Pharmacology
Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase (and thus causes inhibition of prostaglandin production), whereas nonselective NSAIDs (like aspirin, naproxen and ibuprofen) inhibit both COX-1 and COX-2. COX-1, traditionally defined as a constitutively-expressed "housekeeping" enzyme, is the only isoenzyme found in platelets and plays a role in the protection of the gastrointestinal mucosa, renal hemodynamics, and platelet thrombogenesis. COX-2, on the contrary, is extensively expressed in cells involved in inflammation and is upregulated by bacterial lipopolysaccharides, cytokines, growth factors, and tumor promoters. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. It binds with its polar sulfonamide side chain to a hydrophilic side pocket region close to the active COX-2 binding site. In theory, this selectivity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs.
Celecoxib inhibits COX-2 without affecting COX-1. COX-1 is involved in synthesis of prostaglandins and thromboxane, but COX-2 is only involved in the synthesis of prostaglandin. Therefore, inhibition of COX-2 inhibits only prostaglandin synthesis without affecting thromboxane (TxA2) and thus offer no cardioprotective effects of non-selective NSAIDs.
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