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High affinity dihydrofolate reductase inhibitor (Ki = 7 nM). Also inhibits thymidylate synthase, AICART and glycinamide ribonucleotide formyltransferase (Ki values are 109 nM, and 3.5 μM and 9.3 μM, respectively). Indirectly activates AMPK. Inhibits proliferation of cancer cell lines in vitro.
|Storage||Store at +4°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 427.41. 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||2.34 mL||11.7 mL||23.4 mL|
|5 mM||0.47 mL||2.34 mL||4.68 mL|
|10 mM||0.23 mL||1.17 mL||2.34 mL|
|50 mM||0.05 mL||0.23 mL||0.47 mL|
References are publications that support the biological activity of the product.
Shih et al (1997) LY231514, a pyrrolo[2,3-d]pyrimidine-based antifolate that inhibits multiple folate-requiring enzymes. Cancer Res. 57 1116 PMID: 9067281
Rothbart et al (2010) Pemetrexed indirectly activates the metabolic kinase AMPK in human carcinomas. Cancer Res. 70 10299 PMID: 21159649
If you know of a relevant reference for Pemetrexed, please let us know.
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Keywords: Pemetrexed, Pemetrexed supplier, high, affinity, dihydrofolate, reductase, inhibitor, inhibitors, DHFR, thymidylate, synthase, TS, AICART, AICARFT, aminoimidazolecarboxamide, ribonucleotide, formyltransferase, glycinamide, GARFT, chemotherapeutic, antifolate, antimetabolite, Dihydrofolate, Reductase, Other, Transferases, Thymidylate, Synthetase, 6185, Tocris Bioscience
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
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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.