Ibuprofen is eliminated, after biotransformation to glucuronide conjugate metabolites, through urine and feces, with 45-79% as metabolites and 100 mg/L). At doses greater than 600 mg, there is an increase in the unbound faction of the drug leading to an increased clearance. Its primary distribution is in plasma albumin, with a volume of distribution of 0.12L/kg in adults, and significant levels are attained in synovial fluid, which is the proposed NSAID site of action. Ibuprofen is rapidly absorbed, reaching peak serum levels one to two hours after administration, and has a half-life of 1.8 to two hours. Its anti-inflammatory effect has been attributed almost entirely to the S-(+)-enantiomer. There are two stereo-forms of the drug, however the S-(+)-enantiomer accounts for the majority of the pharmacological activity, and has been found, in in vitro studies, to be 160 times more potent than its racemate, R-(-)-ibuprofen, in inhibiting prostaglandin synthesis, and two times more potent in inhibiting platelet aggregation and thromboxane generation. While the exact mechanism remains unknown, ibuprofen is known to be a potent inhibitor of prostaglandin synthesis, which controls pain, inflammation and fever. It became available by prescription in the United States in 1974, over-the-counter in Britain in 1983, and over-the-counter in the United States in 1984.Īs an NSAID, ibuprofen is a non-selective inhibitor of cyclo-oxygenase-1 (COX-1) and cyclo-oxygenase-2 (COX-2). Ibuprofen was originally developed as an anti-rheumatic drug in 1961 and was first introduced by prescription in 1969 in Great Britain as Bufren.
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