Oncogene Fusion Protein
A small individual group of tyrosine kinase inhibitors is specifically targeting oncogenic fusion proteins. The expression of these proteins is caused by a reciprocal translocation between chromosomes, 9 and 22 in case of the BCR-ABL fusion protein. 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[1],[2]. Our product line includes both the very first drug registered on the market inhibiting this specific tyrosine kinase (Axon 1394: STI 571 or 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.)[3]
[1] The molecular genetics ofPhiladelphia chromosome-positive leukemias. Kurzrock, R., Gutterman, J. Talpaz, M. N. Engl. J. Med. 1988, 319, 990-998.
[2] Dasatinib in imatinib-resistantPhiladelphia chromosome-positive leukemias. Talpaz M, Shah NP, Kantarjian H, et al. N. Engl. J. Med. 2006, 354 2531–2541.
[3] 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.
| Axon ID | Name | Description | From price | |
|---|---|---|---|---|
| 1660 | Crizotinib | c-MET Inhibitor; NPM-ALK inhibitor | €70.00 | |