AI Article Synopsis
- Acute myeloid leukemia (AML) is characterized by the malignant growth of defective precursor cells, often involving FLT3 mutations, which worsen prognosis.
- Quizartinib is a second-generation FLT3 inhibitor approved by the FDA for treating relapsed or refractory AML with FLT3/ITD mutations and has been effective in clinical trials since 2013.
- This review covers Quizartinib's working mechanism, its effectiveness alone or with chemotherapy, potential drug interactions, side effects, resistance issues, and future research avenues.
Article Abstract
Acute myeloid leukemia (AML) is caused by a defective precursor leading to malignant clonal expansion, often with FMS-like tyrosine kinase-3 receptor (FLT3) mutations, particularly internal tandem duplication (ITD), which has a poor prognosis. Quizartinib, a second-generation FLT3 inhibitor, has FDA approval for relapsed/refractory AML with FLT3/ITD mutation. It has shown promise in clinical studies since 2013 due to its excellent oral absorption and potent activity on FLT3. This review explores Quizartinib's mechanism of action, efficacy in monotherapy or combination with chemotherapy, drug interactions, adverse events, resistance mechanisms and future research directions.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11572082 | PMC |
| http://dx.doi.org/10.1080/14796694.2024.2399425 | DOI Listing |
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