LFS-1107
LFS-1107 is a reversible CRM1 inhibitor (Kd: 12.5 pM). LFS-1107 can selectively eliminate extranodal natural killer/T cell lymphoma (ENKTL) cells and can be used for cancer research.
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- CAS 番号: 1799330-91-8
- 分子式: C12H11N5OS2
- 分子量:305.38
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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
製品説明
IC50 & Target
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COX-2 |
体外実験
LFS-1107 (4-9 μM, 72 h) can selectively eliminate ENKTL cells while sparing normal human PBMC with good safety profile in PBMC cell lines[1].
LFS-1107 (0.15-500 μM, 24 h) barely exhibits any effects in human platelets[1].
LFS-1107 (50-200 nM, 3 h) can lead to nuclear accumulation IκBα in 293T cells[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:SNK6, HANK-1
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Concentration:0-800 nM
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Incubation Time:72 h
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Result:Achieved IC50 value of 26 nM in SNK6 cell line and 36 nM in HANK-1 cell line.
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Cell Line:SNK6
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Concentration:62.5 nM, 125 nM, 250 nM, 500 nM, 1000 nM
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Incubation Time:3 h
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Result:Suppressed the expression of CRM1 in a dose-dependent manner. Downregulated the expression of proinflammatory and proliferative proteins p65, COX-2, c-Myc, and Survivin in a dose dependent manner.
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Cell Line:293T cells
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Concentration:50 nM, 100 nM, 200 nM
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Incubation Time:3 h
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Result:Could lead to nuclear accumulation of IκBα in a dose dependent manner.
体内実験
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:SNK6 cell xenograft mouse model[1]
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Dosage:10 mg/kg
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Administration:Intraperitoneal injection (i.p.), once a week
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Result:Extended mouse survival and Eliminated tumor cells.
化学情報
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CAS 番号 1799330-91-8
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分子量 305.38
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分子式 C12H11N5OS2
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SMILES
O=S(C1=NN=NN1C2=CC=CC=C2)/C=C/CCN=C=S
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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.
プロトコル
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Research Protocol for Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
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)