Exact Mass: 379.2511
Exact Mass Matches: 379.2511
Found 182 metabolites which its exact mass value is equals to given mass value 379.2511,
within given mass tolerance error 0.05 dalton. Try search metabolite list with more accurate mass tolerance error
0.01 dalton.
Sphingosine 1-phosphate
Sphingosine 1-phosphate (S1P), also known as sphing-4-enine-1-phosphate, is classified as a member of the phosphosphingolipids. Phosphosphingolipids are sphingolipids with a structure based on a sphingoid base that is attached to a phosphate head group. They differ from phosphonospingolipids which have a phosphonate head group. S1P is a compound with potent bioactive actions in sphingolipid metabolism, the calcium signalling pathway, and neuroactive ligand-receptor interaction. Generated by sphingosine kinases and ceramide kinase, S1P control numerous aspects of cell physiology, including cell survival and mammalian inflammatory responses. S1P is involved in cyclooxygenase-2 induction (COX-2) and regulates the production of eicosanoids (important inflammatory mediators). S1P functions mainly via G-protein-coupled receptors and probably also has intracellular targets (PMID: 16219683). S1P is considered to be practically insoluble (in water) and acidic. Sphingosine-1-phosphate. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=26993-30-6 (retrieved 2024-07-15) (CAS RN: 26993-30-6). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0).
Celabenzine
A cyclic spermidine alkaloid that is 2-phenyl-1,5,9-triazacyclotridecan-4-one in which the amino hydrogen at position 9 has been replaced by a benzoyl group.
Aurachin B
An A-type aurachin that is quinoline N-oxide which is substituted by a methyl group at position 2, a hydroxy group at position 3, and a triprenyl group at position 4.
Aurachin C
A C-type aurachin that is quinolin-4-one which is substituted by a hydroxy group at positions 1, a methyl group at position 2, and a triprenyl group at position 3.
Donepezil
Donepezil, marketed under the trade name Aricept (Eisai), is a centrally acting reversible acetyl cholinesterase inhibitor. Its main therapeutic use is in the treatment of Alzheimers disease where it is used to increase cortical acetylcholine. It has an oral bioavailability of 100\\% and easily crosses the blood-brain barrier. Because it has a half life of about 70 hours, it can be taken once a day. Initial dose is 5 mg per day, which can be increased to 10 mg per day after an adjustment period of at least 4 weeks. Donepezil is a centrally acting reversible acetyl cholinesterase inhibitor. Its main therapeutic use is in the treatment of Alzheimers disease where it is used to increase cortical acetylcholine. It is well absorbed in the gut with an oral bioavailability of 100\\% and easily crosses the blood-brain barrier. Because it has a half life of about 70 hours, it can be taken once a day. Currently, there is no definitive proof that use of donepezil or other similar agents alters the course or progression of Alzheimers disease. However, 6-12 month controlled studies have shown modest benefits in cognition and/or behavior. Pilot studies have reported that donepezil therapy may potentially have effects on markers of disease progression, such as hippocampal volume. Therefore, many neurologists, psychiatrists, and primary care physicians use donepezil in patients with Alzheimers disease. In 2005, the UK National Institute for Clinical Excellence (NICE) withdrew its recommendation for use of the drug for mild-to-moderate AD, on the basis that there is no significant improvement in functional outcome; Currently, there is no definitive proof that use of donepezil or other similar agents alters the course or progression of Alzheimers disease. However, 6-12 month controlled studies have shown modest benefits in cognition and/or behavior. Pilot studies have reported that donepezil therapy may potentially have effects on markers of disease progression, such as hippocampal volume. Therefore, many neurologists, psychiatrists, and primary care physicians use donepezil in patients with Alzheimers disease. In 2005, the UK National Institute for Clinical Excellence (NICE) withdrew its recommendation for use of the drug for mild-to-moderate AD, on the basis that there is no significant improvement in functional outcome; of quality of life or of behavioral symptoms. However, NICE revised its guidelines to suggest that donepezil be used in moderate stage patients for whom the evidence is strongest. While the drug is currently indicated for mild to moderate Alzheimers, there is also evidence from 2 trials that it may be effective for moderate to severe disease. An example of this is a Karolinska Institute paper published in The Lancet in early 2006, which states that donepezil improves cognitive function even in patients with severe Alzheimers disease symptoms. of quality of life or of behavioral symptoms. However, NICE revised its guidelines to suggest that donepezil be used in moderate stage patients for whom the evidence is strongest. While the drug is currently indicated for mild to moderate Alzheimers, there is also evidence from 2 trials that it may be effective for moderate to severe disease. An example of this is a Karolinska Institute paper published in The Lancet in early 2006, which states that donepezil improves cognitive function even in patients with severe Alzheimers disease symptoms. D018377 - Neurotransmitter Agents > D018678 - Cholinergic Agents > D002800 - Cholinesterase Inhibitors N - Nervous system > N06 - Psychoanaleptics > N06D - Anti-dementia drugs > N06DA - Anticholinesterases D002491 - Central Nervous System Agents > D018697 - Nootropic Agents C471 - Enzyme Inhibitor > C47792 - Acetylcholinesterase Inhibitor D004791 - Enzyme Inhibitors
Leukotriene B4 ethanolamide
Leukotriene B4 ethanolamide is a synthetic agonist of leukotriene B4 (LTB4), that interacts with both leukotriene B4 receptors and Vanilloid TRPV1 receptors. 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 17623009, 16207832)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. Leukotriene B4 ethanolamide is a synthetic agonist of leukotriene B4 (LTB4), that interacts with both leukotriene B4 receptors and Vanilloid TRPV1 receptors. 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 17623009, 16207832)
N-palmitoyl-phosphoethanolamine
N-palmitoyl-phosphoethanolamine is a substrate for: HRAS-like suppressor 2.
C18-Sphingosine 1-phosphate; D-erythro-Sphingosine-1-phosphate
4-Hydroxy-N-phenyl-3,5-bis(1-pyrrolidinylmethyl)benzamide
4-Isopropylphenserine
Oxypertine
N - Nervous system > N05 - Psycholeptics > N05A - Antipsychotics > N05AE - Indole derivatives C78272 - Agent Affecting Nervous System > C66883 - Dopamine Antagonist
celiprolol
C - Cardiovascular system > C07 - Beta blocking agents > C07A - Beta blocking agents > C07AB - Beta blocking agents, selective C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C72900 - Adrenergic Antagonist D018373 - Peripheral Nervous System Agents > D001337 - Autonomic Agents > D013566 - Sympathomimetics D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D018674 - Adrenergic Antagonists D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents CONFIDENCE standard compound; EAWAG_UCHEM_ID 3015
CP-401387
CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 5359; ORIGINAL_PRECURSOR_SCAN_NO 5357 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 5369; ORIGINAL_PRECURSOR_SCAN_NO 5367 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 5321; ORIGINAL_PRECURSOR_SCAN_NO 5316 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 5361; ORIGINAL_PRECURSOR_SCAN_NO 5360 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 5360; ORIGINAL_PRECURSOR_SCAN_NO 5359 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 5358; ORIGINAL_PRECURSOR_SCAN_NO 5353 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9878; ORIGINAL_PRECURSOR_SCAN_NO 9873 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9917; ORIGINAL_PRECURSOR_SCAN_NO 9915 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9936; ORIGINAL_PRECURSOR_SCAN_NO 9935 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9980; ORIGINAL_PRECURSOR_SCAN_NO 9978 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9987; ORIGINAL_PRECURSOR_SCAN_NO 9985 CONFIDENCE standard compound; INTERNAL_ID 733; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 10000; ORIGINAL_PRECURSOR_SCAN_NO 9999
(2R,6S,2S)-2-O-acetyllobeline|(2R,6S,2??S)-2??-O-acetyl lobeline|(S)-2-[(2R,6S)-6-(2-acetyloxy-2-phenylethyl)-1-methylpiperidin-2-yl]-1-phenylethanone|(S)-2-[(2S,6R)-1-methyl-6-(2-oxo-2-phenylethyl)piperidin-2-yl]-1-phenylethyl acetate|[(S)-2-[(2S,6R)-1-methyl-6-(2-oxo-2-phenylethyl)piperidin-2-yl]-1-phenylethyl acetate]
3-O-Acetyl greenwayodendrin|3-O-acetylgreenwayodendrin|greenwayodendrin-3beta-yl acetate
(6Z,9Z,12Z,15Z)-1-(phenethylamino)octadeca-6,9,12,15-tetraen-3-one|(6Z,9Z,12Z,15Z)-1-[(2-phenylethyl)amino]octadeca-6,9,12,15-tetraen-3-one
(+/-)-julandine|3-(4-Methoxy-phenyl-2-(3,4-dimethoxy-phenyl)-1,6,7,8,9,9a-hexahydro-4H-chinolizin|8-(3,4-dimethoxy-phenyl)-7-(4-methoxy-phenyl)-1,3,4,6,9,9a-hexahydro-2H-quinolizine|Julandin|julandine
Val-Tyr-Val
A tripeptide formed from L-valine, L-tyrosine and L-valine residues joined in sequence.
donepezil
D018377 - Neurotransmitter Agents > D018678 - Cholinergic Agents > D002800 - Cholinesterase Inhibitors N - Nervous system > N06 - Psychoanaleptics > N06D - Anti-dementia drugs > N06DA - Anticholinesterases D002491 - Central Nervous System Agents > D018697 - Nootropic Agents C471 - Enzyme Inhibitor > C47792 - Acetylcholinesterase Inhibitor D004791 - Enzyme Inhibitors Donepezil, marketed under the trade name Aricept (Eisai), is a centrally acting reversible acetyl cholinesterase inhibitor. Its main therapeutic use is in the treatment of Alzheimers disease where it is used to increase cortical acetylcholine. It has an oral bioavailability of 100\\% and easily crosses the blood-brain barrier. Because it has a half life of about 70 hours, it can be taken once a day. Initial dose is 5 mg per day, which can be increased to 10 mg per day after an adjustment period of at least 4 weeks.; Donepezil is a centrally acting reversible acetyl cholinesterase inhibitor. Its main therapeutic use is in the treatment of Alzheimers disease where it is used to increase cortical acetylcholine. It is well absorbed in the gut with an oral bioavailability of 100\\% and easily crosses the blood-brain barrier. Because it has a half life of about 70 hours, it can be taken once a day.; Currently, there is no definitive proof that use of donepezil or other similar agents alters the course or progression of Alzheimers disease. However, 6-12 month controlled studies have shown modest benefits in cognition and/or behavior. Pilot studies have reported that donepezil therapy may potentially have effects on markers of disease progression, such as hippocampal volume. Therefore, many neurologists, psychiatrists, and primary care physicians use donepezil in patients with Alzheimers disease. In 2005, the UK National Institute for Clinical Excellence (NICE) withdrew its recommendation for use of the drug for mild-to-moderate AD, on the basis that there is no significant improvement in functional outcome; Currently, there is no definitive proof that use of donepezil or other similar agents alters the course or progression of Alzheimers disease. However, 6-12 month controlled studies have shown modest benefits in cognition and/or behavior. Pilot studies have reported that donepezil therapy may potentially have effects on markers of disease progression, such as hippocampal volume. Therefore, many neurologists, psychiatrists, and primary care physicians use donepezil in patients with Alzheimers disease. In 2005, the UK National Institute for Clinical Excellence (NICE) withdrew its recommendation for use of the drug for mild-to-moderate AD, on the basis that there is no significant improvement in functional outcome; of quality of life or of behavioral symptoms. However, NICE revised its guidelines to suggest that donepezil be used in moderate stage patients for whom the evidence is strongest. While the drug is currently indicated for mild to moderate Alzheimers, there is also evidence from 2 trials that it may be effective for moderate to severe disease. An example of this is a Karolinska Institute paper published in The Lancet in early 2006, which states that donepezil improves cognitive function even in patients with severe Alzheimers disease symptoms.; of quality of life or of behavioral symptoms. However, NICE revised its guidelines to suggest that donepezil be used in moderate stage patients for whom the evidence is strongest. While the drug is currently indicated for mild to moderate Alzheimers, there is also evidence from 2 trials that it may be effective for moderate to severe disease. An example of this is a Karolinska Institute paper published in The Lancet in early 2006, which states that donepezil improves cognitive function even in patients with severe Alzheimers disease symptoms. [HMDB]
2,2-dimethyl-7-(3-methyloctan-2-yl)-4-pyridin-4-ylchromen-5-ol
Dibucaine hydrochloride
C78272 - Agent Affecting Nervous System > C245 - Anesthetic Agent
(1S)-(S)-pinanediol 1-ammonium trifluoroacetate-3-methylbutane-1-boronate
1-BENZYL-4-(5-(4,4,5,5-TETRAMETHYL-1,3,2-DIOXABOROLAN-2-YL)PYRIDIN-2-YL)PIPERAZINE
5,11-Dihydro-1-(phenylmethyl)-spiro[6H-indolo[3,2-c]quinoline-6,4-piperidine]
(S)-3-cyclohexylpropyl 1-(3,3-diMethyl-2-oxopentanoyl)piperidine-2-carboxylate
(aR,3aS,4S,6S,7aR)-Hexahydro-3a,8,8-trimethyl-alpha-(2-methylpropyl)-4,6-methano-1,3,2-benzodioxaborole-2-methanamine 2,2,2-trifluoroacetate
2-(4-diphenylmethyl-1-piperazinyl)ethyl 3-aminocrotonate
6-(4-Benzyl-1-piperazino)pyridine-3-boronic acid pinacol ester
1-[4-(4.4.5.5-tetramethyl-[1.3.2]dioxaborolan-2-yl)-biphenyl-4-yl]-cyclopropanecarboxylic acid methyl ester
3-(dodecenyl)-2,5-dioxo-1-Pyrrolidinehexanoic acid
n-[3-(n-Hydroxycarboxamido)-2-(2-methylpropyl)-propanoyl]-o-tyrosine-n-methylamide
D004791 - Enzyme Inhibitors > D011480 - Protease Inhibitors > D061965 - Matrix Metalloproteinase Inhibitors
2-((trans-2-(4-(Benzyloxy)phenyl)cyclopropyl)amino)-1-(4-methylpiperazin-1-yl)ethanone
oxypertine
N - Nervous system > N05 - Psycholeptics > N05A - Antipsychotics > N05AE - Indole derivatives C78272 - Agent Affecting Nervous System > C66883 - Dopamine Antagonist
Sphingosine 1-phosphate
A phosphosphingolipid that consists of sphingosine having a phospho group attached at position 1 Sphingosine 1-phosphate (S1P) is a phosphorylated sphingolipid metabolite with potent bioactive actions in the Sphingolipid metabolism, Calcium signaling pathway and Neuroactive ligand-receptor interaction. Generated by sphingosine kinases and ceramide kinase, S1P control numerous aspects of cell physiology, including cell survival and mammalian inflammatory responses. S1P is involved in cyclooxygenase-2 induction (COX-2), and regulate production of eicosanoids (important inflammatory mediators). S1P functions mainly via G-protein-coupled receptors and probably also has intracellular targets. (PMID 16219683) [HMDB]
