PTGS1 (cyclooxygenase-1) is a dual cyclooxygenase/peroxidase enzyme that catalyzes the first committed step in prostanoid biosynthesis from arachidonic acid, converting it to prostaglandin H2 (PGH2), the precursor for all 2-series prostaglandins and thromboxanes [UniProt]. The enzyme abstracts hydrogen at carbon 13 of arachidonic acid and sequentially inserts two oxygen molecules to form the characteristic endoperoxide bridge, with peroxidase activity then reducing the intermediate to PGH2 [UniProt]. PTGS1 is constitutively expressed in the stomach and platelets, where it generates cytoprotective prostaglandins (particularly PGE2) and prothrombotic thromboxane A2, respectively [UniProt]. Clinically, PTGS1 is the primary target of nonsteroidal anti-inflammatory drugs (NSAIDs), whose inhibition contributes to gastrointestinal damage through multiple mechanisms including barrier dysfunction and increased intestinal permeability 1. PTGS1 polymorphisms influence individual responses to NSAID therapy and may modulate cancer risk, with specific variants showing altered metabolic activity and indomethacin sensitivity 23. Gene expression is dynamically regulated by nutritional factors (omega-3 supplementation) and signaling pathways implicated in cancer progression 45. PTGS1 expression occurs early in human embryonic development, suggesting roles in embryogenesis and implantation 6.