Current status of agents active against the T315I chronic myeloid leukemia phenotype

Aine Carol Burke, Ronan T. Swords, Kevin Kelly, Francis J. Giles

Research output: Contribution to journalReview articlepeer-review

8 Scopus citations


Introduction: T315I is a genetic mutation of the Bcr-Abl tyrosine kinase, the pathogenetic abnormality in chronic myeloid leukemia (CML). It accounts for 10 15% of clinically relevant CML mutations. Licensed tyrosine kinase inhibitors are ineffective against this mutation and its development reduces life expectancy of CML in chronic phase from 10 years to just 22 months. Extensive work is ongoing to establish the most effective therapy to overcome this mutation, including the development of novel specific agents and also re-examination of established therapies. Areas covered: This review examines the agents in development, dividing them into Bcr-Abl-dependant and -independent groups. It looks at the progress of this research, updating the reader on the status of agents previously reported and introducing emerging therapeutic possibilities only recently announced. Expert opinion: Development of the T315I mutation is a devastating event for some patients with CML. There are potential therapeutic agents at all stages of the drug development cycle to target this patient subpopulation. Clinical activity has been demonstrated and a number of agents are on the cusp of being licensed and available for use.

Original languageEnglish (US)
Pages (from-to)85-103
Number of pages19
JournalExpert Opinion on Emerging Drugs
Issue number1
StatePublished - Mar 2011


  • T315I
  • chronic myeloid leukemia
  • drug development
  • imatinib resistance

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology


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