Abstract

The emergence of resistance to molecular target therapies such as ABL-kinase inhibitors in chronic myeloid leukemia (CML) has become a significant problem despite the remarkable clinical results. The most common cause of resistance is the selection of leukemic clones with point mutations in the kinase domain, and overexpression of target molecules is another reason of resistance. I focus the novel generation of molecular target therapies for CML: STAMP (Specifically Targeting the ABL Myristoyl Pocket) inhibitor, Asciminib.

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