Quantitative metabolomics services for biomarker discovery and validation.
Specializing in ready to use metabolomics kits.
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Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Prostaglandin G/H synthase 1 Bromfenac Transporter Prostaglandin E synthase Prostacyclin synthase Thromboxane-A synthase Cytosolic phospholipase A2 Bromfenac Bromfenac 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 Extracellular space Bromfenac 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. Inflamed Eye Cell
Endoplasmic Reticulum PTGS1 PTGS2 PTGS1 Unknown PTGES PTGIS TBXAS1 PLA2G4A Bromfenac Bromfenac Prostaglandin H2 Prostaglandin E2 Prostaglandin I2