For research use only.
Licensed by Pfizer Catalog No.S1576 Synonyms: Azulfidine, Salazopyrin, Sulphasalazine, NSC 667219
CAS No. 599-79-1
Sulfasalazine (Azulfidine, Salazopyrin, Sulphasalazine, NSC 667219) is a sulfa derivative of mesalazine, used as an anti-inflammatory agent to treat bowel disease and rheumatoid arthritis. Sulfasalazine is a potent and specific inhibitor of nuclear factor kappa B (NF-κB), TGF-β and COX-2. Sulfasalazine induces ferroptosis, apoptosis and autophagy.
Selleck's Sulfasalazine has been cited by 5 publications
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|Description||Sulfasalazine (Azulfidine, Salazopyrin, Sulphasalazine, NSC 667219) is a sulfa derivative of mesalazine, used as an anti-inflammatory agent to treat bowel disease and rheumatoid arthritis. Sulfasalazine is a potent and specific inhibitor of nuclear factor kappa B (NF-κB), TGF-β and COX-2. Sulfasalazine induces ferroptosis, apoptosis and autophagy.|
Sulfasalazine, like methotrexate, enhances adenosine release at an inflamed site and that adenosine diminishes inflammation via occupancy of A2 receptors on inflammatory cells.  Sulfasalazine treatment for 4 hours inhibits kappaB-dependent transcription with an IC50 value of approximately 0.625 mM. Sulfasalazine (2.5 mM) results in cell death of T-lymphocytes in a dose- and time-dependent manner. Sulfasalazine but not 5ASA or sulfapyridine, strongly inhibits NF-kappaB activation and potently induces apoptosis in T-lymphocytes.  Sulfasalazine is cleaved into sulfapyridine and 5-aminosalicylic acid (5-ASA; mesalamine) by colonic bacteria, and the latter, too, is reported to suppress NF-kappaB activity. Sulfasalazine but not its cleaved form 5-ASA causes a dose-dependent inhibition of glioma growth, this effect is entirely attributable to the inhibition of cystine uptake via the system x(c)(-) cystine-glutamate transporter. Sulfasalazine inhibits cystine uptake causing a chronic depletion of intracellular GSH and consequently compromised cellular redox defense which stymied tumor growth. 
Sulfasalazine markedly decreases the number of leukocytes that accumulated in the inflamed (carrageenan, 2 mg/ml) air pouch in the murine air pouch model of inflammation. Sulfasalazine treatment promotes a marked increase in splenocyte 5-aminoimidazole-4-carboxamidoribonucleotide (AICAR) concentration, which is consistent with the in vitro observation that sulfasalazine inhibits AICAR transformylase. 
|In vitro||DMSO||80 mg/mL (200.8 mM)|
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|Synonyms||Azulfidine, Salazopyrin, Sulphasalazine, NSC 667219|
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03487926||Active not recruiting||Radiation: [18F]FEPPA||Major Depressive Episode|Inflammatory Bowel Diseases||Centre for Addiction and Mental Health|McMaster University||January 1 2019||--|
|NCT01577966||Completed||Drug: Sulfasalazine||Brain Tumor||University of Alabama at Birmingham||January 2012||Not Applicable|
|NCT01474291||Completed||Biological: Tocilizumab||Rheumatoid Arthritis||Hoffmann-La Roche||January 2012||--|
|NCT00637780||Terminated||Drug: Sulfasalazine||Arthritis Juvenile Rheumatoid||Pfizer||June 2010||Phase 4|
|NCT00356356||Completed||Drug: Etanercept||Ankylosing Spondylitis||Amgen|Immunex Corporation||April 2002||Phase 3|
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