Soluflazine
目录号 : GC37663
Soluflazine 是一种具有抗惊厥作用的核苷转运 (nucleoside transport) 抑制剂。Soluflazine 可用作抗癫痫药。
Cas No.:112415-83-5
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
Soluflazine is a nucleoside transport inhibitor with anticonvulsant action. Soluflazine can be used as an antiepileptic agent[1].
[1]. Ashton D, et al. Anticonvulsant action of the nucleoside transport inhibitor, soluflazine, on synaptic and non-synaptic epileptogenesis in the guinea-pig hippocampus. Epilepsy Res. 1988 Mar-Apr;2(2):65-71.
| Cas No. | 112415-83-5 | SDF | |
| Canonical SMILES | O=C(NC1=C(Cl)C=CC=C1Cl)CN2CC(C(N)=O)N(CCCC(C3=CC=C(F)C=C3)C4=CC=CN=C4)CC2.[H]Cl.[H]Cl | ||
| 分子式 | C28H32Cl4FN5O2 | 分子量 | 631.4 |
| 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。 | ||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5838 mL | 7.9189 mL | 15.8378 mL |
| 5 mM | 0.3168 mL | 1.5838 mL | 3.1676 mL |
| 10 mM | 0.1584 mL | 0.7919 mL | 1.5838 mL |
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| 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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Anticonvulsant action of the nucleoside transport inhibitor, Soluflazine, on synaptic and non-synaptic epileptogenesis in the guinea-pig hippocampus
Epilepsy Res 1988 Mar-Apr;2(2):65-71.PMID:3197688DOI:10.1016/0920-1211(88)90021-6.
The effects of the nucleoside transport inhibitor, Soluflazine, were examined on synaptic and non-synaptic epileptogenesis, and on paired-pulse facilitation and inhibition in the CA1 region of the guinea-pig hippocampal slice. In the model of synaptic epileptogenesis, excitation was enhanced by omitting Mg2+ from the artificial cerebrospinal fluid (ACSF). This procedure induced a second epileptogenic population spike (PS) after orthodromic stimulation, which was inhibited by Soluflazine (IC50 value 1.2 x 10(-6) M). In the non-synaptic model of epileptogenesis spontaneous depolarizing 'burst' discharges were induced in CA1 by lowering the concentration of Ca2+ and increasing the concentration of K+ and Mg2+. The IC50 value of Soluflazine was 6.0 x 10(-7) M for antagonizing 'burst' frequency and 7.5 x 10(-6) M for 'burst' amplitude, indicating a preferential effect on 'burst' initiation. After paired orthodromic stimuli to stratum radiatum, the amount of synaptic facilitation of PS amplitude was significantly increased by Soluflazine. This was mainly due to a decrease in the size of the PS induced by the conditioning pulse. The amount of PS inhibition after antidromic/orthodromic stimulation was not significantly altered by Soluflazine. With the exception of the failure of Soluflazine to attenuate inhibition, the results obtained with Soluflazine resemble those reported for adenosine. This strengthens the hypothesis that Soluflazine increases the extracellular concentration of adenosine. Further, the results indicate that centrally active nucleoside transport inhibitors may be a new class of antiepileptic drug.
The effect of Soluflazine on sleep in rats
Neuropharmacology 1991 Jun;30(6):671-4.PMID:1922685DOI:10.1016/0028-3908(91)90089-t.
Soluflazine, a specific adenosine transport inhibitor, was intracerebroventricularly administered to rats in a dose range of 10, 25, and 50 nmoles. At a dose of 50 nmoles, Soluflazine decreased waking and increased sleep during the first hour of EEG recording. Our previous work has shown that chronic intracerebroventricular administration of Soluflazine to rats decreased radioligand binding to adenosine A1 and A2 receptors in specific brain regions. The present data show that administration of an adenosine transport inhibitor to rats produces a transient hypnotic effect presumably through increases in synaptic adenosine levels.
Effects of dipyridamole, Soluflazine and related molecules on adenosine uptake and metabolism by isolated human red blood cells
Fundam Clin Pharmacol 1994;8(5):446-52.PMID:7875639DOI:10.1111/j.1472-8206.1994.tb00824.x.
The suggestion that adenosine may have beneficial effects on post reperfusion survival following cardiac ischaemia has led to the search for agents which increase the concentration of this substance in the ischemic region as a possible therapeutic approach to the treatment of angina and myocardial infarction. In the present study, dipyridamole, Soluflazine and lidoflazine, known inhibitors of the nucleotide exchange system, have been shown using an HPLC method to prevent the decrease in the concentration od added adenosine outside human red blood cells in vitro. However, the results suggest that this effect was due to inhibition of adenosine deaminase rather than inhibition of nucleotide exchange as had previously been suggested. The selective inhibitor of adenosine deaminase erythro-9-(2-hydroxy-3-nonyl adenosine) exhibited the same profile of activity in the human red blood cell assay. pIC50 values for the four compounds named above were found to be 6.80 +/- 0.09, 6.95 +/- .03, 6.10 +/- 0.14 and 7.39 +/- 0.05 vs adenosine disapearance observed in the extracellular incubation medium respectively. Thus, as the disappearance of adenosine outside the cells was not due to its uptake but to its catabolism, this in vitro method does not appear to be predictive for the ability of compounds to act on adenosine uptake into cardiac myocytes. Any antiischemic action of these agents is more readily explained by an inhibition of the catabolism of adenosine and not by the inhibition of its transport across the membrane of cardiac myocytes.
The nucleoside-transport inhibitor Soluflazine (R 64 719) increases the effects of adenosine in the guinea-pig hippocampal slice and is antagonized by adenosine deaminase
Eur J Pharmacol 1987 Oct 27;142(3):403-8.PMID:3428353DOI:10.1016/0014-2999(87)90079-3.
Field EPSP slope and population spike (PS) amplitude were measured in the CA1 pyramidal cell region after double-pulse stimulation of the striatum radiatum in hippocampal slices of guinea-pig. Iontophoresis of adenosine reduced the EPSP slope to 77.9 +/- 5.0% (mean +/- S.E.M.) and PS amplitude to 32.9 +/- 9.7% of the control values. Recovery was 98.7 +/- 3% for the EPSP and 82.9 +/- 7.0% for the PS 1.5 min after iontophoresis was stopped. In the presence of Soluflazine 10(-6) M the effects of adenosine iontophoresis on the PS amplitude were significantly increased and the recovery of the EPSP and PS was significantly delayed. Soluflazine perfusion alone gradually decreased EPSP slope and PS amplitude as with adenosine. The reductions in EPSP slope and PS amplitude produced by Soluflazine were antagonized by adenosine deaminase. An increase in EPSP slope and PS amplitude was seen when adenosine deaminase was given first. This increase was not reduced by exposure to Soluflazine. These results are compatible with the hypothesis that Soluflazine acts as a nucleoside transport inhibitor in the CNS, where it may increase the extracellular concentration of adenosine.
The effect of Soluflazine on adenosine receptors in the rat brain
Neuropharmacology 1991 Jan;30(1):93-5.PMID:2046882DOI:10.1016/0028-3908(91)90048-g.
Soluflazine, a potent adenosine transport inhibitor, was intracerebroventricularly administered to rats via ALZET mini osmotic pumps (4nmole, 0.5 L/hr) for 14 days and the effect on adenosine receptors was determined in specific brain areas. Soluflazine decreased adenosine A1 radioligand binding in the hippocampus as measured by [3H]R-PIA, and lowered adenosine A2 binding sites in the striatum, as estimated by the "NECA minus R-PIA" assay. Previous work from our lab has shown the ability of diazepam and triazolam to decrease adenosine binding in the same brain areas. The data show that a specific adenosine transport inhibitor produces the same effect on adenosine receptors as benzodiazepines, and suggest a role for adenosine in the CNS effects of benzodiazepines.