Background Over-expression of Aurora kinases promotes the tumorigenesis of cells. IC50 10 M) in inhibiting the experience of ALK, CHK1, cMET, EGFR, FLT3, VEGFR1 and VEGFR2 when compared with Aurora-A and Aurora-B kinase (Desk 1). The mobile activity of BPR1K653 was also analyzed. Activation of Aurora-A kinase needs an auto-phosphorylation in the Thr288 residue, whereas… Continue reading Background Over-expression of Aurora kinases promotes the tumorigenesis of cells. IC50