QUIZARTINIB IN AMLFrom Potent FLT3 Inhibition to Real World Practice
FLT3 inhibition could improve standard chemotherapy outcomes in patients with AML, even in the absence of FLT3 mutations. In nonclinical models, quizartinib has shown high binding affinity to WT FLT3 receptors and potent inhibition of FLT3 autophosphorylation in FLT3 WT cell lines. Quizartinib has also shown early clinical activity as monotherapy in patients with relapsed/refractory FLT3-ITD-negative (FLT3-ITD–) AML.1
By reviewing this infographic, you will be able to:
- Describe quizartinib’s development background, including its mechanism of action, selectivity, and activity as a type II FLT3 inhibitor, and summarize its current approval status in Canada.
- Review key efficacy and safety outcomes from the QuANTUM‑First trial and their relevance in newly diagnosed FLT3‑ITD positive AML.
- Describe the evidence supporting quizartinib’s development beyond FLT3‑ITD–positive AML and outline the ongoing clinical development plan from QUIWI to QuANTUM‑WILD, including current enrollment in Canada.
Download the infographic to optimize treatment strategies for patients diagnosed with (FLT3-ITD+) AML.
This program has been made possible through unrestricted support from Daiichi Sankyo.