Atropine methyl bromide
(Synonyms: 甲溴阿托品; Methylatropine bromide) 目录号 : GC35427
A muscarinic acetylcholine receptor antagonist
Cas No.:2870-71-5
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
Methylatropine is an antagonist of muscarinic acetylcholine receptors (IC50 = <0.1 nM in a radioligand binding assay using isolated porcine brain membranes) and a derivative of atropine .1,2 It reduces acetylcholine-induced decreases in blood pressure in rats when administered intravenously with an ED50 value of 5.5 ?g/kg.2 Methylatropine reduces salivation, induces mydriasis, and increases heart rate in dogs.3
1.Schmeller, T., Sporer, F., Sauerwein, M., et al.Binding of tropane alkaloids to nicotinic and muscarinic acetylcholine receptorsPharmazie50(7)493-495(1995) 2.Brezenoff, H.E., Xiao, Y.-F., and Vargas, H.A comparison of the central and peripheral antimuscarinic effects of atropine and methylatropine injected systemically and into the cerebral ventriclesLife Sci.42(8)905-911(1988) 3.Albanus, L.Central and peripheral effects of anticholinergic compoundsActa Pharmacol. Toxicol. (Copenh)28(4)305-326(1970)
| Cas No. | 2870-71-5 | SDF | |
| 别名 | 甲溴阿托品; Methylatropine bromide | ||
| Canonical SMILES | C[N+]1([C@H]2C[C@H](OC(C(C3=CC=CC=C3)CO)=O)C[C@@H]1CC2)C.[Br-] | ||
| 分子式 | C18H26BrNO3 | 分子量 | 384.31 |
| 溶解度 | DMSO: 150 mg/mL (390.31 mM) | 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。 |
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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 | 2.6021 mL | 13.0103 mL | 26.0207 mL |
| 5 mM | 0.5204 mL | 2.6021 mL | 5.2041 mL |
| 10 mM | 0.2602 mL | 1.301 mL | 2.6021 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。
Post-exposure treatment with nasal Atropine methyl bromide protects against microinstillation inhalation exposure to sarin in guinea pigs
Toxicol Appl Pharmacol 2009 Sep 15;239(3):251-7.PMID:19523969DOI:10.1016/j.taap.2009.06.002.
We evaluated the protective efficacy of nasal Atropine methyl bromide (AMB) which does not cross the blood-brain barrier against sarin inhalation exposure. Age and weight matched male guinea pigs were exposed to 846.5 mg/m(3) sarin using a microinstillation inhalation exposure technique for 4 min. The survival rate at this dose was 20%. Post-exposure treatment with nasal AMB (2.5 mg/kg, 1 min) completely protected against sarin induced toxicity (100% survival). Development of muscular tremors was decreased in animals treated with nasal AMB. Post-exposure treatment with nasal AMB also normalized acute decrease in blood oxygen saturation and heart rate following sarin exposure. Inhibition of blood AChE and BChE activities following sarin exposure was reduced in animals treated with nasal AMB, indicating that survival increases the metabolism of sarin or expression of AChE. The body weight loss of animals exposed to sarin and treated with nasal AMB was similar to saline controls. No differences were observed in lung accessory lobe or tracheal edema following exposure to sarin and subsequent treatment with nasal AMB. Total bronchoalveolar lavage fluid (BALF) protein, a biomarker of lung injury, showed trends similar to saline controls. Surfactant levels post-exposure treatment with nasal AMB returned to normal, similar to saline controls. Alkaline phosphatase levels post-exposure treatment with nasal AMB were decreased. Taken together, these data suggest that nasal AMB blocks the copious airway secretion and peripheral cholinergic effects and protects against lethal inhalation exposure to sarin thus increasing survival.
Autonomic and cholinergic mechanisms mediating cardiovascular and temperature effects of donepezil in conscious mice
Am J Physiol Regul Integr Comp Physiol 2021 Jun 1;320(6):R871-R884.PMID:33851543DOI:10.1152/ajpregu.00360.2019.
Donepezil is a centrally acting acetylcholinesterase (AChE) inhibitor with therapeutic potential in inflammatory diseases; however, the underlying autonomic and cholinergic mechanisms remain unclear. Here, we assessed effects of donepezil on mean arterial pressure (MAP), heart rate (HR), HR variability, and body temperature in conscious adult male C57BL/6 mice to investigate the autonomic pathways involved. Central versus peripheral cholinergic effects of donepezil were assessed using pharmacological approaches including comparison with the peripherally acting AChE inhibitor, neostigmine. Drug treatments included donepezil (2.5 or 5 mg/kg sc), neostigmine methyl sulfate (80 or 240 μg/kg ip), atropine sulfate (5 mg/kg ip), Atropine methyl bromide (5 mg/kg ip), or saline. Donepezil, at 2.5 and 5 mg/kg, decreased HR by 36 ± 4% and 44 ± 3% compared with saline (n = 10, P < 0.001). Donepezil, at 2.5 and 5 mg/kg, decreased temperature by 13 ± 2% and 22 ± 2% compared with saline (n = 6, P < 0.001). Modest (P < 0.001) increases in MAP were observed with donepezil after peak bradycardia occurred. Atropine sulfate and Atropine methyl bromide blocked bradycardic responses to donepezil, but only atropine sulfate attenuated hypothermia. The pressor response to donepezil was similar in mice coadministered atropine sulfate; however, coadministration of Atropine methyl bromide potentiated the increase in MAP. Neostigmine did not alter HR or temperature, but did result in early increases in MAP. Despite the marked bradycardia, donepezil did not increase normalized high-frequency HR variability. We conclude that donepezil causes marked bradycardia and hypothermia in conscious mice via the activation of muscarinic receptors while concurrently increasing MAP via autonomic and cholinergic pathways that remain to be elucidated.
Physiological assay of liposome-mediated transport of a drug across Xenopus intestine: cell-liposome interaction
Biochim Biophys Acta 1987 Oct 2;903(2):248-56.PMID:3651461DOI:10.1016/0005-2736(87)90213-6.
(1) The antagonistic effect of Atropine methyl bromide entrapped in liposomes on contraction of Xenopus intestine in vitro induced by acetylcholine was studied. The results provided some insight into cell-liposome interaction. (2) Acetylcholine (0.1 mM) was added to the medium in the bath (serosal solution), while liposomes containing Atropine methyl bromide in their internal and external phases were added on the mucosal side of the intestine. Large multilamellar liposomes were prepared from egg lecithin (phosphatidylcholine, PC) and cholesterol in various molar ratios. Atropine methyl bromide had most effect in liposomes composed of PC and cholesterol in a ratio of 7:3, less in those with a ratio of 4:5, and none in those with a ratio of 9:1. These effects were parallel with the sizes of these liposomes, determined by quasi-elastic light-scattering; that is, the larger the liposomes, the greater was their effect. Addition (to the liposomes) of phosphatidic acid, the negative charge of which increases the distance between the lamellar layers, increased the effect, indicating that Atropine methyl bromide in the space between lamellar layers was effective. Another type of liposomes in which Atropine methyl bromide was present only in the external phase of liposomes was as effective as liposomes in which Atropine methyl bromide was present in both the internal and external phases. (3) From these results the following new model for liposome-mediated stimulation of transport of Atropine methyl bromide is proposed. Large multilamellar liposomes have structural defects in their external lamellae through which Atropine methyl bromide in the mucosal solution can penetrate into the space between the external lamellar layers and move into intestinal cells through regions of fusion between the outermost layers of the liposomes and the cell membrane.
Central muscarinic receptors signal pilocarpine-induced salivation
J Dent Res 2003 Dec;82(12):993-7.PMID:14630901DOI:10.1177/154405910308201211.
Although cholinergic agonists such as pilocarpine injected peripherally can act directly on salivary glands to induce salivation, it is possible that their action in the brain may contribute to salivation. To investigate if the action in the brain is important to salivation, we injected pilocarpine intraperitoneally after blockade of central cholinergic receptors with Atropine methyl bromide (atropine-mb). In male Holtzman rats with stainless steel cannulas implanted into the lateral ventricle and anesthetized with ketamine, atropine-mb (8 and 16 nmol) intracerebroventricularly reduced the salivation induced by pilocarpine (4 micro mol/kg) intraperitoneally (133 + 42 and 108 + 22 mg/7 min, respectively, vs. saline, 463 + 26 mg/7 min), but did not modify peripheral cardiovascular responses to intravenous acetylcholine. Similar doses of atropine-mb intraperitoneally also reduced pilocarpine-induced salivation. Therefore, systemically injected pilocarpine also enters the brain and acts on central muscarinic receptors, activating autonomic efferent fibers to induce salivation.
Pharmacologic evidence for a parasympathetic role in seizure-induced neurocardiac regulatory abnormalities
Epilepsy Behav 2004 Feb;5(1):28-30.PMID:14751203DOI:10.1016/j.yebeh.2003.10.007.
Purpose: We evaluated whether postictal cardiac arrhythmia can be prevented by pharmacologic blockage of peripheral muscarinic receptors in an experimental model of epilepsy in rats. Methods: Rats were prepared for chronic electrocardiograph recording and pretreated with Atropine methyl bromide (2 or 10mg/kg i.p.) or saline prior to exposure to maximal electroshock (MES). The resulting seizure severity and duration of cardiac arrhythmia were measured. Results: Atropine methyl bromide did not significantly affect seizure severity in comparison to control animals but reduced the arrhythmia at a dose of 2mg/kg, and completely suppressed arrhythmia at 10mg/kg. Conclusions: Postictal arrhythmia following MES-induced seizures may be blocked by pretreatment with Atropine methyl bromide, a peripherally acting parasympatholytic agent. Our findings support previous observations that suggest strong participation of the parasympathetic system in postictal arrhythmia. This may be important for clinical suppression of cardiac arrhythmia in persons with uncontrolled epilepsy, who are at risk for sudden unexpected death.