ABL

ABL

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. 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. 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.)

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More About ABL

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]

[1] D.S. Goodsell. The molecular perspective: c-Abl tyrosine kinase. Oncologist. 2005, 10, 758-759.
[2] The molecular genetics ofPhiladelphia chromosome-positive leukemias. Kurzrock, R., Gutterman, J. Talpaz, M. N. Engl. J. Med. 1988, 319, 990-998.
[3] Dasatinib in imatinib-resistantPhiladelphia chromosome-positive leukemias. Talpaz M, Shah NP, Kantarjian H, et al. N. Engl. J. Med. 2006, 354 2531–2541.
[4]BCR-ABL tyrosine kinase inhibitors in the treatment ofPhiladelphia chromosome positive chronic myeloid leukemia: a review. An, X.; Tiwari, A.; Sun, Y.; Ding, P.; Ashby Jr, C.; Chen, Z. Leukemia research 2010, 34, 1255–1268.

 

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