NSAIDs such as dexibuprofen act by inhibiting cyclooxygenase (COX) enzymes, which convert arachidonic acid to prostaglandins. These act as the mediators of pain, inflammation and fever. It also inhibits the formation of thromboxane A2 (which stimulates platelet aggregation, leading to the formation of blood clots). Dexibuprofen is a non-selective COX inhibitor because it inhibits both isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory effects of NSAIDs appear to act primarily by inhibiting COX-2. Inhibition of COX-1 is instead responsible for the adverse effects on the gastrointestinal tract.
The pharmacokinetics are very similar to those of ibuprofen. After oral administration, the maximum serum concentration is reached after 2.25-5 hours. Up to 99% of the drug is bound to plasma proteins. Most of the drug is metabolized in the liver and excreted in the urine within 24 hours; 1% of the given dose is excreted in the stool.
Drinking alcohol while taking Dexibuprofen may increase the risk of stomach bleeding.
Dexibuprofen may possibly interfere with the antiplatelet effect of low-dose aspirin (acetylsalicylic acid), possibly making aspirin less effective when used for cardioprotection and stroke prevention.