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Further information
Mavacoxib is a non-steroidal anti-inflammatory drug (NSAID) of the coxib class. The principal mode of action is inhibition of cyclooxygenase (COX).
COX is a key enzyme in pathways of arachidonic acid metabolism. Its activity culminates in the synthesis of local hormones and inflammatory mediators, termed eicosanoids, which include several prostaglandins. There are two isoforms of COX, COX-1, and COX-2. COX-1 is a widely distributed constitutive enzyme, primarily involved in maintaining organ and tissue function, whilst COX-2 is inducible at sites of tissue damage but in some organs it is also constitutive. COX-2 exerts the major role in synthesising prostaglandins which have pivotal roles as mediators of pain, inflammation and fever. Mavacoxib acts by preferential inhibition of COX-2-mediated prostaglandin synthesis. It therefore possesses analgesic and anti-inflammatory properties. Both COX-1 and COX-2 are present constitutively in the kidney and are assumed to possess protective roles in adverse physiological circumstances.
Mavacoxib is well absorbed after oral administration; bioavailability was 87% in fed dogs and 46 % in fasted conditions and the recommended dose is based on administration with food. Therapeutic concentrations in fed dogs are reached rapidly and peak concentrations are obtained in less than 24 hours after administering a dose. Mavacoxib is approximately 98% bound to plasma proteins. It is extensively distributed throughout the body and almost all the mavacoxib-related residues in plasma comprise parent drug. The rate of body clearance of mavacoxib is slow and the major route of elimination is by biliary excretion of the parent drug.
In laboratory studies with young adult dogs, mean elimination half-life values ranged from 13.8 to 19.3 days. Mavacoxib possessed a longer elimination half-life in client owned animals. Population pharmacokinetic data derived from studies in dogs with a predominately older population with heavier dogs as compared to the experimental studies (mean 9 years of age) showed that the mean elimination half-life was 39 days with a small sub-population (<5%) having an elimination half-life of more than 80 days and correspondingly an increased exposure was recorded in these individuals.