Mioflazine
(Synonyms: 米氟嗪) 目录号 : GC36614
Mioflazine 是具有口服活性的、核苷转运的抑制剂，可用于睡眠障碍的治疗。Mioflazine 抑制核苷摄取。
Cas No.:79467-23-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Mioflazine is an orally active nucleoside transport inhibitor, can be used to treat sleep disorders. Mioflazine inhibits nucleoside uptake[1][2].
[1]. Wauquier A, et al. Sleep improvement in dogs after oral administration of mioflazine, a nucleoside transport inhibitor. Psychopharmacology (Berl). 1987;91(4):434-9. [2]. Pirovano IM, et al. Inhibition of nucleoside uptake in human erythrocytes by a new series of compounds related to lidoflazine and mioflazine. Eur J Pharmacol. 1990 Dec 15;189(6):419-22.
| Cas No. | 79467-23-5 | SDF | |
| 别名 | 米氟嗪 | ||
| Canonical SMILES | O=C(NC1=C(Cl)C=CC=C1Cl)CN2CC(C(N)=O)N(CCCC(C3=CC=C(F)C=C3)C4=CC=C(F)C=C4)CC2 | ||
| 分子式 | C29H30Cl2F2N4O2 | 分子量 | 575.48 |
| 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。 |
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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。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.7377 mL | 8.6884 mL | 17.3768 mL |
| 5 mM | 0.3475 mL | 1.7377 mL | 3.4754 mL |
| 10 mM | 0.1738 mL | 0.8688 mL | 1.7377 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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Potencies of Mioflazine and its derivatives as inhibitors of adenosine transport in isolated erythrocytes from different species
J Pharm Pharmacol 1990 May;42(5):367-9.PMID:1976791DOI:10.1111/j.2042-7158.1990.tb05432.x.
The potency of Mioflazine and related drugs (Janssen Pharmaceutica, Belgium) as inhibitors of adenosine transport in isolated erythrocytes from several species were measured and compared with those of dilazep and 6-(4-nitrobenzylmercapto)purine ribonucleoside (NBMPR). [8-3H]Adenosine was used as the permeant at 1 microM and incubation times were 10 s, and assays were conducted in the presence and absence of varying doses of potential transport inhibitors. The species investigated included mouse, hamster, rabbit, baboon and man. Dilazep was the most potent compound throughout with an IC50 of about 2 nM. In the mouse and hamster Mioflazine and its derivatives were considerably less potent (IC50 values greater than 200 nM) with the exception of R57974 with IC50 values of about 150 and 60 nM in mouse and hamster, respectively. In the man and baboon the derivatives had IC50 values in the same order of magnitude as NBMPR (less than 100 nM), and in the rabbit they had potencies close to that of NBMPR, ranging between 10-60 nM. Nucleoside transport inhibitors are of potential importance as host protectors during treatment of parasitic infections with cytotoxic nucleosides. Present data indicate that Mioflazine and its derivatives are not very potent in some of the preferred animal models for parasitic infections (mouse, hamster) but are more effective in primates such as man and baboon.
The influence of nifedipine and Mioflazine on mitochondrial calcium overload in normoxic and ischaemic guinea-pig hearts
Eur J Pharmacol 1990 Mar 13;178(1):71-8.PMID:2332029DOI:10.1016/0014-2999(90)94794-x.
The influence of nifedipine (20 nM) and Mioflazine (300 nM), i.e. concentrations inducing a 60-70% recovery of cardiac function during reperfusion of globally ischaemic guinea-pig working hearts, on the mitochondrial calcium content was investigated in normoxic, globally ischaemic and reperfused globally ischaemic guinea-pig working hearts. Mitochondrial calcium was determined electronmicroscopically with oxalate-pyroantimonate method. In normoxic hearts both nifedipine and Mioflazine reduced the mitochondrial calcium content. Global ischaemia for 45 min and subsequent reperfusion for 25 min resulted in a pronounced mitochondrial calcium overload and damage to the cellular structure. In ischaemic and in reperfusion hearts the drugs maintained mitochondrial calcium at pre-ischaemic levels and decreased the damage to the cellular structure.
Influence of Mioflazine on canine coronary blood flow and on adenine nucleotide and nucleoside content under normal and ischemic conditions
J Cardiovasc Pharmacol 1987 Aug;10(2):213-21.PMID:2441173DOI:10.1097/00005344-198708000-00012.
Intravenous injection of Mioflazine, a nucleoside transport antagonist, caused maximal coronary vasodilation in canine hearts. This was completely reversed by intravenous injection of the enzyme adenosine deaminase. Coronary vasodilation was induced again by the adenosine deaminase inhibitor EHNA [Erythro-9(2-hydroxy-3-nonyl)adenine]; however, without previous injection of Mioflazine, EHNA did not produce coronary vasodilation. Mioflazine-induced coronary vasodilation was antagonized by theophylline, but it was not associated with increased plasma levels of adenosine. Under the influence of Mioflazine, ischemic myocardium contained adenosine and inosine at a ratio of 65:30, which is the reverse of the control ratio. Total nucleoside content following Mioflazine showed reduced nucleoside losses as compared with control. A significant amount of the accumulated adenosine is extracellular since it was accessible to exogenous adenosine deaminase. Reperfusion of ischemic myocardium did not result in increased rates of adenosine phosphorylation, another indicator of its extracellular accumulation. The data are best explained by assuming release of adenosine by Mioflazine in addition to its known effect of inhibiting nucleoside transport. The adenosine release occurs most probably into the interstitial space where it occupies smooth muscle adenosine receptors. The existence of nonsymmetric transport (uptake is more inhibited than release) is postulated for the myocyte, as well as for the endothelial cell plasma membrane.
Mioflazine, a potentially protective drug against ischaemic damage: a study in dogs
Eur Heart J 1985 Aug;6(8):695-701.PMID:4054139DOI:10.1093/oxfordjournals.eurheartj.a061922.
The protective effect of intravenous Mioflazine pretreatment was examined in intact dogs on cardiopulmonary bypass. The mechanical function of the left ventricle was measured by isovolumic pressure-volume relationships. Mioflazine alone had no inotropic effect. After one hour of normothermic (37 degrees C) global ischaemia of the whole heart, no control hearts, pretreated with solvent, recovered sufficiently to support the animal's circulation; this was not the case with animals pretreated with Mioflazine, they all survived. After the 30-min reperfusion period, the solvent (control) pretreated hearts had a significantly lower (P = 0.05) systolic and higher (P = 0.001) diastolic pressure-volume curve than those given Mioflazine.
Prevention of the "no reflow" phenomenon in the canine heart by Mioflazine
Basic Res Cardiol 1985 Jan-Feb;80(1):27-36.PMID:3985924DOI:10.1007/BF01906741.
The effects of oral pretreatment with Mioflazine (2.5 mg X kg-1) on regional myocardial reflow, infarct size reduction and hemodynamic recovery were studied in 24 anesthetized open-chest dogs undergoing 90 minutes of acute left anterior descending coronary artery (LAD) occlusion followed by 150 minutes of reperfusion. Regional myocardial blood flow was measured with tracer microspheres, and infarct size was determined by triphenyl tetrazolium chloride staining. Pretreatment with Mioflazine resulted in a reduced diastolic aortic pressure (p less than 0.05) and an elevated cardiac output and LV dpdt max (p less than 0.05). These effects persisted throughout the experiment. In control animals (n = 12) a hyperemic reflow response was found in the perfusion area of the LAD during the first minutes of reperfusion. After 150 min of reperfusion, however, the viable myocardium of the LAD area became underperfused, and almost no reflow was found in the infarcted zones. In the animals pretreated with Mioflazine (n = 12) the hyperemic response persisted throughout the reperfusion phase and the no-reflow phenomenon was prevented. Infarct size (expressed as percentage of perfusion area) tended to be smaller in this group: 23.7 +/- 12.4% versus 33.7 +/- 19.2% (p greater than 0.05). Left atrial pressure increased during LAD occlusion in both groups but normalized completely in the drug-pretreated animals (p less than 0.05). It is concluded that pretreatment with Mioflazine prevents the no-reflow phenomenon after reperfusion of an evolving infarction, tends to reduce infarct size and improves hemodynamic recovery.