Evolving paradigms reveal enhanced AML treatment strategies with selective inhibitors and degraders, suggesting improved outcomes.
Abstract FLT3 mutations drive acute myeloid leukemia (AML) progression through aberrant signaling, making FLT3 inhibition a key therapeutic strategy. Current inhibitors show efficacy, yet resistance and toxicity remain challenges. Emerging approaches, including selective inhibitors, proteolysis-targeting chimeras, and protein degraders, offer enhanced potency, sustained suppression, and combinatorial potential, representing a precision-based advancement in AML treatment.
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Thapa et al. (2026) studied this question.
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