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Acute Myeloid Leukemia (AML) is a hematological malignancy known for its aggressive nature, resistance to therapies, and high relapse rates. Approximately one-third of AML cases involve mutations in the FLT3 gene, making it a pivotal target for treatment strategies. Early FLT3 inhibitors demonstrated efficacy initially, yet subsequent issues with drug resistance and disease recurrence underscored the multifaceted challenges of AML management. Immunotherapy and combination therapies are effective strategies to overcome resistance, but there are limitations, such as toxic side effects. In contrast, FLT3 dual-target inhibitors exhibit excellent anti-tumor effects, while being safer and more controllable. Several of these inhibitors have progressed to clinical trials, underscoring their potential in advancing therapeutic options for AML. This review explores the synergistic potential of targeting FLT3 kinase in conjunction with other anti-cancer mechanisms and provides an overview of recent advancements in FLT3 dual-target inhibitors over the past decade.
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