BI-5756
BI-5756 is a CETP inhibitor and cannabinoid receptor 1 (CB1) agonist. BI-5756 can significantly increase HDL-C levels and reduce LDL-C levels. BI-5756 can also enhance the function of regulatory T cells while maintaining T cell-mediated anti-tumor activity. BI-5756 can directly inhibit the growth of tumor cells and upregulate the expression of MHC I, MHC II, and CD80 on tumor cells. BI-5756 has a protective effect in graft-versus-host disease models. BI-5756 can be used in research on tumors, graft-versus-host disease, and metabolic diseases.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
The BI-5756 was designed by Boehringer Ingelheim and could be obtained free of charge through the Boehringer Ingelheim open innovation portal opnMe.com, associated with its negative control.
- CAS. Nr.: 1332485-18-3
- Formel: C27H32F3NO3
- Molecular Weight:475.54
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biologische Aktivität
Beschreibung
Chemical Information
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CAS. Nr. 1332485-18-3
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Molecular Weight 475.54
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Formel C27H32F3NO3
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SMILES
CC(C1=NC(CC(C)(C[C@@H]2O)C)=C2C3=C1[C@@H](C4=CC=C(C=C4)C(F)(F)F)OC35CCOCC5)C
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Protokoll
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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
Reinheit & Dokumentation
Verweise
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)