Exact Mass: 207.1071
Exact Mass Matches: 207.1071
Found 169 metabolites which its exact mass value is equals to given mass value 207.1071,
within given mass tolerance error 0.01 dalton. Try search metabolite list with more accurate mass tolerance error
0.001 dalton.
Miglitol
Miglitol is an oral anti-diabetic drug that acts by inhibiting the ability of the patient to breakdown complex carbohydrates into glucose. It is primarily used in diabetes mellitus type 2 for establishing greater glycemic control by preventing the digestion of carbohydrates (such as disaccharides, oligosaccharides, and polysaccharides) into monosaccharides which can be absorbed by the body. Miglitol inhibits glycoside hydrolase enzymes called alpha-glucosidases. Since miglitol works by preventing digestion of carbohydrates, it lowers the degree of postprandial hyperglycemia. It must be taken at the start of main meals to have maximal effect. Its effect will depend on the amount of non-monosaccharide carbohydrates in a persons diet. In contrast to acarbose (another alpha-glucosidase inhibitor), miglitol is systemically absorbed; however, it is not metabolized and is excreted by the kidneys. A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BF - Alpha glucosidase inhibitors D007004 - Hypoglycemic Agents > D065089 - Glycoside Hydrolase Inhibitors C471 - Enzyme Inhibitor > C2846 - Glucosidase Inhibitor D004791 - Enzyme Inhibitors
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone
4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (also known as NNK) is a potent tobacco-specific nitrosamine derived from nicotine. It plays a key role in human tobacco-related cancers (PMID:24830349). NNK is found in cured tobacco and is also produced during its burning or combustion in cigarettes. NNK is abundantly present in cigarette smoke (20-280 ng/cigarette). Electronic cigarettes (e-cigarettes) do not convert nicotine to NNK due to their lower operating temperatures. NNK is a procarcinogen. This means it must be activated by cytochrome P450 enzymes (CYP2A6 and CYP2B6) to become a carcinogen (PMID:24830349). NNK can also be activated by myeloperoxidase (MPO) and epoxide hydrolase (EPHX1). All activation processes lead to the formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol from NNK, which is called NNAL (PMID:24830349). NNAL can be detoxified via glucuronidation via glucuronidases. Once NNK is activated to NNAL, this compound initiates a cascade of signalling pathways (for example ERK1/2, NFκB, PI3K/Akt, MAPK, FasL, K-ras), resulting in uncontrolled cellular proliferation and tumorigenesis. NNK is known as a mutagen and can cause point mutations that affect cell growth proliferation and differentiation. NNK also targets the SULT1A1, TGF-beta, and angiotensin II genes. NNK plays a key role in gene silencing, gene modification, and carcinogenesis. NNK has been implicated in tumour promotion by activating nicotinic acetylcholine receptors (nAChRs) and β-adrenergic receptors (β-AdrRs), leading to downstream activation of parallel signal transduction pathways that facilitate tumour progression (PMID:24830349). Antioxidants such as EGCG (from green tea) inhibit lung tumorigenesis by NNK. 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent tobacco-specific nitrosamine in animals. It has been suggested to play a role in human tobacco-related cancers. P450 1A2 catalyzed the formation of keto alcohol and 4-oxo-1-(3-pyridyl)-1-butanone (keto aldehyde) from NNK, with the keto alcohol being the major metabolite. Phenethyl isothiocyanate (PEITC0 is an effective inhibitor of the carcinogenicity or toxicity of chemicals that are activated by P450 1A2.( PMID: 8625495) [HMDB] D009676 - Noxae > D002273 - Carcinogens
2-Amino-6-methyl-4-propyl-[1,2,4]triazolo[1,5-a]pyrimidin-5-one
(1E,3E)-1-(4-Fluorophenyl)-2-methyl-1-penten-3-one oxime
1-(2-Hydroxyethyl)-2-(hydroxymethyl)piperidine-3,4,5-triol
4'-(Nitrosomethylamino)-1-(3-pyridyl)-1-butanone
D009676 - Noxae > D002273 - Carcinogens
(2S)-2-(Diaminomethylideneamino)-3-phenylpropanoic acid
2-amino-3-(2,3-dihydroxypropoxy)-3-methylbutanoic acid
(2R,3R,4R,5S,6R)-2,6-bis(hydroxymethyl)-1-methylpiperidine-3,4,5-triol|N-methyl-alpha-homonojirimycin
2-(1,2-Dihydroxypropyl)-5-(hydroxymethyl)pyrrolidine-3,4-diol
Miglitol
A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BF - Alpha glucosidase inhibitors D007004 - Hypoglycemic Agents > D065089 - Glycoside Hydrolase Inhibitors C471 - Enzyme Inhibitor > C2846 - Glucosidase Inhibitor D004791 - Enzyme Inhibitors
Imidodicarbonimidic diamide, N- (4-methoxyphenyl)-
Methyl N-cyclopentyl-β-alaninate hydrochloride (1:1)
(S)-METHYL 2-AMINO-3-CYCLOPENTYLPROPANOATE HYDROCHLORIDE
1-Cyclopropyl-1-(2-thienyl)-N-cyclobutylmethanamine
ETHYL 3-METHYLPIPERIDINE-3-CARBOXYLATE HYDROCHLORIDE
2-amino-2,3,3-trideuterio-3-(1H-indol-3-yl)propanoic acid
(2,6-Dimethyl-1-piperidinyl)acetic acid hydrochloride (1:1)
6-(DIMETHOXYMETHYL)-3-METHYL-3H-IMIDAZO[4,5-B]PYRIDINE
Hydrazinecarboxamide,2-[1-(4-methoxyphenyl)ethylidene]-
ETHYL 3-METHYLPIPERIDINE-4-CARBOXYLATE HYDROCHLORIDE
trans-methyl 4-aminomethyl-cyclohexanecarboxylate hydrochloride
4-(4-METHYLSULFANYL-PHENYL)-PIPERIDINE HYDROCHLORIDE
6-fluorospiro[3,4-dihydrochromene-2,1-cyclobutane]-4-amine
(S)-(-)-2-Hydrazinyl-2-oxo-N-(1-phenylethyl)acetamide
Tricyclo[3.3.1.13,7]decane, 1-isothiocyanato-3-methyl- (9CI)
Benzenamine, 4-(1-aminocyclopropyl)-N-methyl-2-nitro-
4-PIPERIDINOL, 1-METHYL-, PROPANOATE, HYDROCHLORIDE
Cyclohexanecarboxylic acid, 4-(aminomethyl)-, methyl ester, hydrochloride (1:1)
1-AMINO-CYCLOHEXANECARBOXYLIC ACID ETHYL ESTER HCL
1-isopropyl-piperidine-3-carboxylic acid hydrochloride
ETHYL TRANS-2-AMINO-1-CYCLOHEXANECARBOXYLATE HYDROCHLORIDE
Ethyl cis-2-amino-1-cyclohexanecarboxylate hydrochloride
Guanoxan
C - Cardiovascular system > C02 - Antihypertensives > C02C - Antiadrenergic agents, peripherally acting > C02CC - Guanidine derivatives C78274 - Agent Affecting Cardiovascular System > C270 - Antihypertensive Agent
Ethyl 4-methylpiperidine-4-carboxylate hydrochloride
5-amino-6-methoxy-1,3-dimethyl-1,3-dihydro-2H-benzimidazol-2-one(SALTDATA: 1HCl 1.3H2O)
poly(2-methacrylolyloxyethyltrimethylammonium chloride) macromolecule
1H-Benzimidazole-5,6-diol,2-(dimethylamino)-1-methyl-(9CI)
4H-Pyrido[1,2-a]pyrimidine-3-carboxamide, 6,7,8,9-tetrahydro-6-methyl-4-oxo-
1H,2H,3H,4H-3-Tert-butylpyrro(1,2-D)(1,2,4)triazine-1,4-dione
Rivanicline hemioxalate
Rivanicline hemioxalate (RJR-2403 hemioxalate; (E)-Metanicotine hemioxalate) is a neuronal nicotinic receptor agonist, showing high selectivity for the α4β2 subtype (Ki=26 nM); > 1,000 fold selectivity than α7 receptors(Ki= 3.6 μM). IC50 value: 26 nM [1] Target: α4β2 nAChR in vitro: At concentrations up to 1 mM, Rivanicline does not significantly activate nAChRs in PC12 cells, muscle type nAChRs or muscarinic receptors. Dose-response curves for agonist-induced ileum contraction indicate that Rivanicline is less than one-tenth as potent as nicotine with greatly reduced efficacy. Rivanicline does not antagonize nicotine-stimulated muscle or ganglionic nAChR function (IC50 > 1 mM). Chronic exposure of M10 cells to Rivanicline (10 microM) results in an up-regulation of high-affinity nAChRs phenomenologically similar to that seen with nicotine [1]. in vivo: Rivanicline significantly improved passive avoidance retention after scopolamine-induced amnesia and enhanced both working and reference memory in rats with ibotenic acid lesions of the forebrain cholinergic projection system in an 8-arm radial maze paradigm. By comparison, Rivanicline was 15 to 30-fold less potent than nicotine in decreasing body temperature, respiration, Y-maze rears and crosses and acoustic startle response [2]. Metanicotine was about 5-fold less potent than nicotine in the tail-flick test after s.c administration, but slightly more potent after central administration [3].
