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- W2030395635 abstract "Capecitabine (N4-pentyloxycarbonyl-5′-deoxy-5-fluorocytidine) is a novel fluoropyrimidine carbamate that is converted to 5-fluorouracil (5-FUra) by three enzymes located in the liver and tumors; the final step is the conversion of 5′-deoxy-5-fluorouridine (5′-dFUrd) to 5-FUra by thymidine phosphorylase in tumors. The present study compared the efficacy of capecitabine and 5-FUra at their maximum tolerated doses in CXF280, HCT116, COLO205, and WiDr human colon cancer xenograft models, and measured subsequent 5-FUra and 5′-dFUrd levels in tumors and in the plasma and muscle. Capecitabine was effective in the first three models, whereas 5-FUra was effective only in CXF280, which is a cell line highly susceptible to fluoropyrimidines. In the three susceptible models, 5-FUra AUCs in tumors after capecitabine administration were 210 to 303 nmol · hr/g, whereas those after 5-FUra administration were 8.54 to 13.1 nmol · hr/g. In addition, capecitabine gave higher levels of 5-FUra AUC in tumors than in plasma (114- to 209-fold higher) and muscle (21.6-fold higher), whereas 5-FUra was not selectively distributed to tumors. In the refractory model, WiDr, 5-FUra AUC in tumors after capecitabine administration was only 62.8 nmol · hr/g, although the level of the intermediate metabolite 5′-dFUrd was high (AUC: 695 nmol · hr/g). The ratio of 5-FUra/5′-dFUrd levels in the WiDr tumors was 0.09, which was 23.8-fold lower than that in the HCT116 tumors. The mechanism of resistance would be the inefficient conversion of 5′-dFUrd to 5-FUra by thymidine phosphorylase in tumors. Thus, capecitabine might show its high efficacy as a result of delivering high levels of 5-FUra selectively to the tumors." @default.
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- W2030395635 date "1998-04-01" @default.
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- W2030395635 title "Tumor Selective Delivery of 5-Fluorouracil by Capecitabine, a New Oral Fluoropyrimidine Carbamate, in Human Cancer Xenografts" @default.
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- W2030395635 doi "https://doi.org/10.1016/s0006-2952(97)00682-5" @default.
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