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Article

BCR::ABL1 kinase N-lobe mutants confer moderate to high degrees of resistance to asciminib.

Blood - 8 Aug 2024

Leyte-Vidal Ariel, Garrido Ruiz Diego, DeFilippis RosaAnna, Leske Inga B, Rea Delphine, Phan Stacey, Miller Kaeli B, Hu Feifei, Mase Anjeli, Shan Yibing, Hantschel Oliver, Jacobson Matthew P, Shah Neil P

Abstract excerpt

ABSTRACT: Secondary kinase domain mutations in BCR::ABL1 represent the most common cause of resistance to tyrosine kinase inhibitor (TKI) therapy in patients with chronic myeloid leukemia. The first 5 approved BCR::ABL1 TKIs target the adenosine triphosphate (ATP)-binding pocket. Mutations confer resistance to these ATP-competitive TKIs and those approved for other malignancies by decreasing TKI affinity and/or...

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Share to Adenosine Triphosphate
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

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Source

Identifiers

PMID: 38643492
DOI: 10.1182/blood.2023022538

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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BCR::ABL1 kinase N-lobe mutants confer moderate to high degrees of resistance to asciminib.PMID 38643492Read ↗

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