Bcr-Abl Inhibited by STI571 (Imatinib)

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The development of STI571 for the inhibition of Bcr-Abl Tyrosine Kinase revolutionised treatment for chronic myelogenous leukemia (CML), and shows hope for highly specific and effective drug intervention. Bcr-Abl is a constitutively activated, mutated version of Abl, which would normally have highly controlled activity. STI571 or Imatinib has remarkably specific binding to the inactivated conformation of the affected enzyme, and has been shown to be successful in curbing disease progression in up to 93% of cases (Druker, 2008). Druker, BJ 2008, ‘Translation of the Philadelphia chromosome into therapy for CML’, Blood, vol. 112, no. 13, pp. 4808-4817. Structural Information: Schindler, T, Bornmann, W, Pellicena, P, Miller, WT, Clarkson, B & Kuriyan, J 2000, ‘Structural mechanism for STI-571 inhibition of abelson tyrosine kinase’, Science, vol. 289, no. 5486, pp. 1938-1942.