E7016 (GPI 21016) is an orally available PARP inhibitor. E7016 can enhance tumor cell radiosensitivity in vitro and in vivo through the inhibition of DNA repair. E7016 acts as a potential anticancer agent In Vitro E7016 can enhance tumor cell radiosensitivity through the inhibition of DNA repair. E7016 (3 μM)-mediated radiosensitization occurs through an increase in the number of cells undergoing mitotic catastrophe and not an increase in the number of cells undergoing apoptosis. E7016 inhibits PARP by mimicking NAD +. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Apoptosis AnalysisCell Line: The U251 human glioblastoma cell line Concentration: 3 μM Incubation Time: 6 hours prior to irradiation and were stained at 24 and 72 h postirradiation Result: The number of cells in mitotic catastrophe was significantly greater in the E7016-treated irradiated cells than in cells that received radiation only at 24 hours postirradiation. In Vivo E7016 has antitumor efficacy in murine xenograft studies . Administration of E7016 (40 mg/kg; oral gavage) to mice bearing U251 xenografts enhances the effectiveness of the Temozolomide/radiation combination . Mice treated with E7016/irradiation/Temozolomide have an additional growth delay of six days compared with the combination of Temozolomide and irradiation in vivo . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Four- to six-week-old female nude miceDosage: 40 mg/kg Administration: Oral gavage Result: E7016 enhanced the radiation/Temozolomide (3 mg/kg orally)-induced tumor growth delay of U251 xenografts. Form:Solid IC50& Target:PARP