For research use only. Not for therapeutic Use.
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].
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.
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].
| Catalog Number | I003078 |
| CAS Number | 305834-79-1 |
| Synonyms | ethyl 2-amino-6-chloro-4-(1-cyano-2-ethoxy-2-oxoethyl)-4H-chromene-3-carboxylate |
| Molecular Formula | C17H17ClN2O5 |
| Purity | ≥95% |
| InChI | InChI=1S/C17H17ClN2O5/c1-3-23-16(21)11(8-19)13-10-7-9(18)5-6-12(10)25-15(20)14(13)17(22)24-4-2/h5-7,11,13H,3-4,20H2,1-2H3 |
| InChIKey | DXVKFBGVVRSOLI-UHFFFAOYSA-N |
| SMILES | CCOC(=O)C1=C(OC2=C(C1C(C#N)C(=O)OCC)C=C(C=C2)Cl)N |
| Reference | [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. [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. |
