“…2,3 NSAIDs exert their analgesic, antipyretic, anti-inflammatory, and antithrombotic effects by inhibiting both COX-1 and COX-2 activities. [4][5][6] However, the primary responsibility for the synthesis of prostanoids involved in acute and chronic inflammatory states has been credited to COX-2, whereas the gastrointestinal adverse effects have been attributed to COX-1 activity. 1,6 The consequent hypothesis that specific inhibition of this enzyme could have therapeutic effects similar to those of other NSAIDs but without causing gastrointestinal side effects led to the development of COX-2-selective antagonists.…”