144366-40-5

Upstream product

• 3740-52-1 2-(2-nitrophenyl)acetic acid 
• 3342-78-7 2-(2-aminophenyl)acetic acid 
• 18108-55-9 1,3-dihydro-1-hydroxyindole-2-one 

Downstream Products

• 144366-49-4 N-(phenylsulfonyl) N-(2-carboxymethylphenyl)hydroxylamine 
• 1094772-29-8 [2-(2,2-dimethyl-4-oxo-4H-benzo[1,3]dioxin-6-ylazo)-phenyl]-acetic acid 
• 1094772-12-9 5-[2-(2-carboxymethyl)phenylazo]-2-hydroxybenzoic acid tert-butyl ester 
• 18108-55-9 1,3-dihydro-1-hydroxyindole-2-one 
• 150224-32-1 N-formyl-N-(2-carboxymethylphenyl)hydroxylamine 
• 144366-48-3 N-(4-methylphenylsulfonyl) N-(2-carboxymethylphenyl)hydroxylamine 

Relevant academic research and scientific papers

Oxidative cleavage of hydroxamic acid promoted by sodium periodate

A series of hydroxamic acids, involving aliphatic, aromatic and cyclic substrates, were transformed to the corresponding carboxylic acids through NaIO4-mediated oxidative cleavage in mild conditions. Esterification of these acids with TMSCHN2 could result in formation of the corresponding methyl ester. This methodology makes good compensation for the existing methods transforming amides to esters. Our results also pave the way to harness hydroxamic acids as useful synthetic building blocks.

Design, synthesis, and pharmacological effects of a cyclization-activated steroid prodrug for colon targeting in inflammatory bowel disease

Glucocorticoids are used in the treatment of inflammatory bowel disease. A limitation to their use is that they undergo absorption from the GIT before reaching the colon causing severe systemic side effects. We report here on a novel prodrug approach to targeting corticosteroids to the colon. The design involves attaching a 21-ester group that suppresses absorption during transit to the colon. The prodrug is designed to be primed by colonic microflora liberating an amino ester that cyclizes releasing the steroid. One of the prodrugs 5b was as efficacious as prednisolone in the murine DSS model but did not cause thymic atrophy, a marker for systemic steroid effects.

TARGETING DIAZO PRODRUGS FOR THE TREATMENT OF GASTROINTESTINAL DISEASES

Provided herein are compounds, compositions and methods for decreasing NFkB DNA-binding activity in a patient comprising administering of a therapeutically effective amount of a compound or composition of the application to the patient to reduce, alleviate or treat various gastrointestinal diseases, such as inflammatory bowel disease (IBD).

Preparation and study of chemical transformations of N-formyl-N-phenylhydroxylamines

Nitrosobenzenes with CO2H 1b, CO2CH3 3b and CON(CH3)C6H5 4b ortho-substituents were obtained in a "redox" cell from the corresponding nitro compounds.In order to prepare the 3-oxo-1,2-dihydro-2,1-benzisoxazole-1-carbaldehyde from o-substituted N-formyl-N-phenylhydroxylamines, nitroso derivatives were formylated by glyoxylic acid.The N-formylbenzisoxazolone is unstable in the reaction medium and cannot be isolated.In addition to our study, we showed the unstability of N-formyl-N-phenylhydroxylamines and N-formylanilines in the presence of methanol without acetic acid; in an aqueous methanolic medium, formylation of nitrosoderivatives is equivalent to a reduction of the nitroso group.The mechanism was demonstrated by formylation of the nitrosobenzene and the electrogenerated 2-nitrosobenzene acetic acid 2b.Key Words: flow cell electrosynthesis / nitrosobenzenes / glyoxylic acid / formylation / N-formyl-N-phenylhydroxylamines / N-formylanilines / benzisoxazolones

Flow cell electrosynthesis of o-substituted nitrosobenzenes. In situ reaction with sulfinic acids. Attempt to prepare heterocycles.

Nitrosobenzenes with CO2H 1b, CO2CH3 2b, CONR2 3b-6b, CH2CO2H 7b, CHOHCO2H 8b and NHCO2CH3 9b ortho-substituted were prepared, in a "redox" cell, from the corresponding nitro compounds.Addition of sulfinic acids to the solution after electrolyses leads to