231296-92-7

Upstream product

• 103273-01-4 2-bromo-4-tert-butylaniline 
• 292638-85-8 acrylic acid methyl ester 
• 769-92-6 4-tert-Butylaniline 

Downstream Products

• 231296-93-8 methyl (2E)-3-(5-tert-butyl-2-{[(4-methylphenyl)sulfonyl]amino}phenyl)acrylate 

Relevant academic research and scientific papers

Oxidative fluorination of N-arylsulfonamides

We report a late stage oxidative nucleophilic fluorination of N-arylsulfonamides, a class of compounds so far not considered as precursors to 4-fluorophenyl sulfonamides. By installing a para-positioned tert-butyl substituent on the aniline, oxidative fluorination takes place regioselectively in the presence of HF·pyridine and PIDA. This methodology has been shown to give good yields for a variety of ortho- and meta-functionalised N-arylsulfonamides and has been adapted for radiofluorination to give 4-[18F]fluorophenyl sulfonamides under carrier added conditions.

Novel acid-type cyclooxygenase-2 inhibitors: Design, synthesis, and structure-activity relationship for anti-inflammatory drug

Cyclooxygenase (COX) is a key rate-limiting enzyme for prostaglandin (PG) production cascades in the human body. The mechanisms of both the anti-inflammation effects and the side-effects of traditional COX inhibitors are associated with the existence of two COX isoforms. Thus while COX-1 is predominantly expressed ubiquitously and constitutively, and it serves a housekeeping role in processes such as gastrointestinal (GI) mucosa protection, COX-2 is absent or exhibits a low level of expression in most tissues, and is highly upregulated in response to endotoxin, virus, inflammatory or tissue-injury stimuli/signals, and tumour promoter in the various types of organs, tissues, and cells. Furthermore, COX-2 contribution to PGE2 and PGI2 production evokes and sustains systemic or peripheral inflammatory disease, but it is not involved in the COX-1-mediated GI tract events. Also, hypersensitivity of aspirin owing to its inhibitory action against COX-1 is a significant concern clinically. Consequently, highly selective COX-2 inhibitors have been needed for the treatment of inflammatory- and inflammation related-diseases that include pyrexia, inflammation, pain, rheumatoid arthritis, osteoarthritis, and cancers. In this study, a series of novel [2-{[(4-substituted or 4,5-disubstituted)-pyridin-2-yl]carbonyl}-(5- or 6-substituted or 5,6-disubstituted)-1H-indol-3-yl]acetic acid analogues was designed, synthesized, and evaluated to identify potent and selective COX-2 inhibitors as potential agents against inflammatory diseases. As significant findings, the present study clarified unique structure-activity relationship of the analogues toward potent and selective COX-2 inhibition in vitro, and identified 2-{6-fluoro-2-[4-methyl-2-pridinyl)carbonyl]-1H-indol-3-yl}acetic acid as a potent and selective COX-2 inhibitor in vitro that demonstrated orally potent anti-inflammation efficacy against carrageenan-induced oedema formation in the foot of SPF/VAF male SD rats as a peripheral inflammation model in vivo.

2,3-substituted indole compounds as anti-inflammatory and analgesic agents

This invention provides a compound of the following formula: or the pharmaceutically acceptable salts thereof wherein Z is OH, C1-6 alkoxy, —NR2R3 or heterocycle; Q is selected from the following: (a) an optionally substituted phenyl, (b) an optionally substituted 6-membered monocyclic aromatic group containing one, two, three or four nitrogen atom(s), (c) an optionally substituted 5-membered monocyclic aromatic group containing one heteroatom selected from O, S and N and optionally containing one, two or three nitrogen atom(s) in addition to said heteroatom, (d) an optionally substituted C3-7 cycloalkyl and (e) an optionally substituted benzo-fuzed heterocycle; R1 is hydrogen, C1-4 alkyl or halo; R2 and R3 are independently hydrogen, OH, C1-4 alkoxy, C1-4 alkyl or C1-4 alkyl substituted with halo, OH, C1-4 alkoxy or CN; X is independently selected from H, halo, C1-4 alkyl, halo-substituted C1-4 alkyl, OH, C1-4 alkoxy, halo-substituted C1-4 alkoxy, C1-4 alkylthio, NO2, NH2, di-(C1-4 alkyl)amino and CN; and n is 0, 1, 2, 3 and 4.This invention also provides a pharmaceutical composition useful for the treatment of a medical condition in which prostaglandins are implicated as pathogens.