CDK1-IN-9
CDK1-IN-9 is an orally active and selective CDK1 inhibitor with an IC50 of 5.5 nM. CDK1-IN-9 exhibits broad antiproliferative activity, particularly against HCT116 colon cancer cells. CDK1-IN-9 induces G2/M phase arrest and downregulates CDK1, cyclin B1, and the replication initiation factor CDC45. CDK1-IN-9 induces severe DNA replication stress, subsequently activating the p53 signaling pathway to trigger apoptosis. CDK1-IN-9 can be used for research on colon cancer, liver cancer and gastric cancer.
For research use only. We do not sell to patients.
- Formula: C16H17N7O3S2
- Molecular Weight:419.48
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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
All Aurora Kinase Isoforms
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Biological Activity
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CDK1/cyclinB1 5.5 nM (IC50) |
CDK2/cyclinE 25.9 nM (IC50) |
CDK4/cyclin D 402.8 nM (IC50) |
Aurora A 77.8 nM (IC50) |
CDK1-IN-9 (compound 11I) (0.1-5 μM; 24-72 h) exhibits IC50s of 0.023 μM, 0.292 μM, 0.360 μM and 0.566 μM in HCT116 cell line, HepG2 cell line, SGC7901 cell line and normal keratinocyte line HaCaT, respectively[1].
CDK1-IN-9 (0.1-0.5 μM; 3 days) strongly suppresses the clonogenic survival of HCT116 cell line, HepG2 cell line and SGC7901 cell line, respectively[1].
CDK1-IN-9 (0.5 μM; 24-48 h) significantly impairs the migratory ability of HCT116 cells[1].
CDK1-IN-9 (0.01-0.1 μM; 72 h) induces G2/M arrest in the HCT116 cell line[1].
CDK1-IN-9 (0.1-0.5 μM; 72 h) induces G2/M arrest in HepG2 and SGC7901 cell lines[1].
CDK1-IN-9 (0.1-1 μM; 72 h) inhibits the CDK1/cyclin B1 kinase activity through a non-canonical pathway[1].
CDK1-IN-9 (1 μM; 72 h) inhibits cell division cycle protein 45 (CDC45) activity, causes DNA damage, and triggers apoptosis via the p53-mediated mitochondrial pathway, which can be reproduced by CDC45 knockdown in the HCT116 cell line[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HCT116 cell line, HepG2 cell line, SGC7901 cell line
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Concentration:0.1 μM; 0.25 μM; 0.5 μM; 1 μM; 2.5 μM; 5 μM
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Incubation Time:24 h; 48 h; 72 h
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Result:Decreased the viability of HCT116, HepG2, and SGC7901 cells in a dose- and time-dependent manner.
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Cell Line:HCT116 cell line
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Concentration:0.5 μM
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Incubation Time:24 h; 48 h
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Result:Significantly impaired the migratory ability.
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Cell Line:HepG2 cell line, SGC7901 cell line
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Concentration:0.1 μM; 0.5 μM
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Incubation Time:72 h
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Result:Induced G2/M arrest in a concentration-dependent manner.
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Cell Line:HCT116 cell line
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Concentration:0.01 μM; 0.1 μM
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Incubation Time:72 h
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Result:Induced G2/M arrest in a concentration-dependent manner.
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Cell Line:HCT116 cell line, HepG2 cell line, SGC7901 cell line
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Concentration:0.01 μM; 0.1 μM; 0.5 μM
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Incubation Time:72 h
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Result:Induced apoptosis in a concentration-dependent manner.
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Cell Line:HCT116 cell line
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Concentration:0.1 μM; 0.5 μM; 1 μM
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Incubation Time:72 h
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Result:Reduced the protein levels of CDK1 and cyclin B1 in a concentration-dependent fashion.
Significantly reduced CDC45 expression.
Increased γH2AX accumulation.
Elevated both total and phosphorylated levels of p53.
Decreased the ratio of the anti-apoptotic protein Bcl-xL to the pro-apoptotic protein BAX.
Increased Cytochrome c release.
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Cell Line:HCT116 cell line
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Concentration:0.5 μM; 1 μM
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Incubation Time:24 h; 48 h; 72 h
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Result:Downregulated the transcriptional levels of CDK1 and cyclin B1.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Male BALB/c nude mice (4-6 weeks old; 16-20 g) received a subcutaneous injection of 1 × 107 HCT116 cells to establish a xenograft tumor model[1].
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Dosage:3.3 mg/kg; 10 mg/kg; 30 mg/kg
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Administration:i.g.; every day; for 14 days
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Result:Significantly lower tumor volume compared with the control group.
Reduced tumor weight by 56.4% in 30 mg/kg group.
Did not have significant changes in mouse body weight or in the weights of major organs (heart, liver, spleen, lung, and kidney).
Showed no obvious pathological injury or toxicity in these tissues through histological examination.
Did not have significantly effect on serum biochemistry parameters (including ALT and AST).
Chemical Information
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Molecular Weight 419.48
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Formula C16H17N7O3S2
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SMILES
S=C(N1N=C(NC2=CC=C(S(=O)(N)=O)C=C2)N=C1N)NC3=CC=CC=C3OC
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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)
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