Mauro M J, O'Dwyer M E, Druker B J
Leukemia Program, Oregon Health Sciences University, Portland 97201, USA.
Cancer Chemother Pharmacol. 2001 Aug;48 Suppl 1:S77-8. doi: 10.1007/s002800100310.
The deregulated tyrosine kinase activity of the Bcr-Abl fusion protein has been established as the causative molecular event in chronic myelogenous leukemia (CML). Thus the Bcr-Abl tyrosine kinase is an ideal target for pharmacologic inhibition. ST1571 (formerly CGP57148B), is an Abl-specific tyrosine kinase inhibitor that in preclinical studies selectively kills Bcr-Abl-containing cells in vitro and in vivo. The results of clinical studies have demonstrated the potential of molecularly targeted therapies, and ST1571 is emerging as a new therapeutic agent for CML.
Bcr-Abl融合蛋白酪氨酸激酶活性失调已被确认为慢性粒细胞白血病（CML）的致病分子事件。因此，Bcr-Abl酪氨酸激酶是药物抑制的理想靶点。ST1571（原CGP57148B）是一种Abl特异性酪氨酸激酶抑制剂，在临床前研究中，它能在体外和体内选择性杀死含有Bcr-Abl的细胞。临床研究结果证明了分子靶向治疗的潜力，ST1571正成为一种治疗CML的新型治疗药物。
