In the 1990s, researchers discovered that two different COX enzymes exist: COX-1 and COX-2. COX-1 is present in most tissues, including the stomach lining. It’s also involved in kidney function. COX-2 is the enzyme primarily present at sites of inflammation . Both COX-1 and COX-2 convert arachidonic acid to prostaglandin, resulting in pain and inflammation. The anti-inflammatory action of NSAIDs is mainly due to inhibition of COX-2, and their unwanted side effects (like bleeding ulcers) are largely due to inhibition of COX-1. ( 12 )
When and how much to take
NSAIDs should ideally be taken with some food, or at least with milk or yoghurt to avoid irritation of the gastric mucosa (. the inner lining of the stomach). It is important not to exceed the recommended dose to avoid possible serious side-effects. There is also no benefit in taking more than a certain dose, since these drugs have a ceiling effect. This means that above a certain dose, taking even more of this medication will not yield any extra beneficial effects, but will considerably increase the risk for side-effects.
Ibuprofen is administered as a racemic mixture. The R-enantiomer undergoes extensive interconversion to the S-enantiomer in vivo . The S-enantiomer is believed to be the more pharmacologically active enantiomer.  The R-enantiomer is converted through a series of three main enzymes. These enzymes include acyl-CoA-synthetase, which converts the R-enantiomer to (-)-R-ibuprofen I-CoA; 2-arylpropionyl-CoA epimerase, which converts (-)-R-ibuprofen I-CoA to (+)-S-Ibuprofen I-CoA; and hydrolase, which converts (+)-S-ibuprofen I-CoA to the S-enantiomer.  In addition to the conversion of ibuprofen to the S-enantiomer, the body can metabolize ibuprofen to several other compounds, including numerous hydroxyl, carboxyl and glucuronyl metabolites. Virtually all of these have no pharmacological effects.