The structural understanding of BCR-ABL eventually led to the development of imatinib, a CML therapy that works as a potent and selective Abl inhibitor. Although initially skeptical of a any tyrosine kinase inhibitors, imatinib was shown to be a valid and potent treatment for CML. However, challenges remain as imatinib resistance has been shown to occur especially in blast crisis patients who have shown to evolve mutations in BCR-ABL, specifically the Thr315Ile mutation that blocks imatinib activity. Further research into more long-term therapies as well as second generation drugs to combat mutations can lead to longer and lasting remission in CML patients.
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