Exact Mass: 352.2263
Exact Mass Matches: 352.2263
Found 500 metabolites which its exact mass value is equals to given mass value 352.2263,
within given mass tolerance error 0.05 dalton. Try search metabolite list with more accurate mass tolerance error
0.01 dalton.
Prostaglandin E2
The naturally occurring prostaglandin E2 (PGE2) is known in medicine as dinoprostone, and it is the most common and most biologically active of the mammalian prostaglandins. It has important effects during 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 is also the prostaglandin that ultimately induces fever. PGE2 has been shown to increase vasodilation and cAMP production, enhance the effects of bradykinin and histamine, and induce uterine contractions and 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-1α 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). 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 and are 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. 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, induction of uterine contractions and of 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-1α 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) G - Genito urinary system and sex hormones > G02 - Other gynecologicals > G02A - Uterotonics > G02AD - Prostaglandins Chemical was purchased from CAY14010, (Lot 0410966-34); Diagnostic ions: 351.8, 333.1, 271.1, 188.9 D012102 - Reproductive Control Agents > D010120 - Oxytocics C78568 - Prostaglandin Analogue Prostaglandin E2 (PGE2) is a hormone-like substance that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation.
Lipoxin A4
Lipoxin A4 (LXA4) was first identified in 1984 by Serhan and colleagues as 5-lipoxygenase interaction product of activated leukocytes. Endogenous transcellular biosynthesis of LXA4 occurs via interaction of leukocytes with epithelium, endothelium or platelets. Lipoxins (LXs) or the lipoxygenase interaction products are generated from arachidonic acid via sequential actions of lipoxygenases and subsequent reactions to give specific trihydroxytetraene-containing eicosanoids. These unique structures are formed during cell-cell interactions and appear to act at both temporal and spatially distinct sites from other eicosanoids produced during the course of inflammatory responses and to stimulate natural resolution. Lipoxin A4 (LXA4) and lipoxin B4 (LXB4) are positional isomers that each possesses potent cellular and in vivo actions. These LX structures are conserved across species. The results of numerous studies reviewed in this work now confirm that they are the first recognized eicosanoid chemical mediators that display both potent anti-inflammatory and pro-resolving actions in vivo in disease models that include rabbit, rat, and mouse systems. LXs act at specific GPCRs as agonists to regulate cellular responses of interest in inflammation and resolution. Aspirin has a direct impact in the LX circuit by triggering the biosynthesis of endogenous epimers of LX, termed the aspirin-triggered 15-epi-LX, that share the potent anti-inflammatory actions of LX. (PMID: 16005201, 16613568). Lipoxin A4 (LXA4) was first identified in 1984 by Serhan and colleagues as 5-lipoxygenase interaction product of activated leukocytes. Endogenous transcellular biosynthesis of LXA4 occurs via interaction of leukocytes with epithelium, endothelium or platelets. D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D000893 - Anti-Inflammatory Agents D018501 - Antirheumatic Agents
Prostaglandin D2
Prostaglandin D2 (or PGD2) is a prostaglandin that is actively produced in various organs such as the brain, spleen, thymus, bone marrow, uterus, ovary, oviduct, testis, prostate and epididymis, and is involved in many physiological events. PGD2 binds to the prostaglandin D2 receptor (PTGDR) which is a G-protein-coupled receptor. Its activity is mainly mediated by G-S proteins that stimulate adenylate cyclase resulting in an elevation of intracellular cAMP and Ca2+. PGD2 promotes sleep; regulates body temperature, olfactory function, hormone release, and nociception in the central nervous system; prevents platelet aggregation; and induces vasodilation and bronchoconstriction. PGD2 is also released from mast cells as an allergic and inflammatory mediator. Prostaglandin H2 is an unstable intermediate formed from PGG2 by the action of cyclooxygenase (COX) in the arachidonate cascade. In mammalian systems, it is efficiently converted into more stable arachidonate metabolites, such as PGD2, PGE2, PGF2a by the action of three groups of enzymes, PGD synthases (PGDS), PGE synthases and PGF synthases, respectively. PGDS catalyzes the isomerization of PGH2 to PGD2. Two types of PGD2 synthase are known. Lipocalin-type PGD synthase is present in cerebrospinal fluid, seminal plasma and may play an important role in male reproduction. Another PGD synthase, hematopoietic PGD synthase is present in the spleen, fallopian tube, endometrial gland cells, extravillous trophoblasts and villous trophoblasts, and perhaps plays an important role in female reproduction. Recent studies demonstrate that PGD2 is probably involved in multiple aspects of inflammation through its dual receptor systems, DP and CRTH2. (PMID:12148545)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 D2 (or PGD2) is a prostaglandin that is actively produced in various organs such as the brain, spleen, thymus, bone marrow, uterus, ovary, oviduct, testis, prostate and epididymis, and is involved in many physiological events. PGD2 binds to the prostaglandin D2 receptor (PTGDR) which is a G-protein-coupled receptor. Its activity is mainly mediated by G-S proteins that stimulate adenylate cyclase resulting in an elevation of intracellular cAMP and Ca2+. PGD2 promotes sleep; regulates body temperature, olfactory function, hormone release, and nociception in the central nervous system; prevents platelet aggregation; and induces vasodilation and bronchoconstriction. PGD2 is also released from mast cells as an allergic and inflammatory mediator. Chemical was purchased from CAY 12010, (Lot 0436713-1); Diagnostic ions: 351.1, 333.0, 271.3, 233.1, 189.1
Prostaglandin I2
Prostaglandin I2 or prostacyclin (or PGI2) is a member of the family of lipid molecules known as eicosanoids. It is produced in endothelial cells from prostaglandin H2 (PGH2) by the action of the enzyme prostacyclin synthase. It is a powerful vasodilator and inhibits platelet aggregation. Prostaglandin I2 is the main prostaglandin synthesized by the blood vessel wall. This suggests that it may play an important role in limiting platelet-mediated thrombosis. In particular, prostacyclin (PGI2) chiefly prevents formation of the platelet plug involved in primary hemostasis (a part of blood clot formation). The sodium salt (known as epoprostenol) has been used to treat primary pulmonary hypertension. Prostacyclin (PGI2) is released by healthy endothelial cells and performs its function through a paracrine signaling cascade that involves G protein-coupled receptors on nearby platelets and endothelial cells. The platelet Gs protein-coupled receptor (prostacyclin receptor) is activated when it binds to PGI2. This activation, in turn, signals adenylyl cyclase to produce cAMP. cAMP goes on to inhibit any undue platelet activation (in order to promote circulation) and also counteracts any increase in cytosolic calcium levels which would result from thromboxane A2 (TXA2) binding (leading to platelet activation and subsequent coagulation). PGI2 also binds to endothelial prostacyclin receptors and in the same manner raise cAMP levels in the cytosol. This cAMP then goes on to activate protein kinase A (PKA). PKA then continues the cascade by inhibiting myosin light-chain kinase which leads to smooth muscle relaxation and vasodilation. Notably, PGI2 and TXA2 work as antagonists. PGI2 is stable in basic buffers (pH=8), but it is rapidly hydrolyzed to 6-keto PGF1alpha in neutral or acidic solutions. The half-life is short both in vivo and in vitro, ranging from 30 seconds to a few minutes. PGI2 is administered by continuous infusion in humans for the treatment of idiopathic pulmonary hypertension.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 I2 or prostacyclin (or PGI2) is a member of the family of lipid molecules known as eicosanoids. It is produced in endothelial cells from prostaglandin H2 (PGH2) by the action of the enzyme prostacyclin synthase. It is a powerful vasodilator and inhibits platelet aggregation. Prostaglandin I2 is the main prostaglandin synthesized by the blood vessel wall. This suggests that it may play an important role in limiting platelet-mediated thrombosis. In particular, prostacyclin (PGI2) chiefly prevents formation of the platelet plug involved in primary hemostasis (a part of blood clot formation). The sodium salt (known as epoprostenol) has been used to treat primary pulmonary hypertension. Prostacyclin (PGI2) is released by healthy endothelial cells and performs its function through a paracrine signaling cascade that involves G protein-coupled receptors on nearby platelets and endothelial cells. The platelet Gs protein-coupled receptor (prostacyclin receptor) is activated when it binds to PGI2. This activation, in turn, signals adenylyl cyclase to produce cAMP. cAMP goes on to inhibit any undue platelet activation (in order to promote circulation) and also counteracts any increase in cytosolic calcium levels which would result from thromboxane A2 (TXA2) binding (leading to platelet activation and subsequent coagulation). PGI2 also binds to endothelial prostacyclin receptors and in the same manner raise cAMP levels in the cytosol. This cAMP then goes on to activate protein kinase A (PKA). PKA then continues the cascade by inhibiting myosin light-chain kinase which leads to smooth muscle relaxation and vasodilation. Notably, PGI2 and TXA2 work as antagonists. PGI2 is stable in basic buffers (pH=8), but it is rapidly hydrolyzed to 6-keto PGF1alpha in neutral or acidic solutions. The half-life is short both in vivo and in vitro, ranging from 30 seconds to a few minutes. PGI2 is administered by continuous infusion in humans for the treatment of idiopathic pulmonary hypertension. B - Blood and blood forming organs > B01 - Antithrombotic agents > B01A - Antithrombotic agents > B01AC - Platelet aggregation inhibitors excl. heparin C78274 - Agent Affecting Cardiovascular System > C270 - Antihypertensive Agent COVID info from clinicaltrial, clinicaltrials, clinical trial, clinical trials D006401 - Hematologic Agents > D010975 - Platelet Aggregation Inhibitors D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents C78568 - Prostaglandin Analogue Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Prostaglandin H2
Prostaglandin H2 (PGH2) is the first intermediate in the biosynthesis of all prostaglandins. Prostaglandins are synthesized from arachidonic acid by the enzyme COX-1 and COX-2, which are also called PGH synthase 1 and 2. These enzymes generate a reactive intermediate PGH2 which has a reasonably long half-life (90-100 s) but is highly lipophilic. PGH2 is converted into the biologically active prostaglandins by prostaglandin isomerases, yielding PGE2, PGD2, and PGF2, or by thromboxane synthase to make TXA2 or by prostacyclin synthase to make PGI2. Most nonsteroidal anti-inflammatory drugs such as aspirin and indomethacin inhibit both PGH synthase 1 and 2. A key feature for eicosanoid transcellular biosynthesis is the export of PGH2 or LTA4 from the donor cell as well as the uptake of these reactive intermediates by the acceptor cell. Very little is known about either process despite the demonstrated importance of both events. In cells, PGH2 rearranges nonenzymatically to LGs even in the presence of enzymes that use PGH2 as a substrate. When platelets form thromboxane A2 (TXA2) from endogenous arachidonic acid (AA), PGH2 reaches concentrations very similar to those of TXA2 and high enough to produce strong platelet activation. Therefore, platelet activation by TXA2 appears to go along with an activation by PGH2. The agonism of PGH2 is limited by the formation of inhibitory prostaglandins, especially PGD2 at higher concentrations. That is why thromboxane synthase inhibitors in PRP and at a physiological HSA concentration do not augment platelet activation (PMID: 2798452, 15650407, 16968946). 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 and are 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 h2, also known as pgh2 or 9s,11r-epidioxy-15s-hydroxy-5z,13e-prostadienoate, 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. Thus, prostaglandin h2 is considered to be an eicosanoid lipid molecule. Prostaglandin h2 is practically insoluble (in water) and a weakly acidic compound (based on its pKa). Prostaglandin h2 can be found in a number of food items such as gooseberry, evergreen huckleberry, quince, and capers, which makes prostaglandin h2 a potential biomarker for the consumption of these food products. Prostaglandin h2 can be found primarily in human platelet tissue. In humans, prostaglandin h2 is involved in several metabolic pathways, some of which include magnesium salicylate action pathway, ketorolac action pathway, trisalicylate-choline action pathway, and salicylate-sodium action pathway. Prostaglandin h2 is also involved in a couple of metabolic disorders, which include leukotriene C4 synthesis deficiency and tiaprofenic acid action pathway. Prostaglandin h2 is acted upon by: Prostacyclin synthase to create prostacyclin Thromboxane-A synthase to create thromboxane A2 and 12-(S)-hydroxy-5Z,8E,10E-heptadecatrienoic acid (HHT) (see 12-Hydroxyheptadecatrienoic acid) Prostaglandin D2 synthase to create prostaglandin D2 Prostaglandin E synthase to create prostaglandin E2 Prostaglandin h2 rearranges non-enzymatically to: A mixture of 12-(S)-hydroxy-5Z,8E,10E-heptadecatrienoic acid (HHT) and 12-(S)-hydroxy-5Z,8Z,10E-heptadecatrienoic acid (see 12-Hydroxyheptadecatrienoic acid) Use of Prostaglandin H2: regulating the constriction and dilation of blood vessels stimulating platelet aggregation Effects of Aspirin on Prostaglandin H2: Aspirin has been hypothesized to block the conversion of arachidonic acid to Prostaglandin . D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
Thromboxane A2
A thromboxane which is produced by activated platelets and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.
(13E)-11a-Hydroxy-9,15-dioxoprost-13-enoic acid
(13E)-11a-Hydroxy-9,15-dioxoprost-13-enoic acid is a substrate for Carbonyl reductase 1.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. (13E)-11a-Hydroxy-9,15-dioxoprost-13-enoic acid is a substrate for Carbonyl reductase 1.
(5Z)-(15S)-11alpha-Hydroxy-9,15-dioxoprostanoate
(5Z)-(15S)-11alpha-Hydroxy-9,15-dioxoprostanoate is a precursor in producing (5Z)-(15S)-11-a-hydroxy-9,15-dioxoprosta-13-enoate in the presence of NADP+, in this reaction (5Z)-(15S)-11alpha-Hydroxy-9,15-dioxoprostanoate is oxidized. [HMDB] (5Z)-(15S)-11alpha-Hydroxy-9,15-dioxoprostanoate is a precursor in producing (5Z)-(15S)-11-a-hydroxy-9,15-dioxoprosta-13-enoate in the presence of NADP+, in this reaction (5Z)-(15S)-11alpha-Hydroxy-9,15-dioxoprostanoate is oxidized.
15-Keto-prostaglandin F2a
15-Keto-prostaglandin F2a is the oxidized product of prostaglandin F2a by 15-hydroxyprostaglandin dehydrogenase, which is present in lung, kidney, placenta and other tissues and catalyzes the NAD- or NADP-dependent dehydrogenation of 15-dydroxyl group. 15-Keto-prostaglandin F2a is further metabolized by its delta13-reduction, beta-oxidation and omega oxidation. The ultimate metabolite is 5a,7a-dihydroxy-11-keto-tetranorprosta-1,16-dioic acid, and excreted in urine. Prostaglandin F2a (PGF2) is one of the earliest discovered and most common prostaglandins is actively biosynthesized in various organs of mammals and exhibits a variety of biological activities, including contraction of pulmonary arteries. PGF2 is mainly synthesized directly from PGH2 by PGH2 9,11-endoperoxide reductase. A small amount of PGF2 is also produced from PGE2 by PGE2 9-ketoreductase. A PGF2 epimer has been reported to exhibit various biological activities, and its levels are increased in bronchoalveolar lavage fluid, plasma, and urine in patients with mastocytosis and bronchial asthma. PGF2 is synthesized from PGD2 by PGD2 11-ketoreductase. (PMID: 16475787, 184496, 5951401, 12432938)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. 15-Keto-prostaglandin F2a is the oxidized product of prostaglandin F2a by 15-hydroxyprostaglandin dehydrogenase, which is present in lung, kidney, placenta and other tissues and catalyzes the NAD- or NADP-dependent dehydrogenation of 15-dydroxyl group. 15-Keto-prostaglandin F2a is further metabolized by its delta13-reduction, beta-oxidation and omega oxidation. The ultimate metabolite is 5a,7a-dihydroxy-11-keto-tetranorprosta-1,16-dioic acid, and excreted in urine. Prostaglandin F2a (PGF2) is one of the earliest discovered and most common prostaglandins is actively biosynthesized in various organs of mammals and exhibits a variety of biological activities, including contraction of pulmonary arteries. PGF2 is mainly synthesized directly from PGH2 by PGH2 9,11-endoperoxide reductase. A small amount of PGF2 is also produced from PGE2 by PGE2 9-ketoreductase. A PGF2 epimer has been reported to exhibit various biological activities, and its levels are increased in bronchoalveolar lavage fluid, plasma, and urine in patients with mastocytosis and bronchial asthma. PGF2 is synthesized from PGD2 by PGD2 11-ketoreductase. (PMID: 16475787, 184496, 5951401, 12432938)
Lipoxin B4
Lipoxins (LXs) and aspirin-triggered lipoxin (ATL) are trihydroxytetraene-containing eicosanoids generated from arachidonic acid that are distinct in structure, formation, and function from the many other proinflammatory lipid-derived mediators. These endogenous eicosanoids have now emerged as founding members of the first class of lipid/chemical mediators involved in the resolution of the inflammatory response. Lipoxin A4 (LXA4), ATL, and their metabolic stable analogs elicit cellular responses and regulate leukocyte trafficking in vivo by activating the specific receptor, ALX. Many of the eicosanoids derived from arachidonic acid (AA2), including prostaglandins (PGs) and leukotrienes (LTs), play important roles as local mediators exerting a wide range of actions relevant in immune hypersensitivity and inflammation. However, recent observations indicate that other agents derived from the lipoxygenase (LO) pathways are formed and play a key role in initiating the resolution of acute inflammation. This phenomenon is an active process that is governed by specific lipid mediators and involves a series of well-orchestrated temporal events. Thus, potent locally released mediators serve as checkpoint controllers of inflammation. In addition to the well-appreciated ability of aspirin to inhibit PGs, aspirin also acetylates cyclooxygenase (COX)-2, triggering the formation of a 15-epimeric form of lipoxins, termed aspirin-triggered LXA4 (ATL). These eicosanoids (i.e. LXA4 and ATL) with a unique trihydroxytetraene structure function as stop signals in inflammation and actively participate in dampening host responses to bring the inflammation to a close, namely, resolution. LXA4 and ATL elicit the multicellular responses via a specific G protein-coupled receptor (GPCR) termed ALX that has been identified in human (PMID: 16968948, 11478982). Lipoxins (LXs) and aspirin-triggered Lipoxin (ATL) are trihydroxytetraene-containing eicosanoids generated from arachidonic acid that are distinct in structure, formation, and function from the many other proinflammatory lipid-derived mediators. These endogenous eicosanoids have now emerged as founding members of the first class of lipid/chemical mediators involved in the resolution of the inflammatory response. Lipoxin A4 (LXA4), ATL, and their metabolic stable analogs elicit cellular responses and regulate leukocyte trafficking in vivo by activating the specific receptor, ALX. Many of the eicosanoids derived from arachidonic acid (AA2), including prostaglandins (PGs) and leukotrienes (LTs), play important roles as local mediators exerting a wide range of actions relevant in immune hypersensitivity and inflammation. However, recent observations indicate that other agents derived from the lipoxygenase (LO) pathways are formed and play a key role in initiating the resolution of acute inflammation. This phenomenon is an active process that is governed by specific lipid mediators and involves a series of well-orchestrated temporal events. Thus, potent locally released mediators serve as checkpoint controllers of inflammation. D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D000893 - Anti-Inflammatory Agents D018501 - Antirheumatic Agents
Prostaglandin F3a
Prostaglandin F3alpha (PGF3a) 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). 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)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 F3alpha (PGF3a) 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). 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)
Narbonolide
A 14-membererd macrolide containing seven stereocentres carrying one ethyl, one hydroxy and five methyl substituents. It is the aglycone of the antibiotic narbonomycin and an intermediate in the biosynthesis of pikromycin.
Levuglandin E2
Levuglandin E2 is a levuglandin generated in the cyclooxygenase (COX) pathway. Levuglandins (LGs) and their stereo and structural isomers are extraordinarily reactive γ-ketoaldehydes that are generated by rearrangements of prostanoid endoperoxide intermediates of polyene cyclooxygenation. Their rapid adduction with biological nucleophiles results, inter alia, in pathological modifications of proteins and DNA. It also complicates their detection. Cyclooxygenase-promoted lipid oxidation is a pivotal step in the biosynthesis of an array of physiologically active metabolites. COX fosters a highly regio and stereoselective cyclooxygenation of arachidonic acid (AA) to deliver a single, enantiomerically pure endoperoxide, PGH2, that is a branch point in the biosynthesis of numerous hormone-like mediators of cellular activities. Spontaneous rearrangements of PGH2 were known to generate prostaglandins (PG) PGD2 and PGE2. (PMID: 15752459) [HMDB] Levuglandin E2 is a levuglandin generated in the cyclooxygenase (COX) pathway. Levuglandins (LGs) and their stereo and structural isomers are extraordinarily reactive γ-ketoaldehydes that are generated by rearrangements of prostanoid endoperoxide intermediates of polyene cyclooxygenation. Their rapid adduction with biological nucleophiles results, inter alia, in pathological modifications of proteins and DNA. It also complicates their detection. Cyclooxygenase-promoted lipid oxidation is a pivotal step in the biosynthesis of an array of physiologically active metabolites. COX fosters a highly regio and stereoselective cyclooxygenation of arachidonic acid (AA) to deliver a single, enantiomerically pure endoperoxide, PGH2, that is a branch point in the biosynthesis of numerous hormone-like mediators of cellular activities. Spontaneous rearrangements of PGH2 were known to generate prostaglandins (PG) PGD2 and PGE2. (PMID: 15752459).
Levuglandin D2
Levuglandin D2 is one of the products of a non-enzymatically rearrangement of prostaglandin H2 (PGH2) to this highly reactive gamma-keto aldehyde. PGH2 markedly accelerates the formation of dimers and higher oligomers of amyloid beta1-42. This evidence implicates cyclooxygenase activity in the pathogenesis of Alzheimers disease, and is associated with the formation of levuglandin adducts of the peptide. Levuglandins (LGs) and their stereo and structural isomers are extraordinarily reactive γ-ketoaldehydes that are generated by rearrangements of prostanoid endoperoxide intermediates of polyene cyclooxygenation. Their rapid adduction with biological nucleophiles results, inter alia, in pathological modifications of proteins and DNA. It also complicates their detection. Cyclooxygenase-promoted lipid oxidation is a pivotal step in the biosynthesis of an array of physiologically active metabolites. COX fosters a highly regio and stereoselective cyclooxygenation of arachidonic acid (AA) to deliver a single, enantiomerically pure endoperoxide, PGH2, that is a branch point in the biosynthesis of numerous hormone-like mediators of cellular activities. Spontaneous rearrangements of PGH2 were known to generate prostaglandins (PG) PGD2 and PGE2. (PMID: 12358806, 15752459, 3317517, 10224068) [HMDB] Levuglandin D2 is one of the products of a non-enzymatically rearrangement of prostaglandin H2 (PGH2) to this highly reactive gamma-keto aldehyde. PGH2 markedly accelerates the formation of dimers and higher oligomers of amyloid beta1-42. This evidence implicates cyclooxygenase activity in the pathogenesis of Alzheimers disease, and is associated with the formation of levuglandin adducts of the peptide. Levuglandins (LGs) and their stereo and structural isomers are extraordinarily reactive γ-ketoaldehydes that are generated by rearrangements of prostanoid endoperoxide intermediates of polyene cyclooxygenation. Their rapid adduction with biological nucleophiles results, inter alia, in pathological modifications of proteins and DNA. It also complicates their detection. Cyclooxygenase-promoted lipid oxidation is a pivotal step in the biosynthesis of an array of physiologically active metabolites. COX fosters a highly regio and stereoselective cyclooxygenation of arachidonic acid (AA) to deliver a single, enantiomerically pure endoperoxide, PGH2, that is a branch point in the biosynthesis of numerous hormone-like mediators of cellular activities. Spontaneous rearrangements of PGH2 were known to generate prostaglandins (PG) PGD2 and PGE2. (PMID: 12358806, 15752459, 3317517, 10224068).
Cinncassiol D1
Cinncassiol D1 is found in herbs and spices. Cinncassiol D1 is a constituent of cinnamomi cortex, the dried bark of Cinnamomum cassia (Chiense cinnamon) Constituent of cinnamomi cortex, the dried bark of Cinnamomum cassia (Chiense cinnamon). Cinncassiol D1 is found in herbs and spices.
Cinncassiol D4
Cinncassiol D4 is found in herbs and spices. Cinncassiol D4 is a constituent of Cinnamomum cassia (Chinese cinnamon) Constituent of Cinnamomum cassia (Chinese cinnamon). Cinncassiol D4 is found in herbs and spices.
20-Hydroxy-leukotriene B4
20-hydroxy- Leukotriene B4 (20-OH-LTB4) is an omega-hydroxylated metabolite of leukotriene B4 in human neutrophils. Elevated urinary concentrations of 20-OH-LTB4 and LTB4 are found in patients with Sjogren-Larsson syndrome (SLS, OMIM 270220), an autosomal recessively inherited neurocutaneous disorder caused by a deficiency of the microsomal enzyme fatty aldehyde dehydrogenase (FALDH), which as an essential role in LTB4 metabolism. Preterm birth seems to be one of the features of the syndrome. The reason for the preterm birth is unclear. It is hypothesized that it relates to the defective LTB4 degradation in SLS. The pathological urinary excretion of LTB4 and 20-OH-LTB4 is a biochemical marker for SLS. Surprisingly, 20-OH-LTB4 concentrations are normal in CSF. 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 beta-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. (PMID: 12709426, 9799565, 11408337, 17623009). 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-hydroxy- Leukotriene B4 (20-OH-LTB4) is an omega-hydroxylated metabolite of leukotriene B4 in human neutrophils. Elevated urinary concentrations of 20-OH-LTB4 and LTB4 are found in patients with Sjogren-Larsson syndrome (SLS, OMIM 270220), an autosomal recessively inherited neurocutaneous disorder caused by a deficiency of the microsomal enzyme fatty aldehyde dehydrogenase (FALDH), which as an essential role in LTB4 metabolism. Preterm birth seems to be one of the features of the syndrome. The reason for the preterm birth is unclear. It is hypothesized that it relates to the defective LTB4 degradation in SLS. The pathological urinary excretion of LTB4 and 20-OH-LTB4 is a biochemical marker for SLS. Surprisingly, 20-OH-LTB4 concentrations are normal in CSF. 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 beta-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. (PMID: 12709426, 9799565, 11408337, 17623009)
Sterebin B
Sterebin B is a constituent of Stevia rebaudiana (stevia) Constituent of Stevia rebaudiana (stevia)
Thromboxane A2
Thromboxane A2 is an unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).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.
13,14-Dihydro-15-keto-PGE2
13,14-dihydro-15-keto-PGE2 is one of the prostaglandin E2 metabolites. (PMID 7190512) Human fetal lung in vitro has the competence to self-differentiate, as early as 12 weeks gestation and presence of high levels in fetal lung of the inactive metabolite 13,14-dihydro-15-keto-PGE2 relative to PGE2 suggests that active prostaglandin catabolism may be one of the mechanisms to retard this stage of maturation in vivo by limiting PGE2 availability. (PMID 8835315)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. 13,14-dihydro-15-keto-PGE2 is one of the prostaglandin E2 metabolites. (PMID 7190512) Human fetal lung in vitro has the competence to self-differentiate, as early as 12 weeks gestation and presence of high levels in fetal lung of the inactive metabolite 13,14-dihydro-15-keto-PGE2 relative to PGE2 suggests that active prostaglandin catabolism may be one of the mechanisms to retard this stage of maturation in vivo by limiting PGE2 availability. (PMID 8835315)
13,14-Dihydro-15-keto-PGD2
13,14-dihydro-15-keto Prostaglandin D2 (13,14-dihydro-15-keto PGD2), (CAS 59894-07-4), is a metabolite of PGD2 which is formed through the 15-hydroxy PGDH pathway. 13,14-dihydro-15-keto PGD2 was recently identified as a selective agonist for the CRTH2/DP2 receptor. It also inhibits ion flux in a canine colonic mucosa preparation. In humans, 13,14-dihydro-15-keto PGD2 is further metabolized to give 11β-hydroxy compounds which have also undergone β-oxidation of one or both side chains. Virtually no 13,14-dihydro-15-keto PGD2 survives intact in the urine. (http://www.caymanchem.com)
3-(4-Methoxy-2-methylphenyl)-2,5-dimethyl-N-pentan-3-ylpyrazolo[1,5-a]pyrimidin-7-amine
(E,Z,E)-1,16-Dihydroxy-3,11-bis(hydroxymethyl)-15-methyl-7-methylene-2,10,14-hexadecatrien-6-one
7alpha,9alpha,11alpha-trihydroxyabiet-8(14)-en-18-oic acid
methyl 2-(1beta-geranyl-5beta-hydroxy-4beta-methoxy-2-oxocyclohexyl)acetate|Methyl 2-(1??-geranyl-5??-hydroxy-4??-methoxy-2-oxocyclohexyl)acetate
7beta,8,14beta-trihydroxy-15-isopimaren-18-oic acid
7alpha,13beta,15-trihydroxyabiet-8(14)-en-18-oic acid
4-O-acetyl hygrophorone C12|cis-4-acetoxy-5-hydroxy-5-tridecanoyl-2-cyclopenten-1-one
4alpha,11-dihydroxy-3beta-(2-methylbutyryloxy)-eudesm-6-en-8-one
12R,13R,14S-trihydroxylabda-12,15-epoxy-8(17)-en-19-oic acid
botryosphaerin E|rel-(1S,4aR,5S,8aR)-5-(4-carboxy-3-hydroxy-3-methylbutyl)-decahydro-1,4a-dimethyl-6-methylidenenaphthalene-1-carboxylic acid
17beta-hydroxy-17alpha-methyl-2,3-seco-5alpha-androstane-2,3-dioic acid
3??,15xi,16-Trihydroxy-isopimaric acid|Wulingzhic acid
3beta,5beta,6beta,16alpha,17-pentahydroxygrayan-10(20)-ene|craiobiotoxin I
3beta,5beta,16-trihydroxyhalima-13-en-15,16-olide|3beta,5beta,16alpha-trihydroxyhalima-13(14)-en-15,16-olide|4-{2-[(2S,3R,8S,6R)-6,8-dihydroxy-2,3,7,7-tetramethylbicyclo[4.4.0]dec-2-yl]ethyl}-(5S)-5-hydroxy-5-hydrofuran-2-one
(ent-3alpha,6alpha,14alpha,16beta)-3,6,14,16-Tetrahydroxy-5,10-seco-1(10)-kauren-5-one
methyl (3S*,6S*,14E,16E)-3,6-epidioxy-6-methoxyoctadeca-4,14,16-trienoate
(3beta,5beta,10a,13beta,14beta)-3,14,15,16-tetrahydroxyisopimar-8-en-11-one|agallochaol B
2,3-epoxy-5beta,6beta,10alpha,16alpha-tetrahydroxygrayanane|craiobiotoxin II
(1R,3S,4S,8R,11Z)-3,15-epoxycembr-11-ene-18,19-dioic acid
8beta,14alpha-dihydroxy-12,13alpha-epoxyabietan-18-oic acid|abiesadine C
8,13-epoxy-1alpha,6beta,7beta-trihydroxy-labd-14-en-11-one|8,13-epoxy-1alpha,6beta,7beta-trihydroxylabd-14-en-11-one|9-deoxy-deacetylforskolin
ent-16xi-hydroxy-labdan-3alpha,8beta-dihydroxy,13(14)-en-15,16-olide
7alpha,12alpha,14beta,15beta,18-pentahydroxy-ent-kaur-16-ene|wikstroemioidin I
1beta,7beta,15alpha,16-tetrahydroxy-ent-pimara-8-en-14-one|pedinophyllol J
15,19-Dihydroxy-9-ketoprosta-10,13-diencarbonsaeure
15,19-Dihydroxy-9-ketoprosta-8(12),13-diencarbonsaeure
3,15,19-trihydroxy-ent-labda-8(17),13-dien-16-oic acid
2beta,16alpha,17-trihydroxy-ent-kauran-19-oic acid
5-oxo-15,18(R and S),19-trihydroxyspata-13,16(E)-diene
3beta,16alpha,17-trihydroxy-ent-kauran-19-oic acid
2alpha,15R,16-trihydroxy-8(14)-isopimarene-18-oic acid|wulingzhic acid A
16xi-Hydroxy-3,4-Dihydroxy-13-cleroden-15,16-olide|3alpha,4beta,16-trihydroxy-5beta,10beta-cis-17alpha,20alpha-cleroda-13(14)-en-15,16-olide
(1S*,3R*,4S*,6R*,7R*,8R*,11Z)-4,6,8-trihydroxy-11-capnosene-2,10-dione
Lipoxin A4
A C20 hydroxy fatty acid having (5S)-, (6R)- and (15S)-hydroxy groups as well as (7E)- (9E)-, (11Z)- and (13E)-double bonds. D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D000893 - Anti-Inflammatory Agents D018501 - Antirheumatic Agents Chemical was purchased from CAY90410 (Lot D433602-40); Diagnostic ions: 351.2, 251.1, 235,1, 145.6, 114.9
LXA4-[19,19,20,20,20-d5]
Chemical was purchased from CAY10007737 (Lot. 0410966-34); Diagnostic ions: 356.1, 251.0, 240.2, 115.0
PGE2-[3,3,4,4-d4]
Chemical was purchased from CAY314010 (Lot 0437217-27); Diagnostic ions: 355.0, 337.3, 275.2, 193.0
[(1R,2S,3S,4R,4aS)-2,3-dihydroxy-3,4a,8,8-tetramethyl-4-[(E)-3-oxobut-1-enyl]-2,4,5,6,7,8a-hexahydro-1H-naphthalen-1-yl] acetate
PGE2-[d9]
CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0164.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_1min0164.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 STD_neg_MSMS_1min0164.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_0001321.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 QExHF03_NM_0001321.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_0001321.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_0001321.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_0001321.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_0001321.mzML; PROCESSING averaging of repeated ion fragments at 20.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ]
Prostacyclin
CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0196.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_1min0196.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 STD_neg_MSMS_1min0196.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_0000127.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 QExHF03_NM_0000127.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_0000127.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_0000127.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_0000127.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_0000127.mzML; PROCESSING averaging of repeated ion fragments at 20.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ]
PGD2-[d4]
CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0151.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_1min0151.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 STD_neg_MSMS_1min0151.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_0001311.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 QExHF03_NM_0001311.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_0001311.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_0001311.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_0001311.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_0001311.mzML; PROCESSING averaging of repeated ion fragments at 20.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ]
PGE2-[d4]
CONFIDENCE standard compound; NATIVE_RUN_ID STD_neg_MSMS_1min0241.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_1min0241.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 STD_neg_MSMS_1min0241.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_0001313.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 QExHF03_NM_0001313.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_0001313.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_0001313.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_0001313.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_0001313.mzML; PROCESSING averaging of repeated ion fragments at 20.0 NCE within 5 ppm window [MS, MS:1000575, mean of spectra, ]
9,13-Epoxy-3,18-dihydroxy-15,16-labdanolide
Origin: Plant; SubCategory_DNP: Diterpenoids, Labdane diterpenoids
[(1R,2S,3S,4R,4aS)-2,3-dihydroxy-3,4a,8,8-tetramethyl-4-[(E)-3-oxobut-1-enyl]-2,4,5,6,7,8a-hexahydro-1H-naphthalen-1-yl] acetate_major
13,14-dihydro-15-keto-PGD2
5,14,15-trihydroxy-6,8,10,12-Eicosatetraenoic acid
Sterebin B
Sterebin C
(ent-6alpha,7alpha,16alphaH)-6,7,17-Trihydroxy-19-kauranoic acid
FA 20:4;O3
D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D000893 - Anti-Inflammatory Agents D018501 - Antirheumatic Agents
Prostin E2
G - Genito urinary system and sex hormones > G02 - Other gynecologicals > G02A - Uterotonics > G02AD - Prostaglandins D012102 - Reproductive Control Agents > D010120 - Oxytocics C78568 - Prostaglandin Analogue Prostaglandin E2 (PGE2) is a hormone-like substance that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation.
Prostaglandin D2
A member of the class of prostaglandins D that is prosta-5,13-dien-1-oic acid substituted by hydroxy groups at positions 9 and 15 and an oxo group at position 11 (the 5Z,9alpha,13E,15S- stereoisomer).
Prostaglandin H2
D009676 - Noxae > D016877 - Oxidants > D010545 - Peroxides
lipoxin B4
A C20 hydroxy fatty acid having (5S)-, (14R)- and (15S)-hydroxy groups as well as (6E)- (8Z)-, (10E)- and (12E)-double bonds. D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D000893 - Anti-Inflammatory Agents D018501 - Antirheumatic Agents
5-E2t-IsoP
Ectocarpin D
7-((1R,2R,3R)-3-HYDROXY-2-((S,1E,5E)-3-HYDROXYOCTA-1,5-DIEN-1-YL)-5-OXOCYCLOPENTYL)HEPTANOIC ACID
(Z)-7-[(1R,2R,5S)-5-hydroxy-2-[(E,3R)-3-hydroxyoct-1-enyl]-3-oxocyclopentyl]hept-5-enoic acid
(E)-7-[(1R,2R,5S)-5-hydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]-3-oxocyclopentyl]hept-5-enoic acid
7,9a-Methano-9aH-cyclopenta[b]heptalene-2,8,11,11a,12(1H)-pentol, dodecahydro-1,1,8-trimethyl-4-methylene-, (2S,3aS,4aS,7R,8R,9aS,11R,11aR,12R)-
(1R,2R,5R,6S,8aS)-6-hydroxy-5-(hydroxymethyl)-2,5,8a-trimethyl-octahydro-2H-dispiro[naphthalene-1,2:5,3-bis(oxolane)]-5-one
[2,3-Dihydroxy-3,4a,8,8-tetramethyl-4-(3-oxobut-1-enyl)-2,4,5,6,7,8a-hexahydro-1H-naphthalen-1-yl] acetate
(5S,15S)-5-hydroperoxy-15-HETE
A 5-hydroperoxy-15-HETE stereoisomer that has 5S,15S configuration.
(5S,7E,9E,11Z,13E,15S)-15-hydroperoxy-5-hydroxyicosa-7,9,11,13-tetraenoic acid
(5S,6E,8Z,11Z,13E,15R)-5-hydroperoxy-15-hydroxyicosa-6,8,11,13-tetraenoic acid
7-[(1R,2R,3R)-3-Hydroxy-2-[(3S)-3-hydroxyoct-1-enyl]-5-oxocyclopentyl]-5-heptenoic acid
5,6,15-Trihydroxy-7,9,11,13-eicosatetraenoic acid
D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D000893 - Anti-Inflammatory Agents D018501 - Antirheumatic Agents
5-hydroperoxy-15-HETE
An icosanoid that is (6E,8Z,11Z,13E)-icosa-6,8,11,13-tetraenoic acid substituted at positions 5 and 15 by hydroperoxy and hydroxy groups respectively.
(6E,8E,10E,14E)-5,12,20-trihydroxyicosa-6,8,10,14-tetraenoic acid
(5E)-5-[5-hydroxy-4-[(E)-3-hydroxyoct-1-enyl]-3,3a,4,5,6,6a-hexahydrocyclopenta[b]furan-2-ylidene]pentanoic acid
(E)-7-[5-hydroxy-3-oxo-2-(3-oxooctyl)cyclopentyl]hept-5-enoic acid
(5S)-hydroperoxy-(14R,15S)-epoxy-(6E,8Z,11Z)-icosatrienoic acid
A hydroperoxy fatty acid that is (14R,15S)-epoxy-(6E,8Z,11Z)-icosatrienoic acid in which the hydroperoxy group is located at position 5S.
(8S)-hydroperoxy-(14S,15R)-epoxy-(5Z,9E,11Z)-icosatrienoic acid
A hydroperoxy fatty acid that is (14S,15R)-epoxy-(5Z,9E,11Z)-icosatrienoic acid in which the hydroperoxy group is located at position 8S.
(12S)-hydroperoxy-(14R,15S)-epoxy-(5Z,8Z,10E)-icosatrienoic acid
A hydroperoxy fatty acid that is (14R,15S)-epoxy-(5Z,8Z,10E)-icosatrienoic acid in which the hydroperoxy group is located at position 12S.
(12S)-hydroperoxy-(14S,15R)-epoxy-(5Z,8Z,10E)-icosatrienoic acid
A hydroperoxy fatty acid that is (14S,15R)-epoxy-(5Z,8Z,10E)-icosatrienoic acid in which the hydroperoxy group is located at position 12S.
20-hydroxy-6-trans-leukotriene B4
A member of the class of leukotrienes that is 6-trans-leukotriene B4 bearing an additional hydroxy substituent at position 20.
(5S,6Z,8E,10E,12R,14Z)-5,12,18-trihydroxyicosa-6,8,10,14-tetraenoic Acid
(1R,3R,4S,11S,12R)-3,4,11-trihydroxy-4,8,12-trimethyl-15-methylidene-13-oxabicyclo[10.3.2]heptadec-7-en-14-one
(E)-7-[(1R,2R,3R)-3-hydroxy-2-[(3S)-3-hydroxyoct-1-enyl]-5-oxocyclopentyl]hept-5-enoic acid
(5S,6E,8Z,11Z,13E,15S)-15-hydroperoxy-5-hydroxyicosa-6,8,11,13-tetraenoic acid
(5Z,8Z,11Z)-12-[(1S,2R,3R,5R)-2,3-dihydroxy-5-[(1S)-1-hydroxypropyl]cyclopentyl]dodeca-5,8,11-trienoic acid
(13E,15S)-15,20-dihydroxy-9-oxoprosta-10,13-dien-1-oic acid
(E)-7-[(1S,2S,5S)-5-hydroxy-2-[(3S)-3-hydroxyoct-1-enyl]-3-oxocyclopentyl]hept-5-enoic acid
(5S,6E,8Z,10E,12S,14Z)-5-hydroperoxy-12-hydroxyicosa-6,8,10,14-tetraenoic acid
Dinoprostone
G - Genito urinary system and sex hormones > G02 - Other gynecologicals > G02A - Uterotonics > G02AD - Prostaglandins D012102 - Reproductive Control Agents > D010120 - Oxytocics C78568 - Prostaglandin Analogue Prostaglandin E2 (PGE2) is a hormone-like substance that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation.
(1R,2R,3S,6S,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-3,9,14-triol
(1R,2S,3S,4S,6R,10S,11S,13S,14S)-3,7,10-Trimethyl-11-propan-2-yl-15-oxapentacyclo[7.5.1.02,6.07,13.010,14]pentadecane-4,6,9,14-tetrol
15-epi-lipoxin A4
A C20 hydroxy polyunsaturated fatty acid having (5S)-, (6R)- and (15R)-hydroxy groups as well as (7E)- (9E)-, (11Z)- and (13E)-double bonds.
15-Epi-lipoxin b4
A C20 hydroxy fatty acid having (5S)-, (14R)- and (15R)-hydroxy groups as well as (6E)- (8Z)-, (10E)- and (12E)-double bonds.
6-epi-lipoxin A4
A C20 hydroxy fatty acid having (5S)-, (6S)- and (15S)-hydroxy groups as well as (7E)- (9E)-, (11Z)- and (13E)-double bonds.
8-isoprostaglandin E2
D002317 - Cardiovascular Agents > D014662 - Vasoconstrictor Agents
9S,11R-dihydroxy-15-oxo-5Z,13E-prostadienoic acid-cyclo[8S,12R]
15-oxo-5S,6R-dihydroxy-7E,9E,11Z-eicosatrienoic acid
18-hydroxyleukotriene B4
A leukotriene that is leukotriene B4 carrying an additional hydroxy substituent at position 18.
(5S)-hydroxy-(15S)-hydroperoxy-(6E,8Z,11Z,13E)-icosatetraenoic acid
A hydroperoxy(hydroxy)icosatetraenoic acid that is (6E,8Z,11Z,13E)-icosatetraenoic acid in which the hydroxy and hydroperoxy substituents are located at positions 5S and 15S respectively.
8-epi-prostaglandin E2
A prostanoid that is prostaglandin E2 having inverted stereochemistry at the 8-position.
19-hydroxyleukotriene B4
A leukotriene that is leukotriene B4 carrying an additional hydroxy substituent at position 19.
13,14-dihydro-15-oxolipoxin A4
A C20 hydroxy fatty acid obtained by formal hydrogenation across the 13,-14-double bond of 15-oxolipoxin A4.
13,14-dihydro-15-oxo-prostaglandin E2
The 13,14-dihydro derivative of 15-oxo-prostaglandin E2.
Prostaglandin E2
Prostaglandin F2alpha in which the hydroxy group at position 9 has been oxidised to the corresponding ketone. Prostaglandin E2 is the most common and most biologically potent of mammalian prostaglandins.
(1s,5s)-5-hydroxy-4-oxo-5-tridecanoylcyclopent-2-en-1-yl acetate
(1s,2r,4s,5s,9r,10s,13s,14r,15r,16r)-2,15,16-trihydroxy-5-(hydroxymethyl)-5,9,14-trimethyltetracyclo[11.2.1.0¹,¹⁰.0⁴,⁹]hexadecan-12-one
7-[(1r,2r,5s)-5-hydroxy-2-[(1e,3s)-3-hydroxyoct-1-en-1-yl]-3-oxocyclopentyl]hept-5-enoic acid
(4s,5e,7s,10r,11r,13s)-7,10,11-trihydroxy-4-isopropyl-7,11-dimethyl-14-oxabicyclo[11.2.1]hexadeca-1(16),5-dien-15-one
4-hydroxy-1-[5-hydroxy-3-(hydroxymethyl)pent-3-en-1-yl]-1-(hydroxymethyl)-2,5-dimethyl-2,3,4,7,8,8a-hexahydroazulene-3a-carbaldehyde
6-hydroxy-5-(5-hydroxy-3-methylidene-4-oxopentyl)-1,4a,6-trimethyl-hexahydro-2h-naphthalene-1-carboxylic acid
5-hydroxy-4-oxo-5-tridecanoylcyclopent-2-en-1-yl acetate
(3s,4r,5e,9s,10r,11e,13s,14s)-14-ethyl-4,10-dihydroxy-3,5,9,11,13-pentamethyl-1-oxacyclotetradeca-5,11-diene-2,7-dione
methyl 8-[(5r)-2-[(2r)-2-hydroxypent-3-en-1-yl]-5-methoxy-3-oxocyclopent-1-en-1-yl]octanoate
(2e,6r)-6-[(4e)-6-hydroxy-4-methylhex-4-en-1-yl]-2-(4-methylpent-3-en-1-yl)hept-2-enedioic acid
(2s,3s,3ar,5ar,6r,7r,10ar)-8-(hydroxymethyl)-1-isopropyl-3a,5a-dimethyl-2h,3h,4h,5h,6h,7h,10h,10ah-cyclohepta[e]indene-2,3,6,7-tetrol
7-[(1r,2r,3r)-3-hydroxy-2-[(1e,3s)-3-hydroxyoct-1-en-1-yl]-5-oxocyclopentyl]hept-5-enoic acid
(2e,10z,14e)-1,16-dihydroxy-3,11-bis(hydroxymethyl)-15-methyl-7-methylidenehexadeca-2,10,14-trien-6-one
4-[2-(5,6-dihydroxy-1,2,4a,5-tetramethyl-hexahydro-2h-naphthalen-1-yl)ethyl]-5-hydroxy-5h-furan-2-one
3,4,11-trihydroxy-4,8,12-trimethyl-15-methylidene-13-oxabicyclo[10.3.2]heptadec-7-en-14-one
(1s,3r,3as,5's,7as)-4,4,5',7a-tetramethyl-3-(2-oxopropyl)-tetrahydro-3h-spiro[2-benzofuran-1,2'-oxolan]-5'-ylacetic acid
(1r,2r,3ar,4r,8ar)-4-hydroxy-1-[(3z)-5-hydroxy-3-(hydroxymethyl)pent-3-en-1-yl]-1-(hydroxymethyl)-2,5-dimethyl-2,3,4,7,8,8a-hexahydroazulene-3a-carbaldehyde
(1r,2s,4s,4as,5'r,5''s,8as)-4,5''-dihydroxy-2,5,5,8a-tetramethyl-hexahydrodispiro[naphthalene-1,2':5',3''-bis(oxolane)]-3-one
(1r,4as,4br,7r,8r,8ar,9s,10ar)-7-ethenyl-8,8a,9-trihydroxy-1,4a,7-trimethyl-decahydrophenanthrene-1-carboxylic acid
5-(4-carboxy-3-methylbutyl)-7-hydroxy-1,4a-dimethyl-6-methylidene-hexahydro-2h-naphthalene-1-carboxylic acid
(1ar,2s,2as,5's,6as,7ar)-1a-(hydroxymethyl)-2a,5',6,6-tetramethyl-hexahydrospiro[naphtho[2,3-b]oxirene-2,2'-oxolan]-5'-ylacetic acid
3-(acetyloxy)-2-hydroxypropyl 3,7,11-trimethyldodeca-2,6,10-trienoate
5-(4-carboxy-3-methylbutyl)-8a-(hydroxymethyl)-5,6-dimethyl-3,4,4a,6,7,8-hexahydronaphthalene-1-carboxylic acid
(3s,5s)-1-(3,4-dimethoxyphenyl)-5-hydroxydecan-3-yl acetate
(5s,6r,13e,15s)-5,6,15-trihydroxyicosa-7,9,11,13-tetraenoic acid
(2e)-5-[(4r,4ar,5s,6r,8as)-4,6-dihydroxy-5-(hydroxymethyl)-2,5,8a-trimethyl-3,4,4a,6,7,8-hexahydronaphthalen-1-yl]-3-methylpent-2-enoic acid
3-{2-[(1r,2s,4as,8as)-2,5,5-tris(hydroxymethyl)-8a-methyl-octahydronaphthalen-1-yl]ethyl}-5h-furan-2-one
(1r,4s,6s,10s,13s,14r,17s)-10,13-dihydroxy-4,13,17-trimethyl-9-methylidene-5,15-dioxatricyclo[12.3.1.0⁴,⁶]octadecan-16-one
(1r,2r,3s,4s,5r,9s,10s,13r,14r)-2,3-dihydroxy-14-(hydroxymethyl)-5,9-dimethyltetracyclo[11.2.1.0¹,¹⁰.0⁴,⁹]hexadecane-5-carboxylic acid
7-[3,5-dihydroxy-2-(3-oxooct-1-en-1-yl)cyclopentyl]hept-5-enoic acid
15-epileopersin c
{"Ingredient_id": "HBIN001673","Ingredient_name": "15-epileopersin c","Alias": "NA","Ingredient_formula": "C20H32O5","Ingredient_Smile": "CC1C(C(=O)C2C(CCCC2(C13CCC4(O3)CC(OC4)O)C)(C)C)O","Ingredient_weight": "352.5 g/mol","OB_score": "NA","CAS_id": "NA","SymMap_id": "SMIT15263","TCMID_id": "6946","TCMSP_id": "NA","TCM_ID_id": "NA","PubChem_id": "15548655","DrugBank_id": "NA"}
15-epi-leopersin j
{"Ingredient_id": "HBIN001674","Ingredient_name": "15-epi-leopersin j","Alias": "NA","Ingredient_formula": "C20H32O5","Ingredient_Smile": "CC1C(=O)C(C2C(CCCC2(C13CCC4(O3)CC(OC4)O)C)(C)C)O","Ingredient_weight": "NA","OB_score": "NA","CAS_id": "NA","SymMap_id": "NA","TCMID_id": "6947","TCMSP_id": "NA","TCM_ID_id": "NA","PubChem_id": "NA","DrugBank_id": "NA"}
3β,15xi,16-trihydroxy-isopimaricacid
{"Ingredient_id": "HBIN008021","Ingredient_name": "3\u03b2,15xi,16-trihydroxy-isopimaricacid","Alias": "NA","Ingredient_formula": "C20H32O5","Ingredient_Smile": "Not Available","Ingredient_weight": "NA","OB_score": "NA","CAS_id": "NA","SymMap_id": "NA","TCMID_id": "21736","TCMSP_id": "NA","TCM_ID_id": "NA","PubChem_id": "NA","DrugBank_id": "NA"}
3-hydroxyportulol ether; 3-deoxy,19-oxo
{"Ingredient_id": "HBIN008742","Ingredient_name": "3-hydroxyportulol ether; 3-deoxy,19-oxo","Alias": "NA","Ingredient_formula": "C20H32O5","Ingredient_Smile": "NA","Ingredient_weight": "352.47","OB_score": "NA","CAS_id": "98263-93-5","SymMap_id": "NA","TCMID_id": "NA","TCMSP_id": "NA","TCM_ID_id": "8073","PubChem_id": "NA","DrugBank_id": "NA"}
