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A working model of antitumor effects of OPC-B2 through direct binding and inhibition of AKT. OPC-B2 directly binds to AKT and inhibits its phosphorylation, thereby promoting cyclin D1 degradation through ubiquitination to induce cell cycle arrest. Inhibiting AKT activity also leads to the decreased HK1 expressions and inhibition of glycolysis and TCA cycle metabolism.The net outcome of OPC-B2 treatment is the suppression oftumor growth.
