APAP or acetaminophen has analgesic and antipyretic properties, but it has no clinically significant anti-inflammatory activity. The likely mechanism of its analgesic action is related to N-arachidonoyl-phenolamine (AM404), a metabolite of APAP, which appears to inhibit the cellular uptake of anandamide leading to increased cannabinoid receptor activity.24,25 Its antipyretic effect also appears to be related AM404, which inhibits cyclooxygenase activity in the CNS.27-29
The absorption of APAP following oral administration is rapid and complete. The onset of analgesia is about 30 minutes. Plasma protein binding is low (< 25%); consequently, APAP is readily distributed throughout the body. APAP is metabolized primarily by hepatic conjugation. About 10-15% of APAP is metabolized by the CYP450 isoenzyme 2E1 into a hepatotoxic intermediate metabolite, which must be detoxified by glutathione conjugation.30 Inactive metabolites of APAP are eliminated in the kidney.
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