Its precise mechanism of action is unknown, although it is believed that inhibiting brain and spinal cord prostaglandin (fat-like molecules that are involved in inflammation, pain and fever) synthesis might be involved. Recently, researchers uncovered another mechanism involving<unk>  being a prodrug. In this proposal, not yet verified by other researchers, the<unk>  itself breaks down into other chemicals that are the actual active agents. The result is a pair of cannabinoid and NSAID arachidonic acid conjugates (although not in the strict chemical meaning of the word) of<unk> 's breakdown products. Despite this, studies in animals have found that the CB1 cannabinoid receptor is not involved in the analgesia induced by<unk> . Although it seems to inhibit fevers caused by prostaglandins, especially prostaglandin E2,<unk>  appears to produce its therapeutic effects by means of its metabolites, especially N-methyl-4-aminoantipyrine (MAA) and 4-Aminoantipyrine (AA). + Pharmacokinetics of<unk> 's major metabolites Metabolite Acronym Biologically active? Pharmacokinetic properties 200pxN-methyl-4-aminoantipyrine MAA Yes Bioavailability≈90%. Plasma protein binding: 58%. Excreted in the urine as 3±1% of the initial (oral) dose 200px4-aminoantipyrine AA Yes Bioavailability≈22.5%. Plasma protein binding: 48%. Excreted in the urine as 6±3% of the initial (oral) dose 200pxN-formyl-4-aminoantipyrine FAA No Plasma protein binding: 18%. Excretion in the urine as 23±4% of the initial oral dose 200pxN-acetyl-4-aminoantipyrine AAA No Plasma protein binding: 14%. Excretion in the urine as 26±8% of the initial oral dose
Metamizole
Astemizole
Sodium azide
Eflornithine
Miproxifene phosphate
Fursultiamine
Mesocarb
Amifampridine