Q0632
Quinapril hydrochloride
≥98% (HPLC), solid
别名:
(3S)-2-[(2S)-2-[[(1S)-1-(Ethoxycarbonyl)-3-phenylpropyl]amino]-1-oxopropyl]-1,2,3,4-tetrahydro-3-isoquinolinecarboxylic acid hydrochloride
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所有图片(1)
About This Item
经验公式（希尔记法）:
C25H30N2O5 · HCl
CAS号:
分子量:
474.98
MDL编号:
UNSPSC代码:
41116107
PubChem化学物质编号:
NACRES:
NA.77
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质量水平
方案
≥98% (HPLC)
表单
solid
颜色
white
溶解性
H2O: >10 mg/mL
储存温度
2-8°C
SMILES字符串
Cl.CCOC(=O)[C@H](CCc1ccccc1)N[C@@H](C)C(=O)N2Cc3ccccc3C[C@H]2C(O)=O
InChI
1S/C25H30N2O5.ClH/c1-3-32-25(31)21(14-13-18-9-5-4-6-10-18)26-17(2)23(28)27-16-20-12-8-7-11-19(20)15-22(27)24(29)30;/h4-12,17,21-22,26H,3,13-16H2,1-2H3,(H,29,30);1H/t17-,21-,22-;/m0./s1
InChI key
IBBLRJGOOANPTQ-JKVLGAQCSA-N
基因信息
human ... ACE(1636)
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应用
Quinapril hydrochloride has been used as an angiotensin-converting enzyme (ACE) inhibitor to study its effects on renal tubular epithelial cell proliferation in human renal tubular epithelial cells. It has also been used as an ACE inhibitor to evaluate its effects on the expression of angiotensin II (AII) in patient-derived Atheroma samples.
生化/生理作用
Quinapril has been studied to exhibit therapeutic effects against hypertension and congestive heart failure.
Quinapril is a short-acting angiotensin converting enzyme (ACE) inhibitor.
警示用语：
Danger
危险声明
危险分类
Repr. 2 - STOT RE 1
储存分类代码
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
法规信息
新产品
D Lyons et al.
European journal of clinical pharmacology, 51(5), 373-378 (1997-01-01)
Different ACE inhibitors can be distinguished in vitro by their affinity for converting enzyme in vascular and other tissues. Quinapril appears to be amongst the more effective inhibitors of vascular tissue ACE in vitro. This study assesses the in vivo
Tomoe Fujita et al.
The Journal of pharmacology and experimental therapeutics, 341(3), 626-633 (2012-03-06)
Indoxyl sulfate (IS) is an organic anion uremic toxin that accumulates in patients with chronic kidney disease (CKD). The aims of this study were to examine the kinetic profiles of IS in humans at a steady state after multiple doses
Marcel Ruzicka et al.
American journal of hypertension, 23(11), 1179-1182 (2010-07-17)
Angiotensin-converting enzyme (ACE) inhibitors differ in their lipophilic/hydrophilic index that determines their tissue bioavailability and affinity to ACE, which may result in major differences in the degree of blockade of cardiac ACE. We evaluated the hypothesis that in patients with
Dinko Susic et al.
American journal of physiology. Heart and circulatory physiology, 298(4), H1177-H1181 (2010-02-02)
This study examined the role of the renin-angiotensin-aldosterone system (RAAS) in mediating cardiovascular and renal damage in spontaneously hypertensive rats (SHR) given salt excess. Since the circulating RAAS is inhibited in this model, it permits examination of the role of
Zalan Nemeth et al.
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 24(12), 3640-3651 (2009-08-12)
Blockade of the renin-angiotensin-aldosterone system (RAAS) does not completely prevent progression of renal disease. Mineralocorticoid receptor blockade provides additional renoprotection over ACE-inhibition monotherapy. We examined the mechanisms underlying superior renoprotection in the subtotal nephrectomy (SNX) model. Sprague-Dawley rats were randomized
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