Sulfasalazine-d₃,¹⁵N

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].
Treatment of SW620 colon cells with sulfasalazine inhibits TNFα-, LPS-, or phorbol ester-induced NFκB activation. NFκB-dependent transcription is inhibited by sulfasalazine at micro- to millimolar concentrations. TNFα-induced nuclear translocation of NFκB is prevented by sulfasalazine through inhibition of IκBα degradation^[2]. Pre-incubation with 5 mM of sulfasalazine alone significantly increases basal mRNA expression of all pro-inflammatory cytokines with levels of IL-6 mRNA increased by 80-fold compared with vehicle control^[3]. Once digested, sulfasalazine is cleaved into sulfapyridine and 5-aminosalicylic acid by colonic bacteria, and the latter, too, is reported to suppress NF-kappaB activity^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.