Exact Mass: 383.0997
Exact Mass Matches: 383.0997
Found 69 metabolites which its exact mass value is equals to given mass value 383.0997
,
within given mass tolerance error 0.01 dalton. Try search metabolite list with more accurate mass tolerance error
0.001 dalton.
Tebipenem
D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D047090 - beta-Lactams D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D007769 - Lactams
Atropine methobromide
D018373 - Peripheral Nervous System Agents > D001337 - Autonomic Agents > D010276 - Parasympatholytics Atropine methyl bromide, a muscarinic receptor (mAChR) antagonist, is a quaternary ammonium salt of atropine and a mydriatic for dilation of the pupil during ophthalmic examination. It is introduced for relieving pyloric spasm in infants for its highly polar nature. It penetrates less readily into the central nervous system than atropine[1][2].
N6-succinyladenosine
Succinyladenosine (SAdo) is one of the dephosphorylated enzyme substrate that accumulates in body fluids of patients with adenylosuccinate lyase (ADSL) deficiency, the other being 5-amino-4-imidazole-N-succinocarboxamide riboside (SAICAr). ADSL is an inherited metabolic disease characterized by various degrees of psychomotor retardation (PMID 15902552). The severity of the clinical presentation correlates with a low S-Ado/SAICAr ratio in body fluids (PMID: 15571235). Normally Succinyladenosine is not found in blood or CSF but may be detected in trace amounts in urine (OMIM 103050). Succinyladenosine is also found to be associated with fumarase deficiency, another inborn error of metabolism. Succinyladenosine (SAdo) is one of the dephosphorylated enzyme substrate that accumulates in body fluids of patients with adenylosuccinate lyase (ADSL) deficiency, the other being 5-amino-4-imidazole-N-succinocarboxamide riboside (SAICAr). ADSL is an inherited metabolic disease characterized by various degrees of psychomotor retardation. (PMID 15902552)
N6-Succinyl Adenosine
N6-Succinyl Adenosine (Succinyl-AMP) is a nucleotide derivative that possesses a unique chemical structure and plays significant roles in various biological processes. Its chemical structure consists of adenosine, a nucleoside composed of the nitrogenous base adenine and ribose sugar, with an additional succinyl group attached to the N6 position of the adenine base. This succinyl group is derived from succinic acid, a four-carbon dicarboxylic acid. The presence of the succinyl group at the N6 position of adenine alters the physicochemical properties of adenosine, influencing its interactions with enzymes and other molecules in the cell. This modification is biologically relevant, as N6-succinyl adenosine is involved in several metabolic pathways and regulatory mechanisms. Biologically, N6-succinyl adenosine is known for its role in the regulation of gene expression. It can serve as a substrate for the formation of N6-threonylcarbamoyladenosine (t6A), a key modification found in the wobble position of certain tRNAs. This modification is critical for the efficiency of translation initiation and the accuracy of decoding the genetic code. Moreover, N6-succinyl adenosine is involved in the transsulfuration pathway, a metabolic route that interconverts sulfur-containing amino acids. It acts as a precursor for the synthesis of cysteine, an essential amino acid that plays a vital role in protein structure and function, as well as in the synthesis of glutathione, a major antioxidant in the cell. Additionally, N6-succinyl adenosine has been implicated in the process of protein succinylation, a novel post-translational modification where the succinyl group is transferred to lysine residues of proteins. This modification can affect protein function, stability, and cellular signaling pathways. 2-({9-[3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-9H-purin-6-yl}amino)butanedioic acid belongs to the class of organic compounds known as purine nucleosides. Purine nucleosides are compounds comprising a purine base attached to a ribosyl or deoxyribosyl moiety. Based on a literature review very few articles have been published on 2-({9-[3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]-9H-purin-6-yl}amino)butanedioic acid. This compound has been identified in human blood as reported by (PMID: 31557052 ). N6-succinyl adenosine is not a naturally occurring metabolite and is only found in those individuals exposed to this compound or its derivatives. Technically N6-Succinyl Adenosine is part of the human exposome. The exposome can be defined as the collection of all the exposures of an individual in a lifetime and how those exposures relate to health. An individual's exposure begins before birth and includes insults from environmental and occupational sources.
Tebipenem
D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D047090 - beta-Lactams D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D007769 - Lactams
Nitidine chloride
Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6]. Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6]. Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6].
Chelerythrine
Chelerythrine chloride is a potent, cell-permeable inhibitor of protein kinase C, with an IC50 of 660 nM. Chelerythrine chloride inhibits the Bcl-XL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax from Bcl-XL. Chelerythrine chloride induces apoptosis and autophagy. Chelerythrine chloride is a potent, cell-permeable inhibitor of protein kinase C, with an IC50 of 660 nM. Chelerythrine chloride inhibits the Bcl-XL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax from Bcl-XL. Chelerythrine chloride induces apoptosis and autophagy.
Nitidine
Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6]. Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6]. Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6].
N-(2,3-Dihydro-1H-indol-1-ylcarbothioyl)-5-(2-phenylethynyl)nicotinamide
13a-hydroxy-9,10-dimethoxy-2,3-(methylenedioxy)-8,13-dioxo-5,6,13,13a-tetrahydro-8H-dibenzoquinolizine|13a-hydroxy-9,10-dimethoxy-5,13a-dihydro-6H-[1,3]dioxolo[4,5-g]isoquino[3,2-a]isoquinoline-8,13-dione|8,13-dioxo-14-hydroxy-2,3-methylenedioxy-9,10-dimethoxytetrahydroprotoberberine|8,13-Dioxo-14-hydroxycanadin|prechilenine
Chelerythrine
Chelerythrine chloride is a potent, cell-permeable inhibitor of protein kinase C, with an IC50 of 660 nM. Chelerythrine chloride inhibits the Bcl-XL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax from Bcl-XL. Chelerythrine chloride induces apoptosis and autophagy. Chelerythrine chloride is a potent, cell-permeable inhibitor of protein kinase C, with an IC50 of 660 nM. Chelerythrine chloride inhibits the Bcl-XL-Bak BH3 peptide binding with IC50 of 1.5 μM and displaces Bax from Bcl-XL. Chelerythrine chloride induces apoptosis and autophagy.
Nitidine
Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6]. Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6]. Nitidine chloride, a potential anti-malarial lead compound derived from Zanthoxylum nitidum (Roxb) DC, exerts potent anticancer activity through diverse pathways, including inducing apoptosis, inhibiting STAT3 signaling cascade, DNA topoisomerase 1 and 2A, ERK and c-Src/FAK associated signaling pathway. Nitidine chloride inhibits LPS-induced inflammatory cytokines production via MAPK and NF-kB pathway[1][2][3][4][5][6].
tert-Butyl 4-(4-bromo-3,5-dimethylphenoxy)piperidine-1-carboxylate
1,3,4,6-TETRA-O-ACETYL-2-AMINO-2-DESOXY-BETA-D-GLUCOPYRANOSE HYDROCHLORIDE
b-D-Glucopyranose,2-amino-2-deoxy-, 1,3,4,6-tetraacetate, hydrochloride (1:1)
Metampicillin sodium
D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D047090 - beta-Lactams D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D010406 - Penicillins D000890 - Anti-Infective Agents > D000900 - Anti-Bacterial Agents > D007769 - Lactams
2-(4-chlorophenoxy)-N-[5-(5,6,7,8-tetrahydronaphthalen-2-yl)-1,3,4-oxadiazol-2-yl]acetamide
1-(chloroacetyl)-3-(1H-indol-3-yl)-5-(4-methoxyphenyl)-4,5-dihydro-1H-pyrazol-4-ol
2-[[3-cyano-6-(2-furanyl)-4-(trifluoromethyl)-2-pyridinyl]thio]-N,N-diethylacetamide
(2S)-2-[[9-[(2S,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]purin-6-yl]amino]butanedioic acid
N-[(2-naphthalen-2-yloxypropanoylamino)carbamothioyl]furan-2-carboxamide
6-Chloro-4-phenyl-3-(1-phenyl-5-tetrazolyl)quinoline
2-[(5,7-dimethyl-[1,2,4]triazolo[1,5-a]pyrimidin-2-yl)sulfanyl]-N-(1,1-dioxothiolan-3-yl)-N-ethylacetamide
5-(1-Phenyl-5-tetrazolyl)-2-pyridin-4-yl-4-thiophen-2-ylpyrimidine
3-Pyridin-2-yl-2-(4-quinolin-4-ylphenyl)-1,3-thiazolidin-4-one
3-[3-[(E)-(2-acetamido-4-oxo-1,3-thiazol-5-ylidene)methyl]-2,5-dimethylpyrrol-1-yl]benzoic acid
6-Bromo-3-methyl-9-[2-(6-methylpyridin-3-yl)ethyl]-1,2,3,4-tetrahydro-gamma-carboline
atropine methyl bromide
D018373 - Peripheral Nervous System Agents > D001337 - Autonomic Agents > D010276 - Parasympatholytics Atropine methyl bromide, a muscarinic receptor (mAChR) antagonist, is a quaternary ammonium salt of atropine and a mydriatic for dilation of the pupil during ophthalmic examination. It is introduced for relieving pyloric spasm in infants for its highly polar nature. It penetrates less readily into the central nervous system than atropine[1][2].
chromopyrrolate(2-)
A dicarboxylic acid dianion obtained by deprotonation of both carboxy groups of chromopyrrolic acid; major microspecies at pH 7.3.
Succinyladenosine
An aspartic acid derivative that is L-aspartic acid in which one of the amine hydrogens is substituted by a 9-beta-D-ribofuranosyl-9H-purin-6-yl group.