Inhibitor of NF-κB activation. Inhibits in vitro growth of the human pancreatic cancer cell lines MIA PaCa-2 and PANC-1, and induces apoptosis in glioblastoma cell lines. Also inhibits the cystine-glutamate antiporter, system Xc (SXC). Anti-inflammatory. Induces ferroptosis.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 398.39. Batch specific molecular weights may vary from batch to batch due to solvent 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||2.51 mL||12.55 mL||25.1 mL|
|5 mM||0.5 mL||2.51 mL||5.02 mL|
|10 mM||0.25 mL||1.26 mL||2.51 mL|
|50 mM||0.05 mL||0.25 mL||0.5 mL|
References are publications that support the products' biological activity.
Robe et al (2004) In vitro and in vivo activity of the nuclear factor-κB inhbitor sulfasalazine in human glioblastomas. Clin.Cancer Res. 10 5595 PMID: 15328202
Lo et al (2010) Potential use fo the anti-inflammatory drug, sulfasalazine, for targeted therapy of pancreatic cancer. Curr.Oncol. 17 9 PMID: 20567622
Sontheimer and Bridges (2012) Sulfasalazine for brain cancer fits. Expert Opin.Invest.Drugs 21 575 PMID: 22404218
If you know of a relevant reference for Sulfasalazine, please let us know.
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Keywords: Sulfasalazine, supplier, antirheumatic, antiinflammatories, antiinflammatory, arthritis, system, XC, SXC, cysteine-glutamate, antiporters, NF-kappaB, NF-kB, NF-κB, inhibitors, inhibits, ferroptosis, inducers, induces, NF-kB/IkB, Ferroptosis, NF-kB/IkB, Tocris Bioscience
1 Citation for Sulfasalazine
Citations are publications that use Tocris products. Selected citations for Sulfasalazine include:
Yeligar et al (2009) Ethanol augments RANTES/CCL5 expression in rat liver sinusoidal endothelial cells and human endothelial cells via activation of NF-kappa B, HIF-1 alpha, and AP-1. J Immunol 183 5964 PMID: 19828633
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