313346-23-5

Basic information

• Product Name: 5-(chlorosulfonyl)-2,4-dimethylbenzoic acid
• Synonyms: 5-(chlorosulfonyl)-2,4-dimethylbenzoic acid
• CAS NO: 313346-23-5
• Molecular Formula: C₉H₉ClO₄S
• Molecular Weight: 248.68336
• Mol File: 313346-23-5.mol

Chemical Properties

• Appearance: /
• CAS DataBase Reference: 5-(chlorosulfonyl)-2,4-dimethylbenzoic acid(CAS DataBase Reference)
• NIST Chemistry Reference: 5-(chlorosulfonyl)-2,4-dimethylbenzoic acid(313346-23-5)
• EPA Substance Registry System: 5-(chlorosulfonyl)-2,4-dimethylbenzoic acid(313346-23-5)

Safety Data

• Hazardous Substances Data: 313346-23-5(Hazardous Substances Data)

Upstream product

• 611-01-8 2,4-dimethyl-benzoic acid 

Downstream Products

• 176641-71-7 5-Methanesulfonyl-2,4-dimethyl-benzoic acid methyl ester 

Relevant articles and documents

PHENYL mTORC INHIBITORS AND USES THEREOF

The present invention provides compounds, compositions thereof, and methods of using the same.

Small Molecule Microarray Based Discovery of PARP14 Inhibitors

Poly(ADP-ribose) polymerases (PARPs) are key enzymes in a variety of cellular processes. Most small-molecule PARP inhibitors developed to date have been against PARP1, and suffer from poor selectivity. PARP14 has recently emerged as a potential therapeutic target, but its inhibitor development has trailed behind. Herein, we describe a small molecule microarray-based strategy for high-throughput synthesis, screening of >1000 potential bidentate inhibitors of PARPs, and the successful discovery of a potent PARP14 inhibitor H10 with >20-fold selectivity over PARP1. Co-crystallization of the PARP14/H10 complex indicated H10 bound to both the nicotinamide and the adenine subsites. Further structure–activity relationship studies identified important binding elements in the adenine subsite. In tumor cells, H10 was able to chemically knockdown endogenous PARP14 activities.

(2-methyl-5-(methylsulfonyl)benzoyl)guanidine Na+/H+ antiporter inhibitors

The inhibition of the Na+/H+ exchanger during cardiac ischemia and reperfusion has been shown to be beneficial for the preservation of the cellular integrity and functional performance. The aim of the present investigation was to come up with potent and selective benzoylguanidines as NHE inhibitors for their use as an adjunctive therapy in the treatment of acute myocardial infarction. During the course of our investigations it became clear that the substitution ortho to the acylguanidine was of crucial importance for the potency of the compounds. 4-Chloro and 4-fluoro-2- methylbenzoic acids 6 and 7 were prepared using the directed ortho metalation technique with the carboxylic acid as the directing group. With the LDA/methyl iodide system the 2-methyl group could be extended to an ethyl group. 4-Alkyl groups were inserted by the palladium-catalyzed cross-coupling reaction into the 4-bromo-2-methylbenzoic acid methyl ester (20). Starting with benzoic acids 6-19, the methylsulfonyl group was introduced by a sequence of standard reactions (sulfochlorination, reduction, and methylation). 4-Aryl derivatives 6875 were synthesized by the palladium- catalyzed Suzuki reaction. A large number of nucleophilic displacement reactions in the 4-position were carried out with S-, O-, and N-nucleophiles as well as with the cyano and trifluoromethyl group. Using the ester method, acid chlorides, or Mukaiyama's procedure, the 5-(methylsulfonyl)benzoic acid derivatives were finally converted to the (5- (methylsulfonyl)benzoyl)guanidines 165-267 with excessive guanidine. In some cases nucleophilic substitutions with pyridinols and piperidine derivatives were carried out at the end of the reaction sequence with the 4-halo-N- (diaminomethylene)-5-(methylsulfonyl)benzamides. Variations in the 4-position were most reasonable, but the volume of the substituents was of crucial importance. Substitution in the 3- and particularly in the 6-position led to considerable worsening of the inhibitory effects of the Na+/H+ exchanger. The 2-methyl compounds, however, showed without exception higher in vitro activities than their respective demethyl counterparts as they are exemplified by the reference compounds 266 and 267, obviously caused by a conformational restriction of the acylguanidine chain. The development compound (2-methyl-5-(methylsulfonyl)-4-pyrrolobenzoyl)guanidine, methanesulfonate (246) is a NHE-1 subtype specific NHE inhibitor, being 27- fold more potent toward the NHE-1 than the NHE-2 isoform, 246 was found to act cardioprotectively not only when given before an experimentally induced ischemia, but also curatively after the onset of symptoms of acute myocardial infarction when given prior to the induction of reperfusion.