MedChemExpress - Model Sulfasalazine-d4 - 1346606-50-5
Sulfasalazine-d4 is the deuterium labeled Sulfasalazine. Sulfasalazine (NSC 667219) is an anti-rheumatic agent for the research of rheumatoid arthritis and ulcerative colitis. Sulfasalazine can suppress NF-κB activity. Sulfasalazine is a type 1 ferroptosis inducer[1][2][3][4].MCE products for research use only. We do not sell to patients.
Sulfasalazine-d4
MCE China：Sulfasalazine-d4
Brand：MedChemExpress (MCE)
Cat. No.HY-14655S
CAS：1346606-50-5
Purity：99.28%
Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Shipping：Room temperature in continental US; may vary elsewhere.
Description：Sulfasalazine-d4 is the deuterium labeled Sulfasalazine. Sulfasalazine (NSC 667219) is an anti-rheumatic agent for the research of rheumatoid arthritis and ulcerative colitis. Sulfasalazine can suppress NF-κB activity. Sulfasalazine is a type 1 ferroptosis inducer[1][2][3][4].
In Vitro：Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
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References：
[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216. [Content Brief]
[2]. Wahl C, et al. Sulfasalazine: a potent and specific inhibitor of nuclear factor kappa B. J Clin Invest. 1998 Mar 1;101(5):1163-74. [Content Brief]
[3]. Sykes L, et al. Sulfasalazine augments a pro-inflammatory response in interleukin-1β-stimulated amniocytes and myocytes. Immunology. 2015 Dec;146(4):630-44. [Content Brief]
[4]. Chung WJ, et al. Sulfasalazine inhibits the growth of primary brain tumors independent of nuclear factor-kappaB. J Neurochem. 2009 Jul;110(1):182-93. [Content Brief]
[5]. Mao C, et al. DHODH-mediated ferroptosis defence is a targetable vulnerability in cancer. Nature. 2021;593(7860):586-590. [Content Brief]
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