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Prostaglandins are a group of physiologically active lipid compounds derived enzymatically from arachidonic acid, a 20-carbon fatty acid. They are synthesized in nearly all tissues and exert diverse and potent hormone-like effects, including the regulation of inflammation, pain, vascular tone, platelet function, immune responses, and cell growth. Prostaglandins mediate their biological activities via specific G protein-coupled receptors (such as EP, DP, FP, IP, and TP subtypes), and their biosynthesis is catalyzed by cyclooxygenase (COX) enzymes. Clinical agents (NSAIDs, COX-2 inhibitors, prostaglandin analogs) act either by inhibiting their biosynthesis or by mimicking/inhibiting specific prostaglandin-receptor interactions. While not themselves canonical drug targets, their metabolic and signaling pathways are central therapeutic nodes in many diseases.
Not applicable for prostaglandins themselves, but drugs affecting them include: Inhibition of biosynthesis (e.g., COX inhibitors such as NSAIDs, blocking prostaglandin formation); Agonism or antagonism at prostaglandin receptors (e.g., EP2 agonists or antagonists for pain or inflammation); Use of prostaglandin analogs to stimulate or inhibit specific pathways (e.g., misoprostol for gastric protection)
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