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• 64264-20-6 3-(p-Phenoxymethyl-phenyl)-propionaldehyd 
• 91718-22-8 1-iodo-4-(phenoxymethyl)benzene 

Relevant academic research and scientific papers

TETRACYCLIC INHIBITORS OF FATTY ACID AMIDE HYDROLASE

Certain tetracyclic compounds are described, which may be used in pharmaceutical compositions and methods for treating disease states, disorders, and conditions mediated by fatty acid amide hydrolase (FAAH) activity. Thus, the compounds may be administered to treat, e.g., anxiety, pain, inflammation, sleep disorders, eating disorders, or movement disorders (such as multiple sclerosis).

Structure-activity relationships of α-ketooxazole inhibitors of fatty acid amide hydrolase

A systematic study of the structure-activity relationships of 2b (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed targeting the C2 acyl side chain. A series of aryl replacements or substituents for the terminal phenyl group provided effective inhibitors (e.g., 5c, aryl = 1-napthyl, K, - 2.6 nM), with 5hh (aryl -3-ClPh, Ki = 900 pM) being 5-fold more potent than 2b. Conformationally restricted C2 side chains were examined, and many provided exceptionally potent inhibitors, of which 11j (ethylbiphenyl side chain) was established to be a 750 pM inhibitor. A systematic series of heteroatoms (O, NMe, S), electron-withdrawing groups (SO, SO2), and amides positioned within and hydroxyl substitutions on the linking side chain were investigated, which typically led to a loss in potency. The most tolerant positions provided effective inhibitors (12p, 6-position S, Ki = 3 nM, or 13d, 2-position OH, Ki = 8 nM) comparable in potency to 2b. Proteome-wide screening of selected inhibitors from the systematic series of >100 candidates prepared revealed that they are selective for FAAH over all other mammalian serine proteases.

Metabolism of the local anaesthetic fomocaine by rat liver mitochondria

Fomocaine (Erbocain) is metabolized by different routes in rat and beagle. By highly purified rat liver mitochondria it was metabolized to its N-oxide only. The N-oxide was reduced to fomocaine by a reductase localised in the matrix or in the inner membrane of the mitochondria. C-Hydroxylation with subsequent conjugation reactions as well as oxidative N- or O-dealkylation found in intact animals were not observed in mitochondria.