Viquidil
(Synonyms: 维喹地尔,Quinotoxine) 目录号 : GC37912Viquidil (LM 192) 是一种脑血管扩张剂。
Cas No.:84-55-9
Sample solution is provided at 25 µL, 10mM.
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Viquidil (LM 192) is a cerebral vasodilator agent [1].
[1]. Lecrubier C,et al. [Effect of a new cerebral vasodilator agent, viquidil, on the aggregation of blood platelets]. Arzneimittelforschung. 1972 Aug;22(8):1334-6.
Cas No. | 84-55-9 | SDF | |
别名 | 维喹地尔,Quinotoxine | ||
Canonical SMILES | C=C[C@@H](CNCC1)[C@@H]1CCC(C2=CC=NC3=CC=C(OC)C=C23)=O | ||
分子式 | C20H24N2O2 | 分子量 | 324.42 |
溶解度 | DMSO: 125 mg/mL (385.30 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。 |
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1 mg | 5 mg | 10 mg | |
1 mM | 3.0824 mL | 15.4121 mL | 30.8242 mL |
5 mM | 0.6165 mL | 3.0824 mL | 6.1648 mL |
10 mM | 0.3082 mL | 1.5412 mL | 3.0824 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。
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The antithrombotic activity of Viquidil, a cerebral vasodilator
Arzneimittelforschung 1979;29(3):508-11.PMID:582736doi
1-(6-Methoxy-4-quinolyl)-3-(3-vinyl-4-piperidyl)-1-propanone (Viquidil, Desclidium) when administered parenterally was a potent inhibitor of thrombus formation in the microvasculature of the hamster cheek pouch. The drug was active at a minimum dose level of approximately 2.5 X 10(-4) mg/kg and appeared to be more potent than papaverine in the same test system. Papaverine was shown to be toxic at higher dose levels with intermittent vasodilatation and haemorrhage. Viquidil, however, appeared to be approximately twice as potent as papaverine and was apparently without toxic side-effects.
Effects of agents used in the pharmacotherapy of cerebrovascular disease on the oxygen consumption of isolated cerebral mitochondria
J Cereb Blood Flow Metab 1982;2(1):33-40.PMID:7061602DOI:10.1038/jcbfm.1982.4.
A number of drugs used in the pharmacotherapy of cerebral metabolic and vascular disease have been studied for their effects on the respiration of mitochondria isolated from the rat brain. Some of these agents increased the respiratory control ratio by more than 5% from base-line values (at p less than 0.05), namely, aminophylline, dihydroergotoxine, ifenprodil, nicergoline, raubasine, and vincamine. The ability of these agents to increase the efficiency of mitochondrial respiration could be correlated with two other attributes peculiar to these five drugs: their ability to contract cerebrovascular smooth muscle when studied in vitro and their ability to decrease the volume of infarcted brain tissue following experimental occlusion of the middle cerebral artery in the cat. Papaverine and its derivatives (naftidrofuryl, Viquidil, YC-93) decreased respiratory control, an effect that might correlate with their capacity to effect a vasodilatation of the cerebral vessels and their inefficacy in models of acute cerebral infarction. There is a considerable body of evidence suggesting that one of the earliest and most fundamental perturbations of cerebral ischaemia is a loss of respiratory control. Ifenprodil, vincamine, and some related "anti-ischaemic" compounds are capable of increasing respiratory control in normal cerebral mitochondria, and this capacity might well help to explain their therapeutic potential in cerebrovascular disorders in which energy supply to the brain is limited.
Influence of hypercapnia on the cerebrovascular activities of some drugs used in the treatment of cerebral ischemia
Arzneimittelforschung 1977;27(8):1566-9.PMID:578747doi
The effects of twelve substances on local cerebral blood flow (LCBF) were studied in the normocapnic and hypercapnic conscious rabbit. In normocapnia, an increase in LCBF was observed after naftidrofuryl (NAF), cinnarizine (CI), Viquidil (VI) and heptaminol acefyllinate (HA). The LCBF was only slightly increased or unchanged after hydrogenated ergot alkaloids (HEA), cyclandelate (CY), hexobendine (HE), ifenprodil (IF), piridoxilate (PI), vincamine (VC) and xantinol niacate (XN). It was reduced by theophylline (TH). In hypercapnia, a more pronounced increase in LCBF than in normocapnia was seen with CY, HE, NAF, and VI and a decrease or lesser effect with HA, IF, VC and XN. The decrease in LCBF with TH was enhanced by hypercapnia. The effects of CI, HEA and PI were not modified. The therapeutic implication of these modifications of drug effects by hypercapnia, is discussed.