Cyclooxygenase (COX), officially known as prostaglandin-endoperoxide synthase (PTGS), is an enzyme that is responsible for formation of important biological mediators called prostanoids, including prostaglandins, prostacyclin and thromboxane. Pharmacological inhibition of COX can provide relief from the symptoms of inflammation and pain. Drugs, like Aspirin, that inhibit cyclooxygenase activity have been available to the public for about 100 years. Two cyclooxygenase isoforms have been identified and are referred to as COX-1 and COX-2. Under many circumstances the COX-1 enzyme is produced constitutively (i.e., gastric mucosa) whereas COX-2 is inducible (i.e., sites of inflammation). Non-steroidal anti-inflammatory drugs (NSAID), such as aspirin and ibuprofen, exert their effects through inhibition of COX. The main COX inhibitors are the non-steroidal anti-inflammatory drugs (NSAIDs).
Acetaminophen (paracetamol) is a selective cyclooxygenase-2 (COX-2) inhibitor with an IC50 of 25.8 μM; is a widely used antipyretic and analgesic drug.
Ibuprofen (Motrin) is an anti-inflammatory inhibitor targeting COX-1 and COX-2, of which is used for pain relief, fever reduction and for reducing swelling.
NS-398 is a COX-2 inhibitor. The COX-1 activity is completely unaffected by 100 μM NS-398, whereas the COX-2 activity was concentration-dependently inhibited, the IC50 value being 3.8 μM.
Rofecoxib(MK 966) is a potent inhibitor of the COX-2-dependent production of PGE2 in human osteosarcoma cells (IC50= 26±10 nM) and Chinese hamster ovary cells expressing human COX-2 (IC50=18±7 nM).
Iguratimod(T-614) is a selective inhibitor of cyclo-oxygenase-2 (COX-2), and inhibits the production of interleukin-1 (IL-1), IL-6, IL-8 and tumour necrosis factor.
Sulindac (Clinoril) is a non-steroidal anti-inflammatory agent of the arylalkanoic acid class; it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.
