CDK4/6-IN-29
CDK4/6-IN-29 is an orally active and highly selective CDK4/6 inhibitor, with an IC50 of 3.17 nM against CDK4 and an IC50 of 4.91 nM against CDK6. CDK4/6-IN-29 induces apoptosis in non-small cell lung cancer cells, inhibits cancer cell migration, induces G1-phase cell cycle arrest, and exhibits anti-tumor efficacy in vivo. CDK4/6-IN-29 can be used for research related to non-small cell lung cancer.
For research use only. We do not sell to patients.
- Formula: C25H17Br3N2O
- Molecular Weight:601.13
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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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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CDK4 3.17 nM (IC50) |
CDK6 4.91 nM (IC50) |
CDK4/6-IN-29 (Compound 3p) (0.1-30 μM; 48 h) potently inhibits the proliferation of human non-small cell lung cancer A549 (IC50 = 1.77 μM) and H1299 (IC50 = 3.50 μM) cell lines in vitro[1].
CDK4/6-IN-29 (Compound 3p) (72 h) potently inhibits the 3D multicellular spheroid proliferation of human non-small cell lung cancer A549 cells (IC50 = 7.78 μM) and H1299 cells (IC50 = 8.50 μM)[1].
CDK4/6-IN-29 (2.5-7.5 μM; 24 h) induces dose-dependent G1 phase cell cycle arrest in human non-small cell lung cancer A549 cells[1].
CDK4/6-IN-29 (0.1-10 μM; 24 h) regulates cell cycle-related proteins in a p53-dependent manner, inhibits Rb phosphorylation in A549 and H1299 cells, downregulates p21 and Cyclin E1 in A549 cells, but has no effect on p21 in H1299 cells[1].
CDK4/6-IN-29 (72 h) exhibits moderate cytotoxicity against human HepG2 cells (LD50 = 4.71 μM) and HK-2 cells (LD50 = 4.55 μM), and shows a favorable selectivity window between cancer cells and normal cells[1].
CDK4/6-IN-29 (2-8 μM; 48 h) dose-dependently inhibits the migration of human non-small cell lung cancer A549 cells in vitro[1].
CDK4/6-IN-29 (5-15 μM; 24 h) induces robust, dose-dependent late apoptosis in human non-small cell lung cancer A549 cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:human non-small cell lung cancer A549 cells
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Concentration:2, 4 and 8 μM
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Incubation Time:48 h
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Result:Induced dose-dependent inhibition of cell migration.
Reduced the wound closure rate to 6.52% compared to vehicle control at 8 μM.
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Cell Line:human non-small cell lung cancer A549 cells
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Concentration:5, 10 and 15 μM
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Incubation Time:24 h
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Result:Induced dose-dependent apoptosis.
Increased total apoptosis rate from 19.3% (vehicle control) to 54.9% at 5 μM.
Increased total apoptosis rate from 19.3% (vehicle control) to 82.6% at 10 μM.
Increased total apoptosis rate from 19.3% (vehicle control) to 87.1% at 15 μM.
The majority of apoptotic cells were in late apoptosis.
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Cell Line:human non-small cell lung cancer A549 cells
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Concentration:2.5, 5 and 7.5 μM
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Incubation Time:24 h
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Result:Induced dose-dependent accumulation of cells in the G1 phase.
Resulted in a robust G1 arrest at 7.5 μM, increasing the G1 population while reducing S and G2/M phase cells.
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Cell Line:human non-small cell lung cancer A549 (p53 wild-type), H1299 (p53-null) cells
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Concentration:0.1, 1 and 10 μM
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Incubation Time:24 h
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Result:Dose-dependently reduced p21 and Cyclin E1 expression in A549 cells.
Fully suppressed Rb phosphorylation at 10 μM in A549 cells.
Inhibited Rb phosphorylation in H1299 cells.
Triggered compensatory Cyclin E1 upregulation in H1299 cells.
Showed no significant effect on p21 expression in H1299 cells.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (female, 6-7 weeks old, 15-20 g, subcutaneous xenograft model)[1]
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Dosage:10 mg/kg; 25 mg/kg; 50 mg/kg
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Administration:p.o.; daily; 21 days
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Result:Achieved a tumor growth inhibition (TGI) of 28.8% with mean tumor volume of 684 mm3 at 10 mg/kg.
Achieved a tumor growth inhibition (TGI) of 45.9% with mean tumor volume of 550 mm3 at 25 mg/kg.
Achieved a tumor growth inhibition (TGI) of 54.4% with mean tumor volume of 482 mm3 at 50 mg/kg.
Caused no significant body weight loss, with final body weight increases of 6.9% (10 mg/kg), 12.0% (25 mg/kg), and 3.1% (50 mg/kg).
Chemical Information
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Molecular Weight 601.13
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Formula C25H17Br3N2O
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SMILES
BrC(C=C1)=CC=C1C(C[N+](C(C2=CC=C(Br)C=C2)=C3)=CC4=C3C5=CC=CC=C5N4)=O.[Br-]
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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)
CDK4/6-IN-29 Related Classifications
HY-184707 Related Classifications
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