1-Methylhistamine (hydrochloride)
(Synonyms: 1-甲基组胺二对甲苯磺酸盐) 目录号 : GC41999
A major metabolite of histamine
Cas No.:6481-48-7
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
1-Methylhistamine is a major metabolite of histamine by histamine N-methyltransferase in the pathway of histidine metabolism.[1] It has been used as a biomarker of histaminergic system activity in the brains of Alzheimer’s disease patients as well as those with hypersomnia and other neurological conditions.[2] [3]
Reference:
[1]. Lindell, S.E., and Schayer, R.W. Metabolism of injected [14C] histamine in the kidney of the dog. Br.J.Pharmacol.Chemother. 13(1), 52-53 (1958).
[2]. Motawaj, M., Peoc'h, K., Callebert, J., et al. CSF levels of the histamine metabolite tele-methylhistamine are only slightly decreased in Alzheimer’s disease. J.Alzheimers Dis. 22(3), 861-871 (2010).
[3]. Dauvilliers, Y., Delallée, N., Jaussent, I., et al. Normal cerebrospinal fluid histamine and tele-methylhistamine levels in hypersomnia conditions. Sleep 35(10), 1359-1366 (2016).
| Cas No. | 6481-48-7 | SDF | |
| 别名 | 1-甲基组胺二对甲苯磺酸盐 | ||
| 化学名 | 1-methyl-H-imidazole-4-ethanamine, dihydrochloride | ||
| Canonical SMILES | CN1C=NC(CCN)=C1.Cl.Cl | ||
| 分子式 | C6H11N3•2HCl | 分子量 | 198.1 |
| 溶解度 | 1mg/mL in ethanol, 20mg/mL in DMSO, 62.5 mg/mL in Water (Need ultrasonicr) | 储存条件 | Store at -20°C |
| 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.048 mL | 25.2398 mL | 50.4796 mL |
| 5 mM | 1.0096 mL | 5.048 mL | 10.0959 mL |
| 10 mM | 0.5048 mL | 2.524 mL | 5.048 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。
BF2.649 [1-{3-[3-(4-Chlorophenyl)propoxy]propyl}piperidine, hydrochloride], a nonimidazole inverse agonist/antagonist at the human histamine H3 receptor: Preclinical pharmacology
J Pharmacol Exp Ther 2007 Jan;320(1):365-75.PMID:17005916DOI:10.1124/jpet.106.111039.
Histamine H3 receptor inverse agonists are known to enhance the activity of histaminergic neurons in brain and thereby promote vigilance and cognition. 1-{3-[3-(4-Chlorophenyl)propoxy]propyl}piperidine, hydrochloride (BF2.649) is a novel, potent, and selective nonimidazole inverse agonist at the recombinant human H3 receptor. On the stimulation of guanosine 5'-O-(3-[35S]thio)triphosphate binding to this receptor, BF2.649 behaved as a competitive antagonist with a Ki value of 0.16 nM and as an inverse agonist with an EC50 value of 1.5 nM and an intrinsic activity approximately 50% higher than that of ciproxifan. Its in vitro potency was approximately 6 times lower at the rodent receptor. In mice, the oral bioavailability coefficient, i.e., the ratio of plasma areas under the curve after oral and i.v. administrations, respectively, was 84%. BF2.649 dose dependently enhanced tele-methylhistamine levels in mouse brain, an index of histaminergic neuron activity, with an ED50 value of 1.6 mg/kg p.o., a response that persisted after repeated administrations for 17 days. In rats, the drug enhanced dopamine and acetylcholine levels in microdialysates of the prefrontal cortex. In cats, it markedly enhanced wakefulness at the expense of sleep states and also enhanced fast cortical rhythms of the electroencephalogram, known to be associated with improved vigilance. On the two-trial object recognition test in mice, a promnesiant effect was shown regarding either scopolamine-induced or natural forgetting. These preclinical data suggest that BF2.649 is a valuable drug candidate to be developed in wakefulness or memory deficits and other cognitive disorders.
Histamine turnover in the brain of different mammalian species: implications for neuronal histamine half-life
J Neurochem 1984 Dec;43(6):1544-9.PMID:6491668DOI:10.1111/j.1471-4159.1984.tb06076.x.
The turnover of neuronal histamine (HA) in nine brain regions and the spinal cord of the guinea pig and the mouse was estimated and the values obtained were compared with data previously obtained in rats. The size of the neuronal HA pool was determined from the decrease in HA content, as induced by (S)-alpha-fluoro-methylhistidine (alpha-FMH), a suicide inhibitor of histidine decarboxylase. The ratios of neuronal HA to the total differed with the brain region. Pargyline hydrochloride increased the tele-methylhistamine (t-MH) levels linearly up to 2 h after administration in both the guinea pig and the mouse whole brain. Regional differences in the turnover rate of neuronal HA, calculated from the pargyline-induced accumulation of t-MH, as well as in the size of the neuronal HA pool, were more marked in the mouse than in the guinea pig brain. The hypothalamus showed the highest rate in both species. There was a good correlation between the steady-state t-MH levels and the turnover rate in different brain regions. Neither the elevation of the t-MH levels by pargyline nor the reduction of HA by alpha-FMH was observed in the spinal cord, thereby suggesting that the HA present in this region is of mast cell origin. The half-life of neuronal HA in different brain regions was in the range of 13-38 min for the mouse and 24-37 min for the guinea pig, except for HA from the guinea pig hypothalamus, which had an extraordinarily long value of 87 min. These results suggest that there are species differences in the function of the brain histaminergic system.
Changes in histamine metabolism in the mouse hypothalamus induced by acute administration of ethanol
J Neurochem 1985 Dec;45(6):1880-5.PMID:4056796DOI:10.1111/j.1471-4159.1985.tb10547.x.
The effect of acute ethanol administration on histamine (HA) dynamics was examined in the mouse hypothalamus. The steady-state level of HA did not change after intraperitoneal administration of ethanol (0.5-5 g/kg), whereas the level of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, increased when 3 and 5 g/kg of ethanol was given. Pargyline hydrochloride (80 mg/kg, i.p.) increased the level of t-MH by 72.2% 90 min after the treatment. Ethanol at any dose given did not significantly affect the t-MH level in the pargyline-pretreated mice. Decrease in the t-MH level induced by metoprine (10 mg/kg, i.p.), an inhibitor of HA-N-methyltransferase, was suppressed by ethanol (5 g/kg), thereby suggesting inhibition of the elimination of brain t-MH. Ethanol (5 g/kg) significantly delayed the depletion of HA induced by (S)-alpha-fluoromethylhistidine (50 mg/kg, i.v.), a specific inhibitor of histidine decarboxylase. Therefore, a large dose of ethanol apparently decreases HA turnover in the mouse hypothalamus.
Phencyclidine and the dynamics of mouse brain histamine
J Pharmacol Exp Ther 1985 Dec;235(3):788-92.PMID:4078733doi
The effects of phencyclidine (PCP) on the dynamics of brain histamine (HA) were examined in the mouse brain. PCP (2-10 mg/kg i.p.) dose-dependently elevated the level of tele-methylhistamine (t-MH), a predominant metabolite of brain HA, without altering the HA level. PCP also enhanced the accumulation of t-MH after administration of pargyline hydrochloride (80 mg/kg i.p.). PCP at 5 mg/kg facilitated the HA depletion produced by (S)-alpha-fluoromethylhistidine markedly (50 mg/kg i.v.), a specific inhibitor of histidine decarboxylase. Metoprine (10 mg/kg i.p.), an inhibitor of HA-N-methyltransferase, decreased the t-MH level and increased the HA level. In the metoprine-treated mice, PCP at 10 mg/kg had no significant effect on the t-MH level, whereas it significantly increased the HA level. The increase in the t-MH level after administration of PCP (5 mg/kg) was observed in various brain regions except the pons-medulla oblongata. These results suggest that, in mice, PCP increases the brain HA turn-over possibly by facilitating the release of HA.