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Diclofenac is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC50s of 4 nM, 1.3 nM for human COX-1 and COX-2 in CHO cells, and 5.1, 0.84 μM for ovine COX-1 and COX-2, respectively.

Diclofenac is a potent COX inhibitor, with IC50s of 4 nM and 1.3 nM for human COX-1 and COX-2 in the CHO cells, respectively. Diclofenac effectively blocks COX-1 mediated prostanoid production from U937 cell microsomes, with an IC50 of 7 ± 3 nM[1]. Diclofenac sodium exihibits inhibition on COX-1 and COX-2 enzyme with IC50s of 5.1 and 0.84 μM, respectively[2].

Diclofenac (3 mg/kg, b.i.d., for 5 days) significantly increases faecal 51Cr excretion in rats, and such effect is also observed in squirrel monkeys after administrated of 1 mg/kg twice daily for 4 days[1]. Diclofenac (10 mg/kg) shows anti-inflammatory activity in mice[2]. Diclofenac (10 mg/kg) decreases oxidized low-densitylipoprotein (Ox-LDL), but shows no effects on the kinetics parameters of catalase and glutathione peroxidase via intramuscularly injection into rats[3].

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