N-Methylbenzylamine
(Synonyms: N-甲基苄胺) 目录号 : GC61136
N-methylbenzylamine是一种苯基甲基胺化合物。N-methylbenzylamine存在于胡萝卜中，N-methylbenzylamine可作为潜在的生物标记。
Cas No.:103-67-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N-methylbenzylamine is a member of phenylmethylamines. N-methylbenzylamine can be found in carrot, which makes N-methylbenzylamine a potential biomarker for the consumption of these food products[1].
| Cas No. | 103-67-3 | SDF | |
| 别名 | N-甲基苄胺 | ||
| Canonical SMILES | CNCC1=CC=CC=C1 | ||
| 分子式 | C8H11N | 分子量 | 121.18 |
| 溶解度 | 储存条件 | 4°C, protect from light | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 8.2522 mL | 41.2609 mL | 82.5219 mL |
| 5 mM | 1.6504 mL | 8.2522 mL | 16.5044 mL |
| 10 mM | 0.8252 mL | 4.1261 mL | 8.2522 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Metabolism of monoamine oxidase inhibitors
Cell Mol Neurobiol 1999 Jun;19(3):411-26.PMID:10319194DOI:10.1023/a:1006901900106.
1. The principal routes of metabolism of the following monoamine oxidase inhibitors (MAOIs) are described: phenelzine, tranylcypromine, pargyline, deprenyl, moclobemide, and brofaromine. 2. Acetylation of phenelzine appears to be a minor metabolic pathway. Phenelzine is a substrate as well as an inhibitor of MAO, and major identified metabolites of phenelzine include phenylacetic acid and p-hydroxyphenylacetic acid. Phenelzine also elevates brain GABA levels, and as yet unidentified metabolites of phenelzine may be responsible for this effect. beta-Phenylethylamine is a metabolite of phenelzine, and there is indirect evidence that phenelzine may also be ring-hydroxylated and N-methylated. 3. Tranylcypromine is ring-hydroxylated and N-acetylated. There is considerable debate about whether or not it is metabolized to amphetamine, with most of studies in the literature indicating that this does not occur. 4. Pargyline and R(-)-deprenyl, both propargylamines, are N-demethylated and N-depropargylated to yield arylalkylamines (benzylamine, N-Methylbenzylamine, and N-propargylbenzylamine in the case of pargyline and amphetamine, N-methylamphetamine and N-propargylamphetamine in the case of deprenyl). These metabolites may then undergo further metabolism, e.g., hydroxylation. 5. Moclobemide is biotransformed by C- and N-oxidation on the morpholine ring and by aromatic hydroxylation. An active metabolite of brofaromine is formed by O-demethylation. It has been proposed that another as yet unidentified active metabolite may also be formed in vivo. 6. Preliminary results indicate that several of the MAOIs mentioned above are substrates and/or inhibitors of various cytochrome P450 (CYP) enzymes, which may result in pharmacokinetic interactions with some coadministered drugs.
New potential AChE inhibitor candidates
Eur J Med Chem 2009 Sep;44(9):3754-9.PMID:19446931DOI:10.1016/j.ejmech.2009.03.045.
We have theoretically studied new potential candidates of acetylcholinesterase (AChE) inhibitors designed from cardanol, a non-isoprenoid phenolic lipid of cashew Anacardium occidentale nut-shell liquid. The electronic structure calculations of fifteen molecule derivatives from cardanol were performed using B3LYP level with 6-31G, 6-31G(d), and 6-311+G(2d,p) basis functions. For this study we used the following groups: methyl, acetyl, N,N-dimethylcarbamoyl, N,N-dimethylamine, N,N-diethylamine, piperidine, pyrrolidine, and N,N-Methylbenzylamine. Among the proposed compounds we identified that the structures with substitution by N,N-dimethycarbamoyl, N,N-dimethylamine, and pyrrolidine groups were better correlated to rivastigmine, and represent possible AChE inhibitors against Alzheimer disease.
N-sulphoconjugation of alicyclic, alkyl- and aryl-amines in vivo and in vitro
Xenobiotica 1986 Jul;16(7):651-9.PMID:3019024DOI:10.3109/00498258609043555.
Radioactive 35S in 3'-phosphoadenosine 5'-phosphosulphate was incorporated into alicyclic, alkyl- and aryl- amines in the presence of hepatic 105 000 g supernatants of female rats. 4-Phenylpiperazine, 4-phenyl-1,2,3,6-tetrahydropyridine (PTHP), 1,2,3,4-tetrahydroisoquinoline, N-Methylbenzylamine, desmethylzotepine and desmethylzimeldine showed the highest conjugation with 35SO3 among the amines tested. Incorporation of 35SO3 into alicyclic and alkyl-amines was higher at pH 10.0 than at pH 7.4 but the incorporation into arylamines was the opposite. A greater amount of 35SO3 was incorporated into the secondary alkylamines than the corresponding primary amines. Radioactive reaction products were identified as N-sulphoconjugates of amines by comparison on t.l.c. with synthetic authentic compounds. Reaction products of desmethylimipramine (DMI) and PTHP in vitro were isolated as their sulphoconjugates, identified by comparison of field desorption mass spectra, u.v. spectra, retention time on h.p.l.c. and RF values on t.l.c. with synthetic standards. DMI N-sulphonate and PTHP N-sulphonate were detected in the body of female rats treated orally with DMI and PTHP, respectively. These results indicate that N-sulphoconjugation is a common metabolic pathway of alicyclic, alkyl- and aryl-amines in vivo and in vitro.
Reactions of amines with ozone and chlorine: Two novel oxidative methods to evaluate the N-DBP formation potential from dissolved organic nitrogen
Water Res 2021 Nov 13;209:117864.PMID:34847390DOI:10.1016/j.watres.2021.117864.
The composition of oxidant-reactive dissolved organic nitrogen (DON) is poorly characterized, although its ozonation is likely to form a great variety of disinfection by-products containing a nitrogen-oxygen bond (N-DBPs). In this study, two chemical oxidation procedures were developed: continuous ozonation at pH 7.0 and free available chlorine (FAC) titrations at pH 9.2. The formation of two oxidation products (nitrate (NO3-) and chloramines, respectively) was used to quantify and characterize oxidant-reactive nitrogenous moieties in DON. In addition, batch experiments were conducted to study the NO3- yields of 30 selected nitrogenous model compounds upon ozonation. The NO3- yields of 12 primary and secondary amines were highly variable (17-100%, specific ozone dose of 20 molO3/molN), 7 amino acids had high NO3- yields (≥90%), and tertiary amines as well as pyrrole, acetamide and urea had low NO3- yields (≤15%). The mechanisms of NO3- formation were further examined with benzylamine and N-Methylbenzylamine as model compounds. Our results show that nitroalkanes are the last intermediate products before the formation of NO3-, both for primary and secondary amines. The presence of an electron-withdrawing group in the vicinity of the N-atom facilitates the formation of NO3- from nitroalkanes. Therefore, the formation of NO3- is attributed to amino acids and activated primary and secondary amines. In contrast, all primary and secondary amines were transformed to chloramines upon chlorination, which was determined by a novel oxidative titration with chlorine. To further support the selectivity of this assay, it was demonstrated by derivatization of amine moieties that chloramine formation could be inhibited. 13-45% of the DON of 4 dissolved organic matter isolates and 2 wastewater effluents formed NO3- and 0-39% formed chloramines, indicating that the potential for N-DBP formation is high (µMN/mgC-level). From differences in the formation of NO3- and chloramines the nature of the precursors can be hypothesized (e.g., activated or non-activated primary and secondary amines, partially oxidized nitrogenous compounds). This study highlights the capacity of two novel methods to characterize the oxidant-reactive DON fraction. Our results suggest that this fraction is significant and could form a variety of potentially toxic N-DBPs.
N-propargylbenzylamine, a major metabolite of pargyline, is a potent inhibitor of monoamine oxidase type B in rats in vivo: a comparison with deprenyl
Br J Pharmacol 1987 Feb;90(2):335-45.PMID:3103805DOI:10.1111/j.1476-5381.1987.tb08963.x.
In an effort to explore the contribution of the metabolites of pargyline towards the in vivo inhibition of monoamine oxidase (MAO), the effects of pargyline and its major metabolites on the production and metabolism of a number of biogenic amines were studied in rats. The administration of pargyline gave rise to three major ethyl acetate extractable metabolites: benzylamine, N-Methylbenzylamine and N-propargylbenzylamine (NPB). Only NPB demonstrated in vivo monoamine oxidase inhibitory properties at an acute dose of 30 mg kg-1. The acute effects of pargyline, NPB, and deprenyl on urine and brain concentrations of a number of biogenic amines (phenylethylamine (PEA), m- and p-tyramine, noradrenaline (NA), dopamine, and 5-hydroxytryptamine (5-HT) and their metabolites were evaluated. Increased urine and brain concentrations of PEA were considered to represent in vivo inhibition of type B MAO while decreased concentrations of NA and 5-HT metabolites were regarded as indicators of an in vivo inhibition of MAO type A. NPB, like deprenyl and pargyline, significantly increased urine and brain PEA while only pargyline reduced 5-HT metabolism, suggesting that the metabolism of pargyline to NPB may contribute towards the MAO type B inhibitory effects of pargyline in vivo. Since the therapeutic benefits of MAO inhibitors in clinical practice usually require some period of chronic treatment, the chronic effects of repeated 14 daily doses of the above MAO inhibitors on central and peripheral biogenic amines were evaluated at the following times: during treatment, one day and five days after termination of treatment. The biochemical changes observed during the course of chronic NPB, pargyline and deprenyl treatments generally follow the expected in vitro characteristics of these drugs, but the detailed changes observed suggest clear differences. For example, the in vivo effect of pargyline on urine 5-hydroxyindoleacetic acid excretion was considerably weaker than its effect on the excretion of NA and dopamine metabolites. These changes are opposite to the in vitro effects of pargyline on 5-HT, dopamine and NA oxidative deamination. Inhibitions of the metabolism of all the amines studied were clearly observed during chronic MAOI treatments, but these effects were less evident five days after the end of treatment, suggesting an almost normal metabolism of biogenic amines. It is concluded that while MAO inhibitors may be the primary compound responsible for MAO inhibition, the effects of their metabolites in some cases may also play equally important roles in the regulation of monoamines both in the periphery and the brain. Thus, as demonstrated here, NPB was found to be as potent as pargyline and deprenyl with regard to its in vivo MAO type B inhibitory properties.