NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)

NSAIDs are drugs that inhibit the activity of the cyclooxygenase (COX) enzyme that produces prostaglandins from arachidonic acid. By inhibiting COX, NSAIDs decrease prostaglandin production. Prostaglandins (PG), particularly prostaglandin E2, are responsible for inflammation and, subsequently, fever, pain and swelling.  NSAIDs relieve mild to moderate acute and chronic pain and are clinically applied most commonly as adjunctive post-operative pain relief and for osteoarthritis, although other applications exist.

The first chemically derived NSAID was acetylsalicylic acid (ASA) in 1897 (Aspirin) discovered by Felix Hoffman at Bayer, Germany. ASA is related to salicin which is a substance contained in willow bark. Willow bark extract is touted to have been used for medicinal purposes as far back as Egyptian times. 

The NSAID group includes drugs like aspirin, ibuprofen, meloxicam, carprofen, robenacoxib, deracoxib, firocoxib, tepoxalin and etodolac. Tepoxalin is an exception to the others NSAIDs in that it also inhibits the 5-Lipoxygenase (5-LOX) enzyme pathway. They relieve mild to moderate acute and chronic pain. 

NSAIDs are further differentiated based upon their selectivity for particular COX receptors. Presently, two isoforms of COX are known to be present in eukaryotic organisms: COX-1 and COX-24. COX-1 is involved in cellular homeostasis5, 6 while COX-2 is expressed or induced at sites of inflammation through actions of cytokines, growth factors, tumor promoters and bacterial lipopolysaccharide7,8,9. NSAIDs having greater “selectivity” for the COX-2 enzyme have been demonstrated to be safer during chronic therapy especially with respect to gastrointestinal and renal toxicity. Today, both non-selective and selective COX 2 inhibitors are registered and available for veterinary use.  

COX inhibitor classification****




Preferential or selective COX-1 inhibitors

ASA, carprofen**, ketoprofen*, vedaprofen*, tepoxalin

COX-1 inhibitor potency at least 5X greater than COX-2 inhibition

Nonspecific COX inhibitors

carprofen**, flunixin, ketoprofen*, meloxicam*, phenylbutazone, tolfenamic acid*, vedaprofen*

No significant biological or clinical difference in drug concentrations producing COX-1 or COX-2 inhibition

Preferential and moderately selective COX-2 inhibitors

carprofen, deracoxib, etodolac, meloxicam, tolfenamic acid, mavacoxib

COX-2 inhibition potency at least 5-100X COX-1 inhibition

Highly selective COX-2 inhibitors

firocoxib, robenacoxib


 The tradenames in the chart above are the exclusive properties of their respective manufacturers.