BMS-37 hydrochloride
BMS-37 hydrochloride is a PD-1/PD-L1 immune checkpoint inhibitor with an IC50 towards the PD-L1/PD-1 complex in the range of 18 to 200 nM. BMS-37 hydrochloride shows unspecific toxicity against modified Jurkat T cells with an EC50 between 3 and 6 µM. BMS-37 hydrochloride can be used for the study of the PD-L1-induced exhaustion of T-cells or as PD-L1 ligand to synthesize PROTAC molecules.
For research use only. We do not sell to patients.
- CAS No.: 2108101-94-4
- Formula: C27H33ClN2O4
- Molecular Weight:485.01
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Chemical Information
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CAS No. 2108101-94-4
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Molecular Weight 485.01
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Formula C27H33ClN2O4
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SMILES
O=C(C)NCCNCC1=C(OC)C=C(OCC2=CC=CC(C3=CC=CC=C3)=C2C)C=C1OC.Cl
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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.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
Purity & Documentation
References
[2]. Zak KM, et al. Structural basis for small molecule targeting of the programmed death ligand 1 (PD-L1). Oncotarget. 2016 May 24;7(21):30323-35. [Content Brief]
[3]. Skalniak L, et al. Small-molecule inhibitors of PD-1/PD-L1 immune checkpoint alleviate the PD-L1-induced exhaustion of T-cells. Oncotarget. 2017 Aug 7;8(42):72167-72181. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)