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Usage

Uses

Used in Pharmaceutical Research and Drug Development:
4-AMINO-N-(4-IODO-PHENYL)-BENZENESULFONAMIDE is utilized as a key component in the synthesis of potential therapeutic agents due to its unique structure and properties. It serves as a chemical intermediate in organic synthesis, facilitating the development of new drugs with improved efficacy and safety profiles.
Used in Chemical Synthesis:
In the chemical synthesis industry, 4-AMINO-N-(4-IODO-PHENYL)-BENZENESULFONAMIDE is employed as a versatile intermediate, enabling the creation of a variety of chemical compounds with diverse applications. Its reactivity and functional groups make it a valuable asset in the synthesis of complex organic molecules.
Used in Biological Research:
4-AMINO-N-(4-IODO-PHENYL)-BENZENESULFONAMIDE is also used in biological research to study its potential pharmacological effects. Its biological activity has been investigated for possible applications in medicine, including its interaction with biological targets and its impact on cellular processes.
Used in Medicinal Chemistry:
In the field of medicinal chemistry, 4-AMINO-N-(4-IODO-PHENYL)-BENZENESULFONAMIDE is applied as a starting material or a modifying agent in the design and synthesis of novel drug candidates. Its unique structural features allow for the exploration of new chemical space and the optimization of drug-like properties, such as potency, selectivity, and pharmacokinetics.

InChI:InChI=1/C12H11IN2O2S/c13-9-1-5-11(6-2-9)15-18(16,17)12-7-3-10(14)4-8-12/h1-8,15H,14H2

Upstream product

• 19837-94-6 N-{4-[(4-iodophenyl)sulfamoyl]phenyl}acetamide 
• 332025-19-1 N-(4'-nitrophenylsulfonyl)-4-iodoaniline 
• 121-60-8 p-acetylaminobenzenesulfonyl chloride 
• 540-37-4 p-aminoiodobenzene 
• 98-74-8 4-Nitrobenzenesulfonyl chloride 

Relevant academic research and scientific papers

Design, synthesis, and evaluation of substituted nicotinamide adenine dinucleotide (NAD+) synthetase inhibitors as potential antitubercular agents

Nicotinamide adenine dinucleotide (NAD+) synthetase catalyzes the last step in NAD+ biosynthesis. Depletion of NAD+ is bactericidal for both active and dormant Mycobacterium tuberculosis (Mtb). By inhibiting NAD+ synthetase (NadE) from Mtb, we expect to eliminate NAD+ production which will result in cell death in both growing and nonreplicating Mtb. NadE inhibitors have been investigated against various pathogens, but few have been tested against Mtb. Here, we report on the expansion of a series of urea-sulfonamides, previously reported by Brouillette et al. Guided by docking studies, substituents on a terminal phenyl ring were varied to understand the structure–activity-relationships of substituents on this position. Compounds were tested as inhibitors of both recombinant Mtb NadE and Mtb whole cells. While the parent compound displayed very weak inhibition against Mtb NadE (IC50 = 1000 μM), we observed up to a 10-fold enhancement in potency after optimization. Replacement of the 3,4-dichloro group on the phenyl ring of the parent compound with 4-nitro yielded 4f, the most potent compound of the series with an IC50 value of 90 μM against Mtb NadE. Our modeling results show that these urea-sulfonamides potentially bind to the intramolecular ammonia tunnel, which transports ammonia from the glutaminase domain to the active site of the enzyme. This hypothesis is supported by data showing that, even when treated with potent inhibitors, NadE catalysis is restored when treated with exogenous ammonia. Most of these compounds also inhibited Mtb cell growth with MIC values of 19–100 μg/mL. These results improve our understanding of the SAR of the urea-sulfonamides, their mechanism of binding to the enzyme, and of Mtb NadE as a potential antitubercular drug target.

Analgesic agents without gastric damage: Design and synthesis of structurally simple benzenesulfonanilide-type cyclooxygenase-1-selective inhibitors

In order to create novel analgesic agents without gastric disturbance, structurally simple cyclooxygenase-1 (COX-1) inhibitors with a benzenesulfonanilide skeleton were designed and synthesized. As a result, compounds 11f and 15a, which possess a p-amino group on the benzenesulfonyl moiety and p-chloro group on the anilino moiety, showed COX-1-selective inhibition. Moreover compound 11f, which is the most potent compound in this study showed more potent analgesic activity than that of aspirin at 30 mg/kg by po. The anti-inflammatory activity and gastric damage, however, were very weak or not detectably different from aspirin. Since the structure of our COX-1 inhibitors are very simple, they may be useful as lead compounds for superior COX-1 inhibitors as analgesic agents without gastric disturbance.