Diclofenac (potassium)

Diclofenac potassium is a potent and nonselective anti-inflammatory agent, acts as a COX inhibitor, with IC₅₀s of 4 and 1.3 nM for human COX-1 and COX-2 in CHO cells^[1], and 5.1 and 0.84 μM for ovine COX-1 and COX-2, respectively^[2]. Diclofenac potassium induces apoptosis of neural stem cells (NSCs) via the activation of the caspase cascade^[3]. In Vitro: Diclofenac effectively blocks COX-1 mediated prostanoid production from U937 cell microsomes, with an IC₅₀ of 7±3 nM^[1].
Diclofenac (1-60 μM; 1 day) induces neural stem cells (NSCs) death in a concentration-dependent manner^[3].
Diclofenac (10-60 μM; 6 hours) increases the expression of cleaved (activated) caspase-3^[3]. 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; administered via oral route just prior to induction of inflammation) shows in vivo anti-inflammatory activity in Wistar rats^[1].