Ketorolac tromethamine, COX-1 inhibitor

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Cyclooxygenase 2 also known as COX2 is an enzyme involved in the conversion of arachidonic acid to prostaglandins which are lipid compounds with hormone-like effects. It has alternative names including prostaglandin-endoperoxide synthase 2. The molecular weight of COX2 is approximately 72 kDa. This enzyme is expressed in various tissues including the brain kidneys and areas of inflammation. COX2 expression increases during inflammatory responses and is induced by pro-inflammatory cytokines.

Biological function summary

COX2 plays a significant role in the inflammatory response and is part of the complex process of synthesizing prostaglandins. These compounds mediate inflammation and pain making COX2 an important target for understanding these processes. COX2 is not ubiquitously expressed but rather is induced in activated macrophages and other cells during inflammatory conditions. Its function is also important for normal physiological processes like ovulation and implantation.

Pathways

COX2 is essential in the prostaglandin biosynthesis pathway connecting it to the arachidonic acid metabolism pathway. Cyclooxygenase 2 works with phospholipase A2 which releases arachidonic acid from the phospholipid membrane. COX2 then converts this acid to prostaglandin H2 a precursor for other prostaglandins. COX1 the other isoform of cyclooxygenase is closely related to COX2 and while they have different expression patterns they share some functional similarities in these pathways.

COX2 is connected to inflammatory conditions like arthritis and cancer. Its expression often increases in various cancer types contributing to tumor growth and metastasis by promoting angiogenesis and suppressing immune responses. The enzyme is also linked to rheumatoid arthritis where its overexpression exacerbates inflammation. COX2 inhibitors like ketorolac tromethamine or naproxen structure mitigate symptoms by decreasing prostaglandin synthesis. These inhibitors also interact with COX1 but selective inhibition of COX2 targets inflammation more effectively with fewer gastric side effects associated with COX1 inhibition.