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- 详细信息
- 文献和实验
- 技术资料
- 保存条件：
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 保质期：
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 英文名：
Diazoxide
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- CAS号：
364-98-7
- 规格：
100mg
| 基本信息 | |
| CAS | No.364-98-7 |
| 中文名称 | 氯Xylazine |
| 英文名称 | Diazoxide |
| 别名 | Sch-6783;SRG-95213;Proglycem;二氮嗪 |
| 分子式 | C8H7ClN2O2S |
| 分子量 | 230.67 |
| 溶解性 | Soluble in DMSO ≥5mg/mL;Soluble in Water ＜ 0.1mg/mL |
| 纯度 | ≥98% |
| 外观(性状) | White to off-white Solid |
| 储存条件 | Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| EC | EINECS 206-668-1 |
| MDL | MFCD00078578 |
| SMILES | CC(NC1=CC=C(Cl)C=C12)=NS2(=O)=O |
| InChIKey | GDLBFKVLRPITMI-UHFFFAOYSA-N |
| InChI | InChI=1S/C8H7ClN2O2S/c1-5-10-7-3-2-6(9)4-8(7)14(12,13)11-5/h2-4H,1H3,(H,10,11) |
| PubChem CID | 3019 |
| 靶点 | Potassium Channel |
| 通路 | Membrane Transporter&Ion Channel |
| 背景说明 | Diazoxide是一种ATP敏感性的钾离子通道激活剂; 可用于治疗高胰岛素血症。 |
| 生物活性 | Diazoxide (Sch-6783) is an ATP-sensitive potassium channel activator， has the potential for hyperinsulinism treatment.[1-4] |
| In Vitro | Diazoxide effectively protects NSC-34 motoneurons from glutamatergic， oxidative and inflammatory damage. Moreover， diazoxide decreased neuronal death in organotypic hippocampal slice cultures after exicitotoxicity and preserved myelin sheath in organotypic cerebellar cultures exposed to pro-inflammatory demyelinating damage. In addition， we demonstrated that one of the mechanisms of actions implied in the neuroprotective role of diazoxide is mediated by the activation of Nrf2 expression and nuclear translocation. Nrf2 expression was increased in NSC-34 neurons in vitro as well as in the spinal cord of experimental autoimmune encephalomyelitis Animals orally administered with diazoxide. Thus， diazoxide is a neuroprotective agent against oxidative stress-induced damage and cellular dysfunction that can be beneficial for diseases such as multiple sclerosis.[2] |
| 细胞实验 | The K(ATP) channel subunits SUR2B， K(ir)6.1， and K(ir)6.2 were identified in all tissues within mouse eyes. Treatment with diazoxide in wild-type mice decreased IOP by 21.5 ± 3.2% with an absolute IOP reduction of 3.9 ± 0.6 mm Hg (P = 0.002). Nicorandil also decreased IOP (18.9 ± 1.8%) with an absolute IOP reduction of 3.4 ± 0.4 mm Hg (P = 0.002). Treatment with diazoxide in K(ir)6.2((-/-)) mice had no effect on IOP. No morphological abnormalities were observed in diazoxide- or nicorandil-treated eyes.[4] |
| 细胞实验 | Diazoxide is dissolved in DMSO to prepare 50 mM stock solution. NSC-34 cells are allowed to differentiate for 8 weeks under reduced serum conditions and then seeded in 24-well plates. Glutamate is dissolved in culture medium and added to cultures at concentration of 10 μM for 24 h. Cell treatment with 100 μM diazoxide starts 2 h before glutamate exposure. Cell viability is measured by the MTT assay[2]. |
| 动物实验 | Rats: Adult male Sprague-Dawley rats with induced cerebral ischemia (n=10 per group) receive an intraperitoneal injection of 0.1% DMSO (1?mL; vehicle group)， diazoxide (10?mg/kg; DZ group)， or diazoxide (10?mg/kg) plus 5-hydroxydecanoate (5?mg/kg; DZ + 5-HD group) 30?min after CPR. The control group (sham group， n=5) undergoes sham operation， without cardiac arrest. Mitochondrial respiratory control rate (RCR) is determined. Brain cell apoptosis is assessed using TUNEL staining. Expression of Bcl-2， Bax， and protein kinase C epsilon (PKCε) in the cerebral cortex is determined by Western blotting and immunohistochemistry[3].Mouse: Diazoxide is prepared by diluting a 100 mM stock solution in 10% polyethoxylated castor oil in PBS. In C57BL/6 wild-type and Kir6.2(?/?) mice， a 5 μL drop of 5 mM diazoxide is topically administered to one eye of each mouse while the fellow control eye received vehicle (DMSO and 10% polyethoxylated castor oil in the same proportion as the treated eye). IOP is measured daily at 1 hour， 4 hours， and 23 hours following treatment. Treatment with diazoxide and vehicle is continued daily for 14 consecutive days[4]. |
| 数据来源文献 | [1]. Coetzee WA， et al. Multiplicity of effectors of the cardioprotective agent， diazoxide. Pharmacol Ther. 2013 Nov;140(2):167-75. [2]. Virgili N， et al. K(ATP) channel opener diazoxide prevents neurodegeneration: a new mechanism of action viaantioxidative pathway activation. PLoS One. 2013 Sep 11;8(9):e75189. [3]. Wu H， et al. Diazoxide Attenuates Postresuscitation Brain Injury in a Rat Model of Asphyxial Cardiac Arrest by Opening Mitochondrial ATP-Sensitive Potassium Channels. Biomed Res Int. 2016;2016:1253842. [4]. Chowdhury UR， et al. ATP-sensitive potassium (K(ATP)) channel openers diazoxide and nicorandil lower intraocular pressure in vivo. Invest Ophthalmol Vis Sci. 2013 Jul 22;54(7):4892-9. |
| 单位 | 瓶 |
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