined as an FLT3-ITD variant allelic frequency [VAF] ≤ 0.1% or a nucleophosmin 1 [NPM1] mutant VAF ≤ 0.01%) were associated with better OS and LFS. Prior FLT3 inhibitor exposure and 2 or more inductions were associated with inferior LFS.

Conclusions: SOME was safe and effective for R/R and newly diagnosed FLT3-ITD AML.

Keywords: acute myeloid leukemia (AML); internal tandem duplication of Fms-like tyrosine kinase 3 (FLT3-ITD); minimal residual disease; omacetaxine mepesuccinate; sorafenib.

Publication types

  • Clinical Trial, Phase II
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Antineoplastic Combined Chemotherapy Protocols / administration & dosage*
  • Antineoplastic Combined Chemotherapy Protocols / adverse effects
  • Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics
  • Disease Progression
  • Disease-Free Survival
  • Drug Administration Schedule
  • Drug Resistance, Neoplasm
  • Drug Synergism
  • Exons / genetics
  • Female
  • Gene Duplication
  • Hematopoietic Stem Cell Transplantation
  • Homoharringtonine / administration & dosage*
  • Homoharringtonine / adverse effects
  • Homoharringtonine / pharmacokinetics
  • Humans
  • Leukemia, Myeloid, Acute / genetics
  • Leukemia, Myeloid, Acute / mortality
  • Leukemia, Myeloid, Acute / pathology
  • Leukemia, Myeloid, Acute / therapy*
  • Male
  • Middle Aged
  • Neoplasm Recurrence, Local / genetics
  • Neoplasm Recurrence, Local / mortality
  • Neoplasm Recurrence, Local / pathology
  • Neoplasm Recurrence, Local / therapy*
  • Nucleophosmin
  • Remission Induction / methods
  • Sorafenib / administration & dosage*
  • Sorafenib / adverse effects
  • Sorafenib / pharmacokinetics
  • Transplantation, Homologous
  • Young Adult
  • fms-Like Tyrosine Kinase 3 / antagonists & inhibitors
  • fms-Like Tyrosine Kinase 3 / genetics*
  • fms-Like Tyrosine Kinase 3 / pharmacokinetics

Substances

  • NPM1 protein, human
  • Nucleophosmin
  • Homoharringtonine
  • Sorafenib
  • FLT3 protein, human
  • fms-Like Tyrosine Kinase 3