Flt3-itd. Clinical (sorafenib/ac220)

Jorge Eduardo Cortes, Naveen Pemmaraju

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

A plethora of new molecular abnormalities has been identified to be associated with acute myelogenous leukemia (AML). These markers have contributed to a more accurate prognostic stratification of these patients, and have nurtured hopes for effective targeted therapies. One such abnormality is the FMS-like tyrosine kinase 3, or FLT3 gene mutation, present in approximately 30 % of AML patients. The presence of the FLT3 internal tandem duplication (FLT3-ITD) confers a poorer prognosis with higher risk of relapse for this subset of AML patients. Rapid development of a large number of FLT3 tyrosine kinase inhibitors (TKIs) has enabled an exciting era of research and treatment for patients with these abnormalities. The expectation is that FLT3 inhibition may offer improvements in outcomes in this poor prognosis group of patients. Early data suggest that this promise may be materializing for patients. This chapter will focus on two of these FLT3 inhibitors, sorafenib (Nexavar®) and AC220 (quizartinib).

Original languageEnglish (US)
Title of host publicationTargeted Therapy of Acute Myeloid Leukemi
PublisherSpringer New York
Pages233-249
Number of pages17
ISBN (Electronic)9781493913930
ISBN (Print)9781493913923
DOIs
StatePublished - Jan 1 2015
Externally publishedYes

Keywords

  • AML
  • FLT3
  • Quizartinib
  • Sorafenib
  • Tyrosine kinase inhibitor

ASJC Scopus subject areas

  • Medicine(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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  • Cite this

    Cortes, J. E., & Pemmaraju, N. (2015). Flt3-itd. Clinical (sorafenib/ac220). In Targeted Therapy of Acute Myeloid Leukemi (pp. 233-249). Springer New York. https://doi.org/10.1007/978-1-4939-1393-0_12