| Size | Price | Stock | Qty |
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| 50mg |
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| 100mg |
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| 250mg |
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| Other Sizes |
| Targets |
STING inhibitor 1 targets STING (Stimulator of Interferon Genes), binding to its cyclic dinucleotide (CDN) binding pocket with a Ki value of 0.4 μM (ITC assay) [1]
STING inhibitor 1 inhibits human STING (WT) activation induced by 2'3'-cGAMP with an IC₅₀ of 0.7 μM (IFN-β luciferase reporter assay); IC₅₀ values for human STING mutants R284S, R281Q, and A262T are 0.9 μM, 1.1 μM, and 1.3 μM, respectively [1] STING inhibitor 1 shows no significant binding to other innate immune receptors (e.g., TLR4, MDA5) at concentrations up to 10 μM [1] |
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| ln Vitro |
Targeting the human STING's cyclic dinucleotide binding pocket is SN-001 [1]. In a dose-dependent manner, SN-001 (5–20 μM; 6 hours) significantly reduces the induction of Ifnb mRNA in L929 cells [1]. Cytosolic DNA-induced STING signaling is inhibited by SN-001 (10 μM; 3 hours) [1].
STING-mediated signaling inhibition: STING inhibitor 1 (0.1–10 μM) dose-dependently inhibited 2'3'-cGAMP-induced STING activation in THP-1 monocytes and HEK293T cells, reducing IFN-β mRNA levels by 55–88% and IRF3 phosphorylation by 48–82% (qRT-PCR/Western blot) [1] - Proinflammatory cytokine suppression: 2 μM reduced 2'3'-cGAMP-induced IL-6 and TNF-α production by 72% and 65% in THP-1 cells (ELISA); 5 μM inhibited CXCL10 secretion by 78% [1] - CDN binding competition: 1 μM displaced [³H]-2'3'-cGAMP binding to recombinant human STING by 85% (radioligand binding assay) [1] - No effect on cell proliferation: Cell viability >95% in THP-1, HEK293T, and normal human PBMCs at concentrations up to 10 μM (MTT assay) [1] - Cross-species activity: Inhibits mouse STING activation with an IC₅₀ of 1.5 μM (IFN-β reporter assay in RAW264.7 cells) [1] |
| ln Vivo |
Anti-inflammatory activity (mouse STING-induced inflammation model): C57BL/6 mice were intraperitoneally injected with STING inhibitor 1 (5, 10 mg/kg) 1 hour before intraperitoneal administration of 2'3'-cGAMP (1 mg/kg). The compound dose-dependently reduced serum IFN-β levels by 45% (5 mg/kg) and 68% (10 mg/kg) (ELISA); reduced hepatic IL-6 and TNF-α mRNA levels by 52–70% (qRT-PCR) [1]
- Tissue inflammation suppression: 10 mg/kg STING inhibitor 1 reduced immune cell infiltration in the liver and spleen by 65% (histopathological analysis); decreased STING dimerization in hepatic tissues by 72% (Western blot) [1] - No obvious toxicity: Treated mice showed no significant body weight loss (<4% change) or histopathological abnormalities in liver, kidney, or spleen; serum ALT/AST and creatinine levels were within normal ranges [1] |
| Enzyme Assay |
ITC-based STING binding assay: Recombinant human STING protein (residues 1–341) was dialyzed into binding buffer. STING inhibitor 1 (0.01–20 μM) was titrated into STING solution at 25°C, and heat changes were recorded to measure binding affinity (Ki value) [1]
- Radioligand displacement assay: Recombinant STING protein was incubated with [³H]-2'3'-cGAMP (0.5 nM) and serial dilutions of STING inhibitor 1 (0.01–10 μM) in binding buffer at 4°C for 16 hours. Bound and free radioligand were separated by filtration, and radioactivity was quantified to assess CDN binding competition [1] - STING activation inhibition assay (luciferase reporter): HEK293T cells were transfected with human STING (WT or mutants) and IFN-β luciferase reporter plasmid. After 24 hours, cells were treated with STING inhibitor 1 (0.01–10 μM) for 1 hour, then stimulated with 2'3'-cGAMP (1 μM) for 16 hours. Luciferase activity was measured to calculate IC₅₀ [1] |
| Cell Assay |
Western Blot Analysis[1]
Cell Types: L929 Cell Tested Concentrations: 10 μM Incubation Duration: 3 hrs (hours) Experimental Results: Cytoplasmic DNA-induced reduction in STING, TBK1, IRF3, IκBα and p65 phosphorylation and nuclear translocation of IRF3 and p65. IFN-β reporter gene assay: HEK293T or RAW264.7 cells were seeded in 96-well plates, transfected with STING and IFN-β luciferase reporter constructs. Cells were pretreated with STING inhibitor 1 (0.01–10 μM) for 1 hour, stimulated with 2'3'-cGAMP (1 μM) for 16 hours, and luciferase activity was detected [1] - Cytokine production assay: THP-1 monocytes were seeded in 24-well plates, pretreated with STING inhibitor 1 (0.1–10 μM) for 1 hour, then stimulated with 2'3'-cGAMP (1 μM) for 24 hours. Culture supernatants were collected for IFN-β, IL-6, and CXCL10 quantification by ELISA [1] - Western blot and qRT-PCR: Drug-treated/stimulated cells were lysed to extract protein/RNA. Western blot detected STING dimerization and IRF3 phosphorylation; qRT-PCR quantified IFN-β, IL-6, and TNF-α mRNA levels [1] - Cytotoxicity assay: THP-1, HEK293T, and normal human PBMCs were treated with STING inhibitor 1 (0.1–10 μM) for 24 hours. MTT reagent was added to measure cell viability and calculate CC₅₀ [1] |
| Animal Protocol |
STING-induced inflammation model: 6–8 weeks old C57BL/6 mice were randomly divided into vehicle group, STING inhibitor 1 5 mg/kg group, and 10 mg/kg group [1]
- Drug formulation: STING inhibitor 1 was dissolved in dimethyl sulfoxide (DMSO) and diluted with 0.5% carboxymethylcellulose sodium (CMC-Na) to a final DMSO concentration of ≤5% [1] - Administration and sample collection: Mice were administered STING inhibitor 1 via intraperitoneal injection 1 hour before intraperitoneal administration of 2'3'-cGAMP (1 mg/kg). Mice were euthanized 6 hours post-2'3'-cGAMP injection; serum was collected for cytokine ELISA; liver and spleen tissues were collected for qRT-PCR, Western blot, and histopathological analysis [1] |
| Toxicity/Toxicokinetics |
In vitro toxicity: CC₅₀ > 10 μM in THP-1, HEK293T cells and normal human peripheral blood mononuclear cells (PBMCs) [1]
- Acute in vivo toxicity: Mice injected intraperitoneally with doses up to 100 mg/kg of STING inhibitor 1 did not show death or obvious toxic symptoms (drowsiness, diarrhea) [1] - Subacute toxicity (7 days, mice): STING inhibitor 1 (10 mg/kg, intraperitoneal injection, once daily) did not cause significant changes in hematological parameters or liver and kidney function indicators (ALT, AST, creatinine) [1] - Plasma protein binding: 91% (human plasma, ultrafiltration) [1] |
| References | |
| Additional Infomation |
STING inhibitor 1 is a synthetic small molecule STING inhibitor screened through structure-based drug design, targeting the CDN binding pocket [1]. Its mechanism of action includes competitive binding to the CDN binding pocket of STING, thereby preventing the binding of CDN (e.g., 2'3'-cGAMP), STING dimerization, and activation of downstream IRF3 and NF-κB pathways, thereby inhibiting the production of type I interferon and pro-inflammatory cytokines [1]. STING overactivation is associated with autoinflammatory diseases, autoimmune diseases, and neuroinflammation; STING inhibitor 1 targets this pathway to alleviate pathological inflammation [1]. This compound has higher selectivity for STING than other innate immune receptors, good in vitro and in vivo anti-inflammatory activity, and low toxicity, supporting its potential as a therapeutic drug for STING-related diseases [1].
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| Molecular Formula |
C26H21FN2O4S
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|---|---|
| Molecular Weight |
476.5193
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| Exact Mass |
476.121
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| Elemental Analysis |
C, 65.53; H, 4.44; F, 3.99; N, 5.88; O, 13.43; S, 6.73
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| CAS # |
727699-84-5
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| PubChem CID |
5020799
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| Appearance |
White to off-white solid powder
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| LogP |
4.8
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
7
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| Heavy Atom Count |
34
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| Complexity |
751
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| Defined Atom Stereocenter Count |
0
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| SMILES |
S(C1C([H])=C([H])C(=C([H])C=1[H])F)(N([H])C1=C(C([H])=C([H])C(=C1[H])N([H])C(C1C([H])=C([H])C(=C([H])C=1[H])C1C([H])=C([H])C([H])=C([H])C=1[H])=O)OC([H])([H])[H])(=O)=O
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| InChi Key |
DVLMVJILWFSRPS-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C26H21FN2O4S/c1-33-25-16-13-22(17-24(25)29-34(31,32)23-14-11-21(27)12-15-23)28-26(30)20-9-7-19(8-10-20)18-5-3-2-4-6-18/h2-17,29H,1H3,(H,28,30)
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| Chemical Name |
N-[3-[(4-fluorophenyl)sulfonylamino]-4-methoxyphenyl]-4-phenylbenzamide
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| Synonyms |
DUN99845; DUN-99845; DUN 99845;
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~250 mg/mL (~524.64 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.36 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.0985 mL | 10.4927 mL | 20.9855 mL | |
| 5 mM | 0.4197 mL | 2.0985 mL | 4.1971 mL | |
| 10 mM | 0.2099 mL | 1.0493 mL | 2.0985 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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