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Indomethacin is a potent and nonselective inhibitor of COX1 and COX2, with IC50s of 18 nM and 26 nM for human COX-1 and COX-2, respectively, in CHO cells.

Indomethacin is a potent and nonselective inhibitor of COX1 and COX2, with IC50s of 18 nM and 26 nM for human COX-1 and COX-2, respectively, in CHO cells. Indomethacin inhibits lipopolysaccharide (LPS)-induced PGE2 production (COX-2) in a human whole blood assay with a potency (IC50=0.68±0.17 μM), and suppresses coagulation-induced TXB2 production (COX-1) (IC50=0.19±0.02 μM). Indomethacin blocks COX-1 with an IC50 of 20±1 nM in U937 cell microsomes at a low arachidonic acid concentration (0.1 μM)[1].

Indomethacin dose-dependently inhibits both the carrageenan-induced rat paw oedema (ED50, 2.0 mg/kg), hyperalgesia (ED50, 1.5 mg/kg), and is also effective at reversing LPS-induced pyrexia in rats (ED50, 1.1 mg/kg)[1]. Indomethacin (2.5 mg/kg, i.p) decreases the number of NeuN+ cells in the animals at 8 days after ET-1 injection. Indomethacin also reduces microglia/macrophage activation at 14 days. Indomethacin significantly increases the number of SVZ DCX+ cells/field at 14 days post stroke[2]. Indomethacin (22.9 mg/kg, p.o.) produces 8 to 10 linear mucosal lesions extended from the fundic to pyloric area of stomach wall[3].

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