Exact Mass: 189.0399114
Exact Mass Matches: 189.0399114
Found 500 metabolites which its exact mass value is equals to given mass value 189.0399114,
within given mass tolerance error 0.05 dalton. Try search metabolite list with more accurate mass tolerance error
0.01 dalton.
Quisqualic_acid
Quisqualic acid is a non-proteinogenic alpha-amino acid. Quisqualic acid is an agonist at two subsets of excitatory amino acid receptors, ionotropic receptors that directly control membrane channels and metabotropic receptors that indirectly mediate calcium mobilization from intracellular stores. The compound is obtained from the seeds and fruit of Quisqualis chinensis. An agonist at two subsets of excitatory amino acid receptors, ionotropic receptors that directly control membrane channels and metabotropic receptors that indirectly mediate calcium mobilization from intracellular stores. The compound is obtained from the seeds and fruit of Quisqualis chinensis. D018377 - Neurotransmitter Agents > D018683 - Excitatory Amino Acid Agents > D018690 - Excitatory Amino Acid Agonists Acquisition and generation of the data is financially supported in part by CREST/JST. KEIO_ID Q003 Quisqualic acid (L-Quisqualic acid), a natural analog of glutamate, is a potent and pan two subsets (iGluR and mGluR) of excitatory amino acid (EAA) agonist with an EC50 of 45 nM and a Ki of 10 nM for mGluR1R. Quisqualic acid is isolated from the fruits of Quisqualis indica[1][2]. Quisqualic acid (L-Quisqualic acid), a natural analog of glutamate, is a potent and pan two subsets (iGluR and mGluR) of excitatory amino acid (EAA) agonist with an EC50 of 45 nM and a Ki of 10 nM for mGluR1R. Quisqualic acid is isolated from the fruits of Quisqualis indica[1][2]. Quisqualic acid (L-Quisqualic acid), a natural analog of glutamate, is a potent and pan two subsets (iGluR and mGluR) of excitatory amino acid (EAA) agonist with an EC50 of 45 nM and a Ki of 10 nM for mGluR1R. Quisqualic acid is isolated from the fruits of Quisqualis indica[1][2].
Kynurenic acid
Kynurenic acid is a quinolinemonocarboxylic acid that is quinoline-2-carboxylic acid substituted by a hydroxy group at C-4. It has a role as a G-protein-coupled receptor agonist, a NMDA receptor antagonist, a nicotinic antagonist, a neuroprotective agent, a human metabolite and a Saccharomyces cerevisiae metabolite. It is a monohydroxyquinoline and a quinolinemonocarboxylic acid. It is a conjugate acid of a kynurenate. Kynurenic Acid is under investigation in clinical trial NCT02340325 (FS2 Safety and Tolerability Study in Healthy Volunteers). Kynurenic acid is a natural product found in Ephedra foeminea, Ephedra intermedia, and other organisms with data available. Kynurenic acid is a uremic toxin. Uremic toxins can be subdivided into three major groups based upon their chemical and physical characteristics: 1) small, water-soluble, non-protein-bound compounds, such as urea; 2) small, lipid-soluble and/or protein-bound compounds, such as the phenols and 3) larger so-called middle-molecules, such as beta2-microglobulin. Chronic exposure of uremic toxins can lead to a number of conditions including renal damage, chronic kidney disease and cardiovascular disease. Kynurenic acid (KYNA) is a well-known endogenous antagonist of the glutamate ionotropic excitatory amino acid receptors N-methyl-D-aspartate (NMDA), alphaamino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainate receptors and of the nicotine cholinergic subtype alpha 7 receptors. KYNA neuroprotective and anticonvulsive activities have been demonstrated in animal models of neurodegenerative diseases. Because of KYNAs neuromodulatory character, its involvement has been speculatively linked to the pathogenesis of a number of neurological conditions including those in the ageing process. Different patterns of abnormalities in various stages of KYNA metabolism in the CNS have been reported in Alzheimers disease, Parkinsons disease and Huntingtons disease. In HIV-1-infected patients and in patients with Lyme neuroborreliosis a marked rise of KYNA metabolism was seen. In the ageing process KYNA metabolism in the CNS of rats shows a characteristic pattern of changes throughout the life span. A marked increase of the KYNA content in the CNS occurs before the birth, followed by a dramatic decline on the day of birth. A low activity was seen during ontogenesis, and a slow and progressive enhancement occurs during maturation and ageing. This remarkable profile of KYNA metabolism alterations in the mammalian brain has been suggested to result from the development of the organisation of neuronal connections and synaptic plasticity, development of receptor recognition sites, maturation and ageing. There is significant evidence that KYNA can improve cognition and memory, but it has also been demonstrated that it interferes with working memory. Impairment of cognitive function in various neurodegenerative disorders is accompanied by profound reduction and/or elevation of KYNA metabolism. The view that enhancement of CNS KYNA levels could underlie cognitive decline is supported by the increased KYNA metabolism in Alzheimers disease, by the increased KYNA metabolism in downs syndrome and the enhancement of KYNA function during the early stage of Huntingtons disease. Kynurenic acid is the only endogenous N-methyl-D-aspartate (NMDA) receptor antagonist identified up to now, that mediates glutamatergic hypofunction. Schizophrenia is a disorder of dopaminergic neurotransmission, but modulation of the dopaminergic system by glutamatergic neurotransmission seems to play a key role. Despite the NMDA receptor antagonism, kynurenic acid also blocks, in lower doses, the nicotinergic acetycholine receptor, i.e., increased kynurenic acid levels can explain psychotic symptoms and cognitive deterioration. Kynurenic acid levels are described to be higher in the cerebrospinal fluid (CSF) and in critical central nervous system (CNS) regions of schizophrenics as compared to controls. (A3279, A3280).... Kynurenic acid (KYNA) is a well-known endogenous antagonist of the glutamate ionotropic excitatory amino acid receptors N-methyl-D-aspartate (NMDA), alphaamino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainate receptors and of the nicotine cholinergic subtype alpha 7 receptors. KYNA neuroprotective and anticonvulsive activities have been demonstrated in animal models of neurodegenerative diseases. Because of KYNAs neuromodulatory character, its involvement has been speculatively linked to the pathogenesis of a number of neurological conditions including those in the ageing process. Different patterns of abnormalities in various stages of KYNA metabolism in the CNS have been reported in Alzheimers disease, Parkinsons disease and Huntingtons disease. In HIV-1-infected patients and in patients with Lyme neuroborreliosis a marked rise of KYNA metabolism was seen. In the ageing process KYNA metabolism in the CNS of rats shows a characteristic pattern of changes throughout the life span. A marked increase of the KYNA content in the CNS occurs before the birth, followed by a dramatic decline on the day of birth. A low activity was seen during ontogenesis, and a slow and progressive enhancement occurs during maturation and ageing. This remarkable profile of KYNA metabolism alterations in the mammalian brain has been suggested to result from the development of the organisation of neuronal connections and synaptic plasticity, development of receptor recognition sites, maturation and ageing. There is significant evidence that KYNA can improve cognition and memory, but it has also been demonstrated that it interferes with working memory. Impairment of cognitive function in various neurodegenerative disorders is accompanied by profound reduction and/or elevation of KYNA metabolism. The view that enhancement of CNS KYNA levels could underlie cognitive decline is supported by the increased KYNA metabolism in Alzheimers disease, by the increased KYNA metabolism in downs syndrome and the enhancement of KYNA function during the early stage of Huntingtons disease. Kynurenic acid is the only endogenous N-methyl-D-aspartate (NMDA) receptor antagonist identified up to now, that mediates glutamatergic hypofunction. Schizophrenia is a disorder of dopaminergic neurotransmission, but modulation of the dopaminergic system by glutamatergic neurotransmission seems to play a key role. Despite the NMDA receptor antagonism, kynurenic acid also blocks, in lower doses, the nicotinergic acetycholine receptor, i.e., increased kynurenic acid levels can explain psychotic symptoms and cognitive deterioration. Kynurenic acid levels are described to be higher in the cerebrospinal fluid (CSF) and in critical central nervous system (CNS) regions of schizophrenics as compared to controls. (PMID: 17062375 , 16088227). KYNA has also been identified as a uremic toxin according to the European Uremic Toxin Working Group (PMID: 22626821). Kynurenic acid (KYNA) is a well-known endogenous antagonist of the glutamate ionotropic excitatory amino acid receptors N-methyl-D-aspartate (NMDA), alphaamino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainate receptors and of the nicotine cholinergic subtype alpha 7 receptors. KYNA neuroprotective and anticonvulsive activities have been demonstrated in animal models of neurodegenerative diseases. Because of KYNAs neuromodulatory character, its involvement has been speculatively linked to the pathogenesis of a number of neurological conditions including those in the ageing process. Different patterns of abnormalities in various stages of KYNA metabolism in the CNS have been reported in Alzheimers disease, Parkinsons disease and Huntingtons disease. In HIV-1-infected patients and in patients with Lyme neuroborreliosis a marked rise of KYNA metabolism was seen. In the ageing process KYNA metabolism in the CNS of rats shows a characteristic pattern of changes throughout the life span. A marked increase of the KYNA content in the CNS occurs before the birth, followed by a dramatic decline on the day of birth. A low activity was seen during ontogenesis, and a slow and progressive enhancement occurs during maturation and ageing. This remarkable profile of KYNA metabolism alterations in the mammalian brain has been suggested to result from the development of the organisation of neuronal connections and synaptic plasticity, development of receptor recognition sites, maturation and ageing. There is significant evidence that KYNA can improve cognition and memory, but it has also been demonstrated that it interferes with working memory. Impairment of cognitive function in various neurodegenerative disorders is accompanied by profound reduction and/or elevation of KYNA metabolism. The view that enhancement of CNS KYNA levels could underlie cognitive decline is supported by the increased KYNA metabolism in Alzheimers disease, by the increased KYNA metabolism in downs syndrome and the enhancement of KYNA function during the early stage of Huntingtons disease. Kynurenic acid is the only endogenous N-methyl-D-aspartate (NMDA) receptor antagonist identified up to now, that mediates glutamatergic hypofunction. Schizophrenia is a disorder of dopaminergic neurotransmission, but modulation of the dopaminergic system by glutamatergic neurotransmission seems to play a key role. Despite the NMDA receptor antagonism, kynurenic acid also blocks, in lower doses, the nicotinergic acetycholine receptor, i.e., increased kynurenic acid levels can explain psychotic symptoms and cognitive deterioration. Kynurenic acid levels are described to be higher in the cerebrospinal fluid (CSF) and in critical central nervous system (CNS) regions of schizophrenics as compared to controls. (PMID: 17062375, 16088227) [HMDB] D018377 - Neurotransmitter Agents > D018683 - Excitatory Amino Acid Agents > D018691 - Excitatory Amino Acid Antagonists A quinolinemonocarboxylic acid that is quinoline-2-carboxylic acid substituted by a hydroxy group at C-4. [Raw Data] CBA11_Kynurenic-acid_pos_30eV_1-3_01_673.txt [Raw Data] CBA11_Kynurenic-acid_pos_50eV_1-3_01_675.txt [Raw Data] CBA11_Kynurenic-acid_pos_40eV_1-3_01_674.txt [Raw Data] CBA11_Kynurenic-acid_neg_30eV_1-3_01_726.txt [Raw Data] CBA11_Kynurenic-acid_pos_20eV_1-3_01_672.txt [Raw Data] CBA11_Kynurenic-acid_pos_10eV_1-3_01_671.txt [Raw Data] CBA11_Kynurenic-acid_neg_20eV_1-3_01_725.txt [Raw Data] CBA11_Kynurenic-acid_neg_50eV_1-3_01_728.txt [Raw Data] CBA11_Kynurenic-acid_neg_40eV_1-3_01_727.txt [Raw Data] CBA11_Kynurenic-acid_neg_10eV_1-3_01_724.txt Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8.
N-acetylglutamate
N-Acetyl-L-glutamic acid or N-Acetylglutamate, belongs to the class of organic compounds known as N-acyl-alpha amino acids. N-acyl-alpha amino acids are compounds containing an alpha amino acid which bears an acyl group at its terminal nitrogen atom. N-Acetyl-L-glutamate can also be classified as an alpha amino acid or a derivatized alpha amino acid. Technically, N-Acetyl-L-glutamate is a biologically available N-terminal capped form of the proteinogenic alpha amino acid L-glutamic acid. N-Acetyl-L-glutamic acid is found in all organisms ranging from bacteria to plants to animals. N-acetyl amino acids can be produced either via direct synthesis of specific N-acetyltransferases or via the proteolytic degradation of N-acetylated proteins by specific hydrolases. N-terminal acetylation of proteins is a widespread and highly conserved process in eukaryotes that is involved in protection and stability of proteins (PMID: 16465618). About 85\\\\% of all human proteins and 68\\\\% of all yeast proteins are acetylated at their N-terminus (PMID: 21750686). Several proteins from prokaryotes and archaea are also modified by N-terminal acetylation. The majority of eukaryotic N-terminal-acetylation reactions occur through N-acetyltransferase enzymes or NAT’s (PMID: 30054468). These enzymes consist of three main oligomeric complexes NatA, NatB, and NatC, which are composed of at least a unique catalytic subunit and one unique ribosomal anchor. The substrate specificities of different NAT enzymes are mainly determined by the identities of the first two N-terminal residues of the target protein. The human NatA complex co-translationally acetylates N-termini that bear a small amino acid (A, S, T, C, and occasionally V and G) (PMID: 30054468). NatA also exists in a monomeric state and can post-translationally acetylate acidic N-termini residues (D-, E-). NatB and NatC acetylate N-terminal methionine with further specificity determined by the identity of the second amino acid. N-acetylated amino acids, such as N-acetylglutamate can be released by an N-acylpeptide hydrolase from peptides generated by proteolytic degradation (PMID: 16465618). In addition to the NAT enzymes and protein-based acetylation, N-acetylation of free glutamic acid can also occur. In particular, N-Acetyl-L-glutamic acid can be biosynthesized from glutamate and acetylornithine by ornithine acetyltransferase, and from glutamic acid and acetyl-CoA by the enzyme known as N-acetylglutamate synthase. N-Acetyl-L-glutamic acid is the first intermediate involved in the biosynthesis of arginine in prokaryotes and simple eukaryotes and a regulator of the urea cycle in vertebrates. In vertebrates, N-acetylglutamic acid is the allosteric activator molecule to mitochondrial carbamyl phosphate synthetase I (CPSI) which is the first enzyme in the urea cycle. It triggers the production of the first urea cycle intermediate, a compound known as carbamyl phosphate. Notably the CPSI enzyme is inactive when N-acetylglutamic acid is not present. A deficiency in N-acetyl glutamate synthase or a genetic mutation in the gene coding for the enzyme will lead to urea cycle failure in which ammonia is not converted to urea, but rather accumulated in the blood leading to the condition called Type I hyperammonemia. Excessive amounts N-acetyl amino acids can be detected in the urine with individuals with aminoacylase I deficiency, a genetic disorder (PMID: 16465618). These include N-acetylalanine (as well as N-acetylserine, N-acetylglutamine, N-acetylglutamate, N-acetylglycine, N-acetylmethionine and smaller amounts of N-acetylthreonine, N-acetylleucine, N-acetylvaline and N-acetylisoleucine. Aminoacylase I is a soluble homodimeric zinc binding enzyme that catalyzes the formation of free aliphatic amino acids from N-acetylated precursors. In humans, Aminoacylase I is encoded by the aminoacylase 1 gene (ACY1) on chromosome 3p21 that consists of 15 exons (OMIM 609924). Individuals with aminoacylase I deficiency w... N-acetyl-l-glutamate, also known as L-N-acetylglutamic acid or ac-glu-oh, belongs to glutamic acid and derivatives class of compounds. Those are compounds containing glutamic acid or a derivative thereof resulting from reaction of glutamic acid at the amino group or the carboxy group, or from the replacement of any hydrogen of glycine by a heteroatom. N-acetyl-l-glutamate is soluble (in water) and a weakly acidic compound (based on its pKa). N-acetyl-l-glutamate can be found in a number of food items such as cardoon, almond, butternut squash, and avocado, which makes N-acetyl-l-glutamate a potential biomarker for the consumption of these food products. N-acetyl-l-glutamate may be a unique S.cerevisiae (yeast) metabolite. Acquisition and generation of the data is financially supported in part by CREST/JST. KEIO_ID A031 N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1]. N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1].
Tricyclazole
Rice fungicid
Thiotepa
C6H12N3PS (189.04895219999997)
N,NN-triethylenethiophosphoramide (ThioTEPA) is a cancer chemotherapeutic member of the alkylating agent group, now in use for over 50 years. It is a stable derivative of N,N,N- triethylenephosphoramide (TEPA). It is mostly used to treat breast cancer, ovarian cancer and bladder cancer. It is also used as conditioning for Bone marrow transplantation. Its main toxicity is myelosuppression. L - Antineoplastic and immunomodulating agents > L01 - Antineoplastic agents > L01A - Alkylating agents > L01AC - Ethylene imines C274 - Antineoplastic Agent > C186664 - Cytotoxic Chemotherapeutic Agent > C2842 - DNA Binding Agent D000970 - Antineoplastic Agents > D019653 - Myeloablative Agonists D007155 - Immunologic Factors > D007166 - Immunosuppressive Agents D009676 - Noxae > D000477 - Alkylating Agents
1-Nitronaphthalene-5,6-oxide
This compound belongs to the family of Nitronaphthalenes. These are polycyclic aromatic compounds containing a naphthalene moiety substituted by one or more nitro groups.
1-Nitronaphthalene-7,8-oxide
This compound belongs to the family of Nitronaphthalenes. These are polycyclic aromatic compounds containing a naphthalene moiety substituted by one or more nitro groups.
(E)-3-(4-hydroxyphenyl)-2-isocyanoprop-2-enoic acid
1-Isothiocyanato-6-(methylthio)hexane
1-Isothiocyanato-6-(methylthio)hexane is found in brassicas. Flavour compound of Japanese horseradish (Wasabia japonica
Pyrrolidino-[1,2E]-4H-2,4-dimethyl-1,3,5-dithiazine
Pyrrolidino-[1,2E]-4H-2,4-dimethyl-1,3,5-dithiazine is used as a food additive [EAFUS] ("EAFUS: Everything Added to Food in the United States. [http://www.eafus.com/]")
Glutarylglycine
Glutarylglycine is an acyl glycine. Acyl glycines are normally minor metabolites of fatty acids. However, the excretion of certain acyl glycines is increased in several inborn errors of metabolism. In certain cases the measurement of these metabolites in body fluids can be used to diagnose disorders associated with mitochondrial fatty acid beta-oxidation. Acyl glycines are produced through the action of glycine N-acyltransferase (EC 2.3.1.13) which is an enzyme that catalyzes the chemical reaction:. acyl-CoA + glycine < -- > CoA + N-acylglycine. Glutarylglycine is involved in lysine metabolism. An elevated level of glutarylglycine occurs in patients with glutaric acidemia type II, which is an autosomal recessive inborn error of metabolism due to a mitochondrial respiratory electron chain transport defect. (http://www.pediatricneuro.com/alfonso/pg75.htm). Glutarylglycine is an acyl glycine. Acyl glycines are normally minor metabolites of fatty acids. However, the excretion of certain acyl glycines is increased in several inborn errors of metabolism. In certain cases the measurement of these metabolites in body fluids can be used to diagnose disorders associated with mitochondrial fatty acid beta-oxidation. Acyl glycines are produced through the action of glycine N-acyltransferase (EC 2.3.1.13) which is an enzyme that catalyzes the chemical reaction:
Lanthionine ketimine
Lanthionine ketimine binds specifically and with high affinity to brain membranes and belong to a class of endogenous sulfur-containing cyclic products provided with a possible neurochemical function (PMID 1761027) [HMDB] Lanthionine ketimine binds specifically and with high affinity to brain membranes and belong to a class of endogenous sulfur-containing cyclic products provided with a possible neurochemical function (PMID 1761027).
2-aminophenol sulphate
2-aminophenol sulphate is a metabolite found in urine of individuals that have consumed whole grains. It is a particularly strong biomarker for whole grain rye bread consumption (PMID: 23307617).
Fluoromisonidazole
D011838 - Radiation-Sensitizing Agents
Quisqualic acid
Quisqualic acid (L-Quisqualic acid), a natural analog of glutamate, is a potent and pan two subsets (iGluR and mGluR) of excitatory amino acid (EAA) agonist with an EC50 of 45 nM and a Ki of 10 nM for mGluR1R. Quisqualic acid is isolated from the fruits of Quisqualis indica[1][2]. Quisqualic acid (L-Quisqualic acid), a natural analog of glutamate, is a potent and pan two subsets (iGluR and mGluR) of excitatory amino acid (EAA) agonist with an EC50 of 45 nM and a Ki of 10 nM for mGluR1R. Quisqualic acid is isolated from the fruits of Quisqualis indica[1][2]. Quisqualic acid (L-Quisqualic acid), a natural analog of glutamate, is a potent and pan two subsets (iGluR and mGluR) of excitatory amino acid (EAA) agonist with an EC50 of 45 nM and a Ki of 10 nM for mGluR1R. Quisqualic acid is isolated from the fruits of Quisqualis indica[1][2].
α-Cyano-4-hydroxycinnamic acid
Profile spectrum of this record is given as a JPEG file.; [Profile] MCH00005.jpg Profile spectrum of this record is given as a JPEG file.; [Profile] MCH00004.jpg
(+)-(R)-2-(4-hydroxy-2-oxo-2,3-dihydrobenzofuran-3-yl)acetonitrile
Kynurenic acid
MS2 deconvoluted using MS2Dec from all ion fragmentation data, MetaboLights identifier MTBLS1040; HCZHHEIFKROPDY-UHFFFAOYSA-N_STSL_0005_Kynurenic acid_2000fmol_180410_S2_LC02_MS02_66; Spectrum acquired as described in Naz et al 2017 PMID 28641411. Preparation and submission to MassBank of North America by Chaleckis R. and Tada I. MS2 deconvoluted using CorrDec from all ion fragmentation data, MetaboLights identifier MTBLS1040; Spectrum acquired as described in Naz et al 2017 PMID 28641411. Preparation and submission to MassBank of North America by Chaleckis R. and Tada I. D018377 - Neurotransmitter Agents > D018683 - Excitatory Amino Acid Agents > D018691 - Excitatory Amino Acid Antagonists relative retention time with respect to 9-anthracene Carboxylic Acid is 0.374 relative retention time with respect to 9-anthracene Carboxylic Acid is 0.376 relative retention time with respect to 9-anthracene Carboxylic Acid is 0.370 relative retention time with respect to 9-anthracene Carboxylic Acid is 0.372 Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8. Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8. Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8. Transtorine is a quinoline alkaloid, found from Ephedra transitoria, with antibacterial activity[1]. Transtorine is a quinoline alkaloid, found from Ephedra transitoria, with antibacterial activity[1].
N-Acetyl-L-glutamic acid
An N-acyl-L-amino acid that is L-glutamic acid in which one of the amine hydrogens is substituted by an acetyl group. N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1]. N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1].
N-Acetylglutamic acid
N-Acetylglutamic acid (abbreviated NAcGlu) is biosynthesized from glutamic acid and acetyl-CoA by the enzyme NAGS. The reverse reaction, hydrolysis of the acetyl group, is catalyzed by a specific hydrolase. [HMDB] N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1]. N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1].
Kynurenate
D018377 - Neurotransmitter Agents > D018683 - Excitatory Amino Acid Agents > D018691 - Excitatory Amino Acid Antagonists Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8. Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8. Kynurenic acid, an endogenous tryptophan metabolite, is a broad-spectrum antagonist targeting NMDA, glutamate, α7 nicotinic acetylcholine receptor. Kynurenic acid is also an agonist of GPR35/CXCR8. Transtorine is a quinoline alkaloid, found from Ephedra transitoria, with antibacterial activity[1]. Transtorine is a quinoline alkaloid, found from Ephedra transitoria, with antibacterial activity[1].
N-Acetylglutamate
N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1]. N-Acetyl-L-glutamic acid, a glutamic acid, is a component of animal cell culturing media. N-Acetyl-L-glutamic acid is a metabolite of Saccharomyces cerevisiae and human[1].
octopamine
Octopamine ((±)-p-Octopamine) hydrochloride, a biogenic monoamine structurally related to noradrenaline, acts as a neurohormone, a neuromodulator and a neurotransmitter in invertebrates. Octopamine hydrochloride can stimulate alpha2-adrenoceptors (ARs) in Chinese hamster ovary cells transfected with human alpha2-ARs. Octopamine hydrochloride increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure[1][2][3]. Octopamine ((±)-p-Octopamine) hydrochloride, a biogenic monoamine structurally related to noradrenaline, acts as a neurohormone, a neuromodulator and a neurotransmitter in invertebrates. Octopamine hydrochloride can stimulate alpha2-adrenoceptors (ARs) in Chinese hamster ovary cells transfected with human alpha2-ARs. Octopamine hydrochloride increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure[1][2][3]. Octopamine ((±)-p-Octopamine) hydrochloride, a biogenic monoamine structurally related to noradrenaline, acts as a neurohormone, a neuromodulator and a neurotransmitter in invertebrates. Octopamine hydrochloride can stimulate alpha2-adrenoceptors (ARs) in Chinese hamster ovary cells transfected with human alpha2-ARs. Octopamine hydrochloride increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure[1][2][3].
Lanthionine ketimine
A member of the class of 1,4-thiazines that is 3,6-dihydro-2H-1,4-thiazine substituted by carboxy groups at positions 3 and 5. It is a natural but non-proteogenic amino acid found in human urine and brain.
2,4-dimethyl-hexahydropyrrolo[2,1-d][1,3,5]dithiazine
2-Fluoro-4-(methylsulfonyl)aniline
C7H8FNO2S (189.02597599999999)
2-AMINO-1-(3-FLUOROPHENYL)ETHANONE HYDROCHLORIDE
C8H9ClFNO (189.03566659999998)
(Z)-5-(FLUOROMETHYLENE)-4-PHENYL-1H-PYRROL-2(5H)-ONE
(1S)-1-(3-fluoro-2-methylphenyl)ethanamine,hydrochloride
C9H13ClFN (189.07205000000002)
(S)-1-(4-Fluoro-3-methylphenyl)ethanamine hydrochloride
C9H13ClFN (189.07205000000002)
1-[(Aminooxy)methyl]-4-methoxybenzene hydrochloride
3-FLUORO-4-METHYLBENZENESULFONAMID&
C7H8FNO2S (189.02597599999999)
(R)-1-(2-Fluorophenyl)propan-1-amine hydrochloride
C9H13ClFN (189.07205000000002)
(1S)-1-(5-fluoro-2-methylphenyl)ethanamine,hydrochloride
C9H13ClFN (189.07205000000002)
(S)-1-(2-Fluoro-5-Methylphenyl)ethanamine hydrochloride
C9H13ClFN (189.07205000000002)
4-tert-butyl-2-(chloromethyl)-1,3-thiazole
C8H12ClNS (189.03789419999998)
(1R)-1-(5-fluoro-2-methylphenyl)ethanamine,hydrochloride
C9H13ClFN (189.07205000000002)
(R)-1-(2-Fluoro-5-Methylphenyl)ethanamine hydrochloride
C9H13ClFN (189.07205000000002)
(S)-1-(2-Fluorophenyl)propan-1-amine hydrochloride
C9H13ClFN (189.07205000000002)
2-chloro-N-(2,2,2-trifluoroethyl)propanamide
C5H7ClF3NO (189.01682379999997)
4-METHOXY-PYRIDINE-2-CARBOXYLIC ACID HYDROCHLORIDE
(2-fluorophenyl)methanesulfonamide
C7H8FNO2S (189.02597599999999)
4,5,6,7-TETRAHYDROBENZO[B]THIOPHEN-2-AMINE HYDROCHLORIDE
C8H12ClNS (189.03789419999998)
(5-Chloro-2-fluoro-4-methylpyridin-3-yl)boronic acid
1,3-Difluoro-5-methoxy-2-nitrobenzene
C7H5F2NO3 (189.02374840000002)
3-Methyl-5-(pyrrolidin-3-yl)-1,2,4-oxadiazole hydrochloride
C7H12ClN3O (189.06688519999997)
(4-CHLORO-2-METHYLPHENYL)METHYLCYANOCARBONIMIDODITHIOATE
C6H8ClN3S (189.01274379999998)
2-HYDRAZINO-5-METHYL-1,3,4-THIADIAZOLE
C7H8FNO2S (189.02597599999999)
6-fluoro-4-oxochromene-3-carbonitrile
C10H4FNO2 (189.02260560000002)
(3,5-difluoro-4-nitrophenyl)methanol
C7H5F2NO3 (189.02374840000002)
1-(4-fluorophenyl)propan-2-amine hydrochloride
C9H13ClFN (189.07205000000002)
8-Fluoro-3,4-dihydro-2H-benzo[b][1,4]oxazine hydrochloride
C8H9ClFNO (189.03566659999998)
6-Methyl-4-oxo-1,4-dihydropyridine-3-carboxylic acid hydrochloride
1H-Benzimidazole-2-acetaldehyde,alpha-(hydroxyimino)-(9CI)
1-[(Aminooxy)methyl]-3-methoxybenzene hydrochloride
diexo-3-amino-bicyclo[2.2.1]hept-5-ene-2-carboxylic acid hydrochloride
Adenine hydrochloride
C5H8ClN5O (189.04173479999997)
Adenine monohydrochloride hemihydrate is an endogenous metabolite.
1,2,5-Thiadiazole-3-carboxylicacid,4-[(2-hydroxyethyl)amino]-(9CI)
4-Fluoro-2-methylbenzenesulfonamide
C7H8FNO2S (189.02597599999999)
1,5-Difluoro-3-methoxy-2-nitrobenzene
C7H5F2NO3 (189.02374840000002)
2,3-Difluoro-1-methoxy-4-nitrobenzene
C7H5F2NO3 (189.02374840000002)
(1R)-1-(3-fluoro-2-methylphenyl)ethanamine,hydrochloride
C9H13ClFN (189.07205000000002)
2,4(1H,3H)-Pyrimidinedione,5-[(2-chloroethyl)amino]-
2-hydrazinylpyridine-3-carboxylic acid,hydrochloride
2-[(4-amino-6-chloro-1,3,5-triazin-2-yl)amino]ethanol
C5H8ClN5O (189.04173479999997)
Ethyl 2,2-difluoro-3-aminopropanoate hydrochloride
7-Carboxy-1-hydroxyisoquinoline, 7-Carboxy-1-hydroxy-2-azanaphthalene
1-(trifluoromethyl)Cyclopentan-1-amine hydrochloride
1,2-Difluoro-3-methoxy-4-nitrobenzene
C7H5F2NO3 (189.02374840000002)
(2-chloro-5-fluoro-3-methylpyridin-4-yl)boronic acid
2-Amino-1-(2-fluorophenyl)ethanone hydrochloride
C8H9ClFNO (189.03566659999998)
N-(2-Fluorophenyl)methanesulfonamide
C7H8FNO2S (189.02597599999999)
4-Fluoro-2-(methylsulfonyl)aniline
C7H8FNO2S (189.02597599999999)
Benzenethiol,2-amino-3,6-dimethyl-
C8H12ClNS (189.03789419999998)
hydrogen sulfate,tetramethylazanium,hydrate
C4H15NO5S (189.06708999999998)
4-Fluoro-N-methylbenzenesulfonamide
C7H8FNO2S (189.02597599999999)
4(1H)-Pyrimidinone,6-amino-2,3-dihydro-5-nitroso-2-thioxo-, monoammonium salt (9CI)
5-Chloro-2-methyl-4-oxazolecarboxylic acid ethyl ester
3,5-Difluoro-4-methoxynitrobenzene
C7H5F2NO3 (189.02374840000002)
6-fluoro-4-hydroxy-1,7-naphthyridine-3-carbonitrile
2-Fluoro-5-(methylsulfonyl)aniline
C7H8FNO2S (189.02597599999999)
Ethyl 3-hydroxy-2-oxo-3-pyrroline-4-carboxylate monohydrate
2-(Trifluoromethyl)-6,7-dihydro-5H-pyrrolo[3,4-d]pyrimidine
1,2-Difluoro-4-methoxy-5-nitrobenzene
C7H5F2NO3 (189.02374840000002)
Dopamine hydrochloride
D018373 - Peripheral Nervous System Agents > D001337 - Autonomic Agents > D013566 - Sympathomimetics C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist D018377 - Neurotransmitter Agents > D015259 - Dopamine Agents D020011 - Protective Agents > D002316 - Cardiotonic Agents D002317 - Cardiovascular Agents
(2S,4R)-4-(prop-2-ynyl)pyrrolidine-2-carboxylic acid hydrochloride
1,5-Difluoro-2-methoxy-4-nitrobenzene
C7H5F2NO3 (189.02374840000002)
1H-Benzimidazole-5-carbonitrile,2,3-dihydro-3-methoxy-2-oxo-(9CI)
(S)-(-)-2-ISOCYANATO-4-(METHYLTHIO)BUTYRIC ACID METHYL ESTER
1-(Difluoromethoxy)-2-nitrobenzene
C7H5F2NO3 (189.02374840000002)
2-(4-FLUOROPHENYL)ETHANIMIDAMIDE HYDROCHLORIDE
C8H9ClFNO (189.03566659999998)
1-[(Aminooxy)methyl]-2-methoxybenzene hydrochloride
Norfenefrine hydrochloride
C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D000322 - Adrenergic Agonists Norfenefrine hydrochloride is an orally active, endogenously found α-adrenergic agonist and can be used for the research of female stress incontinence[1][2].
5-(2-FURYL)NICOTINIC ACID 975-(2-FURYL)PYRIDINE-3-CARBOXYLIC ACID
3-Fluoro-4-(Methylsulfonyl)aniline
C7H8FNO2S (189.02597599999999)
Fluoromisonidazole F-18
C1446 - Radiopharmaceutical Compound > C2124 - Radioconjugate D011838 - Radiation-Sensitizing Agents
3-(Trimethylsilylamino)thiolan-2-one
C7H15NOSSi (189.06435799999997)
Octopamine hydrochloride
Octopamine ((±)-p-Octopamine) hydrochloride, a biogenic monoamine structurally related to noradrenaline, acts as a neurohormone, a neuromodulator and a neurotransmitter in invertebrates. Octopamine hydrochloride can stimulate alpha2-adrenoceptors (ARs) in Chinese hamster ovary cells transfected with human alpha2-ARs. Octopamine hydrochloride increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure[1][2][3]. Octopamine ((±)-p-Octopamine) hydrochloride, a biogenic monoamine structurally related to noradrenaline, acts as a neurohormone, a neuromodulator and a neurotransmitter in invertebrates. Octopamine hydrochloride can stimulate alpha2-adrenoceptors (ARs) in Chinese hamster ovary cells transfected with human alpha2-ARs. Octopamine hydrochloride increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure[1][2][3]. Octopamine ((±)-p-Octopamine) hydrochloride, a biogenic monoamine structurally related to noradrenaline, acts as a neurohormone, a neuromodulator and a neurotransmitter in invertebrates. Octopamine hydrochloride can stimulate alpha2-adrenoceptors (ARs) in Chinese hamster ovary cells transfected with human alpha2-ARs. Octopamine hydrochloride increased glycogenolysis, glycolysis, oxygen uptake, gluconeogenesis and the portal perfusion pressure[1][2][3].
3-Dehydroquinate
A hydroxy monocarboxylic acid anion that is obtained by removal of a proton from the carboxylic acid group of 3-dehydroquinic acid.
Pyrrolidino-(1,2E)-4H-2,4-dimethyl-1,3,5-dithiazine
(3R)-3,6-Dihydro-2H-1,4-thiazine-3,5-dicarboxylic acid
thiotepa
C6H12N3PS (189.04895219999997)
L - Antineoplastic and immunomodulating agents > L01 - Antineoplastic agents > L01A - Alkylating agents > L01AC - Ethylene imines C274 - Antineoplastic Agent > C186664 - Cytotoxic Chemotherapeutic Agent > C2842 - DNA Binding Agent D000970 - Antineoplastic Agents > D019653 - Myeloablative Agonists D007155 - Immunologic Factors > D007166 - Immunosuppressive Agents D009676 - Noxae > D000477 - Alkylating Agents
Gly-Asp(1-)
A peptide anion obtained by deprotonation of the terminal and side-chain carboxy groups and protonation of the terminal amino group of Gly-Asp; major species at pH 7.3.
Asp-Gly(1-)
A peptide anion obtained by deprotonation of the terminal and side-chain carboxy groups and protonation of the terminal amino group of Asp-Gly; major species at pH 7.3.
gamma-carboxy-L-glutamic acid zwitterion(2-)
A tricarboxylic acid dianion that is obtained from gamma-carboxy-L-glutamic acid by removal of a proton from each of the carboxy groups and protonation of the amino group; the resulting entity has an overall charge of 2-.
1-isothiocyanato-6-(methylsulfanyl)hexane
A isothiocyanate that is hexane in which two of the terminal methyl hydrogens at positions 1 and 6 have been replaced by isothiocyanato and methylsulfanyl groups.
1.2-dihydro-2-oxoduindine-4-carboxylic acid
{"Ingredient_id": "HBIN000795","Ingredient_name": "1.2-dihydro-2-oxoduindine-4-carboxylic acid","Alias": "NA","Ingredient_formula": "C10H7NO3","Ingredient_Smile": "C1=CC=C2C(=C1)C(=CC(=O)N2)C(=O)O","Ingredient_weight": "NA","OB_score": "NA","CAS_id": "NA","SymMap_id": "NA","TCMID_id": "38411","TCMSP_id": "NA","TCM_ID_id": "NA","PubChem_id": "NA","DrugBank_id": "NA"}
1-oxo-1,2-dihydroisoquinoline-4-carboxylic acid
{"Ingredient_id": "HBIN002940","Ingredient_name": "1-oxo-1,2-dihydroisoquinoline-4-carboxylic acid","Alias": "NA","Ingredient_formula": "C10H7NO3","Ingredient_Smile": "C1=CC=C2C(=C1)C(=CNC2=O)C(=O)O","Ingredient_weight": "189.17 g/mol","OB_score": "NA","CAS_id": "NA","SymMap_id": "NA","TCMID_id": "40884","TCMSP_id": "NA","TCM_ID_id": "NA","PubChem_id": "643161","DrugBank_id": "NA"}