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Oxidation of diclofenac sodium produces the metabolite 4'-hydroxy diclofenac) which demonstrates specific inhibition of Cox-2. Inhibition of Cox by diclofenac and 4'-hydroxy diclofenac suppresses prostaglandin E2 synthesis, producing anti-inflammatory and analgesic effects. Diclofenac is also shown to stabilize the native tetrameric conformation of transthyretin (TTR) fibrils, preventing the formation of insoluble amyloidogenic TTR deposits. Diclofenac Sodium is a substrate of CYP2C9. It is also used as an inhibitor of Cox-1 and Cox-2.
Barnett, J., et al. Purification, characterization and selective inhibition of human prostaglandin G/H synthase 1 and 2 expressed in the baculovirus system. Biochim. Biophys. Acta. 1994, 1209, (1), 130-9.
Laneuville, O., et al. Differential inhibition of human prostaglandin endoperoxide H synthases-1 and -2 by nonsteroidal anti-inflammatory drugs. J. Pharmacol. Exp. Ther. 1994, 271, (2), 927-34.
Gefahrenhinweise (EU): H301-H361
Toxic if swallowed. Suspected of damaging fertility or the unborn child.
Do not breathe dust/fume/gas/mist/vapours/spray. Obtain special instructions before use. Wear protective gloves/protective clothing/eye protection/face protection. IF INHALED: Remove to fresh air and keep at rest in a position comfortable for breathing. Store locked up. Dispose of contents/container in accordance with local/regional/national/international regulations.