<unk>  acts as an inhibitor of cyclooxygenase (COX), producing the anti-inflammatory and analgetic (pain relieving) effects. In the body, it is partly metabolized to indometacin, which also acts as a COX inhibitor. The same mechanism is responsible for the antipyretic and antiplatelet effects, which are however not clinically used, as well as for the typical NSAID adverse effects. An advantage of<unk>  is that it reduces gastric damage as compared to indometacin, possibly because<unk>  has less effect on the increase of leukotriene B4 synthesis and tumor necrosis factor (TNF) expression, leading to less induction of leukocyte-endothelial adherence. Pharmacokinetics Metabolism of<unk> . Cleaving of the glycolic acid ester (green) activates the substance to indometacin, cleaving of the methoxy ether or the 4-chlorobenzoate (orange) inactivate it. The substance is quickly and almost completely absorbed from the gut. Highest blood plasma concentrations are reached after two hours. It is bound to plasma proteins to 80–90%. Concentrations in the synovial fluid and membranes, muscle and bone are higher than in the blood. Apart from the active metabolite indometacin, a number of inactive metabolites are found after application of<unk> : the O-desmethyl-, des-4-chlorobenzoyl-, and O-desmethyl-des-4-chlorobenzoyl derivatives of both indometacin and<unk> , as well as all of these substances' glucuronides (mediated at least partly by the enzyme UGT2B7). Elimination half-life is 4.5±2.8 hours (in some individuals up to 16 hours) under steady state conditions. 40% are eliminated via the kidney, and 50% via the faeces.
Acemetacin
Corneal button
Scleral lens
Myopic crescent
Ateronon
Bruch's membrane
Rosenthal fiber
Concha bullosa