PI3K/mTOR-IN-22
PI3K/mTOR-IN-22 is an orally active PI3K/mTOR kinase dual inhibitor with IC50 values of 400.5 nM and 8.2 nM. PI3K/mTOR-IN-22 downregulates phosphorylation of the AKT and mTOR, upregulates pro-apoptotic proteins Bax and caspase-3 and downregulates anti-apoptotic protein Bcl-2. PI3K/mTOR-IN-22 exhibits antiproliferative activity against cancer cells, induces apoptosis and ROS production, and reduces mitochondrial membrane potential. PI3K/mTOR-IN-22 exhibits antitumor activity in breast cancer mice models.
For research use only. We do not sell to patients.
- Formula: C28H34N8O6S
- Molecular Weight:610.68
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Caspase Isoforms
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Biological Activity
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Bax |
Bcl-2 |
Caspase 3 |
PI3K/mTOR-IN-22 (Compound J-33) is a selective dual inhibitor of PI3K and mTOR kinases, with an IC50 of 400.5 nM for PI3Kα and 8.2 nM for mTOR, and forms stable binding interactions with both kinases[1].
PI3K/mTOR-IN-22 potently inhibits proliferation of MCF-7 human breast cancer cells with an IC50 of 1.5 μM, and also inhibits proliferation of H1975, H460, PC-9 cells with IC50 values of 10.7, 2.3 and 13.5 μM[1].
PI3K/mTOR-IN-22 (256 μg/mL) exhibits low hemolytic toxicity in sheep erythrocytes, with a hemolysis rate of 2.60%[1].
PI3K/mTOR-IN-22 (0.75-1.50 μM; 6-12 h) induces concentration-dependent apoptosis in MCF-7 human breast cancer cells, reduces mitochondrial membrane potential and increases intracellular ROS levels[1].
PI3K/mTOR-IN-22 (0.75-1.50 μM; 24 h) dose-dependently inhibits migration of MCF-7 human breast cancer cells in vitro, as shown by the wound healing assay[1].
PI3K/mTOR-IN-22 (0.19-3.00 μM; 14 days) dose-dependently inhibits clonogenicity of MCF-7 human breast cancer cells[1].
PI3K/mTOR-IN-22 (0.75-6.00 μM) dose-dependently downregulates phosphorylation of AKT and mTOR in MCF-7 human breast cancer cells, inhibiting the PI3K-AKT-mTOR signaling pathway[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MCF-7 human breast cancer cells
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Concentration:0.75, 1.50 μM
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Incubation Time:24 h
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Result:Significantly reduced the wound healing rate in cells treated with 0.75 μM relative to the control group.
Significantly reduced the wound healing rate in cells treated with 1.50 μM relative to the control group.
Showed an inhibitory effect that increased with concentration.
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Cell Line:MCF-7 human breast cancer cells
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Concentration:0.75, 1.50 μM
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Incubation Time:6-12 h
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Result:Increased AO red/green fluorescence ratio.
Increased JC-1 red/green fluorescence ratio.
Increased DCFH-DA fluorescence intensity.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Breast cancer BALB/c nude (female, 4-6 weeks old, athymic injected with MCF-7 cells)[1]
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Dosage:75 mg/kg
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Administration:p.o.; every other day; 23 days
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Result:Achieved a tumor inhibition rate of 44.9%.
Significantly reduced phosphorylation of AKT at Ser473 and mTOR in tumor tissue.
Blocked the PI3K-AKT-mTOR signaling pathway.
Upregulated pro-apoptotic proteins Bax and Caspase-3.
Downregulated anti-apoptotic protein Bcl-2 and proliferation marker Ki-67.
Induced tumor cell apoptosis (evidenced by increased TUNEL-positive cells).
Caused no significant organ damage via H&E staining of mouse tissues.
Chemical Information
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Molecular Weight 610.68
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Formula C28H34N8O6S
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SMILES
O=C(OC)C1=CC=C(NC(NC2=CC=C(C3=NC(NC4CCN(S(=O)(C)=O)CC4)=NC(N5CCOCC5)=N3)C=C2)=O)C=C1
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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
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)