Advances in Targeting BCR-ABLT315I Mutation with Imatinib Derivatives and Hybrid Anti-Leukemic Molecules.

Abstract excerpt

Resistance to imatinib remains a therapeutic challenge, largely driven by point mutations within the kinase domain of the BCR-ABL, among which the T315I substitution constitutes the most clinically significant barrier. Ponatinib effectively inhibits this mutant form but is limited by dose-dependent cardiovascular toxicity, prompting efforts to develop safer and more selective agents. Recent advances highlight...

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• Antineoplastic Agents
• Drug Resistance, Neoplasm
• Fusion Proteins, bcr-abl
• BCR gene
• Imatinib Mesylate