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| Other names | 5-fluoro-1-(oxolan-2-yl)pyrimidine-2,4-dione |
| AHFS/Drugs.com | International Drug Names |
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| Routes of administration | Oral |
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| Pharmacokinetic data | |
| Eliminationhalf-life | 3.9-11 hours |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.038.027 |
| Chemical and physical data | |
| Formula | C8H9FN2O3 |
| Molar mass | 200.169 g·mol−1 |
| 3D model (JSmol) | |
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Tegafur is achemotherapeuticprodrug of5-fluorouracil (5-FU) used in the treatment of cancers. It is a component of the combination drugtegafur/uracil. When metabolised, it becomes 5-FU.[1]
It was patented in 1967 and approved for medical use in 1972.[2]
As a prodrug to 5-FU it is used in the treatment of the following cancers:[3]
It is often given in combination with drugs that alter its bioavailability and toxicity such as gimeracil, oteracil or uracil.[3] These agents achieve this by inhibiting the enzymedihydropyrimidine dehydrogenase (uracil/gimeracil) ororotate phosphoribosyltransferase (oteracil).[3]
The major side effects of tegafur are similar to fluorouracil and include myelosuppression, central neurotoxicity and gastrointestinal toxicity (especially diarrhoea).[3] Gastrointestinal toxicity is the dose-limiting side effect of tegafur.[3] Central neurotoxicity is more common with tegafur than with fluorouracil.[3]
Thedihydropyrimidine dehydrogenase (DPD) enzyme is responsible for the detoxifying metabolism of fluoropyrimidines, a class of drugs that includes5-fluorouracil,capecitabine, and tegafur.[5]Genetic variations within the DPD gene (DPYD) can lead to reduced or absent DPD activity, and individuals who areheterozygous orhomozygous for these variations may have partial or completeDPD deficiency; an estimated 0.2% of individuals have completeDPD deficiency.[5][6] Those with partial or complete DPD deficiency have a significantly increased risk of severe or even fatal drug toxicities when treated with fluoropyrimidines; examples of toxicities includemyelosuppression,neurotoxicity andhand-foot syndrome.[5][6]
It is a prodrug to 5-FU, which is athymidylate synthase inhibitor.[3]
It is metabolised to 5-FU byCYP2A6.[7][8]
Click on genes, proteins and metabolites below to link to respective articles.[§ 1]
