Chemical Formula: C20H32O6
Chemical Formula C20H32O6
Found 120 metabolite its formula value is C20H32O6
Prostaglandin G2
Prostaglandin G2 (PGG2) is synthesized from arachidonic acid on a cyclooxygenase (COX) metabolic pathway as a primary step; the COX biosynthesis of prostaglandin (PG) begins with the highly specific oxygenation of arachidonic acid in the 11R configuration and ends with a 15S oxygenation to form PGG2. The COX site activity that catalyzes the conversion of arachidonic acid to PGG2 is the target for nonsteroidal antiinflammatory drugs (NSAIDs). The peroxidase site activity catalyzes the two-electron reduction of the hydroperoxide bond of PGG2 to yield the corresponding alcohol prostaglandin H2 (PGH2). The formation of a phenoxyl radical on Tyr385 couples the activities of the two sites. The Tyr385 radical is produced via oxidation by compound I, an oxoferryl porphyrin -cation radical, which is generated by reaction of the hemin resting state with PGG2 or other hydroperoxides. The tyrosyl radical homolytically abstracts the 13proS hydrogen atom of arachidonic acid which initiates a radical cascade that ends with the stereoselective formation of PGG2. PGG2 then migrates from the cyclooxygenase (COX) site to the peroxidase (POX) site where it reacts with the hemin group to generate PGH2 and compound I. The heterolytic oxygen-oxygen bond cleavage is assisted by the conserved distal residues His207 and Gln203, mutation of which has been shown to severely impair enzyme activity. Compound I, upon reaction with Tyr385, gives compound II, which in turn is reduced to the hemin resting state by one-electron oxidation of reducing cosubstrates or undergoes reactions that result in enzyme self-inactivation. Prostaglandin endoperoxide H synthase (PGHS) 1 is a bifunctional membrane enzyme of the endoplasmic reticulum that converts arachidonic acid into prostaglandin H2 (PGH2), the precursor of all prostaglandins, thromboxanes, and prostacyclins. These lipid mediators are intricately involved in normal physiology, namely, in mitogenesis, fever generation, pain response, lymphocyte chemotaxis, fertility, and contradictory stimuli such as vasoconstriction and vasodilatation, as well as platelet aggregation and quiescence. PGHS is implicated in numerous pathologies, including inflammation, cancers of the colon, lung, and breast, Alzheimers disease, Parkinsons disease, and numerous cardiovascular diseases including atherosclerosis, thrombosis, myocardial infarction, and stroke. (PMID: 14594816, 16552393, 16411757). Prostaglandins are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. Prostaglandin G2 (PGG2) is synthesized from arachidonic acid on a cyclooxygenase (COX) metabolic pathway as a primary step; the COX biosynthesis of prostaglandin (PG) begins with the highly specific oxygenation of arachidonic acid in the 11R configuration and ends with a 15S oxygenation to form PGG2. D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
6-Ketoprostaglandin E1
6-Ketoprostaglandin E1 (6-keto PGE1) is a biologically active and stable prostacyclin (PGI2) metabolite and a substrate for Adenylate cyclase type III. 6-keto PGE1 is a potent coronary vasodilator. 6-keto PGE1 could be elevated in plasma of patients with primary thrombocythaemia. 6-keto-PGE1 has approximately four times less potent antiplatelet activity than PGI2 on a molar basis in man. The cardiovascular and plasma renin activity (PRA) changes are less prominent for 6-keto-PGE1 than PGI2. Salt loading slightly increases urinary 6-keto PGE1. 6-keto-PGE1 elicits the same biological effects as PGI2 in human platelets and in rabbit aorta and mesenteric artery, being, however, less potent. 6-keto-PGE1 dose-dependently stimulates adenylate cyclase activity in membranes of human platelets and cultured myocytes from rabbit aorta and mesenteric artery. The extent of stimulation of the enzyme by 6-keto-PGE1 is the same as elicited by PGI2, while the apparent affinity is lower than that of prostacyclin, both in platelets and in vascular smooth muscle cells. At the level of platelet membranes, 6-keto-PGE1 interacts with the binding sites labelled by PGI2. However, in platelets as well as in mesenteric artery myocytes, 6-keto-PGE1 interacts with only one class of sites as demonstrated either by binding or by adenylate cyclase studies, whereas PGI2 in the same conditions recognizes two different classes. (PMID: 3186779, 3075239, 3472253, 3912001, 3881881, 6391491)Prostaglandins are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 6-Ketoprostaglandin E1(6-keto PGE1) is a biologically active and stable prostacyclin (PGI2) metabolite and a substrate for Adenylate cyclase type III. 6-keto PGE1 is a potent coronary vasodilator. 6-keto PGE1 could be elevated in plasma of patients with primary thrombocythaemia. 6-keto-PGE1 has approximately four times less potent antiplatelet activity than PGI2 on a molar basis in man. The cardiovascular and plasma renin activity (PRA) changes are less prominent for 6-keto-PGE1 than PGI2. Salt loading slightly increases urinary 6-keto PGE1. D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents
11-Dehydro-thromboxane B2
11-Dehydro-thromboxane B2, a stable thromboxane metabolite, is a full agonist of chemoattractant receptor-homologous molecule expressed on TH2 cells (CRTH2) in human eosinophils and basophils. Given its production in the allergic lung, antagonism of the 11-dehydro- thromboxane B2/CRTH2axis may be of therapeutic relevance. (PMID 14668348)Thromboxanes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 11-Dehydro-thromboxane B2, a stable thromboxane metabolite, is a full agonist of chemoattractant receptor-homologous molecule expressed on TH2 cells (CRTH2) in human eosinophils and basophils. Given its production in the allergic lung, antagonism of the 11-dehydro- thromboxane B2/CRTH2axis may be of therapeutic relevance. (PMID 14668348)
Cinncassiol D2
Cinncassiol D2 is found in herbs and spices. Cinncassiol D2 is a constituent of Cinnamomum cassia (Chinese cinnamon) Constituent of Cinnamomum cassia (Chinese cinnamon). Cinncassiol D2 is found in herbs and spices.
Cinncassiol D3
Cinncassiol D3 is found in herbs and spices. Cinncassiol D3 is a constituent of cinnamomi cortex, the dried bark of Cinnamomum cassia (Chinese cinnamon). Constituent of cinnamomi cortex, the dried bark of Cinnamomum cassia (Chinese cinnamon). Cinncassiol D3 is found in herbs and spices.
Thromboxane B3
Thromboxane B3 (TXB3) is a prostanoid that is formed by the hydrolysis of TXA3, a product of dietary eicosapentaenoic acid transformed in humans. Prostanoids are a subclass of the lipid mediator group known as eicosanoids. They derive from C-20 polyunsaturated fatty acids, mainly dihomo-gamma-linoleic (20:3n-6), arachidonic (20:4n-6), and eicosapentaenoic (20:5n-3) acids, through the action of cyclooxygenases-1 and -2 (COX-1 and COX-2). The reaction product of COX is the unstable endoperoxide prostaglandin H (PGH) that is further transformed into the individual prostanoids by a series of specific prostanoid synthases. Prostanoids are local-acting mediators formed and inactivated within the same or neighbouring cells prior to their release into circulation as inactive metabolites (15-keto- and 13,14-dihydroketo metabolites). Non-enzymatic peroxidation of arachidonic acid and other fatty acids in vivo can result in prostaglandin-like substances isomeric to the COX-derived prostaglandins that are termed isoprostanes. Prostanoids take part in many physiological and pathophysiological processes in practically every organ, tissue and cell, including the vascular, renal, gastrointestinal and reproductive systems. Their activities are mediated through prostanoid-specific receptors and intracellular signalling pathways, whilst their biosynthesis and action are blocked by nonsteroidal antiinflammatory drugs (NSAID). Isoprostanes are considered to be reliable markers of oxidant stress status and have been linked to inflammation, ischaemia-reperfusion, diabetes, cardiovascular disease, reproductive disorders and diabetes. (PMID: 16986207, 2996649)Thromboxanes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. Thromboxane B3 (TXB3) is a prostanoid that is formed by the hydrolysis of TXA3, a product of dietary eicosapentaenoic acid transformed in humans. Prostanoids are a subclass of the lipid mediator group known as eicosanoids. They derive from C-20 polyunsaturated fatty acids, mainly dihomo-gamma-linoleic (20:3n-6), arachidonic (20:4n-6), and eicosapentaenoic (20:5n-3) acids, through the action of cyclooxygenases-1 and -2 (COX-1 and COX-2). The reaction product of COX is the unstable endoperoxide prostaglandin H (PGH) that is further transformed into the individual prostanoids by a series of specific prostanoid synthases. Prostanoids are local-acting mediators formed and inactivated within the same or neighbouring cells prior to their release into circulation as inactive metabolites (15-keto- and 13,14-dihydroketo metabolites). Non-enzymatic peroxidation of arachidonic acid and other fatty acids in vivo can result in prostaglandin-like substances isomeric to the COX-derived prostaglandins that are termed isoprostanes. Prostanoids take part in many physiological and pathophysiological processes in practically every organ, tissue and cell, including the vascular, renal, gastrointestinal and reproductive systems. Their activities are mediated through prostanoid-specific receptors and intracellular signalling pathways, whilst their biosynthesis and action are blocked by nonsteroidal antiinflammatory drugs (NSAID). Isoprostanes are considered to be reliable markers of oxidant stress status and have been linked to inflammation, ischaemia-reperfusion, diabetes, cardiovascular disease, reproductive disorders and diabetes. (PMID: 16986207, 2996649)
19-Hydroxy-PGE2
19-Hydroxy-PGE2 is a derivative of PGE2. Both 19-Hydroxy-PGE1 and 19-hydroxy-PGE2 are formed from PGE1 and PGE2 by prostaglandin 19-hydroxylase, a cytochrome P-450 enzyme, in seminal vesicles (PMID: 3196735). 19-Hydroxy-PGE2 is a selective prostanoid EP2-receptor agonist; it doesnt stimulate FP-receptors, and is devoid of activity on thromboxane A2, prostaglandin D2 and prostacyclin sensitive receptors. 19-OH PGE2 is formed in large quantities from PGE2 in human seminal plasma. PGE2 is the most common and most biologically active of the mammalian prostaglandins. It has important effects in labour and also stimulates osteoblasts to release factors which stimulate bone resorption by osteoclasts (a type of bone cell that removes bone tissue by removing the bones mineralized matrix). (PMID: 16978535, 8248550, 817207). Dinoprostone is a naturally occurring prostaglandin E2 (PGE2) and the most common and most biologically active of the mammalian prostaglandins. It has important effects in labour and also stimulates osteoblasts to release factors which stimulate bone resorption by osteoclasts (a type of bone cell that removes bone tissue by removing the bones mineralized matrix). PGE2 has been shown to increase vasodilation and cAMP production, to enhance the effects of bradykinin and histamine, to induce uterine contractions and to activate platelet aggregation. PGE2 is also responsible for maintaining the open passageway of the fetal ductus arteriosus; decreasing T-cell proliferation and lymphocyte migration and activating the secretion of IL-1alpha and IL-2. PGE2 exhibits both pro- and anti-inflammatory effects, particularly on dendritic cells (DC). Depending on the nature of maturation signals, PGE2 has different and sometimes opposite effects on DC biology. PGE2 exerts an inhibitory action, reducing the maturation of DC and their ability to present antigen. PGE2 has also been shown to stimulate DC and promote IL-12 production when given in combination with TNF-alpha. PGE2 is an environmentally bioactive substance. Its action is prolonged and sustained by other factors especially IL-10. It modulates the activities of professional DC by acting on their differentiation, maturation and their ability to secrete cytokines. PGE2 is a potent inducer of IL-10 in bone marrow-derived DC (BM-DC), and PGE2-induced IL-10 is a key regulator of the BM-DC pro-inflammatory phenotype. (PMID: 16978535)Prostaglandins are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 19-Hydroxy-PGE2 is a derivative of PGE2. Both 19-Hydroxy-PGE1 and 19-hydroxy-PGE2 are formed from PGE1 and PGE2 by prostaglandin 19-hydroxylase, a cytochrome P-450 enzyme, in seminal vesicles (PMID: 3196735). 19-Hydroxy-PGE2 is a selective prostanoid EP2-receptor agonist; it doesnt stimulate FP-receptors, and is devoid of activity on thromboxane A2, prostaglandin D2 and prostacyclin sensitive receptors. 19-OH PGE2 is formed in large quantities from PGE2 in human seminal plasma. PGE2 is the most common and most biologically active of the mammalian prostaglandins. It has important effects in labour and also stimulates osteoblasts to release factors which stimulate bone resorption by osteoclasts (a type of bone cell that removes bone tissue by removing the bones mineralized matrix). (PMID: 16978535, 8248550, 817207)
20-Hydroxy-PGE2
20-hydroxy PGE2 is a product of cytochrome P450 metabolism of PGE2. ω-Oxidation at C-20 followed by beta-oxidation and the loss of up to 4 carbons from the lower side chain is a prominent metabolic pathway for PGE2. 20-hydroxy PGE2 is the putative first intermediate in this chain of chemical transformations. -- www.caymanchem.com. Dinoprostone is a naturally occurring prostaglandin E2 (PGE2) and the most common and most biologically active of the mammalian prostaglandins. It has important effects in labour and also stimulates osteoblasts to release factors which stimulate bone resorption by osteoclasts (a type of bone cell that removes bone tissue by removing the bones mineralized matrix). PGE2 has been shown to increase vasodilation and cAMP production, to enhance the effects of bradykinin and histamine, to induce uterine contractions and to activate platelet aggregation. PGE2 is also responsible for maintaining the open passageway of the fetal ductus arteriosus; decreasing T-cell proliferation and lymphocyte migration and activating the secretion of IL-1alpha and IL-2. PGE2 exhibits both pro- and anti-inflammatory effects, particularly on dendritic cells (DC). Depending on the nature of maturation signals, PGE2 has different and sometimes opposite effects on DC biology. PGE2 exerts an inhibitory action, reducing the maturation of DC and their ability to present antigen. PGE2 has also been shown to stimulate DC and promote IL-12 production when given in combination with TNF-alpha. PGE2 is an environmentally bioactive substance. Its action is prolonged and sustained by other factors especially IL-10. It modulates the activities of professional DC by acting on their differentiation, maturation and their ability to secrete cytokines. PGE2 is a potent inducer of IL-10 in bone marrow-derived DC (BM-DC), and PGE2-induced IL-10 is a key regulator of the BM-DC pro-inflammatory phenotype. (PMID: 16978535)Prostaglandins are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 20-hydroxy PGE2 is a product of cytochrome P450 metabolism of PGE2.1 2 ω-Oxidation at C-20 followed by beta-oxidation and the loss of up to 4 carbons from the lower side chain is a prominent metabolic pathway for PGE2. 20-hydroxy PGE2 is the putative first intermediate in this chain of chemical transformations. -- www.caymanchem.com
6,15-Diketo,13,14-dihydro-PGF1a
6,15-diketo,13,14-dihydro-PGF1 alpha is a minor metabolite of prostacyclin (PGI2). Prostacyclin (PGI2) is one of the major vascular protectors against thrombosis and vasoconstriction, caused by thromboxane A(2). PGI2 inhibits platelet aggregation and vasoconstriction. PGI2 synthase (PGIS), a catalyst of PGI2 formation from prostaglandin H2, is widely distributed and predominantly found in vascular endothelial and smooth muscle cells. PGI2 plays an important cardioprotective role increasingly appreciated in recent years in light of adverse effects of COX-2 inhibitors in clinical trials. This cardioprotection is thought to be mediated, in part, by prostacyclin inhibition of platelet aggregation. Multiple lines of evidence suggest that prostacyclin additionally protects from cardiovascular disease by pleiotropic effects on vascular smooth muscle. PGI2 inhibits proliferation of cultured vascular SMCs by inhibiting cell cycle progression from G1 to S phase. Progression through G1 phase is regulated by the sequential activation of the G1 phase cyclin-dependent kinases (cdks). (PMID: 7000774, 6231483, 16303599, 16533160, 17073611, 17164138). 6,15-diketo,13,14-dihydro-PGF1 alpha is a minor metabolite of prostacyclin (PGI2). Prostacyclin (PGI2) is one of the major vascular protectors against thrombosis and vasoconstriction, caused by thromboxane A(2). PGI2 inhibits platelet aggregation and vasoconstriction. PGI2 synthase (PGIS), a catalyst of PGI2 formation from prostaglandin H2, is widely distributed and predominantly found in vascular endothelial and smooth muscle cells. PGI2 plays an important cardioprotective role increasingly appreciated in recent years in light of adverse effects of COX-2 inhibitors in clinical trials. This cardioprotection is thought to be mediated, in part, by prostacyclin inhibition of platelet aggregation. Multiple lines of evidence suggest that prostacyclin additionally protects from cardiovascular disease by pleiotropic effects on vascular smooth muscle. PGI2 inhibits proliferation of cultured vascular SMCs by inhibiting cell cycle progression from G1 to S phase. Progression through G1 phase is regulated by the sequential activation of the G1 phase cyclin-dependent kinases (cdks).
5(6)-Epoxy Prostaglandin E1
Prostaglandins are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs) and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes) and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signaling pathways. [HMDB] Prostaglandins are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways.
20-COOH-10,11-dihydro-LTB4
20-COOH-10,11-dihydro-LTB4 is formed when leukotriene B4 (LTB4) is metabolized by beta-oxidation. LTB4 is the major metabolite in neutrophil polymorphonuclear leukocytes. Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region and phosphorylation to either enhance or inhibit the activity of 5-LO. Biologically active LTB4 is metabolized by w-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the w-carboxy position and after CoA ester formation. (PMID: 8632343, 9667737). Leukotrienes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 20-COOH-10,11-dihydro-LTB4 is formed when leukotriene B4 (LTB4) is metabolized by beta-oxidation. LTB4 is the major metabolite in neutrophil polymorphonuclear leukocytes. Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region and phosphorylation to either enhance or inhibit the activity of 5-LO. Biologically active LTB4 is metabolized by w-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the w-carboxy position and after CoA ester formation. (PMID: 8632343, 9667737)
20-dihydroxyleukotriene B4
20-dihydroxyleukotriene B4 is the metabolite of lipid omega-oxidation of leukotriene B4 (LTB4). LTB4 is the major metabolite in neutrophil polymorphonuclear leukocytes. Omega-oxidation is the major pathway for the catabolism of leukotriene B4 in human polymorphonuclear leukocytes. Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region, and phosphorylation to either enhance or inhibit the activity of 5-LO. Biologically active LTB4 is metabolized by omega-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the omega-carboxy position and after CoA ester formation (PMID: 7649996, 17623009, 2853166, 6088485). Leukotrienes are eicosanoids. The eicosanoids consist of the prostaglandins (PGs), thromboxanes (TXs), leukotrienes (LTs), and lipoxins (LXs). The PGs and TXs are collectively identified as prostanoids. Prostaglandins were originally shown to be synthesized in the prostate gland, thromboxanes from platelets (thrombocytes), and leukotrienes from leukocytes, hence the derivation of their names. All mammalian cells except erythrocytes synthesize eicosanoids. These molecules are extremely potent, able to cause profound physiological effects at very dilute concentrations. All eicosanoids function locally at the site of synthesis, through receptor-mediated G-protein linked signalling pathways. 20-dihydroxyleukotriene B4 is the metabolite of lipid omega-oxidation of leukotriene B4 (LTB4). LTB4 is the major metabolite in neutrophil polymorphonuclear leukocytes. Omega-oxidation is the major pathway for the catabolism of leukotriene B4 in human polymorphonuclear leukocytes. Leukotrienes are metabolites of arachidonic acid derived from the action of 5-LO (5-lipoxygenase). The immediate product of 5-LO is LTA4 (leukotriene A4), which is enzymatically converted into either LTB4 (leukotriene B4) by LTA4 hydrolase or LTC4 (leukotriene C4) by LTC4 synthase. The regulation of leukotriene production occurs at various levels, including expression of 5-LO, translocation of 5-LO to the perinuclear region and phosphorylation to either enhance or inhibit the activity of 5-LO. Biologically active LTB4 is metabolized by w-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the w-carboxy position and after CoA ester formation. (PMID: 7649996, 17623009, 2853166, 6088485)
19-hydroxyprostaglandin H2(1-)
19-hydroxyprostaglandin H2(1-) is considered to be practically insoluble (in water) and acidic
20-hydroxylipoxin A4
20-hydroxylipoxin A4 is considered to be practically insoluble (in water) and acidic
(E)-7-[4-Hydroxy-2-[(E)-3-hydroxyoct-1-enyl]-6-oxooxan-3-yl]hept-5-enoic acid
19-Hydroxyprostaglandin E2
C7FEJ7QWQE
Rhodojaponin III is a natural product found in Rhododendron simsii, Rhododendron catawbiense, and other organisms with data available. Rhodojaponin III is a diterpenoid from the leaves of Rhododendron molle with anti-inflammatory activity[1]. Rhodojaponin III is a diterpenoid from the leaves of Rhododendron molle with anti-inflammatory activity[1].
ent-6alpha,7alpha,16beta,17-Tetrahydroxykauranoic acid
2,3-epoxy-5beta,6cbeta;,10alpha,13beta,16alpha-pentahydroxy-grayanane|craiobiotoxin IX
Rhodojaponin III
Rhodojaponin III is a diterpenoid from the leaves of Rhododendron molle with anti-inflammatory activity[1]. Rhodojaponin III is a diterpenoid from the leaves of Rhododendron molle with anti-inflammatory activity[1].
rhodomollein F,,2,3,6,14,16-pentahydroxyl-5,9-epoxy grayanotoxane
(5S,6E,8Z,11Z,13E,15S)-5,15-Dihydroperoxy-6,8,11,13-eicosatetraenoic acid
C20H32O6_(2E)-2-(1,2-Dihydroxyethyl)-4-[(1R,4aS,5R,8aS)-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylenedecahydro-1-naphthalenyl]-2-butenoic acid
Thromboxane B3
A member of the class of thromboxanes B that is (5Z,13E,17Z)-thromboxa-5,13,17-trien-1-oic acid substituted by hydroxy groups at positions 9, 11 and 15. CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0072.mzML; PROCESSING averaging of repeated ion fragments at 20.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0001323.mzML; PROCESSING averaging of repeated ion fragments at 20.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0001323.mzML; PROCESSING averaging of repeated ion fragments at 30.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0001323.mzML; PROCESSING averaging of repeated ion fragments at 40.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0001323.mzML; PROCESSING averaging of repeated ion fragments at 20.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0001323.mzML; PROCESSING averaging of repeated ion fragments at 30.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0072.mzML; PROCESSING averaging of repeated ion fragments at 30.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0072.mzML; PROCESSING averaging of repeated ion fragments at 10.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ] CONFIDENCE standard compound; NATIVE_RUN_ID QExHF03_NM_0001323.mzML; PROCESSING averaging of repeated ion fragments at 10.0 eV within 5 ppm window [MS, MS:1000575, mean of spectra, ]
5,12-dihydroperoxy-6,8,10,14-eicosatetraenoic acid
5,15-dihydroperoxy-6,8,11,13-eicosatetraenoic acid
8,15-dihydroperoxy-5,9,11,13-eicosatetraenoic acid
6,15-Diketo-13,14-dihydro-PGF1a
20-hydroxy-PGE2
Eganoprost
5,15-diHPETE
D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
8,15-diHPETE
D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
Prostaglandin G2
D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
FA 20:4;O4
D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
20-Hydroxylipoxin B4
A member of the class of lipoxins that is lipoxin B4 carrying an additional hydroxy substituent at position 20.
(5Z,13E,15S)-11alpha,15,19-trihydroxy-6,9alpha-epoxyprosta-5,13-dien-1-oic acid
20-hydroxylipoxin A4
A member of the class of lipoxins that is lipoxin A4 carrying an additional hydroxy substituent at position 20.
11-Dehydro-thromboxane B2
A thromboxane obtained by formal oxidation of the hemiacetal hydroxy function of thromboxane B2.
(E)-7-[6-[(E)-3,7-dihydroxyoct-1-enyl]-2,3-dioxabicyclo[2.2.1]heptan-5-yl]hept-5-enoic acid
19-Hydroxyprostaglandin H2
A prostaglandin H that consists of prostaglandin H2 bearing an additional hydroxy substituent at position 19.
(E)-4-[(1R,4aS,5R,8aS)-6-hydroxy-5-(hydroxymethyl)-5,8a-dimethyl-2-methylidene-3,4,4a,6,7,8-hexahydro-1H-naphthalen-1-yl]-2-(1,2-dihydroxyethyl)but-2-enoic acid
(5Z,13E,15S)-9alpha,11alpha-epoxy-15,18-dihydroxythromboxa-5,13-dien-1-oic acid
(5Z,13E,15S)-9alpha,11alpha-epoxy-15,19-dihydroxythromboxa-5,13-dien-1-oic acid
(5S,6Z,8E,10E,12R,14Z)-5,12,20,20-tetrahydroxyicosa-6,8,10,14-tetraenoic acid
(5Z,8Z,10E,12E,14R,15S)-14,15-bis(hydroperoxy)icosa-5,8,10,12-tetraenoic acid
(5S,6R,7E,9E,11Z,13E,15S)-15-hydroperoxy-5,6-dihydroxyicosa-7,9,11,13-tetraenoic acid
6-Oxoprostaglandin e1
A prostaglandin E that is prostaglandin E1 bearing a keto substituent at the 6-position. D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents
(1R,2S,4S,6R,10S,11S,13S,14S)-11-(1-hydroxypropan-2-yl)-3,7,10-trimethyl-15-oxapentacyclo[7.5.1.02,6.07,13.010,14]pentadecane-4,6,9,14-tetrol
(1R,2R,3S,6R,10S,11S,13S,14S)-11-(1-Hydroxypropan-2-yl)-3,7,10-trimethyl-15-oxapentacyclo[7.5.1.02,6.07,13.010,14]pentadecane-3,6,9,14-tetrol
6,15-diketo,13,14-dihydroprostaglandin F1alpha
A prostaglandin Falpha that is prostaglandin F1alpha bearing keto substituents at positions 6 and 15.
8(S),15(S)-DiHPETE
An icosanoid that is (5Z,9E,11Z,13E)-icosatetraenoic acid carrying two hydroperoxy substituents at positions 8 and 15 (the 8S,15S-stereoisomer).
(5S,15S)-dihydroperoxy-(6E,8Z,11Z,13E)-icosatetraenoic acid
A bis(hydroperoxy)icosatetraenoic acid that is (6E,8Z,11Z,13E)-icosatetraenoic acid in which the two hydroperoxy groups are located at positions 5S and 15S.
14(R),15(S)-DiHPETE
A bis(hydroperoxy)icosatetraenoic acid that is (5Z,8Z,10E,12E)-icosatetraenoic acid carrying two hydroperoxy substituents at positions 14 and 15 (the 14R,15S-stereoisomer).
(5S,6R)-dihydroxy-(15S)-hydroperoxy-(7E,9E,11Z,13E)-icosatetraenoic acid
A hydroperoxy(hydroxy)icosatetraenoic acid that is (7E,9E,11Z,13E)-icosatetraenoic acid carrying 2 hydroxy substituents at positions 5S and 6R as well as a hydroperoxy substituent at position 15S.
19-hydroxyprostaglandin I2
A prostaglandin I that consists of prostaglandin I1 carrying an additional hydroxy substituent at position 19.
19-hydroxythromboxane A2
A thromboxane A that is thromboxane A2 carrying an additional hydroxy substituent at position 19.
18-hydroxythromboxane A2
A thromboxane A that is thromboxane A2 carrying an additional hydroxy substituent at position 18.