2. Immunology/Inflammation NF-κB Metabolic Enzyme/Protease Apoptosis
  3. STING Interleukin Related IFNAR Reactive Oxygen Species (ROS) Apoptosis
  4. STING-IN-16

STING-IN-16 is a STING inhibitor with IC50 values of 44 nM (human) and 32 nM (mice) for cellular STING inhibition. STING-IN-16 effectively inhibits the activation of the STING axis in both human and murine cells. STING-IN-16 can restore renal mitochondrial function, suppress reactive oxygen species (ROS) production, and reduce cell apoptosis. STING-IN-16 shows robust anti-inflammatory efiicacy in vivo. STING-IN-16 can be used for the study of autoimmune and autoinflammatory diseases.

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STING-IN-16 Chemical Structure

STING-IN-16 Chemical Structure

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STING-IN-16 Related Antibodies

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Description

STING-IN-16 is a STING inhibitor with IC50 values of 44 nM (human) and 32 nM (mice) for cellular STING inhibition. STING-IN-16 effectively inhibits the activation of the STING axis in both human and murine cells. STING-IN-16 can restore renal mitochondrial function, suppress reactive oxygen species (ROS) production, and reduce cell apoptosis. STING-IN-16 shows robust anti-inflammatory efiicacy in vivo. STING-IN-16 can be used for the study of autoimmune and autoinflammatory diseases[1].

In Vitro

STING-IN-16 (Compound 5c) (1 μM, 24 h) inhibits the activation of STING with IC50s of 44 nM (THP1-Blue-ISG cells) and 32 nM (RAW-Lucia-ISG cells)[1].
STING-IN-16 (0.3-3 μM, 3-6 h) inhibits the STING signaling pathway activated by STING activators and markedly increases STING thermal stability in THP1 cells, BMDM cells, MEF cells and RAW264.7 murine macrophage cells[1].
STING-IN-16 (1 μM, 6 h) inhibits the activation of the cGAS-STING axis triggered by Cisplatin (HY-17394)-induced DNA damage, which in turn reduces ROS accumulation and cell apoptosis in HK2 cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

STING-IN-16 Related Antibodies

Western Blot Analysis[1]

Cell Line: THP1 cells, BMDM cells, HK2 cells
Concentration: 0.3, 1, 3 μM
Incubation Time: 6 h
Result: Inhibited MSA-2 (HY-136927)-stimulated phosphorylation of STING, TBK1, and IRF3, showing better activity than H151(HY-112693) in THP1 cells.
Inhibited Vadimezan (DMXAA) (HY-10964)-stimulated phosphorylation of STING, TBK1, and IRF3, showing better activity than H151 in BMDM cells.
Inhibited cisplatin-stimulated phosphorylation of STING, TBK1, IRF3, and P65, exhibiting higher potency than H151 in HK2 cells.
Decreased the expression of apoptosis markers such as cleaved-caspase3, cleaved-caspase8, and DNA damage markers (γ-H2A.X and p-CHK1).

Real Time qPCR[1]

Cell Line: THP1 cells, BMDM cells, HK2 cells
Concentration: 0.3, 1, 3 μM
Incubation Time: 3, 6 h
Result: Inhibited MSA-2-triggered gene expression of the cytokines (ISG15, ISG56, IFNβ, CXCL10 and CCL5) dose-dependently in THP1 cells.
Inhibited DMXAA-triggered gene expression of the cytokines (ISG15, ISG56, IFNβ, CXCL10 and CCL5) dose-dependently in BMDM cells.
Inhibited diABZI STING agonist-1 (HY-112921A), cGAMP (HY-12512) and HTDNA-triggered gene expression of the cytokines ( IFNβ, IL6, CXCL10 and ISG15) in THP1 cells and BMDM cells.
Reduced cisplatin-induced gene expression of inflammatory cytokines such as IL6, TNFA, IL8 and CXCL10 in HK2 cells.

ELISA Assay[1]

Cell Line: THP1 cells, BMDM cells
Concentration: 0.3, 1, 3 μM
Incubation Time: 6 h
Result: Decreased MSA-2-induced secretion of IFN-β, CXCL10, and IL-6, showing considerably higher potency than H151 in THP1 cells.
Decreased DMXAA-induced secretion of IFN-β, CXCL10, and IL-6, showing considerably higher potency than H151 in BMDM cells.

Cell Viability Assay[1]

Cell Line: HK2 cells
Concentration: 1 μM
Incubation Time: 6 h
Result: Attenuated Cisplatin-induced cell death.
In Vivo

STING-IN-16 (Compound 5c) (10 mg/kg, i.p., daily for 3 days) alleviates Cisplatin-induced inflammation in mice[1].
STING-IN-16 (10 mg/kg, i.p., single dose) demonstrates anti-inflammatory efficacy in MSA-2-induced inflammatory mouse models[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Cisplatin-induced kidney injury C57BL/6 male mice (8 weeks)[1]
Dosage: 10 mg/kg
Administration: i.p. daily for 3 days
Result: Blocked the expression of Ifnb, Il6, and Tnfa Reduced cisplatin-induced BUN elevation.
Alleviated cisplatin-induced pathological changes (severe tubular dilation, tubular necrosis, and cast formation).
Reduced cisplatin-induced elevation of plasma IL-6, which was better than that of H151.
Restored the expression of such mitochondria-encoded genes(mt-CO1, mt-CO2, mt-CO3, mt-ATP6, mt-ND2 and mt-ND4).
Animal Model: MSA-2-induced inflammation C57BL/6 male mice (8 weeks)[1]
Dosage: 10 mg/kg
Administration: i.p. for a single dose
Result: Decreased MSA-2-induced cytokines secretion in serum, including IFN-β, CXCL10, and IL-6.
Diminished MSA-2-induced expression of Ifnb and Il6 in the kidney tissue.
Lowered MSA-2-stimulated expression of Ifnb, Il6, and Ccl5 in the heart tissue.
Molecular Weight

433.93

Formula

C25H24ClN3O2
SMILES

O=C(N1CCC2C=C(C=CC2C1)C3=CC=C(C=C3)OC)NC4=CNC5=C4C=C(C=C5)Cl
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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STING-IN-16 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

STING-IN-16STINGInterleukin RelatedIFNARReactive Oxygen Species (ROS)ApoptosisStimulator of Interferon GenesTMEM173MITAERISMPYSILInterferon-α/β receptorInterferon-alpha/beta receptor THP1 cellsBMDM cellsMEF cellsRAW264.7 cellsROSapoptosisinflammationInhibitorinhibitorinhibit

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