The exact mechanism of action of acetaminophen is not fully understood, but it is believed to involve inhibition of the enzyme cyclooxygenase (COX), primarily COX-2, in the central nervous system. This inhibition leads to a reduction in the production of prostaglandins, which are chemicals involved in the transmission of pain signals and the regulation of inflammation and fever. Acetaminophen is also thought to have additional mechanisms of action, such as modulation of the endocannabinoid system and activation of the descending serotonergic pathways, which contribute to its analgesic (pain-relieving) and antipyretic (fever-reducing) effects. However, unlike nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen has minimal anti-inflammatory effects and does not significantly inhibit COX-1 in peripheral tissues, which may explain its lack of gastrointestinal side effects commonly associated with NSAIDs.