• N Von Bubnoff, C Peschel, and J Duyster.
• III. Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universität München. n.bubnoff@lrz.tum.de
• Dtsch. Med. Wochenschr. 2004 Oct 1; 129 (40): 2100-3.

Background And ObjectiveThe tyrosinkinase inhibitor Imatinib is active in Philadelphia-positive (Ph+) leukemia. Mutations within the Bcr-Abl kinase domain represent the major cause for clinical resistance toward imatinib. We aimed to examine, whether the alternative Abl Kinaseinhibitor SKI-DV 2 - 43 may be capable of suppressing the growth of cells expressing mutant forms of Bcr-Abl.MethodsThe proliferation of cells expressing wild-type and mutant forms of Bcr-Abl was measured in the presence of imatinib or the pyrido-pyrimidine SKI-DV 2 - 43.ResultsThe growth of a cell line expressing wild-type Bcr-Abl was suppressed with higher potency in the presence of SKI-DV 2 - 43 when compared to imatinib. Moreover, SKI-DV 2 - 43 effectively suppressed mutant forms of Bcr-Abl that cause imatinib resistance in patients.ConclusionTherefore, alternative Abl kinase inhibitors might play an important role in the future therapy of Philadelphia-positive leukemias.

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