Naproxen blocks arachidonic acid binding and competitively inhibits the cyclooxygenase (COX) isoenzymes COX-1 and COX-2, resulting in analgesic and anti-inflammatory effects. COX-1 and COX-2 are catalysts for the conversion of arachidonic acid to prostaglandin G (PGG), the first step in the synthesis of prostaglandins and thromboxanes involved in rapid physiological responses. what is naproxen COX-1 is constitutively expressed in most tissues, whereas COX-2 is only expressed in the brain, kidney, bone, reproductive organs, and specific tumors such as colon and prostate cancers. COX-1 is responsible for the synthesis of prostaglandins in response to stimulation by circulating hormones and maintains healthy renal function, gastric mucosal integrity and hemostasis. COX-2 is induced in many cells in response to specific inflammatory mediators (eg, interleukin 1, tumor necrosis factor, lipopolysaccharide).

The anti-inflammatory mechanism of naproxen is due to the reduction of prostaglandin synthesis through the inhibition of COX-1 and COX-2. Most of the anti-inflammatory effects induced by naproxen are primarily due to inhibition of the COX-2 isoenzyme; however, it should be noted that COX-1 is also expressed at different sites of inflammation. In addition, COX-1 is also expressed in the joints of patients with rheumatoid arthritis or osteoarthritis, especially in the synovial lining. Thus, although naproxen targets both COX-1 and COX2, it is slightly more selective for the former. Additionally, naproxen was most effective in setting pain receptor sensitivity. Prostaglandins, especially prostaglandins E and F, appear to be responsible for sensitizing these pain receptors; thus, naproxen has additional indirect analgesic effects by inhibiting further prostaglandin production. [4]

Naproxen is extensively metabolized by the liver, with approximately 95% of the drug excreted in the urine. Naproxen also has a half-life of 12 to 17 hours.