Radotinib is a selective second generation tyrosine kinase inhibitor that targets both the wild-type and mutant forms of Bcr-Abl, with an IC value of 30.6 nM in Ba/F3 human chronic myeloid leukemia cells expressing the wild-type form. Radotinib also inhibits platelet-derived growth factor receptors (PDGFRs) α and β with IC values of 75.5 and 130 nM, respectively. Binding of radotinib to Bcr-Abl in vitro inhibits the phosphorylation of the downstream signaling mediator CrkL. In acute myeloid leukemia cells, in vitro treatment with radotinib at doses of 10-100 µM reduces viability, activates the mitochondrial apoptosis pathway, and promotes expression of the differentiation marker CD11b.