Cyclooxygenase (COX) (COX)

Cyclooxygenase (COX), also known as prostaglandin-endoperoxide synthase (PTGS), is a key enzyme that catalyzes the conversion of arachidonic acid into prostaglandin H2, a critical precursor for prostaglandins, prostacyclin, and thromboxanes [UniProt: P23219]. It exists in two primary isoforms: COX-1, which is constitutively expressed and maintains physiological functions like gastric mucosal integrity and platelet aggregation, and COX-2, which is induced during inflammation [PubMed: PMC3081099]. These enzymes are the primary therapeutic targets for nonsteroidal anti-inflammatory drugs (NSAIDs), which are used to treat pain, fever, and inflammatory conditions such as rheumatoid arthritis [StatPearls: Physiology, Cyclooxygenase, 2023]. Inhibition of COX-2 provides the desired anti-inflammatory and analgesic effects, while inhibition of COX-1 is often associated with adverse effects like gastrointestinal ulcers and bleeding [NIH: MedlinePlus, NSAIDs]. Additionally, COX-2 is overexpressed in several cancers, making it a target for potential chemopreventive strategies [PubMed: 15034358]. However, selective COX-2 inhibitors have been linked to an increased risk of cardiovascular events, necessitating careful patient selection [PubMed: 15754037]. Overall, the cyclooxygenase pathway is central to both normal physiology and the pathophysiology of inflammation and pain.

Other names

Prostaglandin-endoperoxide synthasePTGSProstaglandin G/H synthasePGHSCyclo-oxygenase

Inhibition of the cyclooxygenase active site, preventing the conversion of arachidonic acid to prostaglandin G2 (PGG2) and subsequently prostaglandin H2 (PGH2) [StatPearls: NSAIDs, 2023].