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Viquidil Sale

(Synonyms: 维喹地尔,Quinotoxine) 目录号 : GC37912

Viquidil (LM 192) 是一种脑血管扩张剂。

Viquidil Chemical Structure

Cas No.:84-55-9

规格 价格 库存
5mg
¥3,150.00
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10mg
¥4,950.00
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50mg
¥14,850.00
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100mg
¥23,850.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

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.

Chemical Properties

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
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溶解性数据

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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
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Research Update

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.