SOHO 2024 | Mechanisms of resistance to the TKI asciminib in CML
Massimo Breccia
• 4 Sep 2024
Massimo Breccia, MD, Sapienza University, Rome, Italy, discusses the mechanisms of resistance to the tyrosine kinase inhibitor (TKI) asciminib, used to treat chronic myeloid leukemia (CML). He notes that mutations to the myristoyl site and other genetic mutations potentially underlie resistance. This interview took place at the Twelfth Annual Meeting of the Society of Hematologic Oncology (SOHO 2024) congress in Houston, TX.
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Transcript
So, it’s an editorial requested by Blood Journal because a group, and in particular the first name of the article is Nirav Shah, published about specific mutations that may drive a resistance to asciminib. Asciminib is the first example of a new TKI because it acts on the mid-historylic site and on the ATP site as all the other available TKIs. So at first in the trial that experimented, asciminib seems that the mechanism of resistance to this drug is the onset of mutations of the mid-historylic site...
So, it’s an editorial requested by Blood Journal because a group, and in particular the first name of the article is Nirav Shah, published about specific mutations that may drive a resistance to asciminib. Asciminib is the first example of a new TKI because it acts on the mid-historylic site and on the ATP site as all the other available TKIs. So at first in the trial that experimented, asciminib seems that the mechanism of resistance to this drug is the onset of mutations of the mid-historylic site. But now indeed we know that other mutations may confer resistance and in particular one of these are more common mutations to the first-line imatinib that is called M244V. So this article and the editorial I believe that open a possible question and shedding a light on the possibility of other mechanisms unfortunately of resistance also to this new drug.
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