Absence of ABL1 exon 2-encoded SH3 residues in BCR::ABL1 destabilizes the autoinhibited kinase conformation and confers resistance to asciminib

Abstract excerpt

The recently approved BCR::ABL1 tyrosine kinase inhibitor (TKI) asciminib has demonstrated considerable activity and tolerability in newly diagnosed chronic phase chronic myeloid leukemia (CML) patients [ 1 ]. In contrast to previously approved BCR::ABL1 TKIs that target the ATP-binding (“orthosteric”) site, asciminib is a first-in-class allosteric TKI that targets the myristoyl-binding pocket in the C-lobe of...

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