NSF-951
NSF-951 (ZINC67299692) is a TLR4 agonist (Kd = 16.01 μM). NSF-951 activates the p38 and JNK kinase pathways. NSF-951 induces IL-6 and TNF-α responses and upregulates CD80 and CD86 expression. In mouse immunization studies, NSF-951 alone or in combination with Alum enhances antigen-specific antibody and T cell responses.
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- CAS No.: 1291868-53-5
- Formule: C23H24N4O3S
- Masse moléculaire:436.53
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
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Activité biologique
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| RAW264.7 | EC50 |
253.4 nM
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Functional potency of NSF-951 for induction of IL-6 production in RAW 264.7 mouse macrophages stimulated for 24 hrs and measured in culture supernatants by sandwich ELISA.
Functional potency of NSF-951 for induction of IL-6 production in RAW 264.7 mouse macrophages stimulated for 24 hrs and measured in culture supernatants by sandwich ELISA.
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41023411 |
In Vitro
NSF-951 binds to the TLR4-MD2 complex of mouse and bovine species with favorable binding energy, and its binding to mTLR4-MD2 is regulated by specific residues including Y122, I68, L101, and L142[1].
NSF-951 (0.244-500 µM) shows direct binding to the mouse TLR4 ectodomain with a KD of 16.01 µM[1].
NSF-951 (1-500 µM; 24 h) shows no cytotoxicity in RAW 264.7 mouse macrophages at concentrations up to 200 µM[1].
NSF-951 (1-500 µM; 24 h) shows no cytotoxicity in THP-1 macrophages at concentrations up to 200 µM[1].
NSF-951 (1-500 µM; 24 h) is not cytotoxic to BoMac bovine macrophages at concentrations up to 200 µM[1].
NSF-951 (2 µM; 24 h) activates the p38 and JNK MAP kinase pathways in RAW 264.7 macrophages[1].
NSF-951 (0.2-20 µM; 24 h) is a potent immunostimulatory molecule that induces pro-inflammatory cytokine production in RAW 264.7 mouse macrophages with an EC50 of 253.4 nM[1].
NSF-951 (2 µM; 24 h) induces the maturation and activation of RAW 264.7 macrophages by upregulating the costimulatory molecules CD80 and CD86 and the maturation marker MHC-II[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:RAW 264.7 mouse macrophage cell line
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Concentration:1-500 µM
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Incubation Time:24 h
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Result:Did not exhibit significant toxicity in the RAW 264.7 cell line at concentrations up to 200 µM.
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Cell Line:THP-1 human macrophage cell line
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Concentration:1-500 µM
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Incubation Time:24 h
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Result:Did not exhibit significant toxicity in the THP-1 cell line at concentrations up to 200 µM.
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Cell Line:BoMac bovine macrophage cell line
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Concentration:1-500 µM
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Incubation Time:24 h
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Result:Did not exhibit significant toxicity in the BoMac cell line at concentrations up to 200 µM.
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Cell Line:RAW 264.7 mouse macrophage cell line
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Concentration:0.2-20 µM
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Incubation Time:24 h
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Result:Induced significant, dose-dependent levels of IL-6 and TNF-α in RAW 264.7 macrophages.
The functional potency for IL-6 induction was determined with an EC50 value of 253.4 nM.
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Cell Line:RAW 264.7 mouse macrophages
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Concentration:2 µM
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Incubation Time:24 h
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Result:Induced strong phosphorylation of p38 and JNK in RAW 264.7 macrophages.
In Vivo
NSF-951 (5 µg/mouse; s.c.; once then boosted on day 21) in AF007 acts as a strong co-adjuvant, amplifying the adjuvant effect of Alum and inducing a Th1-skewed immune response comparable to AS04[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (male, 5-6 weeks old, OVA immunization model)[1]
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Dosage:5 µg/mouse
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Administration:s.c.; once then boosted on day 21
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Result:Induced significantly higher levels of OVA-specific IgG compared to OVA-only group.
Induced significantly higher secretion of IL-4 and IFN-γ cytokines compared to OVA-only group.
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Animal Model:C57BL/6 (male, 5-6 weeks old, OVA immunization model)[1]
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Dosage:5 µg/mouse (NSF-951); 500 µg/mouse (Alum)
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Administration:s.c.; once then boosted on day 21
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Result:Generated significantly higher antibody levels compared to OVA-Alum group.
Induced elevated levels of IgG1 and IgG2c.
Enhanced IL-4 levels and induced significantly higher IFN-γ levels, indicating a Th1-skewed response.
Chemical Information
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CAS No. 1291868-53-5
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Masse moléculaire 436.53
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Formule C23H24N4O3S
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SMILES
O=C(CSC1=NC2=C(C(N1CC3=CC=CO3)=O)NC(C)=C2)NCC4=CC=C(CC)C=C4
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Synonyms
ZINC67299692
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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