Home>>Signaling Pathways>> GPCR/G protein>> Adrenergic Receptor>>(+)-Penbutolol ((R)-Penbutolol)

(+)-Penbutolol ((R)-Penbutolol) Sale

(Synonyms: (R)-Penbutolol; (+)-Isopenbutolol) 目录号 : GC31597

(+)-Penbutolol ((R)-Penbutolol) 是一种 β-adrenoceptor 拮抗剂,IC50 为 0.74 μM。

(+)-Penbutolol ((R)-Penbutolol) Chemical Structure

Cas No.:38363-41-6

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥1,472.00
现货
5mg
¥1,339.00
现货
10mg
¥2,142.00
现货
50mg
¥6,694.00
现货
100mg
¥10,710.00
现货

电话:400-920-5774 Email: sales@glpbio.cn

Customer Reviews

Based on customer reviews.

Sample solution is provided at 25 µL, 10mM.

产品文档

Quality Control & SDS

View current batch:

产品描述

(+)-Penbutolol is a β-adrenoceptor antagonist, with an IC50 of 0.74 μM[1]. (+)-Penbutolol is an optical isomer of l-penbutolol with Na+ channel-blocking action[2].

(+)-penbutolol on the [Ca2+]i-increase induced by LPC is concentration-dependent[1].(+)-penbutolol inhibits the rounding of cells dose dependently (8±4%, 56±4% and 66±2% at the concentrations of 10-6 M, 5×10-6 M and 10-5 M, respectively)[2].

[1]. Chen M, et al. Effects of beta-adrenoceptor antagonists on Ca(2+)-overload induced by lysophosphatidylcholine in rat isolated cardiomyocytes. Br J Pharmacol. 1996 Jun;118(4):865-70. [2]. Hashizume H, et al. Effects of antiischemic drugs on veratridine-induced hypercontracture in rat cardiac myocytes. Eur J Pharmacol. 1994 Dec 12;271(1):1-8.

Chemical Properties

Cas No. 38363-41-6 SDF
别名 (R)-Penbutolol; (+)-Isopenbutolol
Canonical SMILES O[C@@H](COC1=C(C=CC=C1)C2CCCC2)CNC(C)(C)C
分子式 C18H29NO2 分子量 291.43
溶解度 Soluble in DMSO 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。

溶解性数据

制备储备液
1 mg 5 mg 10 mg
1 mM 3.4314 mL 17.1568 mL 34.3136 mL
5 mM 0.6863 mL 3.4314 mL 6.8627 mL
10 mM 0.3431 mL 1.7157 mL 3.4314 mL
  • 摩尔浓度计算器

  • 稀释计算器

  • 分子量计算器

质量
=
浓度
x
体积
x
分子量
 
 
 
*在配置溶液时,请务必参考产品标签上、MSDS / COA(可在Glpbio的产品页面获得)批次特异的分子量使用本工具。

计算

动物体内配方计算器 (澄清溶液)

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
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

Research Update

Mutagenicity of enantiomers of penbutolol

With a view to examine the effect of chirality and the cause of batch-to-batch variation in the mutagenicity of penbutolol, penbutolol enantiomers - isopenbutolol [R(+)-enantiomer] and penbutolol [S(-)-enantiomer] - and two batches of Betapressin were tested employing the Ames Salmonella tester strain TA98. The mutagenic activity of R(+)-enantiomer was found to be similar to that of a batch of penbutolol with a high content of this optical isomer. The pharmaceutical form of penbutolol, Betapressin, exhibited either less or equal mutagenic effectiveness to the S(-)-enantiomer. In the presence of the S9 mix, the mutagenicity of R(+)-enantiomer was only slightly affected in the low dose range of 40 to 160 micrograms/plate. A metabolite of penbutolol, (RS) l"-dehydropenbutolol, did not cause an increase in the number of revertants/plate.

Absence of genotoxic activity of penbutolol in bacterial and mammalian cell screening systems

The genotoxic potential of the beta-adrenergic blocker penbutolol was assessed using the Ames and HGPRT tests, unscheduled DNA synthesis (UDS) and alkaline elution assays. In the Ames test, penbutolol was tested for cytotoxicity and genotoxic activity in concentration ranges of 0.8-500 micrograms/plate and 0.1-125 micrograms/ml in the HGPRT, UDS and alkaline elution assays. In the Ames test penbutolol showed significant toxicity above 500 micrograms/plate. In the mammalian cells (V79) used for the HGPRT test and A459 cells used for alkaline elution and UDS assays, penbutolol was cytotoxic at concentrations above 30 micrograms/ml. In another series of experiments, male Wistar rats were treated i.p. with penbutolol (1, 10 and 100 mg/kg) and after 2 h liver nuclei were isolated and formation of single DNA-strand breaks was measured. The results of the present study demonstrate the absence of genotoxic activity of penbutolol in the 5 strains of Salmonella typhimurium (TA98, TA100, TA1535, TA1537 and TA1538) and in the strain of Escherichia coli WP2 uvrA in the presence or absence of metabolic activation. In V79 cells, penbutolol showed no mutagenic effects at the HGPRT locus in the presence or absence of metabolic activation. Additionally, no significant incorporation of [3H]thymidine into the DNA in the UDS test or formation of DNA-strand breaks in the alkaline elution assay was detected in the non-toxic concentration range of penbutolol with or without metabolic activation. Furthermore, penbutolol did not cause DNA damage in liver nuclei isolated from penbutolol-treated rats.

Plasma protein binding of penbutolol in pregnancy

Penbutolol is a not cardioselective beta-adrenergic blocking drug; it is lipid soluble and differs in its protein binding from the other members of its group because shows linkage to alpha 1-glycoprotein, with no detectable binding to albumin. AAG levels change during pregnancy and so the binding of [3H]-penbutolol was compared in 11 pregnant patients and in 10 healthy women. Binding was obtained by ultrafiltration and measurement of the free fraction by scintillation spectrometry. The free penbutolol fraction was significantly higher in the pregnant women than in the controls (6.06 +/- 0.34 compared with 3.55 +/- 0.29, P less than 0.001). The AAG levels in the pregnant women were significantly lower (0.40 +/- 0.03 g/l) than in the controls (0.77 +/- 0.06 g/l) (P less than 0.001) which showed a significant correlation with the bound/free penbutolol ratio (r = 0.61, P less than 0.005). On the other hand there was no significant correlation with the extent of penbutolol's protein binding even though the albumin levels were lower in the pregnant women (2.83 +/- 0.17 compared with 4.86 +/- 0.17; P less than 0.001). Penbutolol's nK1a for AAG was lower in pregnant women, and this suggests that the fall in AAG levels is not the only factor involved in the reduced binding of penbutolol in pregnancy.

[Extent of beta-blocking action of S- and R-penbutolol during exercise testing (author's transl)]

The effect of 40 mg penbutolol (pure S-form = laevo penbutolol) and 40 mg isopenbutolol (pure R-form) on heart rate and blood pressure during exercise testing was investigated under double-blind, randomized, placebo-controlled conditions in 9 probands. 1.5 and 5.5 hours after ingestion of 40 mg penbutolol, resting, standing, exercise, and recovery heart rate as well as systolic pressure during exercise displayed a significant decline. Diastolic blood pressure rose slightly 1.5 hours after penbutolol. Isopenbutolol had no significant effect on resting and standing heart rate. 1.5 hours after ingestion, a slight reduction in exercise and recovery heart rate could be confirmed. The decline, however, was significantly lower than that achieved with penbutolol. In comparison with its dextrorotatory isomer, isopenbutolol, penbutolol has an approximately 100-fold more potent effect on exercise heart rate. This is also reflected in the drug's duration of action.

Behavioral effect of beta-blocking drugs resulting from the stimulation or the blockade of serotonergic 5-HT1B receptors

The present study was aimed at determining the relative potency of various beta-blocking drugs as agonists or antagonists at 5-HT1B receptors. The behavioral model used (increase in escape attempts of isolated mice) has been previously shown to be exclusively responsive to 5-HT1B agonists such as 1-3-(trifluoromethyl) phenylpiperazine (TFMPP). Beta-blocking drugs acted in three different ways: they were either inactive, or acted as agonists or as antagonists at 5-HT1B receptors. The specific beta-blocking drugs: atenolol and betaxolol (beta-1) and ICI 118,551 (beta-2) were inactive by themselves and in interaction with TFMPP. The mixed beta-1 beta-2 blocking drug 1-penbutolol, (but not d-penbutolol), inactive alone, behaved as an antagonist: it impaired in a dose-dependent way the effect of TFMPP. (+/-)Pindolol and (-)pindolol was inactive. None of the (-), (+), or (+/-)pindolol was able to impair TFMPP effect. The increase in escape attempts induced by (+/-)pindolol was antagonized with 1-penbutolol or after a specific desensitization. Cyanopindolol and S-tertatolol (but not R-tertatolol) acted as agonists. SDZ 21009 was inactive as agonist or antagonist. It may be concluded that all beta-blocking drugs are not equivalent regarding their effect at 5-HT1B receptors. L-penbutolol was the only drug acting as an antagonist.