Diclofenac Sodium (GP 45840) 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. IC50 & Target: IC50: 4 nM (Human COX-1, in CHO cells), 1.3 nM (Human COX-2, in CHO cells)^[1], 5.1 μM (Ovine COX-1), 0.84 μM (Ovine COX-2)^[2] In Vitro: Diclofenac Sodium (GP 45840) 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]. In Vivo: 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].