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Brequinar sodium is a potent and selective dihydroorotate dehydrogenase (DHODH) inhibitor (IC50 = ~20 nM). Causes depletion of pyrimidine nucleotides. Exhibits minimal inhibition against a panel of >400 kinases. Triggers differentiation of AML cell lines (ED50 = ~ 1 μM. Note uridine concentration effects ED50 value). Causes differentiation and depletion of leukemia-initiating cells in vivo. Antimetabolite.
Brequinar sodium is also offered as part of the Tocriscreen 2.0 Max and Tocriscreen Antiviral Library. Find out more about compound libraries available from Tocris.
|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|
The following data is based on the product molecular weight 397.35. 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||2.52 mL||12.58 mL||25.17 mL|
|5 mM||0.5 mL||2.52 mL||5.03 mL|
|10 mM||0.25 mL||1.26 mL||2.52 mL|
|50 mM||0.05 mL||0.25 mL||0.5 mL|
References are publications that support the biological activity of the product.
Arteaga (1989) Phase I clinical and pharmacokinetic trial of Brequinar sodium (DuP 785; NSC 368390). Cancer Res. 49 4648 PMID: 2743343
Sykes et al (2016) Inhibition of dihydroorotate dehydrogenase overcomes differentiation blockade in acute myeloid leukemia. Cell 167 171 PMID: 27641501
Peters et al (1987) Inhibition of pyrimidine de novo synthesis by DUP-785 (NSC 368390). Invest.New Drugs 5 235 PMID: 2822596
If you know of a relevant reference for Brequinar sodium, please let us know.
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Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.