Background

• FMS-like tyrosine kinase 3 (FLT3) is expressed in hematopoietic progenitor cells, and signaling through FLT3 promotes these cells’ proliferation and differentiation. FLT3 is mutated in approximately 30% of patients with acute myeloid leukemia (AML)
• The FLT3-ITD (internal tandem duplication) mutation is associated with
a shorter duration of response, greater cumulative incidence of relapse, and shorter survival after relapse. It has been identified as the worst single prognostic factor for duration of complete remission and relapse-free survival in AML1
• Quizartinib is a novel oral second-generation class III receptor tyrosine kinase inhibitor that has shown potent and selective FLT3 inhibition and high clinical activity in patients with FLT3-ITD–positive relapsed/refractory AML
• Quizartinib has been shown to prolong survival in patients with relapsed/refractory AML (including those with hematopoietic stem cell transplant)1 and is currently being studied along with chemotherapy in the first line

Ninth American Conference on Pharmacometrics (ACoP) Annual Meeting, October 6-12, 2018, San Diego, CA

By Dongwoo Kang, Kuan-ju Lin, Elizabeth A Ludwig, Ophelia Yin