Most NSAIDs, including mefanamic acid, are non-selective prostaglandin G/H synthase (better known as cyclooxygenase or COX) inhibitors that act on both prostaglandin G/H synthase 1 and 2 (COX-1 and -2). Prostaglandin G/H synthase catalyzes the conversion of arachidonic acid to prostaglandin G2 and prostaglandin G2 to prostaglandin H2. Prostglandin H2 is the precursor to a number of prostaglandins involved in fever, pain, swelling and inflammation (e.g. PGE2). Mefanamic acid antagonizes COX by binding to the upper portion of the active site, preventing its substrate, arachidonic acid, from entering the active site. The analgesic, antipyretic and anti-inflammatory effects of mefanamic acid occur as a result of decreased prostaglandin synthesis.