The ABL1 protooncogene encodes a cytoplasmic and nuclear protein tyrosine kinase (ABL1; EC 2.7.10.2) that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. It is a member of the src family of tyrosine kinases, and its DNA-binding activity is regulated by CDC2-mediated phosphorylation. Moreover, the activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene. This translocation results in the head-to-tail fusion of the BCR and ABL1 genes, leading to a fusion gene present in many cases of chronic myelogenous leukemia[1]. About 95% of the patients suffering from chronic myelogenous leukaemia show expression of this particular protein, yet it is also found in two other acute forms of leukaemia[2],[3]. Our product line includes both the very first drug registered on the market inhibiting this specific tyrosine kinase (Axon 1394: STI 571-Imatinib (Novartis)), as well as well-known follow-up inhibitors, being more potent and/or more active against the emerging Gleevec/Glivec resistant BCR-ABL clones that originate from point mutations inside the kinase domain of the Bcr-Abl protein and disrupt the binding site of Imatinib on the tyrosine kinase (e.g. Axon 1392 and Axon 1396 (Dasatinib and Nilotinib resp.)[4]