Indomethacin sodium hydrate |
| Catalog No.GC60935 |
Indomethacin (Indometacin) sodium hydrateis a potent, orally active COX1/2 inhibitor with IC50 values of 18 nM and 26 nM for COX-1 and COX-2, respectively.
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Cas No.: 74252-25-8
Sample solution is provided at 25 µL, 10mM.
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Indomethacin sodium hydrate (Indometacin sodium hydrate) is a potent, blood-brain permeable 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[1]. Indomethacin sodium hydrate disrupts autophagic flux by disturbing the normal functioning of lysosomes[2].
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[3]. Indomethacin (22.9 mg/kg, p.o.) produces 8 to 10 linear mucosal lesions extended from the fundic to pyloric area of stomach wall[4].
[1]. Riendeau D, et al. Biochemical and pharmacological profile of a tetrasubstituted furanone as a highly selective COX-2 inhibitor. Br J Pharmacol. 1997 May;121(1):105-17. [2]. Jorge Vallecillo-HernÁndez, et al. Indomethacin Disrupts Autophagic Flux by Inducing Lysosomal Dysfunction in Gastric Cancer Cells and Increases Their Sensitivity to Cytotoxic Drugs. Sci Rep. 2018 Feb 26;8(1):3593. [3]. Lopes RS, et al. Indomethacin treatment reduces microglia activation and increases numbers of neuroblasts in the subventricular zone and ischaemic striatum after focal ischaemia. J Biosci. 2016 Sep;41(3):381-94. [4]. Afroz S, et al. Concentrated phosphatidic acid in cereal brans as potential protective agents against indomethacin-induced stomach ulcer. J Agric Food Chem. 2016 Aug 26.
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