Figures & data
Figure 1 Metabolic pathways for capecitabine and tegafur. (A) Capecitabine is converted into active metabolite in situ by thymidine phosphorylase or uridine phosphorylase. Further 5-fluorouracil catabolism is initiated by dihydropyrimidine dehydrogenase, eventually yielding FBAL, a catabolite implicated in the etiology of hand-foot syndrome. (B) Tegafur is activated by cytochrome P450 2A6, forming 5-hydroxytegafur, an unstable intermediate which spontaneously converts to 5-fluorouracil. Reprinted by permission from Yen-Revollo JL, Goldberg RM, McLeod HL. Can inhibiting dihydropyrimidine dehydrogenase limit hand-foot syndrome caused by fluoropyrimidines? Clin Cancer Res. 2008;14:8–13.
Abbreviations: FBAL, and α-fluoro-β-alanine; 5′-dFUR, 5′-deoxy-5-fluorouridine; FUPA, 5-fluoro-ureido-propionic acid; 5′-dFCR; 5′-deoxy-5-fluorocytidine.
