Inhibition of aromatic amino acid decarboxylase by a group of non-steroidal anti-inflammatory drugs.
In vitro inhibition of aromatic amino acid decarboxylase (AAD) by eight nonsteroidal anti-inflammatory drugs (NSAIDs) was studied. The most potent inhibitors were fenamates (IC50 for tolfenamate was 4.4 x 10(-5) M), while fluorinated biphenylic compounds (flobufen and 2',4'-difluorobiphenyl-4-yl acetate) and propionic acid derivatives (ibuprofen, ketoprofen, fenoprofen) were one order weaker. The in vitro inhibition of AAD by the compounds studied is probably not strong enough to contribute to their in vivo anti-inflammatory effects.
Pribová
M
M
Department of Biochemical Sciences, Faculty of Pharmacy, Charles University, Hradec Králové, Czechoslovakia.
Gregorová
J
J
Drsata
J
J
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000737:chemistry / Q000494:pharmacology*; D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D002087:Butyrates / Q000494:pharmacology; D005279:Fenoprofen / Q000494:pharmacology; D007052:Ibuprofen / Q000494:pharmacology; D066298:In Vitro Techniques; D007660:Ketoprofen / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D051381:Rats; D013329:Structure-Activity Relationship; D062367:ortho-Aminobenzoates / Q000494:pharmacology
D000894:Anti-Inflammatory Agents, Non-Steroidal; D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D002087:Butyrates; D062367:ortho-Aminobenzoates; C056474:flobufen; C009500:tolfenamic acid; D007660:Ketoprofen; D005279:Fenoprofen; D007052:Ibuprofen