COX-1

COX-1 (cyclooxygenase-1, PTGS1) is a constitutively expressed prostaglandin-endoperoxide synthase that catalyzes the conversion of arachidonic acid into prostaglandin intermediates, thereby initiating prostaglandin and thromboxane biosynthesis essential for physiological homeostasis^[1][2]. Mechanistically, COX-1 participates in the cyclooxygenase and peroxidase reactions that generate prostaglandin H₂, a central precursor for multiple bioactive prostanoids regulating vascular function, platelet activity, renal perfusion, and gastrointestinal integrity^[1][3]. Through sustained prostanoid production, COX-1 contributes to tissue-protective and housekeeping functions across mammalian organs, including maintenance of gastric mucosal defense and thromboxane A₂-dependent platelet aggregation^[3][2]. In disease and pharmacological models, inhibition of COX-1 reduces prostaglandin synthesis and underlies the therapeutic actions of aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), while also contributing to gastrointestinal adverse effects associated with nonselective COX blockade^[1][2][4]. Compared with the inducible isoform COX-2, which is preferentially upregulated by inflammatory stimuli and cellular stress, COX-1 exhibits stable basal expression and is primarily associated with physiological regulation rather than acute inflammatory responses^[3][2][4]. For experimental applications, selective and nonselective COX inhibitors remain important tools for dissecting prostanoid-dependent signaling pathways and distinguishing constitutive versus inducible cyclooxygenase functions in inflammation, thrombosis, and tissue homeostasis^[1][3][4].