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1. Benzylamine Hydrobromide
2. Benzylamine Hydrochloride
3. Benzylamine Monosulfate
1. Phenylmethanamine
2. 100-46-9
3. Benzenemethanamine
4. Monobenzylamine
5. (phenylmethyl)amine
6. Alpha-aminotoluene
7. 1-phenylmethanamine
8. (aminomethyl)benzene
9. N-benzylamine
10. Moringine
11. Phenylmethylamine
12. Sumine 2005
13. 89551-24-6
14. Aminotoluene
15. Benzyl Amine
16. Sumine 2006
17. Omega-aminotoluene
18. .omega.-aminotoluene
19. Benzyl-amine
20. A-aminotoluene
21. 1utj
22. 1utn
23. 2bza
24. Nsc 8046
25. Mfcd00008106
26. .alpha.-aminotoluene
27. Chebi:40538
28. Toluene,alpha-amino
29. Chembl522
30. A1o31ror09
31. Nsc-8046
32. Abn
33. Mfcd00145849
34. Hsdb 2795
35. Einecs 202-854-1
36. Benzylarnine
37. Bezylamine
38. Brn 0741984
39. Unii-a1o31ror09
40. Ai3-15299
41. Aminomethylbenzene
42. N-(phenylmethyl)amine
43. Bnnh2
44. Nh2bn
45. Quadrapure(tm) Bza
46. Bzl-nh2
47. Benzenemethanamine, 9ci
48. Benzylamine [mi]
49. Benzylamine On Polystyrene
50. Benzylamine, Reagent Grade
51. Dsstox_cid_1839
52. Schembl373
53. Benzylamine [hsdb]
54. Epitope Id:141489
55. Ec 202-854-1
56. Quadrapure(tm) Benzylamine
57. Dsstox_rid_76359
58. Nciopen2_007746
59. Dsstox_gsid_21839
60. 4-12-00-02155 (beilstein Handbook Reference)
61. Laquo Omegaraquo -aminotoluene
62. Benzylamine, Analytical Standard
63. Dtxsid5021839
64. Bdbm10999
65. Nsc8046
66. Tetracyclohexylorthosilicate
67. Str00195
68. Zinc6096244
69. Benzylamine, Reagentplus(r), 99%
70. Tox21_300933
71. Mfcd00130502
72. Mfcd00135579
73. Mfcd08561140
74. Stl115534
75. Akos000119096
76. Quadrapure Bza, 400-1100 Micron
77. Db02464
78. Ncgc00166029-01
79. Ncgc00166029-02
80. Ncgc00254835-01
81. Cas-100-46-9
82. Lacosamide Impurity J [ep Impurity]
83. B0406
84. Ft-0622834
85. Ft-0622836
86. Benzylamine, For Gc Derivatization, >=99.0%
87. Benzylamine, Purified By Redistillation, >=99.5%
88. Q424000
89. Brd-k76133116-001-01-2
90. Z54748260
91. F2190-0388
92. 3f830b2a-abaa-4e26-971c-53b1c7485954
93. Aminomethyl Polystyrene (160-200 ?m, 0.8-1.3 Mmol/g)
94. Aminomethyl Polystyrene (rigid, Macroporous 200-400?m, 2-3.5 Mmol/g)
95. Aminomethyl Polystyrene Resin Cross-linked With 1% Dvb (200-400mesh) (2.0-3.0mmol/g)
96. Poly(styrene-divinylbenzene), Aminomethylated, 1% Cross-linked, 100-200 Mesh
97. Quadrapure(r) Bza, 400-1100 Mum, Extent Of Labeling: 20 Mg/g Loading, Macroporous
| Molecular Weight | 107.15 g/mol |
|---|---|
| Molecular Formula | C7H9N |
| XLogP3 | 1.1 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 1 |
| Exact Mass | 107.073499291 g/mol |
| Monoisotopic Mass | 107.073499291 g/mol |
| Topological Polar Surface Area | 26 Ų |
| Heavy Atom Count | 8 |
| Formal Charge | 0 |
| Complexity | 55.4 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Benzylamine is found in Moringa oleifera, a plant used to treat diabetes in traditional medicine.
PMID:20045461 Iffiu-Soltez Z et al; Pharmacol Res 61 (4): 355-63 (2010)
/Experimental Therapy/ Benzylamine/vanadate administration generates peroxovanadium locally in pancreatic islets, which stimulates insulin secretion, and also produces peroxovanadium in adipose tissue, thereby activating glucose metabolism in adipocytes and in neighboring muscle. This opens up the possibility of using the semicarbazide-sensitive amine oxidase (SSAO)/vascular adhesion protein-1 (VAP-1) activity as a local generator of protein tyrosine phosphatase inhibitors in anti-diabetic therapy...
PMID:19246098 Zorzano A et al; J Inorg Biochem 103 (4): 559-66 (2009)
/Experimental Therapy/ ... Benzylamine on its own can improve glucose tolerance in rabbit and mouse, likely by stimulating glucose uptake via amine oxidase activation in insulin-sensitive tissues.
PMID:14978192 Iglesias-Osma MC et al; J Pharmacol Exp Ther 309 (3): 1020-8 (2004)
/Experimental Therapy/ The combination of vanadate plus benzylamine has been reported to stimulate glucose transport in rodent adipocytes and to mimic other insulin actions in diverse studies. However, benzylamine alone activates glucose uptake in human fat cells and increases glucose tolerance in rabbits. The aim of this work was to unravel the benzylamine antihyperglycemic action and to test whether its chronic oral administration could restore the defective glucose handling of mice rendered slightly obese and diabetic by very high-fat diet (VHFD). When VHFD mice were i.p. injected with benzylamine at 0.7 to 700 umol/kg before glucose tolerance test, they exhibited reduced hyperglycemic response without alteration of insulin secretion. Whole body glucose turnover, as assessed by the glucose isotopic dilution technique, was unchanged in mice perfused with benzylamine (total dose of 75 umol/kg). However, their in vivo glycogen synthesis rate was increased. Benzylamine appeared therefore to directly facilitate glucose utilisation in peripheral tissues. When given chronically at 2000 or 4000 micromol/kg/d in drinking water, benzylamine elicited a slight reduction of water consumption but did not change body weight or adiposity and did not modify oxidative stress markers. Benzylamine treatment improved glucose tolerance but failed to normalize the elevated glucose fasting plasma levels of VHFD mice. There was no influence of benzylamine ingestion on lipolytic activity, basal and insulin-stimulated glucose uptake, and on inflammatory adipokine expression in adipocytes. The improvement of glucose tolerance and the lack of adverse effects on adipocyte metabolism, reported here in VHFD mice allow to consider orally given benzylamine as a potential antidiabetic strategy which deserves to be further studied in other diabetic models.
PMID:18457006 Iffiu-Soltesz Z et al; J Physiol biochem 63 (4): 305-15 (2007)
The in vivo and in vitro disposition of benzylamine was investigated in rats. Benzylamine was metabolized to only a small extent by rat liver subcellular fractions. In contrast, it was extensively metabolized in vivo in rats. In vivo studies performed with stable isotope-labeled benzylamine enabled rapid mass spectrometric identification of metabolites present in rat bile and urine. The major metabolite of benzylamine was the hippuric acid formed by glycine conjugation of benzoic acid. LC/MS analysis of bile and urine obtained from rats dosed with 1:1 equimolar mixture of either d(0):d(7)- or d(0):d(2)-benzylamine showed the presence of several glutathione adducts in addition to the hippuric acid metabolite. The presence of various glutathione adducts indicated that benzylamine was metabolized to a number of reactive intermediates. Various metabolic pathways, including those independent of P450, were found to produce these intermediates. A previously undocumented pathway included the formation of a new carbon-nitrogen bond that led to a potentially reactive intermediate, Ar-CH(2)-NH(CO)-X, capable of interacting with various nucleophiles. The origin of this reactive intermediate is postulated to occur via the formation of either a formamide or carbamic acid metabolites. Metabolites which were produced by the reaction of this intermediate, Ar-CH(2)-NH(CO)-X with nucleophiles included S-[benzylcarbamoyl] glutathione, N-acetyl-S-[benzylcarbamoyl]cysteine, S-[benzylcarbamoyl] cysteinylglycine, S-[benzylcarbamoyl] cysteinylglutamate, N-[benzylcarbamoyl] glutamate, and an oxidized glutathione adduct. Bioactivation of amines via this pathway has not been previously described. The oxidative deamination of benzylamine yielding the benzaldehyde was demonstrated to be a precursor to the hippuric acid metabolite and S-benzyl-L-glutathione. The formation of the S-benzyl-L-glutathione conjugate showed that a net displacement of amine from benzylamine had taken place with a subsequent addition of glutathione at the benzylic position. In addition to these novel pathways, a number of other glutathione-derived adducts formed as a result of epoxide formation was characterized. It was demonstrated that benzylamine was converted by rat P450 2A1 and 2E1 to benzamide that was rapidly metabolized to an epoxide. Mechanisms are proposed for the formation of various GSH adducts of benzylamine.
PMID:12230413 Mutlib AE et al; Chem Res Toxicol 15 (9): 1190-207 (2002)
In mammals, benzylamine is metabolized by semicarbazide-sensitive amine oxidase (SSAO) to benzaldehyde and hydrogen peroxide. This latter product has insulin-mimicking action, and is involved in the effects of benzylamine on human adipocytes: stimulation of glucose transport and inhibition of lipolysis.
PMID:20045461 Iffiu-Soltez Z et al; Pharmacol Res 61 (4): 355-63 (2010)
Hippuric acid was excreted after ingestion of benzylamine by humans.
PMID:698137 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1008410 WOOD SG ET AL; BR J IND MED 35 (3): 230-31 (1978)
The activity of monoamine oxidase was studied in the mitochondria fraction of the brain stem of active sleeping, or hibernating ground squirrels. During hibernation, deamination of serotonin and conversion of monoamine oxide serotonin complex decr more than benzylamine deamination and monoamine oxide benzylamine complex conversion.
VOITENKO NN, POPOVA NK; NEIROKHIMIYA 2 (2): 148-55 (1983)
For more Metabolism/Metabolites (Complete) data for Benzylamine (7 total), please visit the HSDB record page.
Glucose, 3-deoxyglucosone (3-DG), and methylglyoxal (MG) oxidatively deaminated benzylamine to benzaldehyde in the presence of Cu(2+) at a physiological pH and temperature but not glyoxal. 3-DG and MG were more effective oxidants than glucose. We have determined the effects of metal ions, pH, oxygen, and radical scavengers on the oxidative deamination. The formation of benzaldehyde was greatest with Cu(2+), and was accelerated at a higher pH and in the presence of oxygen. EDTA, catalase, and dimethyl sulfoxide significantly inhibited the oxidation, suggesting the participation of reactive oxygen species. From these results, we propose a mechanism for the oxidative deamination by the Strecker-type reaction and the reactive oxygen species-mediated oxidation during glycoxidation.
PMID:12628667 Akagawa M et al; Bioorg Med Chem 11 (7)" 1411-7 (2003)
Human semicarbazide-sensitive amine oxidase (SSAO) is a target for novel anti-inflammatory drugs that inhibit enzymatic activity. However, progress in developing such drugs has been hampered by an incomplete understanding of mechanisms involved in substrate turnover. We report here results of a comparative study of human and bovine SSAO enzymes that reveal binding of substrates and other ligands to at least two (human) and up to four (bovine) distinct sites on enzyme monomers. Anaerobic spectroscopy reveals binding of substrates (spermidine and benzylamine) and of an imidazoline site ligand (clonidine) to the reduced active site of bovine SSAO, whereas interactions with oxidized enzyme are evident in kinetic assays and crystallization studies. Radioligand binding experiments with [(3)H]tetraphenylphosphonium, an inhibitor of bovine SSAO that binds to an anionic cavity outside the active site, reveal competition with spermidine, benzylamine, and clonidine, indicating that these ligands also bind to this second anionic region. Kinetic models of bovine SSAO are consistent with one spermidine molecule straddling the active and secondary sites on both oxidized and reduced enzyme, whereas these sites are occupied by two individual molecules of smaller substrates such as benzylamine. Clonidine and other imidazoline site ligands enhance or inhibit activity as a result of differing affinities for both sites on oxidized and reduced enzyme. In contrast, although analyses of kinetic data obtained with human SSAO are also consistent with ligands binding to oxidized and reduced enzyme, ... no apparent requirement for substrate or modulator binding to any secondary site to model enzyme behavior /was observed/.
PMID:17989349 Holt A et al; Mol Pharmacol 73 (2): 525-38 (2008)
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