• The direct binding of AMIGO2 to the PDK1 PH domain enhanced the activation of PDK1 and AKT in the plasma membrane, which regulates endothelial cell (EC) viability, adhesion, migration, and angiogenesis.

• Loss of AMIGO2 attenuated the phosphorylation of PDK1 and AKT and EC survival and adhesion, tumor growth.

• Expected to show efficacy against broad solid tumor, especially lung (NSCLC, SCLC), colorectal, breast, pancreatic cancer

• Prolongs patient survival by significantly increasing expression level in tissues of cancer patients in proximal inflammation stage when the survival rate decreases

• Less toxic to normal cells compared to existing solid tumor