Topoisomerase I-IN-20
Topoisomerase I-IN-20 is a Topoisomerase I inhibitor. Topoisomerase I-IN-20 disrupts DNA synthesis and transcription, thereby inhibiting the proliferation and migration of cancer cells. Topoisomerase I-IN-20 induces S-phase cell cycle arrest and mitochondria-mediated Apoptosis in cancer cells, which is characterized by upregulated expression of p53, Bax, caspase-3 and caspase-9, along with downregulated expression of Bcl-2. Topoisomerase I-IN-20 increases intracellular ROS levels. Topoisomerase I-IN-20 is applicable to lung cancer-related research.
For research use only. We do not sell to patients.
- Formula: C23H34FN5S
- Molecular Weight:431.61
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Topoisomerase I-IN-20 (Compound 11d) (25-100 μM; 30 min) inhibits human topoisomerase I-mediated DNA relaxation[1].
Topoisomerase I-IN-20 potently inhibits the proliferation of human A549 lung cancer cells with an IC50 of 8.06 μM; it exhibits moderate activity against MCF-7, HepG-2 and SGC-7901 cells, and shows extremely low toxicity toward normal HK-2 cells[1].
Topoisomerase I-IN-20 (0-10 μM; 0-48 h) inhibits migration of human lung adenocarcinoma cell line A549[1].
Topoisomerase I-IN-20 (4-16 μM; 48 h) increases the intracellular ROS level in human lung cancer A549 cells in a dose-dependent manner[1].
Topoisomerase I-IN-20 (4-16 μM; 24-48 h) induces S-phase cell cycle arrest and apoptosis in human lung cancer A549 cells[1].
Topoisomerase I-IN-20 (4-16 μM; 24 h) induces DNA double-strand breaks in human lung cancer A549 cells in a dose-dependent manner (by enhancing γ-H2AX phosphorylation), and activates the mitochondria-mediated apoptotic pathway (by upregulating the expressions of p53, Bax, caspase-3 and caspase-9, while downregulating the expression of Bcl-2)[1].
Topoisomerase I-IN-20 (1-10 μM; 48 h) induces DNA damage in human lung cancer A549 cells, with significant damage observed at concentrations of 5 and 10 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:A549 cells
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Concentration:0, 1, 2.5, 5, 10 μM
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Incubation Time:24 h; 48 h
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Result:Reduced wound closure to 46.25% at 2.5 μM after 24 h, with further reduction at higher concentrations.
Reduced wound closure to 21.36% at 10 μM after 48 h, showing a dose-dependent reduction in migration compared to controls.
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Cell Line:A549 human lung carcinoma cells
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Concentration:4, 8, and 16 μM
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Incubation Time:24 h
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Result:Caused a dose-dependent increase in the percentage of cells in S phase, accompanied by proportional reductions in G0/G1 and G2/M phase populations.
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Cell Line:A549 human lung carcinoma cells
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Concentration:4, 8, and 16 μM
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Incubation Time:48 h
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Result:Increased the apoptotic population from 7.38 ± 2.58% (untreated control) to 18.54 ± 1.89% at 16 μM, showing a dose-dependent increase.
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Cell Line:A549 human lung carcinoma cells
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Concentration:4, 8, and 16 μM
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Incubation Time:24 h
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Result:Caused a dose-dependent increase in γ-H2AX phosphorylation, indicating induction of DNA double-strand breaks.
Increased expression of p53, Bax, caspase-3, and caspase-9 in a dose-dependent manner.
Decreased expression of Bcl-2 in a dose-dependent manner.
Chemical Information
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Molecular Weight 431.61
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Formula C23H34FN5S
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SMILES
NC(N/N=C/CCCC1C2C(N3CCC2)C(CCC3)CN1CC4=CC=C(F)C=C4)=S
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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)