67175-12-6

Upstream product

• 67-64-1 acetone 
• 14763-20-3 3-chlorophenyl hydrazine 
• 2312-23-4 m-chlorophenylhydrazine hydrochloride 

Downstream Products

• 335064-86-3 C₁₂H₁₄ClN₃O₂ 
• 872674-95-8 methyl 4-[[2-[4-chloro-(1-diphenylmethyl)-2-methyl-1H-indol-3-yl]ethyl]sulfonyl]benzoate 
• 872674-94-7 methyl 4-[[2-[6-chloro-(1-diphenylmethyl)-2-methyl-1H-indol-3-yl]ethyl]sulfonyl]benzoate 
• 872675-05-3 methyl 4-[2-[6-chloro-1-(diphenylmethyl)-2-methyl-1H-indol-3-yl]ethoxy]benzoate 
• 872674-90-3 methyl 4-[[2-(4-chloro-2-methyl-1H-indol-3-yl)ethyl]sulfonyl]benzoate 
• 872674-89-0 methyl 4-[[2-(6-chloro-2-methyl-1H-indol-3-yl)ethyl]sulfonyl]benzoate 
• 872675-04-2 2-[6-chloro-1-(diphenylmethyl)-2-methyl-1H-indol-3-yl]ethanol 
• 6127-17-9 6-chloro-2-methyl-1H-indole 
• 6127-16-8 4-chloro-2-methyl-1H-indole 

Relevant academic research and scientific papers

Inhibition of cytosolic phospholipase A2α: Hit to lead optimization

Compound 1 was previously reported to be a potent inhibitor of cPLA 2α in both artificial monomeric substrate and cell-based assays. However, 1 was inactive in whole blood assays previously used to characterize cyclooxygenase and lipoxygenase inhibitors. The IC50 of 1 increased dramatically with cell number or lipid/detergent concentration. In an attempt to insert an electrophilic ketone between the indole and benzole acid moieties, we discovered that increasing the distance between the two moieties gave a compound with activity in the GLU (7-hydroxycoumarinyl-γ- linolenate) micelle assay, which contains lipid and detergent. Extensive structure-activity relationship work around this lead identified a potent pharmacophore for cPLA2α inhibition. The IC50s between the GLU micelle and rat whole blood assays correlated highly. No correlation was found for other parameters, including lipophilicity or acidity of the required acid functionality. Compounds 25, 39, and 94 emerged as potent, selective inhibitors of cPLA2α and represent well-validated starting points for further optimization.

Heterocyclic sodium/proton exchange inhibitors and method

Heterocyclic are provided which are sodium/proton exchange (NHE) inhibitors which have the structure wherein n is 1 to 5; X is N or C—R5 wherein R5 is H, halo, alkenyl, alkynyl, alkoxy, alkyl, aryl or heteroaryl; Z is a heteroaryl gorup, R1, R2, R3 and R4 are as defined herein, and where X is N. R1 is preferably aryl or heteroaryl, and are useful as antianginal and cardioprotective agents. In addition, a method is provided for preventing or treating angina pectoris, cardiac dysfunction, myocardial necrosis, and arrhythmia employing the above heterocyclic derivatives.