AKT1-IN-13
AKT1-IN-13 is an orally active AKT1 inhibitor with an IC50 of 5.17 μM. AKT1-IN-13 also exhibits high inhibitory activity against PAK1, PKA, MAP2K1 (MEK1 / MAPKK1) and MAPK1 (ERK2). AKT1-IN-13 induces cell apoptosis, activates the pro-apoptotic protein BAX, inhibits the anti-apoptotic protein Bcl-2, and activates caspase 3 simultaneously. As a cytotoxic agent, AKT1-IN-13 exerts a killing effect on orthotopically transplanted liver cancer in an AKT1-dependent manner. AKT1-IN-13 can be used in studies related to hepatocellular carcinoma.
For research use only. We do not sell to patients.
- Formula: C43H45BrN4O6
- Molecular Weight:793.74
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
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Akt1 5.17 μM (IC50) |
PAK1 |
MEK1 |
ERK2 |
Bax |
Bcl-2 |
Caspase 3 |
AKT1-IN-13 (Compound 17) (1.0 μM; 50 min) is a multi-target kinase inhibitor that potently inhibits AKT1 (with an inhibition rate of 95% at 1 μM), and exhibits an inhibition rate of > 80% against another 4 kinases (PAK1, PKA, MAP2K1, MAPK1) at 1 μM[1].
AKT1-IN-13 (72 h) potently inhibits the proliferation of human hepatocellular carcinoma HepG2 cells, with an IC50 of 2.09 μM and a selectivity index as high as 11.53[1].
AKT1-IN-13 (2-6 μM; 48 h) induces apoptosis in human hepatocellular carcinoma HepG2 cells in a concentration-dependent manner[1].
AKT1-IN-13 (2-6 μM; 48 h) inhibits the migration of human hepatocellular carcinoma HepG2 cells in a concentration-dependent manner[1].
AKT1-IN-13 (2-6 μM; 24 h) inhibits the invasion of human hepatocellular carcinoma HepG2 cells in a concentration-dependent manner[1].
AKT1-IN-13 (2-6 μM; 48 h) reduces the mitochondrial transmembrane potential of human hepatocellular carcinoma HepG2 cells in a concentration-dependent manner in vitro[1].
AKT1-IN-13 (2-6 μM; 48 h) induces G0/G1 cell cycle arrest in human hepatocellular carcinoma HepG2 cells in a concentration-dependent manner in vitro[1].
AKT1-IN-13 (2-6 μM; 48 h) inhibits AKT phosphorylation and activates the apoptotic pathway in a concentration-dependent manner in human hepatocellular carcinoma HepG2 cells in vitro, reduces p-AKT levels, and upregulates the expression of pro-apoptotic proteins[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human liver cancer HepG2 cells
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Concentration:2, 4 and 6 μM
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Incubation Time:48 h
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Result:Induced a concentration-dependent increase in apoptosis rates: early apoptosis rates rose from 2.42% (control) to 19.49% at 6 μM.
Caused morphological changes including loss of cell membrane smoothness and smaller nuclei.
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Cell Line:human liver cancer HepG2 cells
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Concentration:2, 4 and 6 μM
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Incubation Time:48 h
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Result:Inhibited HepG2 cell migration in a concentration-dependent manner, reducing the wound healing rate from 36.49% (control) to 3.43% at 6 μM.
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Cell Line:human liver cancer HepG2 cells
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Concentration:2, 4 and 6 μM
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Incubation Time:24 h
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Result:Inhibited HepG2 cell invasion in a concentration-dependent manner, reducing the percentage of invasive cells from 100% (control) to 19.85% at 6 μM.
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Cell Line:human liver cancer HepG2 cells
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Concentration:2, 4 and 6 μM
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Incubation Time:48 h
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Result:Induced concentration-dependent G0/G1 phase arrest: the percentage of cells in G0/G1 phase increased from 65.30% (control) to 79.77% at 6 μM.
Decreased S phase percentage from 24.03% to 13.62% and G2/M phase percentage from 10.67% to 6.61%.
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Cell Line:human liver cancer HepG2 cells
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Concentration:2, 4 and 6 μM
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Incubation Time:48 h
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Result:Reduced p-AKT (Ser473) levels in a concentration-dependent manner (P < 0.01) while total AKT levels remained unchanged.
Decreased Bcl-2 expression, increased BAX expression, and elevated cleaved-caspase-3 and cleaved-PARP levels in a concentration-dependent manner.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 3-4 weeks old, 16-18 g, orthotopic liver cancer transplantation model via Hepa1-6 cancer tissue implantation)[1]
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Dosage:50 mg/kg; 100 mg/kg
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Administration:i.g.; daily; 14 days
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Result:Reduced average tumor weight to 0.90 g (50 mg/kg group) and 0.86 g (100 mg/kg group) compared to 2.09 g in vehicle control group.
Reduced HCC cell infiltration, disordered arrangement, and multinuclear cell levels in treated groups relative to controls.
Reduced p-AKT levels significantly in both treatment groups compared to controls, with no significant change in total AKT protein levels.
Caused no significant changes in mouse body weight during the study period.
Chemical Information
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Molecular Weight 793.74
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Formula C43H45BrN4O6
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SMILES
COC1=CC(NC2=CC=C(N=C2)Br)=C3C=C1OC4=CC=CC(C[C@H]5C6=C(CCN5C)C=C(C(OC7=C8C(CCN([C@H]8C3)C)=CC(OC)=C7OC)=C6)OC)=C4
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
[1].
Hou H, et al. Design, Synthesis, and Biological Evaluation of Novel Tetrandrine Derivatives Targeting AKT1 for Hepatocellular Carcinoma Therapy: Integration of Network Pharmacology, Molecular Dynamics Simulation, and Experimental Validation. ACS Omega. 2026 May 20;11(21):30812-30833.
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Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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