COX-2 inhibitor mechanism

by Nathan Wei, MD, FACP, FACR

Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.

Click here: Second Opinion Arthritis Treatment Kit

Cox-2 drugs act by selectively blocking the cyclooxygenase-2 pathway. What is meant by that is this...

The membranes of all cells in the body contain a molecule called “arachadonic acid.”

As cells die from old age and new cells take their place, arachadonic acid is released into the blood. An enzyme called cyclooxygenase (“COX”) acts on arachadonic acid to form substances called prostaglandins.

These are a variety of prostaglandins, and they cause many different effects. Some prostaglandins assist the body with normal functions. For example, they help the stomach resist ulcer formation or help maintain normal blood flow to the kidney. Other prostaglandins cause the pain and inflammation of arthritis.

In the early 1990’s it was found that there are actually two forms of COX: COX-1 and COX-2.

COX-1 is more closely associated with prostaglandins that aid the body with normal functioning. COX-2 is more closely associated with prostaglandins that contribute to inflammation.

Traditional non-=steroidal anti-inflammatory drugs (such as ibuprofen, aspirin etc.) interfere with both COX-1 and COX-2.

So… traditional non-steroidal anti-inflammatory drugs combat inflammation, but they also make the body more susceptible to side-effects such as stomach ulcers. The theory behind Cox-2 drugs has been that they block COX-2 but leave COX-1 untouched.

Drugs that do this are referred to as selective “COX-2 inhibitors.” Selective Cox-2 inhibitors appear to have less gastrointestinal toxicity.

However there have been problems. The first is that Cox -2 drugs, when combined with aspirin, do not protect the stomach any more than a non-selective NSAID does. The second is that Cox-2 drugs still have the same adverse effects on kidney function as do the traditional NSAIDS.

Finally, more recently, concerns regarding cardiovascular toxicity (heart attacks and strokes) have led to the removal of rofecoxib (Vioxx) from the market and increased scrutiny of celecoxib (Celebrex). The most recent evidence indicates that all NSAIDS regardless whether they are selective or non-selective, have an increased incidence of cardiovascular events associated with them.

Of note is the potential for Cox-2 drugs to prevent the development of colon cancer.

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