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Nucleoside analog; inhibitor of thymidylate synthase. Incorporation of the triphosphate form into DNA induces DNA fragmentation. Exhibits antitumor activity.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 296.2. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.38 mL||16.88 mL||33.76 mL|
|5 mM||0.68 mL||3.38 mL||6.75 mL|
|10 mM||0.34 mL||1.69 mL||3.38 mL|
|50 mM||0.07 mL||0.34 mL||0.68 mL|
References are publications that support the biological activity of the product.
Okayama et al (2012) Involvement of concentrative nucleoside transporter 1 in intestinal absorption of trifluorothymidine, a novel antitumor nucleoside, in rats. J.Pharmacol.Exp.Ther. 340 457 PMID: 22076553
Emura et al (2005) Potentiation of the antitumor activity of α, α, α-trifluorothymidine by the co-administration of an inhibitor of thymidine phosphorylase at a suitable molar ratio in vivo. Int.J.Oncol. 27 449 PMID: 16010427
Yu et al (2015) Small molecules enhance CRISPR genome editing in pluripotent stem cells. Cell Stem Cell 16 142 PMID: 25658371
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Keywords: Trifluorothymidine, Trifluorothymidine supplier, antitumor, anticancer, nucleoside, analog, thymidylate, synthase, inhibitors, inhibits, DNA,, RNA, and, Protein, Synthesis, Thymidylate, Synthetase, 4460, Tocris Bioscience
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The HeLa human cervical cancer cell line was cultured in EMEM medium with 10% FCS. Anti-tumor activity of Trifluorothymidine was measured.
The rate of tumor growth (IR) inhibition was regarded as a measure of the antitumor efficacy and was calculated using the relative tumor volume (RTV) in the drug-treated groups (T) compared to that in the control group (C) using the following equation: IR (%) = (1 – T/C) × 100.
Literature in this Area
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Cancer Metabolism Poster
Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the main targets for cancer metabolism researchers. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways. These distinct metabolic circuits could provide viable cancer therapeutic targets.
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.