Firocoxib is non-steroidal anti-inflammatory drug (NSAID) belonging to the Coxib group, which acts by selective inhibition of cyclooxygenase-2 (Cox-2)-medicated prostaglandin synthesis. Cyclooxygenase is responsible for generation of prostaglandins. COX-2 is the isoform of the enzyme that has been shown to be induced by pro-inflammatory stimuli and has been postulated to be primarily responsible for the synthesis of prostanoid mediators of pain, inflammation, and fever. Coxibs therefore display analgesic, anti-inflammatory, and antipyretic properties. COX-2 is also thought to be involved in ovulation, implantation and closure of the ductus arteriosus, and central nervous system functions (fever induction, pain perception, and cognitive function). "In "in vitro" equine whole blood assays, firocoxib exhibits 222 to 643 fold selectivity for COX-2 over COX-1. The concentration of firocoxib required to inhibit 50% of the COX-2 enzyme (i.e. the IC50) is 0.0369 to 0.12 μM, whereas the IC50 for COX-1 is 20.14 to 33.1 μM.

Following oral administration in horses at the recommended dose of 1 tablet per horses, firocoxib is rapidly absorbed, and the time to maximal concentration (Tmax) is 2.43 (+ 2.17) hours. The peak concentration (Cmax) is 0.075 (+ 0.021) μg/ml, area under the curve (AUCO-inf) is 3.48 (+1.15) μg x hr/ml. The elimination half-life (t½) after a single dose is 38.7 (+ 7.8) hours. Firocoxib is approximately 97% bound to plasma proteins. Following multiple oral administrations, the steady state is reached by approximately the eighth daily dose. Firocoxib is metabolised predominantly by dealkylation and glucuronidation in the liver. Elimination is principally in the excreta (primarily the urine), with some biliary excretion also observed.