Doxifluridine (5'-deoxy-5-fluorouridine) is a second generation nucleoside analogprodrug developed by Roche and used as a cytostatic agent in chemotherapy in several Asian countries including China and South Korea.[1] Doxifluridine is not FDA-approved for use in the USA. It is currently being evaluated in several clinical trials as a stand-alone or combination therapy treatment.
Biology
5-Fluorouracil (5-FU), the nucleobase of doxifluridine, is currently an FDA-approved antimetabolite.[2] 5-FU is normally administered intravenously to prevent its degradation by dihydropyrimidine dehydrogenase in the gut wall. Doxifluridine is a fluoropyrimidine derivative of 5-FU, thus a second-generation nucleoside prodrug. Doxifluridine was designed to improve oral bioavailability in order to avoid dihydropyrimidine dehydrogenase degradation in the digestive system.[3]
Within a cell, pyrimidine nucleoside phosphorylase or thymidine phosphorylase can metabolize doxifluridine into 5-FU.[4][5] It is also a metabolite of capecitabine.[4] High levels of pyrimidine-nucleoside phosphorylase and thymidine phosphorylase are expressed in esophageal, breast, cervical, pancreatic, and hepatic cancers.[6][7] Liberation of 5-FU is the active metabolite and leads to inhibition of DNA synthesis and cell death.
Side effects
High thymidine phosphorylase expression is also found in the human intestinal tract, resulting in dose-limiting toxicity (diarrhea) in some individuals.[8]
^Schöffski P (February 2004). "The modulated oral fluoropyrimidine prodrug S-1, and its use in gastrointestinal cancer and other solid tumors". Anti-Cancer Drugs. 15 (2): 85–106. doi:10.1097/00001813-200402000-00001. PMID15075664.
^ abIshikawa T, Sekiguchi F, Fukase Y, Sawada N, Ishitsuka H (February 1998). "Positive correlation between the efficacy of capecitabine and doxifluridine and the ratio of thymidine phosphorylase to dihydropyrimidine dehydrogenase activities in tumors in human cancer xenografts". Cancer Research. 58 (4): 685–690. PMID9485021.
^Mori K, Hasegawa M, Nishida M, Toma H, Fukuda M, Kubota T, et al. (July 2000). "Expression levels of thymidine phosphorylase and dihydropyrimidine dehydrogenase in various human tumor tissues". International Journal of Oncology. 17 (1): 33–38. doi:10.3892/ijo.17.1.33. PMID10853015.
^Ogata Y, Sasatomi T, Mori S, Matono K, Ishibashi N, Akagi Y, et al. (Jul 2007). "Significance of thymidine phosphorylase in metronomic chemotherapy using CPT-11 and doxifluridine for advanced colorectal carcinoma". Anticancer Research. 27 (4C): 2605–2611. PMID17695422.
^Lamont EB, Schilsky RL (September 1999). "The oral fluoropyrimidines in cancer chemotherapy". Clinical Cancer Research. 5 (9): 2289–2296. PMID10499595.