SC79 is an inhibitor of Akt-PH domain translocation and a unique specific Akt activator. SC79 enhances Akt phosphorylation and activation in multiple cell types and in both receptor tyrosine kinaseand GPCR-mediated signaling. SC79 suppresses PHAKTM-GFP plasma membrane translocation, and enhances phosphorylation of all three Akt isoforms in HEK293, HeLa, HL60, NB4, and HsSulton (B cells) cells. SC79 reduces neuronal excitotoxicity and prevents stroke-induced neuronal death. SC79 (0.04 mg/g, i.p.) inhibits the cytosolic activation of Akt in the permanent focal cerebral ischemia mouse model, and recapitulates the primary cellular function of Akt signaling, resulting in augmented neuronal survival.
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
|Solubility||DMSO 70 mg/mL|
BRAT1 deficiency causes increased glucose metabolism and mitochondrial malfunction.
So EY, et al. BMC Cancer. 2014 Jul 29;14:548. PMID: 25070371.
Small molecule-induced cytosolic activation of protein kinase Akt rescues ischemia-elicited neuronal death.
Jo H, et al. Proc Natl Acad Sci U S A. 2012 Jun 26;109(26):10581-6. PMID: 22689977.
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