859828-49-2

Upstream product

• 147283-87-2 methyl [3-[[(trifluoromethyl)sulfonyl]oxy]phenyl]-acetate 
• 74-88-4 methyl iodide 
• 42058-59-3 3-hydroxy-benzeneacetic acid, methyl ester 
• 621-37-4 m-hydroxyphenylacetic acid 

Downstream Products

• 859828-57-2 methyl 2-(3-isobutylphenyl)propanoate 
• 1299295-04-7 methyl 2-(3-{[3-methoxy-5-(trifluoromethyl)phenyl]amino}phenyl)propanoate 
• 1299295-03-6 2-(3-{[3-methoxy-5-(trifluoromethyl)phenyl]amino}phenyl)propanoic acid 
• 1299295-05-8 2-(3-{[(trifluoromethyl)sulphonyl]oxy}phenyl)propanoic acid 
• 1299295-19-4 methyl 2-{3-[1-hex-1-en-1-yl]phenyl}propanoate 
• 22161-82-6 α-(3-benzylphenyl)-propionic acid 
• 66622-47-7 Ibuprofen 
• 128984-66-7 2-[3-(1-phenyl-ethyl)-phenyl]-propionic acid methyl ester 
• 129082-19-5 methyl 2-(3-isopropylphenyl)propanoate 
• 946072-98-6 methyl 2-[3-(2-phenylpropyl)phenyl]propanoate 

Relevant academic research and scientific papers

2-ARYL-PROPIONAMIDE DERIVATIVES USEFUL AS BRADYKININ RECEPTOR ANTAGONISTS AND PHARMACEUTICAL COMPOSITIONS CONTAINING THEM

(R,S) 2-aryl-propionamide derivatives, or their single enantiomers (R) and (S) are disclosed useful in the treatment or prevention of symptoms and disorders such as pain and inflammation associated with the bradykinin B 1 pathway.

2-aryl-propionamide derivatives useful as bradykinin receptor antagonists and pharmaceutical compositions containing them

(R,S) 2-aryl-propionamide derivatives, or their single enantiomers (R) and (S) are disclosed useful in the treatment or prevention of symptoms and disorders such as pain and inflammation associated with the bradykinin B1 pathway.

2-Arylpropionic CXC chemokine receptor 1 (CXCR1) ligands as novel noncompetitive CXCL8 inhibitors

The CXC chemokine CXCL8/IL-8 plays a major role in the activation and recruitment of polymorphonuclear (PMN) cells at inflammatory sites. CXCL8 activates PMNs by binding the seven-transmembrane (7-TM) G-protein-coupled receptors CXC chemokine receptor 1 (CXCR1) and CXC chemokine receptor 2 (CXCR2). (R)-Ketoprofen (1) was previously reported to be a potent and specific noncompetitive inhibitor of CXCLS-induced human PMNs chemotaxis. We report here molecular modeling studies showing a putative interaction site of 1 in the TM region of CXCR1. The binding model was confirmed by alanine scanning mutagenesis and photoaffinity labeling experiments. The molecular model driven medicinal chemistry optimization of 1 led to a new class of potent and specific inhibitors of CXCL8 biological activity. Among these, repertaxin (13) was selected as a clinical candidate drug for prevention of post-ischemia reperfusion injury.