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Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Prostaglandin E synthase Prostacyclin synthase Thromboxane-A synthase Cytosolic phospholipase A2 Ocular hydrolase Amfenac Amfenac Nepafenac Nepafenac Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid O2 Prostaglandin G2 H2O Heme Heme Glutathione Heme Phospholipids Acceptor Reduced acceptor Prostaglandin G/H synthase 2 Heme Heme Heme Calcium Endoplasmic Reticulum Cytosol Amfenac inhibits COX-1 (prostaglandin G/H synthase 1) and COX-2 (prostaglandin G/H synthase 2) on the endoplasmic reticulum membrane, preventing the conversion of arachidonic acid into PGH2. Prostaglandin H2 synthesis is reduced COX-1 synthesizes prostaglandins necessary for normal gastrointestinal and renal function. COX-2 is responsible for prostaglandin synthesis during tissue injury and inflammation. Inhibition of COX-2 provides anti-inflammatory activity. Prostaglandin E2 is responsible for inflammation and pain by activating immune cells and stimulating pain fibres. Lower concentrations of prostaglandin E2 lowers inflammatory and pain response, hence an analgesic effect is seen. Decreasing PGE2 in the central nervous system also has an antipyretic effect. Napafenac is available as eye drops. After penetrating the cornea, nepafenac undergoes a rapid bioactivation to amfenac in the choroid and retina cells. Inflamed Uvea Cell Uvea Cell