Flunixin (as meglumine) demonstrates potent inhibition of the cyclo-oxygenase system (COX). The enzyme converts arachidonic acid to unstable cyclic endoperoxides, which are converted to prostaglandins, prostacyclin and thromboxane. Some of these prostanoids, such as prostaglandins are mediators for inflammation, pain and fever. The inhibition of the synthesis of such components would be responsible for the therapeutic effects of flunixin meglumine.

Since prostaglandins also play a part in other physiological processes, COX inhibitors may be responsible for some untoward effects such as gastrointestinal and renal damage.

Prostaglandins are involved in the complex process of endotoxaemic shock

In cattle, after intramuscular injection at a dose of 2 mg/kg, a maximum concentration of 2.5 μg/ml is observed approximately 30 minutes after injection.

After intravenous injection flunixin distributes rapidly. The elimination is slow (approximately 4 hours).

Flunixin is highly bound to plasma proteins (>99%).

In pigs, after intramuscular injection at a dose of 2 mg/kg, a maximum concentration of 4 μg/ml is observed approximately 30 minutes after injection.

After intravenous injection flunixin distributes rapidly. The elimination is slow (approximately 8 hours).

Flunixin is highly bound to plasma proteins (>98%).

In the horse, after intravenous injection at a dose of 1 mg/kg flunixin distributes rapidly. The elimination half-life is 1.6 hours.

Flunixin is eliminated mainly via the kidneys as conjuguated form.

Flunixin is toxic to avian scavengers although foreseen low exposure leads to low risk.