Capecitabine Research Paper
Capecitabine (Xeloda) is an anti-cancer chemotherapy drug. Capecitabine (N4-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine) is a novel fluoropyrimidinecarbamate that is converted to 5-fluorouracil (5-FUra) by three enzymes located in the liver and tumors [1].
In vitro:In antiproliferative assays, both LS174T WT and LS174T-c2 cells were more sensitive to capecitabine when cultivated in the same plates as HepG2 hepatoma. In LS174T WT alone and cultivated with HepG2, IC50values of capecitabine were 890 ± 48 and 630 ± 14 μM respectively. The IC50fell from 330 ± 4 down to 89 ± 6 μMin LS174T-C2 subline when cultivated in the same plates as hepatoma cells.In the LS174T-c2 subclone, whereas little cell death occurred in cells exposed to capecitabine,
both early and late apoptosis were increased by 244 and 262%, respectively [1]. Furthermore, Capecitabine induces apoptosis in a Fas-dependent manner, and shows a 7-fold higher cytotoxicity and markedly stronger apoptotic potential in thymidine phosphorylase (TP)-transfected LS174T-c2 cells [2].
In vivo:Capecitabine was effective in a wider dose range in CXF280, HCT116, COLO205, and WiDr human colon cancer xenograft models [2]. In highly metastatic nude mice model, capecitabine inhibited tumor growth and metastatic recurrence after resection of HCC attributed to the high expression of PD-ECGF in tumors [3].
In vitro:In antiproliferative assays, both LS174T WT and LS174T-c2 cells were more sensitive to capecitabine when cultivated in the same plates as HepG2 hepatoma. In LS174T WT alone and cultivated with HepG2, IC50values of capecitabine were 890 ± 48 and 630 ± 14 μM respectively. The IC50fell from 330 ± 4 down to 89 ± 6 μMin LS174T-C2 subline when cultivated in the same plates as hepatoma cells.In the LS174T-c2 subclone, whereas little cell death occurred in cells exposed to capecitabine,
both early and late apoptosis were increased by 244 and 262%, respectively [1]. Furthermore, Capecitabine induces apoptosis in a Fas-dependent manner, and shows a 7-fold higher cytotoxicity and markedly stronger apoptotic potential in thymidine phosphorylase (TP)-transfected LS174T-c2 cells [2].
In vivo:Capecitabine was effective in a wider dose range in CXF280, HCT116, COLO205, and WiDr human colon cancer xenograft models [2]. In highly metastatic nude mice model, capecitabine inhibited tumor growth and metastatic recurrence after resection of HCC attributed to the high expression of PD-ECGF in tumors [3].