64288-19-3

Upstream product

• 16979-23-0 ethyl 4-((4-chlorobenzylidene)amino)benzoate 
• 104-88-1 4-chlorobenzaldehyde 
• 94-09-7 p-aminoethylbenzoate 
• 622-95-7 4-chlorobenzyl bromide 

Downstream Products

• 63759-94-4 4-((4-chlorobenzyl)amino)benzoic acid 
• 68266-41-1 ethyl N-(4-ethoxycarbonylphenyl)-N-(4-chlorobenzyl)-carbamate 
• 68266-45-5 N-(4-ethoxycarbonylphenyl)-N-(4-chlorobenzyl)-ethylamine 
• 68266-44-4 N-(4-ethoxycarbonylphenyl)-N-(4-chlorobenzyl)-acetamide 
• 68266-40-0 N-(4-ethoxycarbonylphenyl)-N-(4-chlorobenzyl)-formamide 
• 68266-43-3 N-(4-ethoxycarbonylphenyl)-N-(4-chlorobenzyl)-methylamine 
• 1255716-75-6 4-[tert-butoxycarbonyl-(4-chloro-benzyl)-amino]-benzoic acid ethyl ester 
• 1255716-58-5 4-[benzenesulfonyl-(4-chloro-benzyl)-amino]-benzoic acid ethyl ester 

Relevant academic research and scientific papers

Discovery of a benzenesulfonamide-based dual inhibitor of microsomal prostaglandin E2 synthase-1 and 5-lipoxygenase that favorably modulates lipid mediator biosynthesis in inflammation

Leukotrienes (LTs) and prostaglandin (PG)E2, produced by 5-lipoxygenase (5-LO) and microsomal prostaglandin E2 synthase-1 (mPGES-1), respectively, are key players in inflammation, and pharmacological suppression of these lipid mediators (LM) represents a strategy to intervene with inflammatory disorders. Previous studies revealed that the benzenesulfonamide scaffold displays efficient 5-LO-inhibitory properties. Here, we structurally optimized benzenesulfonamides which led to an N-phenylbenzenesulfonamide derivative (compound 47) with potent inhibitory activities (IC50 = 2.3 and 0.4 μM for isolated 5-LO and 5-LO in intact cells, respectively). Compound 47 prevented the interaction of 5-LO with its activating protein (FLAP) at the nuclear envelope in transfected HEK293 cells as shown by in situ proximity ligation assay. Comprehensive assessment of the LM profile produced by human macrophages revealed the ability of 47 to selectively down-regulate pro-inflammatory LMs (i.e. LTs and PGE2) in M1 but to enhance the formation of pro-resolving LMs (i.e. resolvins and maresins) in M2 macrophages. Moreover, 47 strongly inhibited LT formation and cell infiltration in two in vivo models of acute inflammation (i.e., peritonitis and air pouch sterile inflammation in mice). Together, 47 represents a novel LT biosynthesis inhibitor with an attractive pharmacological profile as anti-inflammatory drug that also promotes the biosynthesis of pro-resolving LM.

O -Phenylenediamine: A privileged pharmacophore of ferrostatins for radical-trapping reactivity in blocking ferroptosis

Ferroptosis is a non-apoptotic, iron dependent form of regulated cell death that is characterized by the accumulation of lipid hydroperoxides. It has drawn considerable attention owing to its putative involvement in diverse neurodegenerative diseases. Ferrostatins are the first identified inhibitors of ferroptosis and they inhibit ferroptosis by efficiently scavenging free radicals in lipid bilayers. However, their further medicinal application has been limited due to the deficient knowledge of the lipid peroxyl radical-trapping mechanism. In this study, experimental and theoretical methods were performed to illustrate the possible lipid hydroperoxide inhibition mechanism of ferrostatins. The results show that an ortho-amine (-NH) moiety from ferrostatins can simultaneously interact with lipid radicals, and then form a planar seven-membered ring in the transition state, and finally present greater reactivity. NBO analysis shows that the formed planar seven-membered ring forces ortho-amines into better alignment with the aromatic π-system. It significantly increases the magnitudes of amine conjugation and improves spin delocalization in the transition state. Additionally, a classical H-bond type interaction was discovered between a radical and an o-NH group as another transition state stabilizing effect. This type of radical-trapping mechanism is novel and has not been found in diphenylamine or traditional polyphenol antioxidants. It can be said that o-phenylenediamine is a privileged pharmacophore for the design and development of ferroptosis inhibitors.

Reductive amination catalyzed by iridium complexes using carbon monoxide as a reducing agent

Development of novel, sustainable catalytic methodologies to provide access to amines represents a goal of fundamental importance. Herein we describe a systematic study for the construction of a variety of amines catalyzed by a well-defined homogeneous ir

SULFONAMIDE COMPOUNDS, PHARMACEUTICAL COMPOSITIONS AND USES THEREOF

Compounds are provided according to formula (1), wherein W, X, Z, R1, R2, R3, and ml are as defined herein. Provided compounds and pharmaceutical compositions thereof are useful for the prevention and treatment of a variety of conditions in mammals including humans, including by way of non- limiting example, pain, inflammation, cognitive disorders, anxiety, depression, and others. Provided compounds and pharmaceutical compositions thereof are also useful for the prevention and treatment of a variety of conditions in mammals including humans, including by way of non- limiting example immune-mediated disorders and autoimmune diseases, including multiple sclerosis, type-1 diabetes mellitus, type-2 diabetes mellitus, rheumatoid arthritis, psoriasis, contact dermatitis, obesity, systemic lupus erythematosus, graft-versus host disease, transplant rejection, and others.

Potential antiatherosclerotic agents. 2. (Aralkylamino)- and (alkylamino)benzoic acid analogues of cetaben

The syntheses of a series of (aralkylamino)- and (alkylamino)benzoic acids, as well as the corresponding esters and sodium salts, are described. The compounds were evaluated in vivo in rats for serum sterol and triglyceride lowering activity and in vitro

Hypolipidaemic compounds and compositions

Certain substituted aralkylanilines in which the aromatic aniline ring carries, at the para position to the amino function, a substituent which comprises a carboxylic acid, salt or ester, an alkyl, hydroxyalkyl, cyano or acyl group, have hypolipidaemic ac