SC79 suppresses PH-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 restores proliferation of BRAT1 knockdown cells, and reduces the production of superoxide in mitochondria of MitoSox positive cells.
In vivo
In the permanent focal cerebral ischemia mouse model, SC79 (0.04 mg/g, i.p.) enables the cytosolic activation of Akt, and recapitulates the primary cellular function of Akt signaling, resulting in augmented neuronal survival.