Diclofenac potassiumDiclofenac potassium
MedChemExpress (MCE)
HY-15038
15307-81-0
99.99%
4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
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, and 5.1 and 0.84 μM for ovine COX-1 and COX-2, respectively. Diclofenac potassium induces apoptosis of neural stem cells (NSCs) via the activation of the caspase cascade.
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].
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].
Human COX-2 1.3 nM (IC50, in CHO cells) Human COX-1 4 nM (IC50, in CHO cells) Ovine COX-2 0.84 nM (IC50) Ovine COX-1 5.1 nM (IC50)
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[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. [Content Brief]
[2]. Labib MB, et al. Design, synthesis of novel isoindoline hybrids as COX-2 inhibitors: Anti-inflammatory, analgesic activities and docking study. Bioorg Chem. 2018 Oct
80:70-80. [Content Brief]
[3]. Chiho Kudo, et al. Diclofenac Inhibits Proliferation and Differentiation of Neural Stem Cells. Biochem Pharmacol. 2003 Jul 15
66(2):289-95. [Content Brief]