Cimicoxib is a non-steroidal anti-inflammatory drug belonging to the coxib group and acting by selective inhibition of the enzyme cyclo-oxygenase 2. The cyclo-oxygenase enzyme (COX) is present in two isoforms. COX-1 is usually a constitutive enzyme expressed in tissues, which synthesize products responsible for normal physiologic functions (e.g. in the gastro-intestinal tract and kidneys). COX-2 on the other hand, is mainly inducible and synthesized by macrophages and inflammatory cells after stimulation by cytokines and other mediators of inflammation. COX-2 is involved in the production of mediators, including PGE2, that induce pain, exudation, inflammation and fever.

In an in vivo inflammatory acute pain model, it was shown that the simulated effect of cimicoxib lasted for approximately 10-14 hours.

After oral administration in dogs at the recommended dose of 2 mg/kg without food, cimicoxib is rapidly absorbed and the time to maximal concentration (Tmax) is 2.25 (± 1.24) hours. The peak concentration (Cmax) is 0.3918 (± 0.09021) µg/ml, area under the curve (AUC) is 1.676 (± 0.4735) µg.hr/ml, and oral bioavailability is 44.53 (± 10.26) percent.

The oral administration of cimicoxib with food did not significantly influence the bioavailability but decreased significantly the observed Tmax.

Metabolism of cimicoxib is extensive. The major metabolite, demethylated cimicoxib is mainly eliminated in faeces by the biliary route and, to a lesser extent, in urine. The other metabolite, glucuronide conjugate of the demethylated cimicoxib, is eliminated in urine. The elimination half-life (t1/2) is 1.38 (± 0.24) hours. The metabolising enzymes have not been fully investigated and slower metabolism (up to four-fold increased exposure) has been noted in some individuals.