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Structure optimization, synthesis and bioactivity evaluation of novel BCR-ABL tyrosine kinase inhibitor targeting T315I mutation.

Chemico-biological interactions - 1 Nov 2024

Wang Shuo, Chen Jingjing, Hou Rui, Xiong Yijing, Shi Huaihuai, Chen Zhesheng, Li Jiazhong, Wang Xin

Abstract excerpt

Chronic Myeloid Leukemia (CML) is a malignant hematologic tumor caused by BCR-ABL fusion protein that binds with ATP to exert tyrosinase activity and persistently activates downstream phosphorylation pathways. The tyrosine kinase inhibitors (TKIs) represented by Imatinib are the key clinical therapy to the CML. While the mutations on the target lead to the serious drug resistance problems, especially the T315I...

Topics

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Antineoplastic Agents
Fusion Proteins, bcr-abl
Imidazoles
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Molecular Docking Simulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Protein Kinase Inhibitors

Structure-Activity Relationship

Tyrosine Kinase Inhibitors

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Identifiers

PMID: 39332790
DOI: 10.1016/j.cbi.2024.111248

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

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