In comparison with four tumor cell lines and three non transformed cell types, chronic myeloid leukemia K562 cells were selectively sensitive to proliferation inhibition by the oxoindole derivative XJW20, as determined by the MTT assay. Further investigation revealed that XJW20 selectively induced G2/M arrest and apoptosis in K562 cells. At the molecular level, XJW20-induced G2/M arrest was accompanied by up-regulation of cyclin B1 and phospho (p)-Cdc25C (Ser216) and down-regulation of CDK1. There is no change in the expression of CDK2. The increased apoptotic activity by XJW20 was characterized by an increase in reactive oxygen species (ROS) generation, the mitochondrial transmembrane potential (DeltaPsi(m)) dissipation, cytochrome C releasing, apoptotic nuclei (AO/EB double staining) and nuclei condensation (DAPI-staining). The down-regulation of phosphorylated ERK was also found in XJW20-treated K562 cells. These molecular events induced by XJW20 may provide insight into the mechanism of action that led to growth arrest and apoptosis.