Acetaminophen is an analgesic and antipyretic compound.Unlike many NSAIDs, which inhibit both COX-1 and COX-2, early studies suggested that acetaminophen is a poor inhibitor of both isoforms.However, it does inhibit COX-2 by 83% and COX-1 by 56% in human blood ex vivo, albeit at a high 1,000 mg dose, with IC50 values of 25.8 and 113.7 µM, respectively.Acetaminophen is enzymatically and non-enzymatically converted to several reactive metabolites that contribute to adverse or indirect effects, including liver injury.At toxic doses, the acetaminophen metabolite N-acetyl-4-benzoquinone imine (NAPQI; Cat No. PC-52714) depletes glutathione reserves in the liver, leading to an accumulation of NAPQI and subsequent hepatocyte necrosis.Acetaminophen decreases glutathione levels and reduces glutathione peroxidase activity in mice when administered at a dose of 250 mg/kg and induces ferroptotic cell death in primary mouse hepatocytes, an effect that can be blocked by the ferroptosis inhibitor ferrostatin-1 (Cat No. PC-53956).Acetaminophen has analgesic and antipyretic properties in animal models.

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