Arotinolol
(Synonyms: 阿罗洛尔) 目录号 : GC38887
Arotinolol 是一种非选择性的 α/β-肾上腺素受体 (α/β-adrenergic receptor ) 阻滞剂和一种血管扩张性 β-受体阻滞剂。Arotinolol 是一种抗高血压试剂，可用于治疗各种心血管疾病以及非心血管疾病。
Cas No.:68377-92-4
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
Arotinolol is a nonselective α/β-adrenergic receptor blocker and a vasodilating β-blocker. Arotinolol is an antihypertensive agent for the treatment of a variety of cardiovascular pathologies as well as non-cardiovascular diseases[1].
Arotinolol (oral gavage; 200 mg/kg; 8 weeks) can significantly decrease central arterial pressure (CAP) and pulse wave velocity (PWV), in addition, it reduces aortic collagen depositions and finally improves arterial stiffness in SHR mouse[1]. Animal Model: SHR mice[1]
[1]. Zhou W, et al. Mechanisms of improved aortic stiffness by arotinolol in spontaneously hypertensive rats.PLoS One. 2014 Feb 12;9(2):e88722.
| Cas No. | 68377-92-4 | SDF | |
| 别名 | 阿罗洛尔 | ||
| Canonical SMILES | O=C(C1=CC=C(C2=CSC(SCC(O)CNC(C)(C)C)=N2)S1)N | ||
| 分子式 | C15H21N3O2S3 | 分子量 | 371.54 |
| 溶解度 | DMSO: 250 mg/mL (672.88 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 | 2.6915 mL | 13.4575 mL | 26.915 mL |
| 5 mM | 0.5383 mL | 2.6915 mL | 5.383 mL |
| 10 mM | 0.2692 mL | 1.3458 mL | 2.6915 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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。
Effect of Arotinolol on chronic heart failure: A systematic review and meta-analysis of randomized controlled trials
Front Cardiovasc Med 2022 Dec 14;9:1071387.PMID:36588575DOI:10.3389/fcvm.2022.1071387.
Background: Heart failure is the end stage of all cardiovascular diseases, which brings a heavy burden to the global health network. Arotinolol, as a new type of β Receptor blocker, has a good antihypertensive effect. Many clinical trials have observed the clinical efficacy of Arotinolol in the treatment of essential hypertension. However, so far, there has been no systematic evaluation on the efficacy and safety of Arotinolol in the treatment of chronic heart failure. Objective: The purpose of this review was to systematically evaluate the clinical efficacy of Arotinolol in patients with chronic heart failure. Methods: Randomized controlled trials (RCTs) of Arotinolol in the treatment of chronic heart failure were retrieved from seven databases according to the Cochrane manual, including CNKI (China National Knowledge Infrastructure), Wan fang database, VIP database, PubMed, Sinomed, EMBASE, and the Cochrane Library databases. The main outcomes were the effective rate, left ventricular ejection fraction (LVEF), blood pressure, heart rate, cardiac index, stroke volume (SV), brain natriuretic peptide (BNP), hypersensitive C-reactive protein (Hs-CRP), left ventricular end diastolic volume (LVEDV), left ventricular end diastolic diameter (LVEDD), and adverse events (AEs). Results: A total of 17 trials met the qualification criteria, which included 1,717 patients with heart failure. Most trials had uncertain risks in terms of random sequence generation, allocation hiding, patient loss, and result evaluation. Meta analysis showed that Arotinolol significantly improved the treatment efficiency of patients with heart failure (standardized mean difference (SMD) = 4.07, 95% confidence interval (CI) [2.89, 5.72], p = 0.00, I 2 = 0), LVEF (SMD = 1.59, 95% CI [0.99, 2.19], p = 0.000 0, I 2 = 95.8%), cardiac index (SMD = 0.32, 95% CI [0.11, 0.53], p = 0.03), I 2 = 0), SV (SMD = 2.00, 95% CI [1.57, 2.34], p = 0.000, I 2 = 64.2%), lower BNP (SMD = -0.804, 95% CI [-0.97, -0.64], p = 0.000, I 2 = 94.4%), and LVEDV (SMD = -0.25, 95% CI [-0.45, -0.05], p = 0.015, I 2 = 0). There was no statistical significance for blood pressure (SMDsystolic pressure = -0.09, 95% CI [-0.69, 0.51], p = 0.775, I 2 systolic pressure = 90.2%; SMDdiastolic pressure = -0.16, 95% CI [-0.79, 0.48], P = 0.632, I 2 diastolic pressure = 91.2%), heart rate (SMD = -0.12, 95% CI [-1.00, 0.75], P = 0.787, I 2 = 96.1%), Hs-CRP (SMD = -1.52, 95% CI [-3.43, 0.40], P = 0.121, I 2 = 98.3%), and LVEDD (SMD = -0.07, 95% CI [-0.90, 0.76], P = 0.870, I 2 = 96.5%). Conclusion: Arotinolol can safely and effectively improve the effective rate of patients with chronic heart failure, increase LVEF, increase CI and SV, and reduce BNP and LVEDV. However, because of the low overall quality of the included randomized controlled trials, these findings need to be considered carefully. More high-quality randomized controlled trials are needed for further verification, to provide a more scientific basis for the safety and effectiveness of Arotinolol in the clinical treatment of heart failure. Systematic review registration: [https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=371214], identifier [CRD:420223371214].
Enantiospecific determination of Arotinolol in rat plasma by LC-MS/MS: application to a stereoselective pharmacokinetic study
J Pharm Biomed Anal 2015 Jan;102:299-304.PMID:25459927DOI:10.1016/j.jpba.2014.09.034.
A highly sensitive and selective liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed and fully validated for quantification of Arotinolol enantiomers in rat plasma using haloperidol as the internal standard. After solid phase extraction of 50.0 μL rat plasma in 96 well plate, a baseline resolution of Arotinolol enantiomers was achieved on a CHIRALPAK AD-H column using the mobile phase of n-hexane and ethanol in 0.02% diethylamine (20:80, v/v) at a flow rate of 0.550 mL/min within 11.0 min. Acquisition of mass spectrometric data was performed on a triple-quadrupole mass spectrometer in multiple-reaction-monitoring (MRM) mode with an ESI source using the transition m/z 372.1 → 316.1 for (±)-arotinolol and m/z 376.1 → 165.1 for haloperidol. The calibration curves of both enantiomers were linear over the range of 1.00-200.0 ng/mL (r(2)>0.992) and the lower limit of quantification was 1.00 ng/mL. Intra- and inter-day precision ranged from 5.6% to 8.9% for R-(-)-arotinolol and 4.6-7.4% for S-(+)-arotinolol. Accuracy varied from 0.0% to 7.0% for R-(-)-arotinolol and 5.0-10.0% for S-(+)-arotinolol. For R-(-)-arotinolol, the recovery ranged from 87.2% to 99.2% and the matrix factor was 1.03-1.09; for S-(+)-arotinolol, the recovery ranged from 88.0% to 92.4% and the matrix factor was 0.84-0.95, both were not concentration dependent. The method was demonstrated with acceptable accuracy, precision and specificity for the determination of Arotinolol enantiomers and has been successfully applied to a stereoselective pharmacokinetic study.
Mechanisms of improved aortic stiffness by Arotinolol in spontaneously hypertensive rats
PLoS One 2014 Feb 12;9(2):e88722.PMID:24533142DOI:10.1371/journal.pone.0088722.
Objectives: This study investigates the effects on aortic stiffness and vasodilation by Arotinolol and the underlying mechanisms in spontaneously hypertensive rats (SHR). Methods: The vasodilations of rat aortas, renal and mesenteric arteries were evaluated by isometric force recording. Nitric oxide (NO) was measured in human aortic endothelial cells (HAECs) by fluorescent probes. Sixteen-week old SHRs were treated with metoprolol (200 mg·kg-1·d⁻¹), Arotinolol (30 mg·kg-1·d⁻¹) for 8 weeks. Central arterial pressure (CAP) and pulse wave velocity (PWV) were evaluated via catheter pressure transducers. Collagen was assessed by immunohistochemistry and biochemistry assay, while endothelial nitric oxide synthase (eNOS) and eNOS phosphorylation (p-eNOS) of HAECs or aortas were analyzed by western blotting. Results: Arotinolol relaxed vascular rings and the relaxations were attenuated by Nω-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) and the absence of endothelium. Furthermore, arotinolol-induced relaxations were attenuated by 4-aminopyridine (4-AP, Kv channels blocker). Arotinolol produced more nitric oxide compared to metoprolol and increased the expression of p-eNOS in HAECs. These results indicated that arotinolol-induced vasodilation involves endothelium-derived NO and Kv channels. The treatement with Arotinolol in 8 weeks, but not metoprolol, markedly decreased CAP and PWV. Biochemistry assay and immunohistochemistry showed that aortic collagen depositions in the Arotinolol groups were reduced compared with SHRs with metoprolol. Moreover, eNOS phosphorylation was significantly increased in aortinolol-treated SHR compared with SHRs with metoprolol. Conclusions: Arotinolol improves arterial stiffness in SHR, which involved in increasing NO and decreasing collagen contents in large arteries.
Arotinolol is a weak partial agonist on beta 3-adrenergic receptors in brown adipocytes
Can J Physiol Pharmacol 2001 Jul;79(7):585-93.PMID:11478592doi
Arotinolol, a clinically used alpha/beta-adrenergic blocker, has been demonstrated to be an anti-obesity agent. The anti-obesity effect of Arotinolol was suggested to be the result of direct activation of thermogenesis in brown-fat cells. We tested the ability of Arotinolol to stimulate thermogenesis (oxygen consumption) in isolated brown-fat cells and in intact animals. Arotinolol stimulated thermogenesis in brown-fat cells isolated from mouse and hamster. A relatively low sensitivity to the beta-adrenergic antagonist propranolol (pK(B) approximately 6) indicated that Arotinolol interacted with the beta3-adrenergic receptor. On the beta3-receptor, Arotinolol was a very weak (EC50 approximately 20 microM) and only partial (approximately 50%) agonist, but Arotinolol also demonstrated the properties of being a beta3-receptor antagonist with a pK(B) of 5.7. In intact animals, only the antagonistic action of Arotinolol could be observed. Because Arotinolol is only a very weak and partial agonist on the beta3-receptors, direct stimulation of thermogenesis in brown adipose tissue is unlikely to be sufficient to cause significant weight loss. It may be necessary to invoke additional pathways to explain the anti-obesity effects of chronic treatment with Arotinolol.
Effects of Arotinolol, an alpha- and beta-adrenoceptor antagonist, on renin release from rat kidney cortical slices
Clin Exp Pharmacol Physiol 1986 Jun;13(6):505-10.PMID:2428551DOI:10.1111/j.1440-1681.1986.tb00931.x.
The effects of Arotinolol on changes in renin release in rat kidney cortical slices in response to isoproterenol (IP) or norepinephrine (NE), were studied in comparison with those of AC-623, a main metabolite of Arotinolol, and other typical adrenoceptor antagonists. Arotinolol, at concentrations of 10(-8) to 10(-4) mol/l, inhibited the increasing effect of 10(-6) mol/l IP on renin release, in a concentration-dependent manner. Similar results were observed with AC-623, propranolol or labetalol, although the inhibitory potencies of these agents were considerably lower than that of Arotinolol. The blocking effect of Arotinolol on the 10(-5) mol/l NE-induced decrease in renin release was much less potent than seen with other alpha-adrenoceptor blocking agents such as prazosin, phenoxybenzamine and labetalol. These data suggest that the potent blocking effects of Arotinolol and its metabolite on the increased renin release in response to beta-adrenoceptor stimulation may contribute to the antihypertensive effect of this agent.