Prenalterol
(Synonyms: 普瑞特罗) 目录号 : GC64843
Prenalterol 是一种选择性 β1- 肾上腺素能受体激动剂。Prenalterol 对肠道平滑肌收缩活动无影响。Prenalterol 可用于心血管疾病的研究。
Cas No.:57526-81-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Prenalterol is a selective β1-adrenergic receptor agonist. Prenalterol has no effect on gut smooth muscle contractile activity. Prenalterol can be used for researching cardiovascular disease[1].
[1]. Seiler R, et al. alpha- and beta-adrenergic receptor mechanisms in spontaneous contractile activity of rat ileal longitudinal smooth muscle. J Gastrointest Surg. 2005;9(2):227-235.
| Cas No. | 57526-81-5 | SDF | Download SDF |
| 别名 | 普瑞特罗 | ||
| 分子式 | C12H19NO3 | 分子量 | 225.28 |
| 溶解度 | DMSO : 100 mg/mL (443.89 mM; Need ultrasonic) | 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 | 4.4389 mL | 22.1946 mL | 44.3892 mL |
| 5 mM | 0.8878 mL | 4.4389 mL | 8.8778 mL |
| 10 mM | 0.4439 mL | 2.2195 mL | 4.4389 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。
Cardioselectivity of Prenalterol and isoproterenol
Clin Pharmacol Ther 1983 Dec;34(6):749-57.PMID:6641090DOI:10.1038/clpt.1983.245.
We examined the hemodynamic effects and kinetics of Prenalterol, a new beta-adrenoceptor agonist, in 10 normal subjects. There is some doubt whether Prenalterol is selective for beta 1 adrenoceptors in animals; therefore, we also compared its cardioselectivity with that of the nonselective agonist, isoproterenol, with respect to heart rate (HR) and blood pressure (BP) responses after inhibition of cardiovascular reflexes with atropine, clonidine, and phentolamine. After intravenous (2.5 mg) and oral (10 mg and 100 mg) dosing, t 1/2 beta was 2 to 3 hr. Oral bioavailability averaged 33% and was independent of dose. Oral Prenalterol, 10 mg and 100 mg, increased resting HR, systolic BP, and cardiac index by up to 27% but had no significant effects during graded exercise. Prenalterol infusions were calculated to attain steady-state plasma concentrations of 10, 20, and 40 ng/ml. HR and BP effects of the levels (10.8, 23.6, and 47.4 ng/ml) were compared with those of 0.5, 1.5, and 2.5 micrograms isoproterenol. Before autonomic block, Prenalterol increased HR by 10 bpm at the highest dose and mean arterial pressure (MAP) by 10 mm Hg. In contrast, HR rose and MAP fell after isoproterenol. After block, at the highest doses of Prenalterol and isoproterenol, there was an average rise in HR of 42 and 27 bpm; BP was almost maintained after the former but fell by 33 mm Hg after the latter. Prenalterol is an inotropic drug that has the effects of a full cardioselective beta-adrenoceptor agonist. Its inotropic effects are evident at doses that have little effect on HR because of the modifying effect of cardiovascular reflexes. The hemodynamic effects are most obvious at rest when sympathetic tone is low.
Effect of Prenalterol in asthmatic patients
Eur J Clin Pharmacol 1982 Oct;23(4):297-302.PMID:6129142DOI:10.1007/BF00613609.
The bronchial effects of Prenalterol, a selective inotropic beta-adrenoceptor agonist, were examined to see whether beta 1-adrenoceptor stimulation would produce bronchodilatation, or whether beta 2-adrenoceptor blockade could be demonstrated. In a first investigation 8 asthmatic patients were studied under standardized conditions in a double-blind, randomized, crossover comparison between i.v. doses of Prenalterol and saline infusions. After the fourth dose of Prenalterol/saline, 4 intravenous doses of terbutaline were given. All medication was given at 30 min intervals. In a second study in 7 of the previously studied patients, 5 increasing doses of Prenalterol or saline were inhaled from a bird ventilator, and after the last dose 4 i.v. doses of terbutaline were given as before. Prenalterol and saline caused no change in FEV1 during the intravenous study. Terbutaline infusion produced a dose dependent increase in FEV1 which was not significantly altered after Prenalterol treatment. In the inhalation study, in which a much larger dose was applied to the bronchial tree, there was no significant difference in FEV1, between the saline and Prenalterol inhalations. However, Prenalterol did show beta 2-blocking property, as the dose response curve of terbutaline was shifted to the right. The heart rate increased significantly and to the same degree during both the i.v. and inhaled Prenalterol treatments. Thus, this study revealed no significant beta 2-blocking effect of therapeutic doses of i.v. Prenalterol. However, when the drug was inhaled in a much higher dose, a beta 2-blocking effect on FEV1 was recorded. No significant beta 1-adrenoceptor-mediated bronchodilator effect of Prenalterol could be demonstrated.
Are the clinical benefits of oral Prenalterol in ischaemic heart failure due to beta blockade? A six month randomised double blind comparison with placebo
Br Heart J 1985 Feb;53(2):208-15.PMID:2857088DOI:10.1136/hrt.53.2.208.
The clinical effects of the oral beta 1 partial agonist, Prenalterol, were investigated in 37 patients (29 male, eight female; mean age 57 years) with chronic ischaemic left ventricular failure using a placebo controlled randomised double blind protocol over six months. All patients were limited by dyspnoea (New York Heart Association class III) despite treatment with digoxin and diuretics. Twenty eight patients completed the protocol. Moderate clinical improvement was seen in the Prenalterol group, whereas there was little change in the placebo group. Bicycle exercise capacity increased over six months in the Prenalterol and placebo groups but only achieved statistical significance for Prenalterol when compared with baseline values. Maximum exercise heart rate was significantly reduced in the Prenalterol group compared with placebo. Radionuclide left ventricular ejection fraction at rest and during exercise and cardiothoracic ratio showed no significant improvement in either group over six months. Prenalterol was well tolerated and produced no increase in frequency of angina or ventricular arrhythmias. Prenalterol produced clinical benefits and improved exercise tolerance while reducing exercise heart rate. A moderate placebo response was noted. The apparent beta blocking effect of Prenalterol may be as important as the beta 1 agonist effect in producing these benefits. Prenalterol has, however, been withdrawn because of side effects in animals.
Prenalterol, an oral beta-1 adrenoceptor agonist, in the treatment of chronic heart failure
Eur J Clin Pharmacol 1983;25(4):539-45.PMID:6653650DOI:10.1007/BF00542125.
The haemodynamic effects of Prenalterol, a new beta-1 agonist, were studied in 10 patients with chronic heart failure. Following intravenous Prenalterol infusions of 1 mg, 2.5 mg and 5 mg at 15 min intervals, oral slow release Prenalterol 20 mg, 30 mg and 50 mg was given at 2 h intervals and then 50-100 mg bid for one month. There were no significant changes in heart rate or blood pressure. Cardiac output increased significantly from control of 4.4 +/- 0.91/min to a maximum of 5.8 +/- 1.81/min (p less than 0.01) following the 5 mg Prenalterol infusion and this increase was maintained following oral Prenalterol on Days 1 and 2 and at 1 month. Significant increases in stroke volume and stroke work indices and reduction in systemic vascular resistance were also observed. Maximum increases in cardiac output and stroke work index following intravenous Prenalterol correlated significantly with maximum increases observed following oral Prenalterol on Day 2. Non-invasive evaluation showed no change in echocardiographic left ventricular end-diastolic dimension but a significant reduction in left ventricular end-systolic dimension on Day 30. PEP/LVET was significantly reduced from control of 0.56 +/- 0.15 to 0.47 +/- 0.12 (p less than 0.05) on Day 2 and 0.49 +/- 0.09 (p less than 0.05) at 1 month. Treadmill exercise duration was significantly improved for the group at 1 month and no adverse effects were noted. Oral slow release Prenalterol is a potentially useful new drug for patients with chronic heart failure.
High-dose Prenalterol in beta-blockade intoxication
Acta Med Scand 1985;218(5):525-8.PMID:4091050DOI:10.1111/j.0954-6820.1985.tb08884.x.
This study presents a case of beta-blocker intoxication due to massive overdose of metoprolol (7.5 g). Prenalterol in a dose of 420 mg was given as antidote, in combination with epinephrine in intermittent doses. Resuscitation was performed during 4 hours because of mechanical asystole. The patient regained health in 24 hours after further repeated doses of 30 mg Prenalterol. Prenalterol is valuable in the management of toxic doses of beta-blocking drugs, and a titration to extremely high doses of Prenalterol might be necessary.