Melox Mechanism of Action

Pharmacotherapeutic group: Non-steroidal anti-inflammatory drug (NSAID).
Pharmacology: Pharmacodynamics: Meloxicam is a NSAID of the oxicam group, possessing analgesic, anti-inflammatory, and anti-pyretic activity. In common with other NSAIDS, although the exact mechanism of action remains unknown, it is known that the inhibition of prostaglandin synthesis, known inflammation mediators, plays a role in the anti-inflammatory activity.
Pharmacokinetics: Following oral administration, meloxicam is well absorbed from the gastrointestinal tract, and it has an absolute bioavailability of about 90%. Peak serum levels are reached after 7-8 hours following a single oral dose, with steady state concentration being achieved after 3-5 days administration. Plasma concentrations are proportional to dose over the 7.5 mg-15 mg dosage range.
Plasma protein binding, principally to albumin, is high, 99%.
Meloxicam undergoes extensive metabolism, principally via oxidation of the methyl group of the thiazolyl ring.
Excretion of administered dose is 50% in the urine and 50% in the faeces, principally as metabolites, with only about 3% of the dose being excreted as unchanged meloxicam.
Mean elimination half life is approximately 20 hours. Mean plasma clearance is about 8 ml/minute, and clearance is reduced in the elderly. Meloxicam has a low volume of distribution, about 11 L, although there is considerable interindividual variation.
Patients with terminal renal failure have an increased volume of distribution, and the stipulated maximum daily dosage of 7.5 mg must not be exceeded.
Toxicology: Preclinical Safety Data: Meloxicam exhibits a similar toxicological profile to other NSAIDS. Preclinical studies in animals using chronic administration of high doses resulted in gastrointestinal erosion and ulceration, and renal papillary necrosis. Depending upon the animal species, non toxic doses were 3-10 times greater than those used clinically.
Reproductive toxicological studies in animals demonstrated foetotoxic effects at doses greatly in excess of those used clinically. Foetotoxic effects at the end of the gestation period common to all prostaglandin synthesis inhibitors were found, cardiopulmonary and renal toxic effects.
In vitro and in vivo studies have not shown any evidence of mutagenic or carcinogenic potential.