Celecoxib is a non-steroidal anti-inflammatory drug (NSAID), which selectively inhibits the enzyme cyclo-oxygenase (COX)-2. NSAIDs are widely used to treat pain caused by inflammation-related complications, which are symptomatic in chronic or acute pathologies. Allegedly, NSAIDs prevent pain by inhibiting COX-1 and COX-2, which help to synthesize mediators of pain such as prostaglandins. While COX-1 is normally present in most healthy tissues, COX-2 is expressed only in damaged tissues and is mainly induced by inflammatory factors¹.

The first generation of NSAIDs targeted both COXs. This led to unwanted gastrointestinal side effects due to the inhibition of COX-1. To minimize intervention with COX-1, selective COX-2 inhibitors (coxibs) were then developed. Celecoxib was the first clinically proven coxib. In vitro assays have shown that celecoxib inhibits COX-2 with an IC₅₀ of 15 μmol/L. In addition, it efficiently blocks L-type Ca²⁺ channels (Ca_V1), but enhances the K⁺ voltage-gated channel KCNQ activity^2,3.

Clinical trials have shown that celecoxib is a useful therapy for symptomatic pain relief, usually in various joint-related diseases such as osteoarthritis, rheumatoid arthritis, and Ankylosing Spondylitis. Unfortunately, it increases the risk of cardiovascular diseases, probably due to interfering with cardiac K⁺ channels¹.

It was suggested that the drug might be implicated in other aspects of the COX-2 signaling pathway than the anti-inflammation effects⁴. Celecoxib is also being evaluated as a potential anti-cancer drug as it was found to induce apoptosis via specific pathways independent of COX-2⁵.