STING-IN-8
STING-IN-8 (Compound 15b) emerges as a potent stimulator of interferon gene (STING) inhibitor with an IC50 value of 0.121 μM in human and an IC50 value of 0.033 μM in mouse. STING-IN-8 inhibits MSA-2 (HY-136927) or 2’, 3’ -cGAMP (HY-100564)-stimulated STING signaling and suppresses immune-inflammatory cytokine levels in both human and murine cells. STING-IN-8 is promising for research in the field of STING-associated inflammatory and autoimmune diseases.
For research use only. We do not sell to patients.
- Formula: C18H14F3N3O5S2
- Molecular Weight:473.45
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
STING-IN-8 (0.1, 0.3, 1, 3 μM, 5 h) restrains the MSA-2 (10 μM) or 2’, 3’-cGAMP (10 μM) -induced p-TBK1 and p-IRF3 upregulation expression in both human and murine cells[1]. STING-IN-8 shows negligible cytotoxicity with CC50 of 30 μM in THP1-Dual and RAW-Lucia cells[1]. STING-IN-8 (0.3, 1, 3 μM and 0.1, 1, 3 μM, 9 h) effectively inhibits STING downstream immune-inflammatory cytokines in both human and mouse immune 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:Human monocyte derived THP1-Dual cell line, murine macrophage cells and mouse embryonic fibroblasts
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Concentration:0.1, 0.3, 1, 3 μM
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Incubation Time:5 h
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Result:Significantly down-regulate the the levels of phosphorylated TBK1 and IRF3 induced by MSA-2 (10 μM) and 2’, 3’ -cGAMP (10 μM) in all cell lines with better potency than SN-011 (HY-145010).
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Cell Line:THP1-Dual cell line and RAW-Lucia cells
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Concentration:0.3, 1, 3 μM and 0.1, 1, 3 μM
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Incubation Time:9 h
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Result:Significantly inhibited the MSA-2 (10 μM) or 2’, 3’-cGAMP (10 μM)-induced upregulation of STING signals expression in THP1-Dual cell line and RAW-Lucia cells.
In Vivo
STING-IN-8 (10 mg/kg, i.p., daily for two weeks) attenuates sustainably high levels of immune-inflammatory cytokines in the mice with Trex1 loss-of-function [1].
Pharmacokinetic parameters of STING-IN-8 in mice[1]
| Administration | T1/2 (h) | Tmax(h) | Cmax(ng/mL) | AUC0-∞ (ng·h/mL) | MRT(h) |
| p.o. 10 mg/ kg b | 1.75 | 0.25 | 77.6 | 109 | 2.53 |
| i.p. 5 mg/kgc | 4.86 | 0.18 | 137 | 100 | 4.73 |
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 mice[1]
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Dosage:10 MG/KG
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Administration:i.p., a single dose
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Result:Effectively reduced MSA-2 (10 MG/KG) -stimulated serum IL-6, CXCL10 levels and inhibited the expression of IFNβ, TNFα, ISG15, ISG56, Cxcl10, IL6 in kidney tissues.
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Animal Model:Kidney tissues of Trex1-D18N mice[1]
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Dosage:10 MG/KG
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Administration:i.p. daily for two weeks
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Result:Significantly reduced the ISG 15, ISG 56, CXCL10 levels in kidney and demonstrated anti-inflammatory effects in tongue and other muscle tissues of Trex1-D18N mice.
Chemical Information
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Molecular Weight 473.45
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Formula C18H14F3N3O5S2
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SMILES
CS(=O)(NC1=C(C=CC(NC(C2=NC(C3=CC=C(C=C3)OC(F)(F)F)=CS2)=O)=C1)O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Multiple sequence alignment
Multiple sequence alignment is a computational method for arranging DNA, RNA, or protein sequences so that homologous residues or nucleotides are placed in the same columns, enabling conservation analysis, motif detection, structure prediction, phylogenetic inference, and evolutionary interpretation. MSA accuracy depends on sequence similarity, length variation, insertions and deletions, domain architecture, sequence number, and algorithm choice; therefore, no single aligner is optimal for every dataset. Commonly used MSA tools include MAFFT, MUSCLE, Clustal Omega, and T-Coffee; MAFFT provides multiple strategies for diverse alignment problems, MUSCLE emphasizes speed and accuracy, Clustal Omega scales well to large protein datasets, and T-Coffee uses consistency information to improve alignment reliability. Unresolved issues include alignment uncertainty in divergent sequences, over-alignment of unrelated regions, variable effects of automated trimming, and propagation of alignment er
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)