4-M-HMBPP
4-M-HMBPP is a weak agonist for Vγ9Vδ2 T cell activation and a potent competitive inhibitor of HMBPP. 4-M-HMBPP binds to BTN3A1 with high affinity (KD: 26.2 μM), but fails to induce its complex formation with BTN2A1. 4-M-HMBPP can be used in studies on γδ T cell activation.
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- 화학식: C12H15F3O8P2
- 분자량:406.19
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
제품 설명
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| PBMC | EC50 |
10 μM
Compound: 6e
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Effect on IFN-gamma release in human PBMC incubated for 48 hrs by ELISA
Effect on IFN-gamma release in human PBMC incubated for 48 hrs by ELISA
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[PMID: 39029338] |
In Vitro
4-M-HMBPP (Compound 6e) (100 μM; 24 h) does not significantly activate the interaction between BTN3A1 and BTN2A1 in K562 cells[1].
4-M-HMBPP (0.001-100 μM; stimulated for 3 days, cultured for 11 days) does not induce the proliferation of Vγ9Vδ2 T cells in human peripheral blood mononuclear cells (PBMCs)[1].
4-M-HMBPP (0.01-100 μM; 48 h) inhibits HMBPP-induced IFNγ release in human PBMCs, with an IC50 of 0.63 μM[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 406.19
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화학식 C12H15F3O8P2
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SMILES
O=P(OP(O)(O)=O)(OC/C=C(CC1=CC=C(C=C1)C(F)(F)F)/CO)O
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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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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)