| CAS NO: | 305834-79-1 |
| 包装 | 价格(元) |
| 50mg | 电议 |
| 10mg | 电议 |
| Storage | Store at -20°C |
| M.Wt | 364.78 |
| Cas No. | 305834-79-1 |
| Formula | C17H17ClN2O5 |
| Solubility | ≥36.5 mg/mL in DMSO; insoluble in H2O; ≥9.76 mg/mL in EtOH with gentle warming and ultrasonic |
| Chemical Name | ethyl 2-amino-6-chloro-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate |
| Canonical SMILES | CCOC(C(C(C(C(OCC)=O)=C1N)C2=C(O1)C=CC(Cl)=C2)C#N)=O |
| 运输条件 | 蓝冰运输或根据您的需求运输。 |
| 一般建议 | 为了使其更好的溶解，请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异，仅做参考。若实验所需浓度过大至产品溶解极限，请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存，请尽快用完。 |
IC50：N/A
SC 79是一种Akt活化剂。Akt/PKB（丝氨酸/苏氨酸蛋白激酶）具有抗凋亡活性，是PtdIns P3信号传导通路的主要下游靶点之一。
体外：SC79通过基于细胞的高通量化学遗传筛选鉴定，抑制Akt膜转位。然而，Akt在细胞溶质中可能由SC79活化，特异性结合Akt的PH结构域。结合SC79 的Akt的构象有利于被上游蛋白激酶磷酸化。在缺血性中风的小鼠模型和海马神经元培养系统中，获得神经元存活增加的结果，基于Akt被SC79的胞浆激活，这足以概括Akt信号传导的主要细胞功能。因此，SC79，一种独特的特异性Akt活化剂，可应用于各种生理和病理条件下增强Akt的活性。
体内：SC79在水性环境中相对不稳定。然而有趣的是，去除SC79后，在细胞培养物和体内观察到磷酸化Akt的持续水平，表明SC79可能不可逆地作用。SC79的化学部分（即腈基）可以被修饰和/或与氨基酸反应。尽管如此，SC79，一种相对安全的药物，由下列事实展现。高剂量的SC79治疗（0.4 mg/g体重）并未加速小鼠体重（存活率、外观和行为）任何可检测的变化。腹腔注射获得神经保护作用表明SC79也具有良好的血脑屏障穿透。SC79可作为化学平台开发用于神经系统和其他并发症的新药。
临床试验：目前尚未进行临床研究。
参考文献：
[1] Jo H, Mondal S, Tan D, Nagata E, Takizawa S, Sharma AK, Hou Q, Shanmugasundaram K, Prasad A, Tung JK, Tejeda AO, Man H, Rigby AC, Luo HR. Small molecule-induced cytosolic activation of protein kinase Akt rescues ischemia-elicited neuronal death. Proc Natl Acad Sci U S A. 2012 Jun 26; 109 (26):10581-6.
| Cell experiment:[1] | |
Cell lines | Cortical and hippocampal neurons |
Reaction Conditions | 50 μM SC 79 for 40 min incubation |
Applications | Treatment of cultured cortical neurons with Akt activator SC 79 markedly enhanced Akt phosphorylation without altering total Akt levels. Similarly, SC 79 treatment substantially reduced the death of glutamate-challenged hippocampal neurons |
| Animal experiment:[1] | |
Animal models | Mice subjected to middle cerebral artery occlusion (MCAO) |
Dosage form | 0.04 mg/g Injected intraperitoneally |
Applications | Intraperitoneal pretreatment with SC 79 in mice effectively prevented stroke-induced Akt deactivation, and consequently, provided protection from excitotoxicity-induced brain damage in both the cortical area and striatum. The effect of SC 79 was potent, with a single dose of SC 79 reducing the neocortical lesion size by 35% 24 h after MCAO and more than 40% 1 wk after MCAO. |
Note | The technical data provided above is for reference only. |
References: 1. Jo H, Mondal S, Tan D, et al. Small molecule-induced cytosolic activation of protein kinase Akt rescues ischemia-elicited neuronal death. Proceedings of the National Academy of Sciences of the United States of America, 2012, 109(26): 10581-10586. | |
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