The basic mechanism of action of the COX-2 inhibitors is similar to that of nonsteroidal anti-inflammatory drugs (NSAIDs). Traditional NSAIDs block two enzymes, COX-1 and COX-2. The COX-2 enzyme is the one that needs to be blocked in order to inhibit inflammation.
Unfortunately, the lining of the stomach can be damaged when the COX-1 enzyme is also blocked. There is also the potential for kidney damage and high blood pressure when the COX-1 enzyme is blocked. Initially, it was believed that selectively blocking the COX-2 enzyme would diminish these side effects.
In addition, because the COX-1 enzyme would not be blocked, it would be possible to take a higher dosage of the COX-2 blocker, and thus achieve greater control of inflammation and pain. This worked well in laboratory studies, and also in early human studies.
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