Abstract

Chronic myelogenous leukemia (CML), a type of cancer of the white blood cells, arises due to the constitutive activity of the BCR-ABL1 oncoprotein. Several non-specific ATP competitive tyrosine kinase inhibitors including imatinib (Gleevec), dasatinib (Sprycel), nilotinib (Tasigna), and bosutinib (Bosulif) can enhance the overall survival rate of CML patients. However, many of these drugs became resistant due to mutation of the threonine T315 to isoleucine (T315I). Asciminib binds myristate pocket in an allosteric site, outside the catalytic/ATP-binding site. It inhibits both wide- type and mutated T315I BCR-ABL1 activities in vitro, in vivo and in human clinical trials. This very short review discusses the current CML treatment options and mechanism of action, dosage and administration, pharmacokinetic, drug interaction, and side effects of newly approved acciminib.

Graphical Abstract

Asciminib (Scemblix)

Allosteric Inhibitor of BCR-ABL1; Binding to myristate pocket