MAPK-IN-9
MAPK-IN-9 is a ERK MAPK-MCL-1 inhibitor. MAPK-IN-9 activates caspase-7 and caspase-3, and cleaves poly (ADP-ribose) polymerase (PARP) to induce apoptosis. MAPK-IN-9 inhibits the clonogenic capacity of non-small cell lung cancer cells. MAPK-IN-9 can be used in research related to non-small cell lung cancer.
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研究用途以外に使用した場合、当社は一切の責任を負いかねます。
- 分子式: C21H14BrN5O3
- 分子量:464.27
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保管条件:
Please store the product under the recommended conditions in the Certificate of Analysis.
生物活性
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Caspase-3 |
Caspase-7 |
Mcl-1 |
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| H1975 | IC50 |
1.055 μM
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Inhibition of cell viability against human H1975 non-small cell lung cancer cells incubated for 24 hrs by Cell Counting Kit-8 assay.
Inhibition of cell viability against human H1975 non-small cell lung cancer cells incubated for 24 hrs by Cell Counting Kit-8 assay.
|
42456857 |
MAPK-IN-9 (Compound PPC-15) (1-20 μM; 7 days) potently inhibits the colony-forming ability of H1975 non-small cell lung cancer cells[1].
MAPK-IN-9 (0.1-20 μM; 24 h) inhibits the viability of H1975 non-small cell lung cancer cells, with an IC50 of 1.055 μM after 24 h of treatment[1].
MAPK-IN-9 (10 μM; 24 h) induces significant cell death in H1975 non-small cell lung cancer cells, reducing the viable cell population by more than 48%[1].
MAPK-IN-9 (10 μM; 18 h) induces apoptotic cell death in H1975 non-small cell lung cancer cells after 18 h of treatment, as evidenced by nuclear fragmentation and an increased population of Annexin V-positive cells[1].
MAPK-IN-9 (1-20 μM; 6-24 h) induces apoptosis in H1975, PC-9, HCC827 and A549 non-small cell lung cancer cells by downregulating MCL-1 expression and activating caspase-7, caspase-3 and PARP, which is associated with the selective inhibition of ERK phosphorylation[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:H1975 non-small cell lung cancer cells
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Concentration:0.1, 1, 10, 20 μM
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Incubation Time:24 h
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Result:Reduced cell viability in a dose-dependent manner, with a half-maximal inhibitory concentration (IC50) of 1.055 μM.
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Cell Line:H1975 non-small cell lung cancer cells
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Concentration:10 μM
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Incubation Time:18 h
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Result:Induced nuclear condensation and fragmentation, characteristic of apoptosis.
Increased the proportion of early apoptotic PI-negative/Annexin V-positive cells from 3% to 25%.
Increased late apoptotic/necrotic PI-positive/Annexin V-positive cells from 5% to 75%.
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Cell Line:H1975, PC-9, HCC827, and A549 non-small cell lung cancer cells
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Concentration:1, 10, 20 μM (H1975 dose-dependent); 10 μM (H1975, PC-9, HCC827, A549 time-dependent)
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Incubation Time:24 h (H1975 dose-dependent); 6, 12, 24 h (H1975, PC-9, HCC827, A549 time-dependent)
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Result:Reduced MCL-1 expression and increased cleavage of caspase-7, caspase-3, and PARP in H1975 cells in both dose- and time-dependent manners.
Selectively reduced ERK phosphorylation in H1975 cells in a time-dependent manner, with no significant effect on AKT or MEK phosphorylation.
Reduced ERK phosphorylation, reduced MCL-1 expression, and increased caspase-7 and PARP cleavage in PC-9, HCC827, and A549 cells.
化学情報
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分子量 464.27
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分子式 C21H14BrN5O3
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SMILES
N#CC1=C2N=CC(C(C3=CC(Br)=CC=C3O)=O)=CN2N=C1NC4=CC=CC(OC)=C4
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輸送条件
Room temperature in continental US; may vary elsewhere.
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保管条件
Please store the product under the recommended conditions in the Certificate of Analysis.
純度とドキュメンテーション
参考文献
Calculators
濃度 (開始) × 体積 (開始) = 濃度 (終了) × 体積 (終了)