KF1601, a dual inhibitor of BCR::ABL1 and FLT3, overcomes drug resistance in FLT3+ blast phase chronic myeloid leukemia. (PubMed, Mol Cancer)
Furthermore, KF1601 effectively inhibited the FLT3 signaling pathway in imatinib-resistant K562 cells expressing FLT3 and TAZ, suppressing cell proliferation through dual inhibition of BCR::ABL1 and FLT3. In summary, KF1601 demonstrated promising preclinical efficacy in overcoming resistance mechanisms, including the BCR::ABL1T315I mutation, while also addressing FLT3 signaling implicated in BP-CML progression. Unlike existing therapies such as ponatinib, KF1601 offers a favorable safety profile, potentially minimizing the risk of life-threatening adverse effects.