5-Ethynyluracil (776C85): Protection from 5-fluorouracil-induced neurotoxicity in dogs

Davis, Stephen T.; Joyner, S S; Baccanari, David P.; Spector, Thomas

doi:10.1016/0006-2952(94)90092-2

Cited by 25 publications

(10 citation statements)

References 9 publications

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“…26,27 Because the patterns of toxicity development clearly differ between DIF preparations and non-DIF preprations, 28-31 the possibility cannot be denied that control or inhibition of DPD decreases the degradation products and decreases toxicity. [32][33][34][35] Relation between DPD and sensitivity to 5-FU It is well known that thymidylate synthase (TS), a target enzyme of 5-FU, affects the sensitivity of 5-FU. [36][37][38] It is also reported that DPD determines 5-FU sensitivity.…”

Section: Toxicity Caused By 5-fu Catabolitesmentioning

confidence: 99%

5-Fluorouracil and dihydropyrimidine dehydrogenase

Kubota

2003

International Journal of Clinical Oncology

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Dihydropyrimidine dehydrogenase (DPD) is a rate-limiting enzyme of (fluorinated) pyrimidine degradation that plays a significant role in the pharmacokinetics of 5-fluorouracil (5-FU). In addition, a catabolite of 5-FU induces a certain toxicity, and the sensitivity of 5-FU is determined by DPD activity in tumors. DPD is thus important clinically. Drugs have been developed that control variations of the pharmacokinetics of 5-FU by controlling or inhibiting DPD, thereby reducing toxicity and improving sensitivity. These fluorinated pyrimidines with DPD-inhibiting activity, called DPD-inhibitory fluoropyrimidines, contribute to oral therapy with 5-FU for cancer. This paper summarizes the important role of DPD in cancer chemotherapy with 5-FU.

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Section: Toxicity Caused By 5-fu Catabolitesmentioning

confidence: 99%

5-Fluorouracil and dihydropyrimidine dehydrogenase

Kubota

2003

International Journal of Clinical Oncology

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“…These results suggest that the therapeutic efficacy of FU can be increased by inhibiting DPD. Furthermore, a decrease in FBAL-related toxicity could be expected when DPD in the liver is inhibited, as suggested by the reduced neurotoxicity of FU treatment in dogs when EU is administrated [96]. However, it should be noted that severe neurotoxicity of FU treatment has been described for patients with a genetic DPD deficiency [97][98][99] or for patients receiving a DPD inhibitor [29].…”

Section: Modulation Of Fu Metabolismmentioning

confidence: 97%

Monitoring fluoropyrimidine metabolism in solid tumors with in vivo 19F magnetic resonance spectroscopy

Laarhoven

Punt

Kamm

et al. 2005

Critical Reviews in Oncology/Hematology

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“…4 Clinical studies have demonstrated complete inactivation of peripheral blood mononuclear cell 10,11 and intratumoral 12 DPD by orally administered eniluracil. 10,11 Coadministration of eniluracil with 5-FU results in approximately 100% oral bioavailability of 5-FU, prolonged 5-FU half-life (approximately 5 hrs), and increased renal elimination of unchanged 5-FU.…”

Section: Discussionmentioning

confidence: 99%