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Pharmacology: Pharmacodynamics: Diclofenac inhibits the cyclo-oxygenase (COX) enzyme, an early component of the arachidonic acid cascade, resulting in the reduced formation of prostaglandins, thromboxanes and prostacyclin. Diclofenac, the active component has anti-inflammatory, anti-nociceptive and antipyretic effects.
Pharmacokinetics: Absorption: A study was conducted in 18 healthy male volunteers to evaluate pharmacokinetic parameters. 5 ml DICLOTROY (200 mg of diclofenac) was applied over the back of volunteers. The maximum plasma concentration of diclofenac was 175.93 ± 89.49 ng/ml while time to reach maximum plasma concentration was 5.24 ± 2.59 hours. AUC0-t was found to be 1224.19 ± 445.69 hr.ng/ml while AUC0-inf was 1718.21 ± 740.58 hr.ng/ml.
Distribution: Diclofenac is more than 99% bound to human serum proteins, primarily to albumin. Diclofenac diffuses into and out of the synovial fluid.
Metabolism: The major diclofenac metabolite, 4'hydroxy-diclofenac, has very weak pharmacological action. The formation of 4'-hydroxy-diclofenac is primarily mediated by CPY2C9. Both diclofenac and its metabolites undergo glucuronidation or sulfation followed by biliary excretion. CYP3A4 is responsible for the formation of minor metabolites, 5-hydroxy and 3'-hydroxy-diclofenac.
Elimination: Diclofenac is eliminated through metabolism and subsequent urinary and biliary excretion of the glucuronide and the sulfate conjugates of the metabolites. Little or no free unchanged diclofenac is excreted in the urine.
