产品
编 号：F312897
分子式：C17H17ClN2O5
分子量：364.78
分子式：C17H17ClN2O5
分子量：364.78
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
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询价
50mg
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询价
100mg
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询价
200mg
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结构图
CAS No: 305834-79-1
产品详情
生物活性：
SC79, a unique specific and BBB permeable Akt activator, activates Akt in the cytosol and inhibits Akt membrane translocation. SC79 specifically binds to the PH domain of Akt.
体内研究：
SC79 处理，即使在高得多的剂量 (0.4 mg/g) 下，也不会引起小鼠体重、存活率、外观和行为的任何可检测变化。SC79 (10 mg/kg，ip) 保护 C57BL/6 小鼠免于 fas 诱导的暴发性肝衰竭。 SC79 保护肝细胞免于 TNFα 介导的细胞凋亡和小鼠免于 Gal/LPS 诱导的肝损伤和损伤。Animal Model:Male, age-matched (6- to 8-weekeold) C57BL/6 or BALB/c mice weighing 16 to 18 g.
Dosage:10 mg/kg.
Administration:Intraperitoneally at 0.5 hour before the i.p. administration of an agonistic anti-Fas Jo2 antibody at a lethal dose of 0.5 and 0.4 mg/kg for C57BL/6 and BALB/c mice, respectively.
Result:Treatment of mice with 10 mg/kg of SC79 at 0.5 hour before Jo2 injection increased mouse survival at 12 hours after Jo2 injection from 0% to 35%, and no additional mortality was observed to the end of the 2-month observation period.
Animal Model:Male, age-matched (6 to 8 weeks old) C57BL/6 mice weighing 16-18 g.
Dosage:10 mg/kg.
Administration:Intraperitoneally at 0.5 h before i.p. administration of 400 mg/kg of D-galactosamine (D-Gal) and 60 μg/kg of lipopolysaccharide (LPS) for C57BL/6 mice.
Result:Gal/LPS challenge there was more bleeding on the liver of the vehicle control-treated mice as compared to that of SC79-treated mice. A single dose of SC79 significantly reduced Gal/LPS-mediated liver damage but not an infiltration of inflammatory cells in liver sections.
体外研究：
SC79 在 Thr308 和 S473 位点增强 Akt 磷酸化。 SC79 (10.96 μM) 诱导 Akt 的细胞溶质磷酸化。SC79 增强血清饥饿细胞和富含血清培养基中生长的细胞中 IGF1 诱导的 Akt 磷酸化。 SC79 降低神经元兴奋性毒性并防止中风诱导的神经元死亡。SC79 抑制 PHAKTM-GFP 质膜转位。 SC79 恢复 BRAT1 敲低细胞的增殖，并减少 MitoSox 阳性细胞线粒体中超氧化物的产生。 SC79 上调 FLIPL/S 表达，从而抑制 caspase-8 激活。
SC79, a unique specific and BBB permeable Akt activator, activates Akt in the cytosol and inhibits Akt membrane translocation. SC79 specifically binds to the PH domain of Akt.
体内研究：
SC79 处理，即使在高得多的剂量 (0.4 mg/g) 下，也不会引起小鼠体重、存活率、外观和行为的任何可检测变化。SC79 (10 mg/kg，ip) 保护 C57BL/6 小鼠免于 fas 诱导的暴发性肝衰竭。 SC79 保护肝细胞免于 TNFα 介导的细胞凋亡和小鼠免于 Gal/LPS 诱导的肝损伤和损伤。Animal Model:Male, age-matched (6- to 8-weekeold) C57BL/6 or BALB/c mice weighing 16 to 18 g.
Dosage:10 mg/kg.
Administration:Intraperitoneally at 0.5 hour before the i.p. administration of an agonistic anti-Fas Jo2 antibody at a lethal dose of 0.5 and 0.4 mg/kg for C57BL/6 and BALB/c mice, respectively.
Result:Treatment of mice with 10 mg/kg of SC79 at 0.5 hour before Jo2 injection increased mouse survival at 12 hours after Jo2 injection from 0% to 35%, and no additional mortality was observed to the end of the 2-month observation period.
Animal Model:Male, age-matched (6 to 8 weeks old) C57BL/6 mice weighing 16-18 g.
Dosage:10 mg/kg.
Administration:Intraperitoneally at 0.5 h before i.p. administration of 400 mg/kg of D-galactosamine (D-Gal) and 60 μg/kg of lipopolysaccharide (LPS) for C57BL/6 mice.
Result:Gal/LPS challenge there was more bleeding on the liver of the vehicle control-treated mice as compared to that of SC79-treated mice. A single dose of SC79 significantly reduced Gal/LPS-mediated liver damage but not an infiltration of inflammatory cells in liver sections.
体外研究：
SC79 在 Thr308 和 S473 位点增强 Akt 磷酸化。 SC79 (10.96 μM) 诱导 Akt 的细胞溶质磷酸化。SC79 增强血清饥饿细胞和富含血清培养基中生长的细胞中 IGF1 诱导的 Akt 磷酸化。 SC79 降低神经元兴奋性毒性并防止中风诱导的神经元死亡。SC79 抑制 PHAKTM-GFP 质膜转位。 SC79 恢复 BRAT1 敲低细胞的增殖，并减少 MitoSox 阳性细胞线粒体中超氧化物的产生。 SC79 上调 FLIPL/S 表达，从而抑制 caspase-8 激活。
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