2. Cell Cycle/DNA Damage Epigenetics Apoptosis
  3. CDK Aurora Kinase Apoptosis
  4. 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.

CDK1-IN-9

CDK1-IN-9 Chemical Structure

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CDK1-IN-9 Related Antibodies

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CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85 CDK10 CDK15 CDK17 CDK18 CDK20 PITSLRE

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Aurora Kinase Aurora A Aurora B Aurora C

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Description

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[1].

IC50 & Target[1]

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)

In Vitro

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.

CDK1-IN-9 Related Antibodies

Cell Viability Assay[1]

Cell Line: HCT116 cell line, HepG2 cell line, SGC7901 cell line
Concentration: 0.1 μM; 0.25 μM; 0.5 μM; 1 μM; 2.5 μM; 5 μM
Incubation Time: 24 h; 48 h; 72 h
Result: Decreased the viability of HCT116, HepG2, and SGC7901 cells in a dose- and time-dependent manner.

Cell Migration Assay [1]

Cell Line: HCT116 cell line
Concentration: 0.5 μM
Incubation Time: 24 h; 48 h
Result: Significantly impaired the migratory ability.

Cell Cycle Analysis[1]

Cell Line: HepG2 cell line, SGC7901 cell line
Concentration: 0.1 μM; 0.5 μM
Incubation Time: 72 h
Result: Induced G2/M arrest in a concentration-dependent manner.

Cell Cycle Analysis[1]

Cell Line: HCT116 cell line
Concentration: 0.01 μM; 0.1 μM
Incubation Time: 72 h
Result: Induced G2/M arrest in a concentration-dependent manner.

Apoptosis Analysis[1]

Cell Line: HCT116 cell line, HepG2 cell line, SGC7901 cell line
Concentration: 0.01 μM; 0.1 μM; 0.5 μM
Incubation Time: 72 h
Result: Induced apoptosis in a concentration-dependent manner.

Western Blot Analysis[1]

Cell Line: HCT116 cell line
Concentration: 0.1 μM; 0.5 μM; 1 μM
Incubation Time: 72 h
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.

Real Time qPCR[1]

Cell Line: HCT116 cell line
Concentration: 0.5 μM; 1 μM
Incubation Time: 24 h; 48 h; 72 h
Result: Downregulated the transcriptional levels of CDK1 and cyclin B1.
In Vivo

CDK1-IN-9 (3.3-30 mg/kg; i.g.; every day; for 14 days) markedly suppressed xenograft tumor growth in male BALB/c nude mice, without inducing significant body weight loss or observable organ toxicity[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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].
Dosage: 3.3 mg/kg; 10 mg/kg; 30 mg/kg
Administration: i.g.; every day; for 14 days
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).
Molecular Weight

419.48

Formula

C16H17N7O3S2
SMILES

S=C(N1N=C(NC2=CC=C(S(=O)(N)=O)C=C2)N=C1N)NC3=CC=CC=C3OC
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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CDK1-IN-9 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

CDK1-IN-9CDKAurora KinaseApoptosisCyclin dependent kinaseselective CDK1 inhibitorbroad antiproliferative activityHCT116 colon cancer cellsG2/M phase arrestcyclin B1CDC45DNA replication stressp53 signaling pathwayapoptosiscolon cancerliver cancergastric cancerInhibitorinhibitorinhibit

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