STING agonist-13
Based on 1 publication(s) in Google Scholar
STING agonist-13 is a stimulator of interferon genes (STING) agonist, for cancer immunity via STING-mediated immune activation. STING agonist-13 can stimulate STING downstream signaling and promoting type I interferon immune responses. STING agonist-13 significantly decreases tumor volume and shows immunological memory-derived cancer inhibition.
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- CAS No.: 2816929-48-1
- Formule: C45H53N15O7
- Masse moléculaire:916.00
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) STING agonist-13
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Activité biologique
Description
IC50 & Target
EC50: 7.471 nM (PBMCs), 2.442 nM (RAW264.7)[1]
In Vitro
STING agonist-13 (compound 4c) induces the secretion of IFN-β with an EC50 of 7.471 nM in human primary PBMCs cells[1].
STING agonist-13 (2 μM; 24 hours) induces IP-10 with an EC50 of 2.442 nM and other proinflammatory cytokines such as IL-6 and TNF-α release in RAW264.7 cells[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:PBMCs, RAW264.7
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Concentration:2 μM
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Incubation Time:24 hours
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Result:Showed broad reactivity in PBMCs and RAW264.7 cells.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:8 week-old female BALB/c mice(CT26 tumor mouse models)[1]
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Dosage:1.5 mg/kg
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Administration:Intravenous injection; once a day for 8 days.
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Result:Showed activity of cancer immunity via STING-mediated immune activation.
Chemical Information
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CAS No. 2816929-48-1
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Masse moléculaire 916.00
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Formule C45H53N15O7
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SMILES
CCN1N=C(C=C1C(NC2=NC3=C(N2C/C=C/CN4C(NC(C5=CC(C)=NN5CC)=O)=NC6=CC(C(N)=O)=CC(OCCCNC(C7=CC(C)=NN7CC)=O)=C64)C(OC)=CC(C(N)=O)=C3)=O)C
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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.
Publications (1)
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Journal Impact Factor
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Most Recent
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Signal Transduct Target Ther
Arginase 1 drives mitochondrial cristae remodeling and PANoptosis in ischemia/hypoxia-induced vascular dysfunction. [Abstract]2025 May 28;10(1):167. PMID: 40425583
Protocole
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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)