Alprenolol ((RS)-Alprenolol)
(Synonyms: 阿普洛尔; (RS)-Alprenolol; dl-Alprenolol) 目录号 : GC32905
A non-selective β-AR and 5-HT receptor antagonist
Cas No.:13655-52-2
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: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Alprenolol is a non-selective β-adrenergic receptor (β-AR) antagonist that is also an antagonist of the serotonin (5-HT) receptor subtypes 5-HT1A and 5-HT1B.1,2 It binds to β1-, β2-, and β3-ARs expressed in CHO cells (Kds = 15, 0.91, and 117 nM, respectively, for the human receptors) and to 5-HT1A and 5-HT1B receptors in rat hippocampal and striatal membranes (Kis = 34 and 134 nM, respectively).1,2 In vivo, alprenolol (40 mg/kg, i.v.) completely blocks the hyperactivity response of rats to 2-PCPA and L-tryptophan.3 Alprenolol (10 μg, i.v.) inhibits decreases in heart rate and left ventricular systolic pressure induced by the β2-AR antagonist ICI 118551 in transgenic mice overexpressing the β2-AR.4 It also reduces the level of abnormal prion fibrils (PrPSc) in the brain of mice intracerebrally infected with prion disease to less than 20% of control levels when administered in drinking water at a dose of 50 mg/L.5
1.Baker, J.G.The selectivity of β-adrenoceptor antagonists at the human β1, β2 and β3 adrenoceptorsBr. J. Pharmacol.144(3)317-322(2005) 2.Langlois, M., Brémont, B., Rousselle, D., et al.Structural analysis by the comparative molecular field analysis method of the affinity of β-adrenoreceptor blocking agents for 5-HT1A and 5-HT1B receptorsEur. J. Pharmacol.244(1)77-87(1993) 3.Costain, D.W., and Green, A.R.β-Adrenoceptor antagonists inhibit the behavioural responses of rats to increased brain 5-hydroxytryptamineBr. J. Pharmacol.64(2)193-200(1978) 4.Bond, R.A., Leff, P., Johnson, T.D., et al.Physiological effects of inverse agonists in transgenic mice with myocardial overexpression of the β2-adrenoceptorNature374(6519)272-276(1995) 5.Miyazaki, Y., Ishikawa, T., Kamatari, Y.O., et al.Identification of alprenolol hydrochloride as an anti-prion compound using surface plasmon resonance imagingMol. Neurobiol.(2018)
| Cas No. | 13655-52-2 | SDF | |
| 别名 | 阿普洛尔; (RS)-Alprenolol; dl-Alprenolol | ||
| Canonical SMILES | OC(COC1=CC=CC=C1CC=C)CNC(C)C | ||
| 分子式 | C15H23NO2 | 分子量 | 249.35 |
| 溶解度 | DMSO : ≥ 100 mg/mL (401.04 mM);Water : < 0.1 mg/mL (insoluble) | 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 | 4.0104 mL | 20.0521 mL | 40.1043 mL |
| 5 mM | 0.8021 mL | 4.0104 mL | 8.0209 mL |
| 10 mM | 0.401 mL | 2.0052 mL | 4.0104 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。
Alprenolol-induced thrombocytopenia
Acta Med Scand 1980;207(3):231-3.PMID:7368989DOI:10.1111/j.0954-6820.1980.tb09711.x.
A case of alprenolol-induced thrombocytopenia in a 65-year-old woman is reported. She was admitted to the hospital twice with platelet counts below 10X10(9)/l. The platelet count rapidly returned to normal after discontinuation of Alprenolol. The reason for the thrombocytopenia was increased platelet destruction.
Analysis of the vasodilator action of Alprenolol
Eur J Pharmacol 1978 Feb 1;47(3):341-50.PMID:631185DOI:10.1016/0014-2999(78)90242-x.
The effect of Alprenolol and other beta-adrenoceptor antagonists, including d-isomers, on blood flow in femoral, coronary and mesenteric vascular beds was measured in anesthetized dogs. Under conditions of constant perfusion pressure, intra-arterial injection of beta-adrenoceptor antagonists produced vasodilation. Propranolol and Alprenolol were approximately equipotent in coronary and mesenteric beds but Alprenolol was significantly more potent in the femoral bed. Practolol was virtually inactive in all beds. The vasodilating potency of d-alprenolol and d-propranolol was not significantly different from that of the respective racemic mixtures. The vasodilator response to Alprenolol was not affected by pretreatment with atropine, diphenhydramine or propranolol. In conscious normotensive dogs i.v. injections of d,l- and d-alprenolol produced dose-dependent decreases in blood pressure and increases in heart rate. Under similar conditions, i.v. d,l-propranolol was without effect on either measurement. The results suggest that the hypotensive action of Alprenolol in dogs may derive from its vasodilator activity.
Continuous Alprenolol infusion for control of hypertension in the acute stage of ruptured intracranial aneurysms
Neurol Med Chir (Tokyo) 1991 Jul;31(7):396-400.PMID:1720217DOI:10.2176/nmc.31.396.
The clinical benefits and hemodynamic effects of continuous Alprenolol infusion for control of hypertension in the acute stage of ruptured cerebral aneurysms were investigated. Twenty-five patients manifesting systemic hypertension (greater than 160/100 mmHg) were treated with Alprenolol, a beta-adrenergic antagonist, phentolamine, an alpha-adrenergic antagonist, and trimethaphan camsilate, a ganglionic blocker, given intravenously. All drugs decreased the mean arterial blood pressure significantly. However, Alprenolol decreased the heart rate and cardiac index while phentolamine increased them. Alprenolol also decreased arterial catecholamine and renin activity, but caused no change in central venous pressure, pulmonary capillary wedge pressure, pulmonary vascular resistance, and systemic vascular resistance. The results indicate the usefulness of continuous Alprenolol infusion for the control of acute hypertension in hemorrhagic cerebrovascular disease. The mode of action of Alprenolol is also discussed.
Identification of Alprenolol Hydrochloride as an Anti-prion Compound Using Surface Plasmon Resonance Imaging
Mol Neurobiol 2019 Jan;56(1):367-377.PMID:29704200DOI:10.1007/s12035-018-1088-7.
Prion diseases are transmissible neurodegenerative disorders of humans and animals, which are characterized by the aggregation of abnormal prion protein (PrPSc) in the central nervous system. Although several small compounds that bind to normal PrP (PrPC) have been shown to inhibit structural conversion of the protein, an effective therapy for human prion disease remains to be established. In this study, we screened 1200 existing drugs approved by the US Food and Drug Administration (FDA) for anti-prion activity using surface plasmon resonance imaging (SPRi). Of these drugs, 31 showed strong binding activity to recombinant human PrP, and three of these reduced the accumulation of PrPSc in prion-infected cells. One of the active compounds, Alprenolol hydrochloride, which is used clinically as a β-adrenergic blocker for hypertension, also reduced the accumulation of PrPSc in the brains of prion-infected mice at the middle stage of the disease when the drug was administered orally with their daily water from the day after infection. Docking simulation analysis suggested that Alprenolol hydrochloride fitted into the hotspot within mouse PrPC, which is known as the most fragile structure within the protein. These findings provide evidence that SPRi is useful in identifying effective drug candidates for neurodegenerative diseases caused by abnormal protein aggregation, such as prion diseases.
Labeling of Alprenolol with fluorescent aryl iodide as a reagent based on Mizoroki-Heck coupling reaction
J Chromatogr A 2011 May 20;1218(20):3002-6.PMID:21489541DOI:10.1016/j.chroma.2011.03.030.
A novel fluorescent labeling method for Alprenolol was developed based on Mizoroki-Heck coupling reaction. We designed and synthesized fluorescent aryl iodide, 4-(4,5-diphenyl-1H-imidazol-2-yl)iodobenzene (DIBI) as a labeling reagent. DIBI has a lophine skeleton carrying an iodide atom acting as fluorophore and reactive center, respectively. In order to evaluate the usefulness of DIBI, a high-performance liquid chromatography (HPLC) with fluorescence detection method was developed for the determination of Alprenolol as a model compound of terminal double bond. The fluorescent labeling of Alprenolol with DIBI was achieved in the presence of palladium acetate as a catalyst, and the labeled Alprenolol was detected fluorometrically. In addition, it was found that the fluorescence of DIBI derivative increased and red shifted when compared with that of DIBI. Furthermore, the proposed method could be applied to determine the Alprenolol concentration in rat plasma after administration of Alprenolol without interferences from biological components. The detection limit (S/N=3) for Alprenolol in rat plasma was 0.74 ng/mL (30 fmol on column).