Merck
CN
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文件

R6152

Sigma-Aldrich

雷诺嗪 二盐酸盐

≥98% (HPLC), powder

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别名:
(±)-4- [2-羟基-3-（邻甲氧基苯氧基）丙基]-1-哌嗪乙酰-2′,6'-二甲苯胺 二盐酸盐, N-（2,6-二甲基苯基）-4-[2-羟基-3-（2-甲氧基苯氧基）丙基]-1-哌嗪乙酰胺 二盐酸盐
经验公式（希尔记法）:
C24H33N3O4 · 2HCl
CAS号:
95635-56-6
分子量:
500.46
MDL编号:
MFCD03788770
PubChem化学物质编号:
24278795
NACRES:
NA.77

质量水平

100

检测方案

≥98% (HPLC)

形式

powder

储存条件

desiccated

颜色

white to beige

mp

222-229.5 °C (lit.)

溶解性

H2O: soluble ≥10 mg/mL

创始人

Gilead

SMILES字符串

Cl.Cl.COc1ccccc1OCC(O)CN2CCN(CC2)CC(=O)Nc3c(C)cccc3C

InChI

1S/C24H33N3O4.2ClH/c1-18-7-6-8-19(2)24(18)25-23(29)16-27-13-11-26(12-14-27)15-20(28)17-31-22-10-5-4-9-21(22)30-3;;/h4-10,20,28H,11-17H2,1-3H3,(H,25,29);2*1H

InChI key

RJNSNFZXAZXOFX-UHFFFAOYSA-N

基因信息

human ... SCN4A(6329) , SCN5A(6331)

应用

盐酸雷诺嗪已被用作：
  • 低尖端扭转(TdP)风险药物，以研究其对犬心血管模型QTc延长、心电图（PR和QRS）间期的影响
  • 部分脂肪酸氧化(FAO)抑制剂，以研究其对胶质母细胞瘤细胞的作用
  • 晚期钠(Na+)-电流抑制剂，以研究其对兔心房性心动过速的影响。

生化/生理作用

雷诺嗪是抗局部缺血哌嗪的衍生物，可作为钠(Na+)-电流抑制剂。它具有治疗舒张性心力衰竭和改善心肌舒张功能的潜力。
pFOX（部分脂肪酸氧化）抑制剂是一类新型的抗心绞痛药物，可抑制脂肪酸β-氧化并激活丙酮酸脱氢酶，从而使心脏的能量从脂质转移到葡萄糖，氧气消耗更少，并有助于在缺血时维持心肌功能。

特点和优势

该化合物由Gilead开发。要浏览其他药物开发化合物和批准的药物/候选药物列表，单击此处。

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)

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G-T Wang et al.
European review for medical and pharmacological sciences, 23(21), 9625-9632 (2019-11-28)
To investigate the effects of ranolazine on the cardiac function and myocardial apoptosis in rats with heart failure and its possible mechanisms. Thirty Wistar rats were randomly divided into sham operation (negative control; NC), chronic heart failure (CHF), and ranolazine
Isaac Aidonidis et al.
The Journal of innovations in cardiac rhythm management, 12(3), 4421-4427 (2021-03-30)
Ranolazine (RAN) has previously been shown to lower the onset of cholinergic atrial fibrillation in intact animals; however, its efficacy in the setting of atrial tachycardia (AT) is unknown. The purpose of this study was to investigate the effects of
Leigh D Plant et al.
Cell reports, 30(7), 2225-2236 (2020-02-23)
Acute cardiac hypoxia produces life-threatening elevations in late sodium current (ILATE) in the human heart. Here, we show the underlying mechanism: hypoxia induces rapid SUMOylation of NaV1.5 channels so they reopen when normally inactive, late in the action potential. NaV1.5
Chung-Chuan Chou et al.
Scientific reports, 10(1), 20032-20032 (2020-11-20)
Studies have demonstrated that diabetic (db/db) mice have increased susceptibility to myocardial ischemia-reperfusion (IR) injury and ventricular tachyarrhythmias (VA). We aimed to investigate the antiarrhythmic and molecular mechanisms of ranolazine in db/db mouse hearts with acute IR injury. Ranolazine was
Irene Del-Canto et al.
Frontiers in physiology, 11, 922-922 (2020-08-28)
Mechanical stretch increases Na+ inflow into myocytes, related to mechanisms including stretch-activated channels or Na+/H+ exchanger activation, involving Ca2+ increase that leads to changes in electrophysiological properties favoring arrhythmia induction. Ranolazine is an antianginal drug with confirmed beneficial effects against
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