Methylatropine (nitrate)
(Synonyms: 甲硝阿托品) 目录号 : GC48661
A muscarinic acetylcholine receptor antagonist
Cas No.:52-88-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- 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 µg/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. | 52-88-0 | SDF | |
| 别名 | 甲硝阿托品 | ||
| Canonical SMILES | C[N+]1([C@H](CC[C@H]1C2)C[C@@H]2OC(C(C3=CC=CC=C3)CO)=O)C.O=[N]([O-])=O | ||
| 分子式 | C18H26NO3•NO3 | 分子量 | 366.4 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | -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 | 2.7293 mL | 13.6463 mL | 27.2926 mL |
| 5 mM | 0.5459 mL | 2.7293 mL | 5.4585 mL |
| 10 mM | 0.2729 mL | 1.3646 mL | 2.7293 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。
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Methylatropine blocks the central effects of cholinergic antagonists
Behav Pharmacol 1994 Apr;5(2):167-175.PMID:11224265DOI:10.1097/00008877-199404000-00008.
These studies were conducted in order to establish the dose dependency and relative peripheral versus central activity of four prototypical cholinergic antagonists on the rodent passive avoidance response, a widely used animal model of retention. Subcutaneous administration of 0.1 to 100mg/kg revealed a potency profile of scopolamine > atropine methylscopolamine >/= Methylatropine for the impairment of passive avoidance responding. A series of neurological assessments of the doses used indicated that side effects alone were not sufficient to impair passive avoidance responding. Although inactive when delivered peripherally, Methylatropine was able to produce retention deficits at 10nmol (3.66µg) when administered intracerebrally. To further evaluate whether systemic Methylatropine could enter the central nervous system, either scopolamine or atropine was administered subcutaneously in mice and rats pretreated with 10-100mg/kg Methylatropine. The deficit-producing effects of scopolamine and atropine were abolished with Methylatropine. Thus Methylatropine is an exclusive peripheral antagonist; its ability to block the deficit-producing effects of scopolamine and atropine may occur through a change in blood-brain barrier permeability or through uncharacterized pharmacokinetic properties.
Intracerebroventricular injection of Methylatropine suppresses insulin response to oral glucose load in rats
J Auton Nerv Syst 1996 Feb 5;57(1-2):43-8.PMID:8867084DOI:10.1016/0165-1838(95)00101-8.
Hepatic glucoreceptor-vagal afferent inputs to the central nervous system and pancreatic vagal efferent stimuli are important for insulin secretion. In the present study, we examined the effect of intracerebroventricular (i.c.v.) injection of atropine methyl bromide (Methylatropine) on the insulin response following glucose ingestion in rats. When rats were injected with Methylatropine i.c.v., the plasma glucose concentration increased, the insulin response reduced, and glucagon-like peptide-1 (7-36) amide (tGLP-1) was unchanged following an oral glucose load, compared with the controls. The plasma insulin response following an intravenous glucose load was not affected by i.c.v. or intraperitoneal injection of Methylatropine. A transient increase in plasma insulin after selective hepatic vagotomy was inhibited by i.c.v. injection of Methylatropine. Arterial blood pressure or pulse rate was not changed by i.c.v. injection of Methylatropine. These results show that the central nervous system plays an important role in the vagal control of the insulin response to glucose ingestion. In rats, for the insulin response soon after glucose ingestion (early phase insulin response), direct neural control (hepatic vagal afferent-central nervous system-pancreatic vagal efferent) of the islet B cells seems more important than the intestinal insulinotropic hormone, tGLP-1.
A comparison of the central and peripheral antimuscarinic effects of atropine and Methylatropine injected systemically and into the cerebral ventricles
Life Sci 1988;42(8):905-11.PMID:3343890DOI:10.1016/0024-3205(88)90389-x.
We compared the relative abilities of atropine sulfate and Methylatropine, injected i.v. and into the cerebral ventricles (icv), to block pharmacological responses mediated through central and peripheral muscarinic receptors. The hypotensive response to i.v. injection of acetylcholine (peripheral muscarinic receptors) was inhibited 50% by i.v. injection of 14.3 nmol (5.5 micrograms)/kg Methylatropine and 147.8n molar equivalents (50 micrograms)/kg atropine sulfate. A similar degree of inhibition followed icv injection of 49.4 nmol/kg Methylatropine and 384.2 nmol equivalents/kg atropine sulfate, indicating significant leakage out of the ventricular space. The pressor response to icv injection of neostigmine (central muscarinic receptors) also was inhibited more effectively by icv Methylatropine than by atropine sulfate. Methylatropine was not effective in blocking central muscarinic receptors when injected i.v.
Spectrophotometric determination of strychnine and Methylatropine by extraction with tetrabromophenolphthalein ethyl ester
Talanta 1973 Feb;20(2):222-4.PMID:18961259DOI:10.1016/0039-9140(73)80271-1.
A new application of monoacidic dyes is reported for the determination of strychnine and Methylatropine. The method is based on solvent extraction into 1,2-dichloroethane of the ion-pair or addition compound formed between tetrabromophenolphthalein ethyl ester and quaternary ammonium salts or alkaloids. The absorbance of the extracts is linearly dependent on the concentration of strychnine or Methylatropine initially present in the aqueous solution.
Effect of intravenous atropine and Methylatropine on heart rate and secretion of saliva in man
Eur J Clin Pharmacol 1975 Apr 4;8(3-4):233-40.PMID:786681DOI:10.1007/BF00567121.
Intravenous atropine sulphate (0.25, 0.40, 0.75 and 1.50 mg), atropine methylnitrate (0.08, 0.13 and 0.25 mg) and saline were given to 72 healthy medical students. The effects on heart rate and rhythm, systolic and diastolic blood pressure and salivary secretion were studied. Salivation was inhibited by all the doses of the two drugs. There was a clear dose-response relationship and Methylatropine was about 3 times as potent as atropine. Heart rate was accelerated by 0.75 and 1.50 mg atropine, and 0.25 mg Methylatropine, whereas 0.25 mg atropine and 0.08 and 0.13 mg Methylatropine induced bradycardia, which was considered to be due to a peripheral action. It is suggested that the drugs act as partial agonists at muscarinic receptors. No clear effect on blood pressure was seen, except for the highest dose of atropine, after which the diastolic pressure was increased. 20 out of 59 subjects who received anticholinergics developed supra-ventricular arrhythmias; with both drugs periods of nodal rhythm were most common. They appeared shortly after the injection and usually lasted for a few minutes.