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Titlebook: Antifolate Drugs in Cancer Therapy; Ann L. Jackman Book 1999 Springer Science+Business Media New York 1999 biochemistry.cancer.cancer ther

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C. Guillén,M. C. Romero,I. Galindo 5´-thienyl-dideazatetrahydrofolic acid), which is more potent than lometrexol and has greater antitumor efficacy in vivo (2). Biochemical and pharmacological differences between LY309887 and lometrexol with respect to potency to inhibit GARFT, differential transport and storage in liver, and polygl
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Javier Dóniz-Páez,Rafael Becerra-Ramírezreductase (DHFR) (.). More recently, folate analogs were synthesized that could target other key enzymes in folate metabolism, including thymidylate synthase (TS) (., .) glycinamide ribonucleotide transformylase (GARTFase) (., .) and folylpolyglutamate synthetase (FPGS) (.). A number of these novel
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https://doi.org/10.1007/978-3-031-07289-5ity in several epithelial malignancies (.–.). The rational use of folates as modulators of toxicity or antitumor activity requires an integral understanding of their biochemistry, pharmacokinetics, and pharmacodynamics.
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Folate Biochemistry in Relation to Antifolate Selectivity,r et al. . in 1948. This work depended on knowledge generated at the American Cyanamid Company, Pearl River, NY, on the structure of folic acid and the chemical synthesis of analogs in addition to the insightful clinical observations of the Farber group .. This work was done before the role of tetra
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Raltitrexed (TomudexTM), a Highly Polyglutamatable Antifolate Thymidylate Synthase Inhibitor,f knowledge for the development of the antifolate thymidylate synthase (TS) inhibitors over the last 20 yr (. Chapter 1). For example, it was shown that the cytotoxicity induced by the indirect inhibition of TS by MTX may be antagonized by its inhibitory effects on . purine synthesis .. The antipuri
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Preclinical and Clinical Studies with the Novel Thymidylate Synthase Inhibitor Nolatrexed DihydrochThe folate-based cytotoxic agents are more likely, when compared with their pyrimidine-based counterparts, to have a unique locus of action, not be incorporated into nucleic acids, and not be susceptible to catabolic degradation. The first clinically evaluable folate-based TS inhibitor was CB3717. T
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ZD9331,f more recent interest has been the development of water-soluble acidic, quinazoline-based TS inhibitors that lack FPGS substrate activity but retain high affmity for the RFC. Work from the group of F. Sirotnak (.) has provided evidence that compounds with favorable kinetic parameters for the RFC ma
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