Mel-OD is a nonsteroidal anti-inflammatory drug (NSAID). In contrast with other NSAIDs currently available, it has a greater inhibitory activity against the inducible isoform of cyclooxygenase (COX-2), which is implicated in the anti-inflammatory response than against the constitutive isoform (COX-1), inhibition of which is associated with GI and renal adverse events and inhibition of platelet aggregation.
Pharmacokinetics: Mel-OD is absorbed almost completely when given orally and has an oral bioavailability of 89-93%. Binding to plasma proteins exceeds 99.5% and therefore, the drug has a relatively small volume of distribution of 10.8 L (0.14 L/kg). Linear pharmacokinetics are observed over the entire dose range and steady-state concentrations are reached after 3-5 days. The maximum plasma concentration (Cmax) attained at steady-state range from 0.88-1.92 mg/L.
Meloxicam effectively reaches the synovial fluid in concentrations reflecting 40-50% of the accompanying total plasma concentrations but the free, protein unbound concentrations in synovial fluid are similar to those in plasma. The terminal elimination t½ of Mel-OD is about 20 hrs and total plasma clearance is 0.42-0.48 L/hr. Meloxicam is extensively metabolized by the cytochrome P-450 system in the liver into 4 major inactive metabolites and has a dual excretion, with about half of meloxicam being excreted in the urine and the remainder in the feces. Food intake has no clinically significant impact on the pharmacokinetics of Mel-OD and the drug may therefore be taken concurrently with meals. The pharmacokinetics of Mel-OD are not altered in patients with hepatic dysfunction as well as in patients with mild to moderate renal dysfunction, but a lower dosage is recommended in patients with end-stage renal failure.