Until recently, it has been widely accepted that a common mechanism (COX inhibition) is responsible for both the therapeutic and side effects of NSAIDs. However, this theory has been refined since the discovery of a second, inducible COX isozyme, COX-2. It has been proposed that COX-2 inhibition is the relevant target of for the anti-inflammatory effects of NSAIDs, whereas inhibition of constitutive COX-1 is responsible for the gastric and renal side effects as well as for the anti-thrombotic activity of these agents.
Meloxicam, the active ingredient of Mobitil, is a relatively new NSAID which has consistently shown preferential COX-2 inhibition.

The tolerability and safety of meloxicam 7.5 mg/day and 15 mg/day with regard to the gastrointestinal system in general and to peptic ulcer complications in particular is significantly better than that of recommended doses of the classical NSAIDs such as diclofenac.

This was demonstrated by the analysis of clinical pharmacological investigations, 27 clinical double-blind, randomized therapeutic trials including two large-scale clinical studies, as well as study under controlled pharmacoepidemiological conditions.

The favourable tolerability and safety profile of meloxicam is thought to be related to its preferential COX-2 inhibition relative to COX-1.