aktin2

AKT-IN-2 is a selective, and orally bioavailable AKT inhibitor (IC50: 5 nM for AKT1).

AKT-IN-25 (Compound 14a) is an inhibitor of Akt that prevents the phosphorylation of Akt, thereby hindering the PI3K/Akt/mTOR signaling pathway. It arrests the cell cycle at the G1 phase, inhibits the migration of PANC-1 cells, and suppresses the proliferation of cancer cells PANC-1, PATU-T, and SUIT-2, with IC50 values of 3.05, 1.32, and 3.85 μM, respectively.

VEGFR-2/AKT-IN-2 (Compound 5) is an inhibitor of VEGFR-2/AKT, with an IC50 of 0.061 μM for VEGFR in human liver cancer cells. It reduces total and phosphorylated AKT in cells, increases BAX and caspase-3 levels, and decreases Bcl-2, thereby inducing apoptosis. Additionally, VEGFR-2/AKT-IN-2 halts the cell cycle at the S phase and inhibits the growth of human liver cancer cells.

AKT-IN-24 (Compound M17) is an allosteric inhibitor of AKT exhibiting antitumor activity. In combination with Trametinib, it targets the AKT/mTOR and MEK/ERK signaling pathways while inhibiting epithelial-mesenchymal transition, resulting in a synergistic suppression effect on TNBC. This combination promotes apoptosis and inhibits cell proliferation and migration.

AKT-IN-26 (Compound 453) is an AKT inhibitor that binds to the Pleckstrin Homology (PH) domain of AKT. It is useful for research related to cell proliferation and cancer involving the AKT pathway.

AKT-IN-27 (4a) is a potential anticancer drug that functions by selectively targeting Akt-driven signaling pathways. It induces apoptosis by activating caspase-3, causing G2/M phase cell cycle arrest, and disrupting mitochondrial membrane potential. AKT-IN-27 (4a) is applicable in research on triple-negative breast cancer (TNBC).

AKT-IN-21 (compound C36) is a potent AKT inhibitor with broad-spectrum cytotoxic and anticancer properties. It induces apoptosis in cancer cells by blocking the cell cycle and downregulating the PI3K/AKT pathway.

AKT-IN-28 is an allosteric inhibitor of Akt and a derivative of Shikonin. It effectively binds to Akt's allosteric site through hydrophobic and hydrogen bond interactions, with a Kd value of 2.07 μM. AKT-IN-28 significantly inhibits Akt activity, inducing apoptosis in KRAS-mutant colorectal cancer cells, arresting the cell cycle at the G2/M phase, and suppressing cell proliferation, migration, and metabolism.

PI3K/AKT-IN-2, a dual inhibitor of PI3K and AKT, prevents the epithelial-mesenchymal transition (EMT) and promotes apoptosis. Additionally, it impedes tubulin polymerization.

AKT-IN-22 (compound 0R4) serves as a potent allosteric inhibitor of AKT, exhibiting anticancer properties [1].