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SC79

MCE China：SC79

Brand：MedChemExpress (MCE)

Cat. No.HY-18749

CAS：305834-79-1

Purity：98.0%

Storage：Powder -20°C 3 years 4°C 2 years *The compound is unstable in solutions, freshly prepared is recommended.

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

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]. Note: SC79 is unstable in solution state[6]. It is recommended to freshly prepare in DMSO for preparation and use as needed.

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].

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References：

[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.  [Content Brief]

[2]. So EY, et al. BRAT1 deficiency causes increased glucose metabolism and mitochondrial malfunction. BMC Cancer. 2014 Jul 29;14:548  [Content Brief]

[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.  [Content Brief]

[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.  [Content Brief]

[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.  [Content Brief]

[6]. Shuangying Hao, et al. Phosphorylation of Akt by SC79 Prevents Iron Accumulation and Ameliorates Early Brain Injury in a Model of Experimental Subarachnoid Hemorrhage. Molecules. 2016 Mar 10;21(3):325.  [Content Brief]