Exact Mass: 336.23475520000005
Exact Mass Matches: 336.23475520000005
Found 500 metabolites which its exact mass value is equals to given mass value 336.23475520000005,
within given mass tolerance error 0.05 dalton. Try search metabolite list with more accurate mass tolerance error
0.01 dalton.
Prostaglandin B1
Prostaglandin B1 (PGB1) is a metabolite of PGE1. PGE1 is a prostanoid. Prostanoids is a term that collectively describes prostaglandins, prostacyclines and thromboxanes. 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). PGB1does not inhibit phospholipase activity, but oligomers of PGB1 (PGBx) extracted from human neutrophils inhibit human phospholipases A2 in vitro and in situ in a dose-dependent manner; these oligomers inhibit arachidonic acid mobilization in human neutrophils and endothelial cells. One mechanism for the pharmacological effects of PGBx may be inhibition of cell-associated and extracellular phospholipase A2. PGB1 has the ability to enhance peripheral vascular resistance and elevate blood pressure. The effect is not central in origin and apparently is not the result of changes in cholinergic or alpha-adrenoceptor sensitivity or changes in vascular smooth muscle susceptibility per se. PGB1 blocks S-phase DNA synthesis; inhibition of DNA synthesis does not appear to require elevated levels of cAMP. (PMID: 7667505, 1477202, 2129000, 2597672, 6635328). 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 B1 (PGB1) is a metabolite of PGE1. PGE1 is a prostanoid. Prostanoids is a term that collectively describes prostaglandins, prostacyclines and thromboxanes. 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).
Prostaglandin A1
Prostaglandin A1 (PGA1, a prostaglandin characterized by a cyclopentenone structure) has a fundamental structure common to punaglandin and clavulone, the antitumor eicosanoids discovered in marine organisms such as corals. It is well established that PGA1, which exert potent antiviral activity in several DNA and RNA virus models, induce heat shock protein (hsp)70 syntheses through cycloheximide sensitive activation of heat shock transcription factor. Antitumor prostaglandins are actively incorporated through cell membrane and control gene expression. P53 (protein 53, is a transcription factor that regulates the cell cycle and functions as a tumor suppressor) independent expression of p21 (also known as cyclin-dependent kinase inhibitor 1A or CDKN1A, is a human gene on chromosome 6 (location 6p21.2), that encodes a cyclin-dependent kinase) and gadd 45 (growth arrest and DNA-damage-inducible, alpha 45, a major breast cancer (BRCA1) target is the DNA damage-responsive gene GADD45) activation of peroxisome proliferative activated receptor gamma (PPARgamma) are involved in antitumor mechanism of these prostaglandins. At the low concentration, these prostaglandins exhibit physiological or pathological activity such as osteoblast calcification, promotion of colon cancer cell proliferation. One of the mechanisms of anti-cancer activity of prostaglandins, has been believed to be that these prostaglandins might have p53 like effect in cells lacking p53. (PMID: 7988663, 11104898)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 A1 (PGA1, a prostaglandin characterized by a cyclopentenone structure) has a fundamental structure common to punaglandin and clavulone, the antitumor eicosanoids discovered in marine organisms such as corals. It is well established that PGA1, which exert potent antiviral activity in several DNA and RNA virus models, induce heat shock protein (hsp)70 syntheses through cycloheximide sensitive activation of heat shock transcription factor. Antitumor prostaglandins are actively incorporated through cell membrane and control gene expression. P53 (protein 53, is a transcription factor that regulates the cell cycle and functions as a tumor suppressor) independent expression of p21 (also known as cyclin-dependent kinase inhibitor 1A or CDKN1A, is a human gene on chromosome 6 (location 6p21.2), that encodes a cyclin-dependent kinase) and gadd 45 (growth arrest and DNA-damage-inducible, alpha 45, a major breast cancer (BRCA1) target is the DNA damage-responsive gene GADD45) activation of peroxisome proliferative activated receptor gamma (PPARgamma) are involved in antitumor mechanism of these prostaglandins. At the low concentration, these prostaglandins exhibit physiological or pathological activity such as osteoblast calcification, promotion of colon cancer cell proliferation. One of the mechanisms of anti-cancer activity of prostaglandins, has been believed to be that these prostaglandins might have p53 like effect in cells lacking p53. (PMID: 7988663, 11104898) D000890 - Anti-Infective Agents > D000998 - Antiviral Agents
12(S)-HPETE
12-HPETE is one of the six monohydroperoxy fatty acids produced by the non-enzymatic oxidation of arachidonic acid (Leukotrienes). Reduction of the hydroperoxide yields the more stable hydroxyl fatty acid (+/-)12-HETE. A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system. 12-HPETE is one of the six monohydroperoxy fatty acids produced by the non-enzymatic oxidation of arachidonic acid (Leukotrienes). Reduction of the hydroperoxide yields the more stable hydroxyl fatty acid (+/-)12-HETE. D006401 - Hematologic Agents > D010975 - Platelet Aggregation Inhibitors D002317 - Cardiovascular Agents > D014662 - Vasoconstrictor Agents
Leukotriene B4
A leukotriene composed of (6Z,8E,10E,14Z)-icosatetraenoic acid having (5S)- and (12R)-hydroxy substituents. It is a lipid mediator of inflammation that is generated from arachidonic acid via the 5-lipoxygenase pathway. Chemical was purchased from CAY20110 (Lot 0439924-0).; Diagnostic ions: 335.1, 317.2, 195.1, 129.0, 115.0, 111.5
5(S)-Hydroperoxyeicosatetraenoic acid
5(S)-Hydroperoxyeicosatetraenoic acid is a lipid hydroperoxide precursor of leukotrienes. The first step of biosynthesis of leukotrienes is conversion of arachidonic acid into 5(S)-hydroperoxy-6,8,11,14-(E,Z,Z,Z)-eicosatetraenoic acid [5(S)-HpETE] by 5- lipoxygenases (5-LOX). Lipid hydroperoxides undergo homolytic decomposition into bifunctional electrophiles, which react with DNA bases to form DNA adducts. These DNA modifications are proposed to be involved in the etiology of cancer, cardiovascular disease, and neurodegeneration. 5-LOX, the enzyme responsible for the formation of 5(S)-HpETE in vivo, is expressed primarily in leukocytes, including monocytes and macrophages. Studies have implicated the 5-LOX pathway as an important mediator in the pathology of atherosclerosis. (PMID: 15777099). Endogenously generated 5-hydroperoxyeicosatetraenoic acid is the preferred substrate for human leukocyte leukotriene A4 synthase activity. Thus, the arachidonic acid moiety is preferentially converted to LTA4 in a concerted reaction without dissociation of a 5-HPETE intermediate. (PMID: 3036580). 5(S)-Hydroperoxyeicosatetraenoic acid is a lipid hydroperoxide precursor of leukotrienes. The first step of biosynthesis of leukotrienes is conversion of arachidonic acid into 5(S)-hydroperoxy-6,8,11,14-(E,Z,Z,Z)-eicosatetraenoic acid [5(S)-HpETE] by 5- lipoxygenases (5-LOX). Lipid hydroperoxides undergo homolytic decomposition into bifunctional electrophiles, which react with DNA bases to form DNA adducts. These DNA modifications are proposed to be involved in the etiology of cancer, cardiovascular disease, and neurodegeneration.
Prostaglandin C1
This compound belongs to the family of Prostaglandins and related compounds. These are unsaturated carboxylic acids consisting of of a 20 carbon skeleton that also contains a five member ring, and are based upon the fatty acid arachidonic acid.
(5Z,9E,14Z)-(8xi,11R,12S)-11,12-epoxy-8-hydroxyicosa-5,9,14-trienoic Acid
(5Z,9E,14Z)-(8xi,11R,12S)-11,12-epoxy-8-hydroxyicosa-5,9,14-trienoic Acid, also known as Hepoxilin a3 or 8-EH-2, is classified as a member of the Hepoxilins. Hepoxilins are eicosanoids containing an oxirane group attached to the fatty acyl chain. (5Z,9E,14Z)-(8xi,11R,12S)-11,12-epoxy-8-hydroxyicosa-5,9,14-trienoic Acid is considered to be practically insoluble (in water) and acidic
15(S)-HPETE
15(S)-hydroperoxyeicosatetraenoic acid (15(S)-HPETE) is the corresponding hydroperoxide of 15(S)-HETE and undergoes homolytic decomposition to the DNA-reactive bifunctional electrophile 4-oxo-2(E)-nonenal, a precursor of heptanone-etheno-2-deoxyguanosine. Reactive oxygen species convert the omega-6 polyunsaturated fatty acid arachidonic acid into (15-HPETE); vitamin C mediates 15(S)-HPETE decomposition. 15(S)-HPETE initiates apoptosis in vascular smooth muscle cells. 15(S)-HPETE is a lipoxygenase metabolite that affects the expression of cell adhesion molecules (CAMs) involved in the adhesion of leukocytes and/or the accumulation of leukocytes in the vascular endothelium, these being the initial events in endothelial cell injury. 15(S)-HPETE induces a loss of cardiomyocytes membrane integrity. 15-(S)HPETE is a hydroperoxide that enhances the activity of the enzymes lipoxygenase [EC 1.13.11.12] and Na+, K+-ATPase [EC 3.6.3.9] of brain microvessels. Lipoxygenase(s) and Na+-K+-ATPase of brain microvessels may play a significant role in the occurrence of ischemic brain edema. (PMID: 15964853, 15723435, 8655602, 8595608, 2662983). D002317 - Cardiovascular Agents > D014662 - Vasoconstrictor Agents D004791 - Enzyme Inhibitors > D016859 - Lipoxygenase Inhibitors D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
15H-11,12-EETA
15H-11,12-EETA is an epoxyeicosatrienoic acid (EET). The role of EETs in regulation of the cerebral circulation has become more important, since it was realized that EETs are produced in another specialized cell type of the brain, the astrocytes. It has become evident that EETs released from astrocytes may mediate cerebral functional hyperemia. Molecular and pharmacological evidence hve shown that neurotransmitter release and spillover onto astrocytes can generate EETs. Since these EETs may reach the vasculature via astrocyte foot-processes, they have the same potential as their endothelial counterparts to hyperpolarize and dilate cerebral vessels. P450 enzymes contain heme in their catalytic domain and nitric oxide (NO) appears to bind to these heme moieties and block formation of P450 products, including EETs. Thus, there appears to be crosstalk between P450 enzymes and NO/NO synthase. The role of fatty acid metabolites and cerebral blood flow becomes even more complex in light of data demonstrating that cyclooxygenase products can act as substrates for P450 enzymes. (PMID: 17494091, 17468203, 17434916, 17406062, 17361113, 15581597, 11413051, 10519554, 11893556) [HMDB] 15H-11,12-EETA is an epoxyeicosatrienoic acid (EET). The role of EETs in regulation of the cerebral circulation has become more important, since it was realized that EETs are produced in another specialized cell type of the brain, the astrocytes. It has become evident that EETs released from astrocytes may mediate cerebral functional hyperemia. Molecular and pharmacological evidence hve shown that neurotransmitter release and spillover onto astrocytes can generate EETs. Since these EETs may reach the vasculature via astrocyte foot-processes, they have the same potential as their endothelial counterparts to hyperpolarize and dilate cerebral vessels. P450 enzymes contain heme in their catalytic domain and nitric oxide (NO) appears to bind to these heme moieties and block formation of P450 products, including EETs. Thus, there appears to be crosstalk between P450 enzymes and NO/NO synthase. The role of fatty acid metabolites and cerebral blood flow becomes even more complex in light of data demonstrating that cyclooxygenase products can act as substrates for P450 enzymes. (PMID: 17494091, 17468203, 17434916, 17406062, 17361113, 15581597, 11413051, 10519554, 11893556).
Hepoxilin B3
Hepoxilin B3 is a normal human epidermis eicosanoid. Hepoxilin B3 is dramatically elevated in psoriatic lesions. The primary biological action of the hepoxilins appears to relate to their ability to release calcium from intracellular stores through a receptor-mediated action. The receptor is intracellular, and appears to be G-protein coupled. The conversion of hepoxilin into its omega-hydroxy catabolite has recently been demonstrated through the action of an omega-hydroxylase. This enzyme is different from that which oxidizes leukotriene B4, as the former activity is lost when the cell is disrupted, while leukotriene B4-catabolic activity is recovered in both the intact and disrupted cell. Additionally, hepoxilin catabolism is inhibited by CCCP, a mitochondrial uncoupler, while leukotriene catabolism is unaffected. As hepoxilins cause the translocation of calcium from intracellular stores in the endoplasmic reticulum to the mitochondria, it is speculated that hepoxilin omega-oxidation takes place in the mitochondria, and the omega-oxidation product facilitates accumulation of the elevated cytosolic calcium by the mitochondria. (PMID 10692117, 11851887, 10086189) [HMDB] Hepoxilin B3 is a normal human epidermis eicosanoid. Hepoxilin B3 is dramatically elevated in psoriatic lesions. The primary biological action of the hepoxilins appears to relate to their ability to release calcium from intracellular stores through a receptor-mediated action. The receptor is intracellular, and appears to be G-protein coupled. The conversion of hepoxilin into its omega-hydroxy catabolite has recently been demonstrated through the action of an omega-hydroxylase. This enzyme is different from that which oxidizes leukotriene B4, as the former activity is lost when the cell is disrupted, while leukotriene B4-catabolic activity is recovered in both the intact and disrupted cell. Additionally, hepoxilin catabolism is inhibited by CCCP, a mitochondrial uncoupler, while leukotriene catabolism is unaffected. As hepoxilins cause the translocation of calcium from intracellular stores in the endoplasmic reticulum to the mitochondria, it is speculated that hepoxilin omega-oxidation takes place in the mitochondria, and the omega-oxidation product facilitates accumulation of the elevated cytosolic calcium by the mitochondria. (PMID 10692117, 11851887, 10086189).
11H-14,15-EETA
11H-14,15-EETA is an epoxyeicosatrienoic acid. Epoxyeicosatrienoic acids (EpETrEs) have been reported recently having vasodilatory effects and a role of P-450-dependent arachidonic acid monooxygenase metabolites is suggested in vasoregulation. The physiological role of this compound has not been totally established, although in other tissues EpETrEs are mainly involved in hormone production and in the vascular and renal systems. Some studies have implicated epoxygenase metabolites of arachidonic acid in the control of steroidogenesis in luteinised granulosa cells. (PMID: 12749593, 12361727, 1650001) [HMDB] 11H-14,15-EETA is an epoxyeicosatrienoic acid. Epoxyeicosatrienoic acids (EpETrEs) have been reported recently having vasodilatory effects and a role of P-450-dependent arachidonic acid monooxygenase metabolites is suggested in vasoregulation. The physiological role of this compound has not been totally established, although in other tissues EpETrEs are mainly involved in hormone production and in the vascular and renal systems. Some studies have implicated epoxygenase metabolites of arachidonic acid in the control of steroidogenesis in luteinised granulosa cells. (PMID: 12749593, 12361727, 1650001).
11(R)-HPETE
11R-HPETE is a hydroperoxyeicosatetraenoic acid eicosanoid derived from arachidonic acid. 11R-HPETE is formed from arachidonic acid in the prostaglandin endoperoxide H synthase-1 cyclooxygenase site. 11R-HPETE has been described in other mammalian tissues (rat, sheep). There are two distinct isozymes of prostaglandin H synthase (PGHS), the key enzyme in prostaglandin biosynthesis; PGHS-1 is generally considered to play a housekeeping role, whereas PGHS-2 has been linked to various pathological processes. Both PGHS isozymes have two catalytic activities; they are a cyclooxygenase activity that converts arachidonic acid (AA) to prostaglandin G2 (PGG2) and a peroxidase activity that catalyzes the transformation of PGG2 to prostaglandin H2. Oxygenase activity is completely abolished in aspirin-treated PGHS-1 (ASA-PGHS-1), whereas aspirin-treated PGHS-2 (ASA-PGHS-2) still catalyzes formation of 11(R)-HPETE. (PMID: 12664566, 15292194, 15964853, 12167656) [HMDB] 11R-HPETE is a hydroperoxyeicosatetraenoic acid eicosanoid derived from arachidonic acid. 11R-HPETE is formed from arachidonic acid in the prostaglandin endoperoxide H synthase-1 cyclooxygenase site. 11R-HPETE has been described in other mammalian tissues (rat, sheep). There are two distinct isozymes of prostaglandin H synthase (PGHS), the key enzyme in prostaglandin biosynthesis; PGHS-1 is generally considered to play a housekeeping role, whereas PGHS-2 has been linked to various pathological processes. Both PGHS isozymes have two catalytic activities; they are a cyclooxygenase activity that converts arachidonic acid (AA) to prostaglandin G2 (PGG2) and a peroxidase activity that catalyzes the transformation of PGG2 to prostaglandin H2. Oxygenase activity is completely abolished in aspirin-treated PGHS-1 (ASA-PGHS-1), whereas aspirin-treated PGHS-2 (ASA-PGHS-2) still catalyzes formation of 11(R)-HPETE. (PMID: 12664566, 15292194, 15964853, 12167656).
Hepoxilin A3
Hepoxilin A3 is an electrophilic eicosanoids synthesized during arachidonic acid oxidative metabolism, which can participate in the Michael addition reaction with glutathione (GSH, a major cellular antioxidant) catalyzed by the GSH-S-transferase (GST) family. GSH-adducts have been observed with molecules synthesized through the 12-lipoxygenase pathway. (PMID 12432937). Hepoxilins have biological actions that appear to have, as their basis, changes in intracellular concentrations of ions including calcium and potassium ions as well as changes in second messenger systems. Recent evidence suggests that the biological actions of the hepoxilins may be receptor-mediated as indicated from data showing the existence of hepoxilin-specific binding proteins in the human neutrophils. Such evidence also implicates the association of G-proteins both in hepoxilin-binding as well as in hepoxilin action. (PMID 7947989). Hepoxilin A3 is an electrophilic eicosanoids synthesized during arachidonic acid oxidative metabolism, which can participate in the Michael addition reaction with glutathione (GSH, a major cellular antioxidant) catalyzed by the GSH-S-transferase (GST) family. GSH-adducts have been observed with molecules synthesized through the 12-lipoxygenase pathway. (PMID 12432937)
12(R)-HPETE
12(R)-HPETE is a hydroperoxyeicosatetraenoic acid eicosanoid derived from arachidonic acid. The epidermal lipoxygenases 12R-LOX and eLOX3 act in sequence to convert arachidonic acid via 12(R)-HPETE to 12(R)-HETE and the corresponding epoxyalcohol, 8(R)-hydroxy-11(R),12(R)-epoxyeicosatrienoic acid. The epidermal lipoxygenases 12R-LOX and eLOX3 are the gene products of ALOX12B and ALOXE3. Mutations in ALOXE3 or ALOX12B have been found in families with autosomal-recessive congenital ichthyosis (ARCI). ARCI is a clinically and genetically heterogeneous group of severe hereditary keratinization disorders characterized by intense scaling of the whole integument, and differences in color and shape, often associated with erythema. Mutations in ALOXE3 and ALOX12B on chromosome 17p13, which code for two different epidermal lipoxygenases, were found in patients with ichthyosiform erythroderma. Genetic studies indicated that 12R-lipoxygenase (12R-LOX) or epidermal lipoxygenase-3 (eLOX3) was mutated in six families affected by non-bullous congenital ichthyosiform erythroderma (NCIE), one of the main clinical forms of ichthyosis. (PMID: 16116617, 15629692). 12(R)-HPETE is a hydroperoxyeicosatetraenoic acid eicosanoid derived from arachidonic acid. The epidermal lipoxygenases 12R-LOX and eLOX3 act in sequence to convert arachidonic acid via 12(R)-HPETE to 12(R)-HETE and the corresponding epoxyalcohol, 8(R)-hydroxy-11(R),12(R)-epoxyeicosatrienoic acid.
8(S)-HPETE
8S-HPETE is metabolized from arachidonic acid by the enzyme 8S-lipoxygenase (8-LOX in mouse, ALOX15 and ALOX15B in human). 8S-HPETE will be readily reduced under physiological circumstances to 8S-hydroxyeicosatetraenoic acid (8S-HETE), a natural agonist of peroxisome proliferator-activated receptor alpha (PPAR alpha). (PMID: 16112079) [HMDB] 8S-HPETE is metabolized from arachidonic acid by the enzyme 8S-lipoxygenase (8-LOX in mouse, ALOX15 and ALOX15B in human). 8S-HPETE will be readily reduced under physiological circumstances to 8S-hydroxyeicosatetraenoic acid (8S-HETE), a natural agonist of peroxisome proliferator-activated receptor alpha (PPAR alpha). (PMID: 16112079).
5-HPETE
Arachidonic acid 5-hydroperoxide (5-hydroperoxyeicosatetraenoic acid, 5-HPETE) is an intermediate in the production of leukotriene A4 from arachidonic acid. [HMDB] Arachidonic acid 5-hydroperoxide (5-hydroperoxyeicosatetraenoic acid, 5-HPETE) is an intermediate in the production of leukotriene A4 from arachidonic acid.
8-iso-PGA1
8-iso-PGA1 is an isoprostane. Isoprostanes are arachidonic acid metabolites produced by peroxidative attack of membrane lipids. These accumulate to substantial levels in many clinical conditions characterized in part by accumulation of free radicals and reactive oxygen species, including asthma, hypertension and ischemia reperfusion injury. For this reason, they are frequently used as markers of oxidative stress; however, many are now finding that these molecules are not inert, but in fact evoke powerful biological responses in an increasing array of cell types. In many cases, these biological effects can account in part for the various features and manifestations of those clinical conditions. Thus, it may be possible that the isoprostanes are playing somewhat of a causal role in those disease states. (PMID: 14504139)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. 8-iso-PGA1 is an isoprostane. Isoprostanes are arachidonic acid metabolites produced by peroxidative attack of membrane lipids. These accumulate to substantial levels in many clinical conditions characterized in part by accumulation of free radicals and reactive oxygen species, including asthma, hypertension and ischemia reperfusion injury. For this reason, they are frequently used as markers of oxidative stress; however, many are now finding that these molecules are not inert, but in fact evoke powerful biological responses in an increasing array of cell types. In many cases, these biological effects can account in part for the various features and manifestations of those clinical conditions. Thus, it may be possible that the isoprostanes are playing somewhat of a causal role in those disease states. (PMID: 14504139)
8,15-DiHETE
8,15-DiHETE is a double oxidation product of arachadonic acid. It is generated through the action of 15-lipoxygenase (PMID: 8334154). 8,15-DiHETE is also known as eosinophil chemotactic factor of anaphylaxis (ECF-A). In particular it is able to selectively attract eosinophils and neutrophils from mixed leukocyte populations.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. 8,15-DiHETE is a double oxidation product of arachadonic acid. It is generated through the action of 15-lipoxygenase (PMID: 8334154). 8,15-DiHETE is also known as eosinophil chemotactic factor of anaphylaxis (ECF-A). In particular it is able to selectively attract eosinophils and neutrophils from mixed leukocyte populations.
Leukotriene B4
Leukotriene B4 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 omega-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the omega-carboxy position and after CoA ester formation. Other specific pathways of leukotriene metabolism include the 12-hydroxydehydrogenase/15-oxo-prostaglandin-13-reductase that form a series of conjugated diene metabolites that have been observed to be excreted in human urine. Metabolism of LTC4 occurs by sequential peptide cleavage reactions involving a gamma-glutamyl transpeptidase that forms LTD4 (leukotriene D4) and a membrane-bound dipeptidase that converts LTD4 into LTE4 (leukotriene E4) before omega-oxidation. These metabolic transformations of the primary leukotrienes are critical for termination of their biological activity, and defects in expression of participating enzymes may be involved in specific genetic disease. The term leukotriene was coined to indicate the presence of three conjugated double bonds within the 20-carbon structure of arachidonic acid as well as the fact that these compounds were derived from leucocytes such as PMNNs or transformed mast cells. Interestingly, most of the cells known to express 5-LO are of myeloid origin, which includes neutrophils, eosinophils, mast cells, macrophages, basophils, and monocytes. Leukotriene biosynthesis begins with the specific oxidation of arachidonic acid by a free radical mechanism as a consequence of interaction with 5-LO. The first enzymatic step involves the abstraction of a hydrogen atom from C-7 of arachidonate followed by the addition of molecular oxygen to form 5-HpETE (5-hydroperoxyeicosatetraenoic acid). A second enzymatic step is also catalyzed by 5-LO and involves removal of a hydrogen atom from C-10, resulting in the formation of the conjugated triene epoxide LTA4. LTA4 must then be released by 5-LO and encounter either LTA4-H (LTA4 hydrolase) or LTC4-S [LTC4 (leukotriene C4) synthase]. LTA4-H can stereospecifically add water to C-12 while retaining a specific double-bond geometry, leading to LTB4 [leukotriene B4, 5(S),12(R)-dihydroxy-6,8,10,14-(Z,E,E,Z)-eicosatetraenoic acid]. If LTA4 encounters LTC4-S, then the reactive epoxide is opened at C-6 by the thiol anion of glutathione to form the product LTC4 [5(S)-hydroxy-6(R)-S-glutathyionyl-7,9,11,14- (E,E,Z,Z)-eicosatetraenoic acid], essentially a glutathionyl adduct of oxidized arachidonic acid. Both of these terminal leukotrienes are biologically active in that specific GPCRs recognize these chemical structures and receptor recognition initiates complex intracellular signalling cascades. In order for these molecules to serve as lipid mediators, however, they must be released from the biosynthetic cell into the extracellular milieu so that they can encounter the corresponding GPCRs. Surprising features of this cascade include the recognition of the assembly of critical enzymes at the perinuclear region of the cell and even localization of 5-LO within the nucleus of some cells. Under some situations, the budding phagosome has been found to assemble these proteins. Non-enzymatic proteins such as FLAP are now known as critical partners of this protein-machine assembly. An unexpected pathway of leukotriene biosynthesis involves the transfer of the chemically reactive intermediate, LTA4, from the biosynthetic cell followed by conversion into LTB4 or LTC4 by other cells that do not express ...
12,20-DiHETE
This compound belongs to the family of Hydroxyeicosatetraenoic Acids. These are eicosanoic acids with an attached hydroxyl group and four CC double bonds.......
9alpha-(3-Methylbutanoyloxy)-4S-hydroxy-10(14)-oplopen-3-one
9alpha-(3-Methylbutanoyloxy)-4S-hydroxy-10(14)-oplopen-3-one is found in tea. 9alpha-(3-Methylbutanoyloxy)-4S-hydroxy-10(14)-oplopen-3-one is a constituent of flower buds of Tussilago farfara (coltsfoot). Constituent of flower buds of Tussilago farfara (coltsfoot). 9alpha-(3-Methylbutanoyloxy)-4S-hydroxy-10(14)-oplopen-3-one is found in tea.
14,15-DiHETE
14,15-DiHETE is an oxygenated lipid found in human blood. This fatty acyl belongs to the main class of eicosanoids and the sub class of hydroxy/hydroperoxyeicosatetraenoic acids. (Lipid Maps) [HMDB] 14,15-DiHETE is an oxygenated lipid found in human blood. This fatty acyl belongs to the main class of eicosanoids and the sub class of hydroxy/hydroperoxyeicosatetraenoic acids. (Lipid Maps).
5,15-DiHETE
5,15-DiHETE or 5,15-dihydroxyeicosatetraenoic acid is a double oxidation product of arachadonic acid. (PMID: 6817003). It is produced by the action of lipoxygenases (specifically 5-lipoxygenase and 15 lipoxygenase) in the liver and in neutrophils. [HMDB] 5,15-DiHETE or 5,15-dihydroxyeicosatetraenoic acid is a double oxidation product of arachadonic acid. (PMID: 6817003). It is produced by the action of lipoxygenases (specifically 5-lipoxygenase and 15 lipoxygenase) in the liver and in neutrophils.
17,18-DiHETE
17,18-DiHETE is an oxygenated lipid found in human blood. This fatty acyl belongs to the main class of eicosanoids and sub class of hydroxy/hydroperoxyeicosatetraenoic acids. (Lipid Maps) [HMDB] 17,18-DiHETE is an oxygenated lipid found in human blood. This fatty acyl belongs to the main class of eicosanoids and sub class of hydroxy/hydroperoxyeicosatetraenoic acids. (Lipid Maps).
(14S)-14,15-Dihydroxy-8(17),13(16)-labdadien-19-oic acid
(14S)-14,15-Dihydroxy-8(17),13(16)-labdadien-19-oic acid is found in fruits. (14S)-14,15-Dihydroxy-8(17),13(16)-labdadien-19-oic acid is a constituent of Juniperus communis (juniper) Constituent of Juniperus communis (juniper). (14S)-14,15-Dihydroxy-8(17),13(16)-labdadien-19-oic acid is found in fruits.
6-trans-Leukotriene B4
Leukotriene B4 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 b-oxidation from the w-carboxy position and after CoA ester formation. Other specific pathways of leukotriene metabolism include the 12-hydroxydehydrogenase/ 15-oxo-prostaglandin-13-reductase that form a series of conjugated diene metabolites that have been observed to be excreted into human urine. Metabolism of LTC4 occurs by sequential peptide cleavage reactions involving a gamma-glutamyl transpeptidase that forms LTD4 (leukotriene D4) and a membrane-bound dipeptidase that converts LTD4 into LTE4 (leukotriene E4) before w-oxidation. These metabolic transformations of the primary leukotrienes are critical for termination of their biological activity, and defects in expression of participating enzymes may be involved in specific genetic disease. The term leukotriene was coined to indicate the presence of three conjugated double bonds within the 20-carbon structure of arachidonic acid as well as the fact that these compounds were derived from leucocytes such as PMNNs or transformed mast cells. Interestingly, most of the cells known to express 5-LO are of myeloid origin, which includes neutrophils, eosinophils, mast cells, macrophages, basophils and monocytes. Leukotriene biosynthesis begins with the specific oxidation of arachidonic acid by a free radical mechanism as a consequence of interaction with 5-LO. The first enzymatic step involves the abstraction of a hydrogen atom from C-7 of arachidonate followed by the addition of molecular oxygen to form 5-HpETE (5-hydroperoxyeicosatetraenoic acid). A second enzymatic step is also catalysed by 5-LO and involves removal of a hydrogen atom from C-10, resulting in formation of the conjugated triene epoxide LTA4. LTA4 must then be released by 5-LO and encounter either LTA4-H (LTA4 hydrolase) or LTC4-S [LTC4 (leukotriene C4) synthase]. LTA4-H can stereospecifically add water to C-12 while retaining a specific double-bond geometry, leading to LTB4 [leukotriene B4, 5(S),12(R)-dihydroxy-6,8,10,14-(Z,E,E,Z)-eicosatetraenoic acid]. If LTA4 encounters LTC4-S, then the reactive epoxide is opened at C-6 by the thiol anion of glutathione to form the product LTC4 [5(S)-hydroxy-6(R)-S-glutathyionyl-7,9,11,14- (E,E,Z,Z)-eicosatetraenoic acid], essentially a glutathionyl adduct of oxidized arachidonic acid. Both of these terminal leukotrienes are biologically active in that specific GPCRs recognize these chemical structures and receptor recognition initiates complex intracellular signalling cascades. In order for these molecules to serve as lipid mediators, however, they must be released from the biosynthetic cell into the extracellular milieu so that they can encounter the corresponding GPCRs. Surprising features of this cascade include the recognition of the assembly of critical enzymes at the perinuclear region of the cell and even localization of 5-LO within the nucleus of some cells. Under some situations, the budding phagosome has been found to assemble these proteins. Non-enzymatic proteins such as FLAP are now known as critical partners of this protein-machine assembly. An unexpected pathway of leukotriene biosynthesis involves the transfer of the chemically reactive intermediate, LTA4, from the biosynthetic cell followed by conversion into LTB4 or LTC4 by other cells that do not express 5-LO. (PMID 17... 6-trans-Leukotriene B4 is an enzymatic metabolite of leukotriene B4(LTB4). A greater increase in LTB4 and 6-trans-LTB4 (one of its hydroxylated 5-lipoxygenase metabolic derivatives) occurs after stimulation with calcium-ionophore in asthma patients compared to healthy controls. 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 omega-oxidation carried out by specific cytochrome P450s (CYP4F) followed by beta-oxidation from the w-carboxy position and after CoA ester formation (PMID: 17623009, 2176862, 7649996, 9667737, 2125732). 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.
6-trans-12-epi-Leukotriene B4
6-trans-12-epi-Leukotriene 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. 6-trans-12-epi-Leukotriene 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)
12(S)-Leukotriene B4
12(S)-Leukotriene B4 is an agonist of G-protein-coupled receptors for leukotriene B4 (LTB4), BLT1, and BLT2. 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, 2866160, 15866883). 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. 12(S)-Leukotriene B4 is an agonist of G-protein-coupled receptors for leukotriene B4 (LTB4), BLT1 and BLT2. 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, 2866160, 15866883)
10,11-dihydro-12-oxo-LTB4
10,11-dihydro-12-oxo-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. 10,11-dihydro-12-oxo-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)
6,7-dihydro-5-oxo-12-epi-LTB4
6,7-dihydro-5-oxo-12-epi-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. 6,7-dihydro-5-oxo-12-epi-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)
ent-1(10)-Halimene-15,19-dioic acid
ent-1(10)-Halimene-15,19-dioic acid is found in fruits. ent-1(10)-Halimene-15,19-dioic acid is isolated (as di-Me ester) from seed-pod resin of Hymenaea courbaril. Isol. (as di-Me ester) from seed-pod resin of Hymenaea courbaril. ent-1(10)-Halimene-15,19-dioic acid is found in fruits.
9-Deoxy-delta12-PGD2
This compound belongs to the family of Prostaglandins and related compounds. These are unsaturated carboxylic acids consisting of of a 20 carbon skeleton that also contains a five member ring, and are based upon the fatty acid arachidonic acid.
5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid
5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid is classified as a member of the Leukotrienes. Leukotrienes are eicosanoids containing a hydroxyl group attached to the aliphatic chain of an arachidonic acid. Leukotrienes have four double bonds, three (and only three) of which are conjugated. 5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid is considered to be practically insoluble (in water) and acidic. 5,12-dihydroxy-6,8,10,14-eicosatetraenoic acid is an eicosanoid lipid molecule
10-hydroxy-11S,12S-epoxy-5Z,8Z,14Z-eicosatrienoic acid
10-hydroxy-11S,12S-epoxy-5Z,8Z,14Z-eicosatrienoic acid, also known as Hepoxilin b3 or EPHETA, is classified as a member of the Hepoxilins. Hepoxilins are eicosanoids containing an oxirane group attached to the fatty acyl chain. 10-hydroxy-11S,12S-epoxy-5Z,8Z,14Z-eicosatrienoic acid is considered to be practically insoluble (in water) and acidic
5,20-DiHETE
5,20-DiHETE is also known as 5,20-Dihydroxy-6,8,11,14-eicosatetraenoic acid. 5,20-DiHETE is considered to be practically insoluble (in water) and acidic
5(S),11(R)-DiHETE
5(S),11(R)-DiHETE is also known as 5,11-DiHETE or 5S,11R-Dihydroxy-6E,8Z,12E,14Z-eicosatetraenoate. 5(S),11(R)-DiHETE is considered to be practically insoluble (in water) and acidic. 5(S),11(R)-DiHETE is an eicosanoid lipid molecule
5(S),15(R)-DiHETE(1-)
5(S),15(R)-DiHETE(1-) is considered to be practically insoluble (in water) and acidic
8,20-DiHETE
8,20-DiHETE is also known as 8,20-Dihydroxy-5Z,9E,11Z,14Z-eicosatetraenoate or (5Z,9E,11Z,14Z)-8,20-Dihydroxyicosatetraenoate. 8,20-DiHETE is considered to be practically insoluble (in water) and acidic
15-HPETE
15-HPETE is also known as 15-Hydroperoxy-5,8,11,13-eicosatetraenoic acid or (6E,8Z,11Z,14Z)-15-Hydroperoxyicosatetraenoate. 15-HPETE is considered to be practically insoluble (in water) and acidic. 15-HPETE is an eicosanoid lipid molecule
5(S),15(R)-DiHETE
5(S),15(R)-DiHETE is also known as 5S,15R-DiHETE or 5S,15R-Dihydroxy-6E,8Z,11Z,13E-eicosatetraenoate. 5(S),15(R)-DiHETE is considered to be practically insoluble (in water) and acidic. 5(S),15(R)-DiHETE is an eicosanoid lipid molecule
Prostaglandin C1(1-)
Prostaglandin C1(1-) is also known as Prostaglandin C1 anion. Prostaglandin C1(1-) is considered to be practically insoluble (in water) and acidic
(+/-)-11,12-Dihydroxy-5Z,8Z,14Z,17Z-eicosatetraenoic acid
15-Hydroperoxyicosa-5,8,11,13-tetraenoic acid
5-Hydroperoxyicosa-6,8,11,14-tetraenoic acid
Arachidonic acid 5-hydroperoxide (5-hydroperoxyeicosatetraenoic acid, 5-HPETE) is an intermediate in the production of leukotriene A4 from arachidonic acid. [HMDB]
8S,15S-Dihydroxy-5Z,9E,11Z,13E-eicosatetraenoic acid
(3E,7E,11R,12E)-11-Hydroxy-3,7,11,15-tetramethyl-14-oxohexadeca-3,7,12-trienoic acid
Prostaglandin A-1
Prostaglandin a-1 is a member of the class of compounds known as prostaglandins and related compounds. Prostaglandins and related compounds are unsaturated carboxylic acids consisting of a 20 carbon skeleton that also contains a five member ring, and are based upon the fatty acid arachidonic acid. Prostaglandin a-1 is practically insoluble (in water) and a weakly acidic compound (based on its pKa). Prostaglandin a-1 can be found in garden onion and soft-necked garlic, which makes prostaglandin a-1 a potential biomarker for the consumption of these food products.
Prostaglandin B-1
Prostaglandin b-1 is a member of the class of compounds known as prostaglandins and related compounds. Prostaglandins and related compounds are unsaturated carboxylic acids consisting of a 20 carbon skeleton that also contains a five member ring, and are based upon the fatty acid arachidonic acid. Prostaglandin b-1 is practically insoluble (in water) and a weakly acidic compound (based on its pKa). Prostaglandin b-1 can be found in soft-necked garlic, which makes prostaglandin b-1 a potential biomarker for the consumption of this food product.
[9]-Gingerol
[9]-gingerol is a member of the class of compounds known as gingerols. Gingerols are compounds containing a gingerol moiety, which is structurally characterized by a 4-hydroxy-3-methoxyphenyl group substituted at the C6 carbon atom by a 5-hydroxy-alkane-3-one. [9]-gingerol is practically insoluble (in water) and a very weakly acidic compound (based on its pKa). [9]-gingerol can be found in ginger, which makes [9]-gingerol a potential biomarker for the consumption of this food product.
Methyl-[8]-gingerol
Methyl-[8]-gingerol is a member of the class of compounds known as dimethoxybenzenes. Dimethoxybenzenes are organic aromatic compounds containing a monocyclic benzene moiety carrying exactly two methoxy groups. Methyl-[8]-gingerol is practically insoluble (in water) and an extremely weak acidic compound (based on its pKa). Methyl-[8]-gingerol can be found in ginger, which makes methyl-[8]-gingerol a potential biomarker for the consumption of this food product.
ent-14S,15-Dihydroxy-1(10),13(16)-halimadien-18-oic acid
(E)-ent-3beta-3,18-Dihydroxy-8(17),13-labdadien-15-oic acid
8alphaH,ent-3beta-Hydroxy-17-oxo-13Z-labden-15oic acid
2alpha,3alpha,4beta-Trihydroxy-ent-cleroda-13(16),14-diene-15,16-oxide
(E)-ent-2alpha-17-Dihydroxy-7,13-labdienepentenoic acid
8alpha,12R-Epoxy-6beta,11alpha-dihydroxy-13E-labden-1-one
[1-Acetyloctahydro-4-hydroxy-7-(1-methylethyl)-1H-inden-4-yl]methyl ester 2-methyl-2-butenoic acid
2beta,3beta-Dihydroxy-8(17),13Z-labdadien-15-oic acid
(E,E,E,E)-1,5,15-Trihydroxy-2,6,10,13-phytatetraen-12-one
13R,14R-Epoxy-15S-hydroxy-5Z,8Z,11Z-eicosatrienoic acid
8S,9S-Epoxy-7S-hydroxy-5Z,11Z,14Z-eicosatrienoic acid
Decahydro-alpha,4a-dimethyl-8-methylene-7-(3-methyl-1-oxobutoxy)-2-naphthaleneacetic acid
ent-3beta,7beta-Dihydroxy-8(17),13-labdadiene-15-oic acid
ent-13,14-Epoxy-15-hydroxy-1(10)-halimen-18-oic acid
8S,9S-Epoxy-7R-hydroxy-5Z,11Z,14Z-eicosatrienoic acid
8betaH,ent-3beta-Hydroxy-17-oxo-13Z-labden-15oic acid
ent-14R,15-Dihydroxy-1(10),13(16)-halimadien-18-oic acid methyl ester
ent-16α,17-Dihydroxy-19-kauranoic acid
A ent-kaurane diterpenoid that is ent-kaurane-19-oic acid substituted by hydroxy groups at positions 16 and 17 (the 16beta stereoisomer). It is isolated from Helianthus sp. and Annona squamosa and exhibits anti-HIV activity.
6-Hydroxy-2,6-dimethyl-5-(2-oxoheptyl)-3-(2-oxopentyl)-2-cyclohexen-1-one
(2E,6E,10Z)-12-hydroxy-10-(hydroxymethyl)-6-methyl-2-(4-methylpent-3-enyl)dodeca-2,6,10-trienoic acid
[(2Z)-6-hydroxy-2,6-dimethylocta-2,7-dienyl] 2-(5-ethenyl-5-methyloxolan-2-yl)propanoate
(Z)-5-[(1S,2R,4aR,8aR)-5-(hydroxymethyl)-1,2,4a-trimethyl-2,3,4,7,8,8a-hexahydronaphthalen-1-yl]-3-(hydroxymethyl)pent-2-enoic acid
5(S),6(R)-diHETE
8-O-angeloylshiromodiol|8-O-Tigloylshiromodiol|shiromodiol-8-O-angelate
(16alpha)-16,17,18-trihydroxyphyllocladan-3-one|(4alpha,5alpha,9alpha,10beta,16alpha)-16,17,18-trihydroxykauran-3-one
(4R,5E,8R,9E,11S)-4,8-dimethyl-8-hydroxy-11-isopropyl-14-oxo-5,9-pentadecadien-4-olide
(2R,3R,4aR,7R,8R,8aR)-octahydro-3-hydroxy-3-(hydroxymethyl)-8-methyl-7-(1-methylethenyl)-2H-2,4a-ethanonaphthalene-8-propanoic acid|3-[(1R,4R,5R,6R,8R,9R)-9-hydroxy-9-(hydroxymethyl)-5-methyl-4-(1-methylethenyl)tricyclo[6.2.2.01,6]dodec-5-yl]propanoic acid|agallochaol C
(+)-cis,anti,cis-3-hydroxy-1,8,12,12-tetramethyl-4-oxatricyclo[6.4.0.02,6]-dodecan-9-yl senecioate|(1R,2R,3S,6R,8R,9R)-3-hydroxy-1,8,12,12-tetramethyl-4-oxatricyclo[6.4.0.0(2,6)]dodecan-9-yl 3-methylbut-2-enoate|10-hydroxy-10,11-epoxythapsan-5-yl senecioate|3-Senecioyloxy-14,15-epoxythapsan-14-ol
3,6-Dihydroxy-2-(1-oxo-10-tetradecenyl)-2-cyclohexen-1-one
(ent-3beta,4alpha,5alpha)-3,4-Dihydroxy-13-cleroden-15,16-olide|3alpha,4beta-dihydroxy-5beta,10beta-cis-17alpha,20alpha-cleroda-13(14)-en-15,16-olide
3beta-angeloyloxy-4,5-epoxy-6beta-hydroxygermacr-1(10)-ene
2H-1-Benzoxacyclohexadecin-16(18aH)-one, 3,4,5,6,7,8,9,10,11,12,13,14-dodecahydro-18,18a-dihydroxy-2-methyl-
(ent-4alpha,16R)-4,16-Dihydroxy-13-cleroden-15,16-olide|4beta,16alpha-dihydroxyclerod-13(14)Z-en-15,16-olide
ent-12alpha,16-epoxy-2beta,15alpha,19-trihydroxypimar-8(14)-ene|ent-12??,16-Epoxy-2??,15??,19-trihydroxypimar-8(14)-ene
ent-12alpha,16-epoxy-2beta,15alpha,19-trihydroxypimar-8-ene|ent-12??,16-Epoxy-2??,15??,19-trihydroxypimar-8-ene
(15S)-15,16-Dihydroxy-3,4-seco-enantio-pimara-4(18),7-dien-3-oic acid
grayanototoxin-XVIII|Grayanotoxin XVIII|grayanotoxin-XVIII
13,14-dihydroxy-mulin-11-en-20-oic acid|14-dihydroxymulin-11-en-20-oic acid|mulin-11-ene-13alpha,14alpha-dihydroxy-20-oic acid
12alpha,13beta-dihydroxyabiet-8(14)-en-18-oic acid
(1alpha,4alpha,9alpha)-1,4,9-Trihydroxy-2-dolasten-6-one|(1R*,4S*,5R*,8S*,9S*,12S*,14S*)-trihydroxydolasta-2-en-6-one
(1S*,2R*,3S*,4S*,6R*,7R*,8R*,11R*)-2,11:8,11-diepoxy-12(20)-capnosene-4,6-diol
(2R,3aS,7aR,8S,10aS,10bR)-2-ethenyldecahydro-8-(2-hydroxypropan-2-yl)-2,7a,10a-trimethyloxepino[2,3,4-de]chromen-5(2H)-one|agallochaexcoerin A
18,19-dihydroxy-ent-cleroda-3,13E-dien-15-oic acid
3-ethyl-2-methoxy-5-methyl-6-(9-oxoundecyl)pyran-4-one
ent-3beta,7alpha,18-Trihydroxy-15beta,16-epoxy-kauran
13S,14S-Epoxide-(8alpha,12R,13E)-8,12-Epoxy-13-labdene-15,16-diol
(9beta,16alpha)-9,16,17-trihydroxy-ent-kauran-2-one
(ent-6alpha)-6,17-Dihydroxy-3,4-seco-15-beyeren-3-oic acid|Ent-6alpha.17-dihydroxy-3.4-secobeyer-15-en-3-oic-saeure
(1R*,2S*,3R*,4S*,7S*,8S*,11R*,12S*)-1,3-epoxy-4,8-dihydroxybasman-6-one
(5R,13(15)E,16Z)-13(15),16-Spatadiene-5,14,18,19-tetrol
(ent-2??,7??,13E) 2,7-Dihydroxy-3,13-clerodadien-15-oic acid
2beta,14beta,15alpha,18-tetrahydroxy-ent-kaur-16-ene|pterokaurane M2
ent-17,18-dihydroxykauran-19-oic acid|Siegesbeckic acid
(4R,5R,6R)-4,5-epoxy-11-hydroxygermacr-1(10)-en-6-yl (Z)-2-methylbut-2-enoate
2-Hydroxy-5-methoxy-3-tridecylcyclohexa-2,5-diene-1,4-dione
(10E)-3,12-dihydroxy-3,7,11,15-tetramethyl-1,10,14-hexadecatrien-5,13-dione
(Z)-2-Methylbut-2-enoic acid (1R,2S,4aR,7R,8aR)-1-hydroxy-7-isopropyl-1,4a-dimethyl-6-oxodecahydronaphthalen-2-yl ester|3beta-angeloyloxy-4beta-hydroxy-7alpha-H-eudesman-8-one|3beta-Angeloyloxy-4beta-hydroxyeudesman-8-one
1beta,6alpha,7alpha,9alpha-tetrahydroxypimara-8(14),15-diene|spaeropsidin F|sphaeropsidin F
(5Z,8Z,10E,12S,14Z,19R)-12,19-Dihydroxy-5,8,10,14-eicosatetraenoic acid|(5Z,8Z,10E,12S,14Z,19S)-12,19-Dihydroxy-5,8,10,14-eicosatetraenoic acid
(2S,13R)-2,13-dihydroxy-1(10),14-ent-halimadien-18-oic acid
(13E)-15, 16-Dihydroxy-8(17), 13-labdadien-19-oic acid
7beta,13S-dihydroxylabda-8(17),14-dien-19-oic acid
13beta,15,18-trihydroxyabiet-8(14)-en-7-one|13beta,18-dihydroxy-8(14)-abieten-7-one
3beta,7beta,14-trihydroxy-15,16-epoxylabda-8(17),12Z-dien|coronarin I
(2S,7S,8R,11S,12R,3E)-8,12-dihydroxy-7,11:2,16-bisepoxycembra-1(15),3-diene|crassumol B
(1R,2R,6R,7R,8R,9R,10S,12S)-6-isopropyl-3,9-dimethyl-13-methylene-15-oxatricyclo[6.6.1.02,7]pentadec-3-ene-9,10,12-triol|4alpha-hydroxycladieunicellin A|cladieunicellin B
15,16-epoxy-labda-13(16),14-dieno-6beta,7beta,9alpha-triol|15,16-epoxylabda-13(16),14-diene-6beta,7beta,9alpha-triol
4-Hydroxy-2,5,5,8a-tetramethyl-3,4,4,5-tetrahydrodispiro[decalin-1,2(5H)-furan-5,3(2H)-furan]-2-one
(1R*,3S*,4S*,7S*,8S*,11R*,14R*,12E)-3,4:7,8-diepoxydolabell-12-ene-14,18-diol
3alpha,7alpha,14beta-trihydroxy-16beta-methyl-ent-kaur-15-one|glaucocalyxin J
13beta,14beta-dihydroxyabieta-8(9)-en-19-oic acid|jiadifenoic acid F
(rel-5S,6R,8R,9R,10S,13S)-6-hydroxy-9,13-epoxylabda-15,16-olide|vitextrifolin F
2,3-dihydroxy-haliman-5,13Z-diene-15-oic acid|salicifolic acid
9,13-epoxy-15,16-dihydroxylabd-5-en-7-one|leoleorin I|leonurenone A
(1S,2S,4aS,4bS,8R,8aR,10aS)-4a,10a-epoxy-dodecahydro-1-hydroxy-4b,8-dimethyl-2-(1-methylethyl)-phenanthrene-8-carboxylic acid|(8alpha,13beta,14alpha)-8,9-epoxy-14-hydroxyabietan-18-oic acid|8alpha,9alpha-epoxysuaveolic acid
(1S,2R,4aS,5S,8aR)-octahydro-1-[(3S)-3-hydroxy-3-methylpent-4-en-1-yl]-5,8a-dimethylspiro[naphthalene-2(1H)2?-oxirane]-5-carboxylic acid|8,20-epoxy-13-hydroxy-ent-labd-14-en-18-oic acid|labdorffianic acid B
3,4-seco-12RS,13SR-dihydroxy-4(18),8(17),14(15)-labdatrien-3-oic acid
(rel-3S,5S,8R,9R,10S)-3,9-dihydroxy-13(14)-labden-16,15-olide
2beta,3beta,16-trihydroxy-ent-pimar-8(14)-en-15-one|ent-2alpha, 3alpha, 16-Trihydroxy-8(14)-pimaren-15-one|flickinflimbrol A
(1R,3R,4aS,6aS,8R,10aR,10bR)-3-ethenyldodecahydro-1,8-dihydroxy-3,4a,7,7,10a-pentamethyl-9H-benzo[f]chromen-9-one|agallochaexcoerin C
methyl ent-8alpha,16-dihydroxylabdan-6,13E-dien-15-oate
1alpha,5beta,11beta-trihydroxy-7-oxo-ros-15-ene|1??,5??,11??-Trihydroxy-7-oxo-ros-15-ene
(ent-14alpha,16beta)-14,16,17-Trihydroxy-3-atisanone
2beta,3alpha,9xi,13xi-tetrahydroxy-1(15),8(19)-trinervitadiene
ent-2alpha,13,14alpha,15beta-Tetrahydroxykaur-16-en
ent-3beta,18-Dihydroxylabda-8(17),13E-dien-15-oic acid
(5beta,7alpha,8alpha,9beta,10alpha,11beta,13alpha,14R,16beta)-7,11,14-trihydroxykauran-15-one|(7alpha,11beta,14beta,16R)-7,11,14-trihydroxy-ent-kaur-15-one
6,7-epoxy-19-hydroxy-12-oxo-6,7-dihydrogeranyl nerol
(5R,15xi,16E,18xi)-13,16-Spatadiene-5,15,18,19-tetrol|5(R),15,18(R and S),19-tetrahydroxyspata-13,16(E)-diene|5(R),15,18(R/S)-trihydroxyspata-13,16-diene|5(R),15,18,19-tetrahydroxyspata-13,16(E)-diene
(13S)-ent-7beta-hydroxy-2-oxo-3-cleroden-15-oic acid|ent-7??-Hydroxy-2-oxo-3-cleroden-15-oic acid
5beta,9betaH,10alpha,3,4-seco-labd-7,13(Z)-dien-3,15,dioic acid|ent-3,4-Seco-7,13-labdadiene-3,15-dioic acid
Methyl N-Boc-2-bromo-5-sulfamoylbenzoate
C18H32N4S (336.23475520000005)