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[1][2][3].
IC50 & Target
Akt
体外研究 (In Vitro)
SC79 augmentes Akt phosphorylation at both the Thr308 and S473 sites[1]. SC79 (10.96 μM) induces cytosolic phosphorylation of Akt. SC79 enhances IGF1-induced Akt phosphorylation in both serum-starved cells and cells grown in serum-rich medium[1]. SC79 reduces neuronal excitotoxicity and prevents stroke-induced neuronal death. SC79 suppresses PHAKTM-GFP plasma membrane translocation[1]. SC79 restores proliferation of BRAT1 knockdown cells, and reduces the production of superoxide in mitochondria of MitoSox positive cells[2]. SC79 upregulates FLIPL/S expression and consequently suppresses caspase-8 activation[5].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
Cell Line:
HeLa cells.
Concentration:
4 μg/mL (10.96 μM).
Incubation Time:
30 min.
Result:
Induced cytosolic phosphorylation of Akt.
体内研究 (In Vivo)
SC79 treatment, even at much high dose (0.4 mg/g of body weight), does not induce any detectable changes in body weight, survival rate, appearance, and behavior in mice[1]. SC79 (10 mg/kg, i.p.) Protects C57BL/6 mice from fas-induced fulminant hepatic failure[4]. SC79 protects hepatocytes from TNFα-mediated apoptosis and mice from Gal/LPS-induced liver injury and damage[5].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Male, age-matched (6- to 8-weekeold) C57BL/6 or BALB/c mice weighing 16 to 18 g[4].
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.
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.
分子量
364.78
Formula
C17H17ClN2O5
CAS 号
305834-79-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Jo H, 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):10581-10586.
[2]. So EY, et al. BRAT1 deficiency causes increased glucose metabolism and mitochondrial malfunction. BMC Cancer. 2014 Jul 29;14:548
[3]. Liu X, et al. Activation of Akt by SC79 decreased cerebral infarct in early cerebral ischemia-reperfusion despite increased BBB disruption. Neurosci Lett. 2018 Aug 10;681:78-82.
[4]. Liu W, 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.
[5]. Jing ZT, 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.
