CliMB-325
CliMB-325 is an HSP90 inhibitor that can induce MHC-I (EC50 = 498 nM) expression on the surface of CT26 murine colorectal cancer cells. CliMB-325 enhances T cell activation and exhibits lower toxicity. CliMB-325 can be used for the study of colorectal cancer.
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- 화학식: C15H9Cl2N9
- 분자량:386.20
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
IC50 & Target
[1]|
HSP90 |
MHC I 498 nM (EC50) |
In Vitro
CliMB-325 induces MHC-I (EC50 = 498 nM) expression on the surface of CT26 murine colorectal cancer cells[1].
CliMB-325 exhibits low cytotoxicity against CT26 murine colorectal cancer cells with a CC50 of 1.3 μM[1].
CliMB-325 (1 μM, 48 h) increases T cell activation (measured by β-galactosidase activity) by 1.6-fold when MC38-OVA cells, after a 48-hour incubation, are co-cultured with B3Z T cells[1].
CliMB-325 adds 290 unique MHC-I peptides, five times more than the untreated group, and 81.3% of the peptides are unique to the CliMB-325 group[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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분자량 386.20
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화학식 C15H9Cl2N9
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SMILES
ClC1=C2N=CN(C2=NC(N)=N1)CC3=CN(N=N3)C4=CC=C(C=C4C#N)Cl
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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RNA extraction experimental
By lysing cells, releasing RNA, and removing impurities such as proteins and DNA, high-purity RNA products are finally obtained. The commonly used traditional method is the guanidine isothiocyanate/phenol/chloroform method (Trizol), which is suitable for a variety of animal materials including animal tissues, microorganisms, cultured cells, etc., and most plant materials.
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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
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)