作者: He Liu , Hongyan Li , Zhiqiang Feng , Jun Tai , Yang Meng
DOI: 10.1080/10428190802709438
关键词:
摘要: FB2 is a novel Abl/Src dual tyrosine kinase inhibitor which designed to overcome imatinib resistance. Besides imatinib-sensitive cell lines (K562), significantly inhibited the growth of imatinib-resistant different resistance mechanisms (K562/G5.0 and K562/G01), decreased expression autophosphorylation Bcr/Abl, c-Src Lyn kinases on them. It also proliferation Src over activated cells DU145 MDA-MB-231. Furthermore, potently prolonged survival time non-obese diabetic/severe combined immunodeficient mice harboured K562/G5.0 cells. These results indicated that FB2, an inhibitor, promising candidate for CML cancer.