13029-71-5

Basic information

• Product Name: 2-([(4-FLUOROPHENYL)SULFONYL]AMINO)ACETIC ACID
• Synonyms: 2-([(4-FLUOROPHENYL)SULFONYL]AMINO)ACETIC ACID;AKOS BC-3152;BUTTPARK 31\07-81;(4-Fluoro-benzenesulfonylamino)-acetic acid
• CAS NO: 13029-71-5
• Molecular Formula: C₈H₈FNO₄S
• Molecular Weight: 233.22
• Mol File: 13029-71-5.mol

Chemical Properties

• Melting Point: 158-160°C
• Appearance: /
• CAS DataBase Reference: 2-([(4-FLUOROPHENYL)SULFONYL]AMINO)ACETIC ACID(CAS DataBase Reference)
• NIST Chemistry Reference: 2-([(4-FLUOROPHENYL)SULFONYL]AMINO)ACETIC ACID(13029-71-5)
• EPA Substance Registry System: 2-([(4-FLUOROPHENYL)SULFONYL]AMINO)ACETIC ACID(13029-71-5)

Safety Data

• Hazard Codes: Xi
• HazardClass: IRRITANT
• Hazardous Substances Data: 13029-71-5(Hazardous Substances Data)

Usage

General Description

The chemical 2-([(4-fluorophenyl)sulfonyl]amino)acetic acid is a compound that contains a sulfonyl group and an amino acid moiety. It is often used in medicinal chemistry and drug development as a building block for the synthesis of potential pharmaceutical agents. The presence of the fluorophenyl group in the molecule can impart specific chemical and biological properties to the compound. Additionally, the sulfonyl group can participate in various chemical reactions and interactions with biological targets, making 2-([(4-FLUOROPHENYL)SULFONYL]AMINO)ACETIC ACID potentially useful for therapeutic purposes. Overall, this chemical compound has potential applications in the field of drug discovery and development.

Upstream product

• 349-88-2 4-Fluorobenzenesulfonyl chloride 
• 56-40-6 glycine 
• 346696-78-4 C₉H₁₀FNO₄S 

Downstream Products

• 1160366-94-8 (S)-N-[[3-[3-fluoro-4-[4-[2-(4-fluorophenylsulfonamido)acetyl]piperazin-1-yl]phenyl]-2-oxo-5-oxazolidinyl]methyl]acetamide 
• 391935-66-3 1-[(4-fluorophenyl)sulfonyl]-2-thioxo-4-imidazolidinone 
• 287407-11-8 2-[(4-but-2-ynylthiophenylsulfonyl)methylamino]acetic acid tert-butyl ester 
• 287407-08-3 2-(methyl{[4-(prop-2-ynylamino)phenyl]sulfonyl}-amino)acetic acid, tert-butyl ester 
• 287407-12-9 [(4-but-2-ynylsulfanyl-benzenesulfonyl)-methyl-amino]-acetic acid 
• 287407-09-4 2-(methyl{[4-(prop-2-ynylamino)phenyl]sulfonyl}-amino)acetic acid 
• 287407-07-2 tert-butyl 2-(4-fluoro-N-methylphenylsulfonamido)acetate 
• 213015-69-1 tert-butyl 2-{[(4-fluorophenyl)sulfonyl]amino}acetate 
• 276695-39-7 N-benzyl-N-[(4-fluorophenyl)sulfonyl]glycine 

Relevant articles and documents

Class I/IIb-Selective HDAC Inhibitor Exhibits Oral Bioavailability and Therapeutic Efficacy in Acute Myeloid Leukemia

The HDAC inhibitor 4-tert-butyl-N-(4-(hydroxycarbamoyl)phenyl)benzamide (AES-350, 51) was identified as a promising preclinical candidate for the treatment of acute myeloid leukemia (AML), an aggressive malignancy with a meagre 24% 5-year survival rate. Through screening of low-molecular-weight analogues derived from the previously discovered novel HDAC inhibitor, AES-135, compound 51 demonstrated greater HDAC isoform selectivity, higher cytotoxicity in MV4-11 cells, an improved therapeutic window, and more efficient absorption through cellular and lipid membranes. Compound 51 also demonstrated improved oral bioavailability compared to SAHA in mouse models. A broad spectrum of experiments, including FACS, ELISA, and Western blotting, were performed to support our hypothesis that 51 dose-dependently triggers apoptosis in AML cells through HDAC inhibition.

Development of Piperazinediones as dual inhibitor for treatment of Alzheimer's disease

Novel multifunctional 3,6-Diphenyl-1,4-bis(phenylsulfonyl)piperazine-2,5-dione derivatives were designed and synthesized for the treatment of Alzheimer's disease (AD). The designed scaffold has blood brain barrier penetrating ability, acetylcholinesterase (AChE) and matrix metalloproteinase-2 (MMP-2) inhibition potential. Compounds 52 and 46 showed very significant inhibition against AChE, IC50 = 32.45 ± 0.044, 28.65 ± 0.029, BuChE, IC50 = 157.95 ± 0.264, 160.58 ± 0.082 and MMP-2, IC50 = 36.83 ± 0.015, 19.57 ± 0.005 (nM). In the enzyme kinetics study, lead molecule 46 showed non-competitive inhibition of AChE with Ki = 7 nM and competitive inhibition of MMP-2 with Ki = 20 nM. Compounds 52 and 46 inhibited AChE-induced Aβ aggregation at 20 μM. The compounds also exhibited in-vitro antioxidant potential in DPPH assay. Further, compound 46 was found to be a promising neuroprotective agent in MC65 cells. Lead molecule 46 significantly enhanced working memory in scopolamine induced amnesia animal model at dose of 5 mg/kg dose. The mitochondrial membrane potential was restored in animals when treated with compounds 52 and 46.

Acetylenic TACE inhibitors. Part 1. SAR of the acyclic sulfonamide hydroxamates

The SAR of a series of potent sulfonamide hydroxamate TACE inhibitors, all bearing a butynyloxy P1′ group, was explored. In particular, compound 5j has excellent in vitro potency against isolated TACE enzyme and in cells, good selectivity over MMP-1 and MMP-9, and oral activity in an in vivo model of TNF-α production and a collagen-induced arthritis model.

N-(4-sulfonylaryl)Cyclylamine 2-hydroxyethylamines as beta-3 adrenergic receptor agonists

This invention provides compounds of Formula I having the structure wherein R1, R2, R3, R4, W, X, and Y are as defined hereinbefore or a pharmaceutically acceptable salt thereof, which are useful in treating metabolic disorders related to insulin resistance or hyperglycemia.

Thioaryl sulfonamide hydroxamic acid compounds

PCT No. PCT/US98/04298 Sec. 371 Date Sep. 10, 1999 Sec. 102(e) Date Sep. 10, 1999 PCT Filed Mar. 4, 1998 PCT Pub. No. WO98/39313 PCT Pub. Date Sep. 11, 1998A thioaryl sulfonamide hydroxamic acid compound that inter alia inhibits matrix metalloprotease act

Protease inhibitors - Part 5. Alkyl/arylsulfonyl- and arylsulfonylureido-/arylureido- glycine hydroxamate inhibitors of Clostridium histolyticum collagenase

Reaction of alkyl/arylsulfonyl halides with glycine afforded a series of derivatives which were first N-benzylated by treatment with benzyl chloride, and then converted to the corresponding hydroxamic acids with hydroxylamine in the presence of carbodiimide derivatives. Other derivatives were obtained by reaction of N-benzyl-glycine with aryl isocyanates, arylsulfonyl isocyanates or benzoyl isothiocyanate, followed by conversion of their COOH group into the CONHOH moiety, as mentioned above. The 90 new compounds reported here were assayed as inhibitors of the Clostridium histolyticum collagenase (EC 3.4.24.3), a zinc enzyme which degrades triple helical regions of native collagen. The prepared hydroxamate derivatives were generally 100-500 times more active than the corresponding carboxylates. In the series of synthesized hydroxamates, substitution patterns leading to the best inhibitors were those involving perfluoroalkylsulfonyl- and substituted- arylsulfonyl moieties, such as pentafluorophenylsulfonyl, 3- and 4- carboxyphenylsulfonyl-, 3-trifluoromethyl-phenylsulfonyl or 1- and 2-naphthyl among others. Thus, it seems that similarly to the matrix metalloproteinase (MMP) hydroxamate inhibitors, Clostridium histolyticum collagenase inhibitors should incorporate hydrophobic moieties at the P1, and P2, sites, whereas the α-carbon substituent may be a small and compact moiety (such as H. for the Gly derivatives reported here). Such compounds might lead to the design of collagenase inhibitor-based drugs useful as anti-cancer, anti-arthritis or anti-bacterial agents for the treatment of corneal keratitis. (C) 2000 Editions scientifiques et medicales Elsevier SAS.

SULFONAMIDE INHIBITORS OF MATRIX METALLOPROTEINASES

Sulfonamide compounds are described which are inhibitors of matrix metalloproteinases, particularly stromelysin-1 and gelatinase A (72 kD gelatinase). Also described are methods for the treatment of multiple sclerosis, atherosclerotic plaque rupture, aortic aneurism, heart failure, restenosis, periodontal disease, corneal ulceration, burns, decubital ulcers, chronic ulcers or wounds, cancer metastasis, tumor angiogenesis, arthritis, or other autoimmune or inflammatory disorders dependent upon tissue invasion by leukocytes using the compounds.