SC 79
(Synonyms: 2-氨基-6-氯-ALPHA-氰基-3-(乙氧羰基)-4H-1-苯并吡喃-4-乙酸乙酯) 目录号 : GC11645
SC 79 是大脑中渗透性 Akt 磷酸化的激活剂和 AKT-PH 结构域易位的抑制剂。
Cas No.:305834-79-1
Sample solution is provided at 25 µL, 10mM.
SC 79 is an activator of osmotic Akt phosphorylation in the brain and an inhibitor of AKT-PH domain translocation[1].
SC 79 enhances phosphorylation of all three Akt isotypes and enhances Akt activation in a variety of cell types[1]. Treatment of BRAT1 knockdown cells with Akt activator SC 79 can improve their proliferation and reduces mitochondrial ROS concentration[4]. In both SH-SY5Y cells and primary murine dopaminergic neurons, pre-treatment with SC 79 largely inhibited hydrogen peroxide (H2O2)-induced cell viability reduction, apoptosis and necrosis. SC 79 activated Akt in the neuronal cells, which was required for its neuroprotection against H2O2[5]. In primary murine osteoblasts and osteoblastic MC3T3-E1 cells, pretreatment with SC 79 significantly attenuated Dex-induced cell death. Further, Dex-induced mitochondrial permeability transition pore (mPTP) opening, cytochrome C release and apoptosis activation were dramatically alleviated with SC 79 pretreatment in above cells[6]. The protective role of SC 79 against H/R of hepatocytes or hepatic I/R injury is related to activation of phosphorylation of Akt, resulting in the decrease of pro-apoptotic protein of Bim, Bax, and Bad, and increase of the anti-apoptotic protein Bcl-2 and Bcl-xL induced by cell H/R and hepatic I/R injury[7].
SC 79 enhances Akt activity during neuronal cell death in an in vivo mouse model of ischemia, SC 79 attenuates stroke-induced neuron death[1]. SC 79 protects hepatocytes from apoptosis induced by agonistic anti-Fas antibody CH11 (for humans) or Jo2 (for mice) and significantly prolongs the survival of mice given a lethal dose of Jo2[2]. Akt activator SC 79 protects hepatocytes from TNF-α-induced apoptosis and protects mice from d-galactosamine (d-Gal)/lipopolysaccharide (LPS)-induced TNF-α-mediated liver injury and damage. SC 79 not only enhances the nuclear factor-κB (NF-κB) prosurvival signaling in response to TNF-α stimulation, but also increases the expression of cellular FLICE (FADD-like IL-1β-converting enzyme)-inhibitory protein L and S (FLIPL/S), which consequently inhibits the activation of procaspase-8[2].
References:
[1]: Jo H, Mondal S, et,al. 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. doi: 10.1073/pnas.1202810109. Epub 2012 Jun 11. PMID: 22689977; PMCID: PMC3387065.
[2]: Liu W, Jing ZT, et,al. A Novel AKT Activator, SC79, Prevents Acute Hepatic Failure Induced by Fas-Mediated Apoptosis of Hepatocytes. Am J Pathol. 2018 May;188(5):1171-1182. doi: 10.1016/j.ajpath.2018.01.013. PMID: 29673487.
[3]: Jing ZT, Liu W, et,al. AKT activator SC79 protects hepatocytes from TNF-α-mediated apoptosis and alleviates d-Gal/LPS-induced liver injury. Am J Physiol Gastrointest Liver Physiol. 2019 Mar 1;316(3):G387-G396. doi: 10.1152/ajpgi.00350.2018. Epub 2019 Jan 10. PMID: 30629471.
[4]: So EY, Ouchi T. BRAT1 deficiency causes increased glucose metabolism and mitochondrial malfunction. BMC Cancer. 2014 Jul 29;14:548. doi: 10.1186/1471-2407-14-548. PMID: 25070371; PMCID: PMC4129107.
[5]: Xu Y, Gao YW, et,al. SC79 protects dopaminergic neurons from oxidative stress. Oncotarget. 2017 Dec 20;9(16):12639-12648. doi: 10.18632/oncotarget.23538. PMID: 29560097; PMCID: PMC5849161.
[6]: Li ST, Chen NN, et,al. SC79 rescues osteoblasts from dexamethasone though activating Akt-Nrf2 signaling. Biochem Biophys Res Commun. 2016 Oct 7;479(1):54-60. doi: 10.1016/j.bbrc.2016.09.027. Epub 2016 Sep 7. PMID: 27614310.
[7]: Zhou H, Yu Y,et,al. Protective Effects the Akt Activator SC79 in Hepatic Ischemia-Reperfusion Injury. Med Sci Monit. 2018 Jun 24;24:4346-4354. doi: 10.12659/MSM.911178. PMID: 29936516; PMCID: PMC6049012.
SC 79 是大脑中渗透性 Akt 磷酸化的激活剂和 AKT-PH 结构域易位的抑制剂[1]。
SC 79 增强所有三种 Akt 的磷酸化同种型并增强多种细胞类型中的 Akt 活化[1]。用 Akt 激活剂 SC 79 处理 BRAT1 敲低细胞可以改善它们的增殖并降低线粒体 ROS 浓度 [4]。在 SH-SY5Y 细胞和原代小鼠多巴胺能神经元中，用 SC 79 预处理在很大程度上抑制了过氧化氢 (H2O2) 诱导的细胞活力降低、细胞凋亡和坏死。 SC 79 激活神经元细胞中的 Akt，这是其针对 H2O2 的神经保护作用所必需的 [5]。在原代小鼠成骨细胞和成骨细胞 MC3T3-E1 细胞中，用 SC 79 预处理显着减弱了 Dex 诱导的细胞死亡。此外，SC 79 预处理上述细胞后，Dex 诱导的线粒体通透性转换孔 (mPTP) 打开、细胞色素 C 释放和细胞凋亡激活得到显着缓解 [6]。 SC 79 对肝细胞 H/R 或肝 I/R 损伤的保护作用与激活 Akt 磷酸化有关，导致 Bim、Bax 和 Bad 促凋亡蛋白减少，抗细胞 H/R 和肝 I/R 损伤诱导的凋亡蛋白 Bcl-2 和 Bcl-xL[7]。
SC 79 在体内小鼠缺血模型中增强神经元细胞死亡期间的 Akt 活性， SC 79 可减轻中风引起的神经元死亡[1]。 SC 79 可保护肝细胞免受激动性抗 Fas 抗体 CH11（用于人类）或 Jo2（用于小鼠）诱导的细胞凋亡，并在给予致死剂量的 Jo2[2] 后显着延长小鼠的存活期。 Akt 激活剂 SC 79 保护肝细胞免受 TNF-α 诱导的细胞凋亡，并保护小鼠免受 d-半乳糖胺 (d-Gal)/脂多糖 (LPS) 诱导的 TNF-α 介导的肝损伤和损伤。 SC 79 不仅增强核因子-κ；B (NF-κ；B) 响应 TNF-α 的促存活信号；刺激，但也会增加细胞 FLICE（FADD 样 IL-1β；-转化酶）-抑制蛋白 L 和 S (FLIPL/S) 的表达，从而抑制 procaspase-8 的激活[2].
| Kinase experiment [1]: | |
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Preparation Method |
Hela cells were serum-starved for 1 h, treated with IGF or SC 79 (4 μg/mL) for 30 min, lysed in lysis buffer, supplemented with protease inhibitors, and analyzed for phospho-Akt by Western blotting |
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Reaction Conditions |
SC 79 (4 μg/mL) for 30 min |
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Applications |
SC 79, which inhibits PH AkT-GFP plasma membrane translocation but enhances Akt phosphorylation and activation in the cytosols |
| Cell experiment [1]: | |
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Cell lines |
HsSultan and NB4 cells |
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Preparation Method |
SC 79(8 ug/mL) was added to HsSultan or NB4 cell medium and incubated overnight (16-20 h). |
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Reaction Conditions |
8 ug/mL SC 79 for 16-20 h |
|
Applications |
SC 79 enhances phosphorylation of all three Akt isotypes and enhances Akt activation in a variety of cell types. |
| Animal experiment [1]: | |
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Animal models |
MCAO mice |
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Preparation Method |
SC 79 was administered by intraperitoneal injection at a concentration of 0.04mg/g body weight. |
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Dosage form |
0.04mg/g SC 79 |
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Applications |
SC 79 enhances Akt activity during neuronal cell death in an in vivo mouse model of ischemia, SC 79 attenuates stroke-induced neuron death. |
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References: [1]. Jo H, Mondal S, et,al. 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. doi: 10.1073/pnas.1202810109. Epub 2012 Jun 11. PMID: 22689977; PMCID: PMC3387065. |
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| Cas No. | 305834-79-1 | SDF | |
| 别名 | 2-氨基-6-氯-ALPHA-氰基-3-(乙氧羰基)-4H-1-苯并吡喃-4-乙酸乙酯 | ||
| 化学名 | 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 | ||
| 分子式 | C17H17ClN2O5 | 分子量 | 364.78 |
| 溶解度 | ≥ 36.5mg/mL in DMSO | 储存条件 | Store at -20°C,unstable in solution, ready to use. |
| 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 | 2.7414 mL | 13.7069 mL | 27.4138 mL |
| 5 mM | 0.5483 mL | 2.7414 mL | 5.4828 mL |
| 10 mM | 0.2741 mL | 1.3707 mL | 2.7414 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
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Related Biological Data
Activation of PFK1 and PFKFB3 is due to phosphorylation of AKT and AMPK. (F) Representative images of ARS and ALP staining in MC3T3-E1 cells after treatment with SC79 and PFK15.
MK-2206 dihydrochloride (GC16304) and SC79 (GC11645) were obtained from GLPBIO.
Clin Transl Med 13.9 (2023): e1369. PMID: 37649137 IF: 10.6002 -
Related Biological Data
SC79 partially rescued the inhibitory effect of proliferation and migration caused by the knockdown of HRL-SC. a, b Western blot analysis showed that SC79 increased expression of p-AKT.
The medium was replaced with the medium containing 5 μg/mL of SC79 (10 μM, GlpBio) in AKT activation experiments.
Stem Cell Res Ther 13.1 (2022): 1-16. PMID: 35765088 IF: 7.4996 -
Related Biological Data
Melatonin inhibits the AKT/mTOR signaling to reduce autophagy and the expression of fibrotic proteins in HSFs. (E) Treatment with SC79 to activate the AKT/mTOR signaling rescued the melatonin-decreased AKT/mTOR signaling and fibrotic protein expression in HSFs.
HSFs were treated with vehicle (DMSO) or 200 μM melatonin and/or 10 μM SC79 (Glpbio) for 24 h.
Bba-Mol Basis Dis (2023): 166887. PMID: 37739092 IF: 6.2001 -
Related Biological Data
CST1 enhances SERPINB2 expression via AKT signaling pathway in bronchial epithelial cells. (C) SC-79 has a positive effect on SERPINB2 expression (n = 2).
BEAS-2B cells were stimulated with or without cytokines IL-4, IL-13, and IL-17A,17 stimulated with or without house dust mite, treated with or without E64d, induced with SC-79 (4 μg/mL, AKT activator; GlpBio) or MK2206USA).
Allergy Asthma Immun 15.3 (2023): 374. PMID: 37075800 IF: 4.4 -
Related Biological Data
Rescue experiments were conducted to verify the mechanism of TOP2A regulating OC cell behavior. (a-c) after SC79 treatment of cells in the SH-TOP2A group, WB results suggested that the levels of p-AKT/AKT and p-mTOR/mTOR were increased.
Lyophilized SC79 (GC11645, Glpbio), an activator of AKT, was resuspended in 500 μL of DMSO at 20 μg/μL, followed by storage at −20°C for later use.
Cancer Biol Ther 25.1 (2024): 2325126. PMID: 38445610 IF: 3.5999