C-176 (STING inhibitor 1) |
Catalog No.GC33823
One-Click Copy Product Info
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C-176 (STING inhibitor 1) strongly reduces STING-mediated, but not RIG-I- or TBK1-mediated, IFNβ reporter activity.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 314054-00-7
Sample solution is provided at 25 µL, 10mM.
C-176 (STING inhibitor 1) is a selective and blood-brain-barrier permeable STING inhibitor. C-176 covalently binds to Cys91 of STING via its nitrofuran group. C-176 blocks STING activation-induced palmitoylation. C-176 inhibits STING assembly into multimeric complexes at the Golgi apparatus. C-176 blocks downstream TBK1/IRF3 and NF-κB signaling pathways. C-176 reduces type I interferon production. C-176 reduces inflammatory cytokines including IL-1β, IL-6, TNF-α, and MCP-1. C-176 reduces NLRP3 inflammasome formation. C-176 modulates immune cell polarization. C-176 can be used in studies related to Parkinson's disease-associated neuroinflammation, acute lung injury, traumatic brain injury, subarachnoid hemorrhage, inflammatory bone resorption/osteoarthritis, systemic lupus erythematosus-like autoimmune disease, and Epstein-Barr virus-associated lymphoproliferative disorders[1-4].
In vitro, treatment of 4T1 cells with 2μM C-176 for 12 hours reduced total STING protein levels and phosphorylated STING protein levels[5]. Pretreatment of Lewis lung carcinoma (LLC) cells with 20μM C-176 for 1 hour followed by 4Gy X-ray irradiation inhibited total STING, phosphorylated TBK1, and phosphorylated IRF3 protein expression, and blocked IRF3 translocation from cytoplasm to nucleus[6]. Co-treatment of GMI-R1 cells with 20μM C-176 and 1μg/mL LPS for 24 hours reduced phosphorylated TBK1 and phosphorylated NF-κB protein levels, reduced MHCII protein expression, and increased CD206 protein expression[7].
In vivo, male C57BL/6J mice received intraperitoneal injection of 1mg/mL C-176 at 24h before, 2h after, and 24h after 20Gy whole-thorax irradiation. C-176 ameliorated alveolar wall thickening, alveolar collapse, diffuse inflammatory cell infiltration, and excessive extracellular matrix deposition. This reduced collagen deposition and pulmonary fibrosis[8]. HSV-2 and Candida albicans co-infected BALB/c mice received intraperitoneal injection of 750nmol C-176 daily for 9 consecutive days. C-176 aggravated vulvar ulcer with purulent exudate, vaginal redness and swelling, and body weight loss[9]. C57BL/6J mice bearing subcutaneous LLC1-ISRE-Luc cell xenografts received intraperitoneal injection of 750nmol C-176 daily for 18 consecutive days combined with 20mg/kg Tetrandrine. C-176 reversed Tetrandrine-induced reduction in tumor volume and weight[10].
References:
[1] Haag SM, Gulen MF, Reymond L, et al. Targeting STING with covalent small-molecule inhibitors. Nature. 2018 Jul;559(7713):269-273.
[2] Yu ZC, Fu R, Li Y, et al. The STING inhibitor C-176 attenuates osteoclast-related osteolytic diseases by inhibiting osteoclast differentiation. FASEB J. 2023;37(4):e22855.
[3] Fan MW, Tian JL, Chen T, et al. Role of cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes pathway in diabetes and its complications. World J Diabetes. 2024 Oct 15;15(10):2041-2057.
[4] Huang J, Xie J, Wang Y, et al. STING mediates increased self-renewal and lineage skewing in DNMT3A-mutated hematopoietic stem/progenitor cells. Leukemia. 2025;39(4):929-941.
[5] Bai B, Zhang L, Zhang Y, et al. Astragaloside IV potentiates cisplatin sensitivity in triple-negative breast cancer via STING signaling pathway activation. Phytomedicine. 2025;148:157330.
[6] Zhao X, Hu S, Zeng L, et al. Irradiation combined with PD-L1-/- and autophagy inhibition enhances the antitumor effect of lung cancer via cGAS-STING-mediated T cell activation. iScience. 2022 Aug 19;25(8):104690.
[7] Zhang X, Li X, Wang W, et al. STING Contributes to Cancer-Induced Bone Pain by Promoting M1 Polarization of Microglia in the Medial Prefrontal Cortex. Cancers. 2022 Oct;14(21):5188.
[8] Zhao X, Du L, Ma N, et al. The role of cGAS-STING pathway in the development of radiation-induced lung injury. J Cancer Res Clin Oncol. 2025;151:48.
[9] Jin X, Jiang W, Zhao X, et al. Efficacy and mechanism of topical Chinese herbal formulation JieZe-1 on female lower genital tract co-infection with HSV-2 and Candida albicans via upregulating the cGAS/STING/IFN-I pathway. J Ethnopharmacol. 2026;368:121842.
[10] Tan Y, Zhu Q, Yang M, et al. Tetrandrine activates STING/TBK1/IRF3 pathway to potentiate anti-PD-1 immunotherapy efficacy in non-small cell lung cancer. Pharmacol Res. 2024;207:107314.
| Cell experiment [1]: | |
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Cell lines |
GMI-R1 cells (rat microglia cell line) |
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Preparation Method |
GMI-R1 cells were cultured in H-DMEM with 10% FBS and 1% penicillin-streptomycin at 37°C, 5% CO2. Cells were treated with 1μg/mL LPS alone for 24h, or pretreated with 20μM C-176 followed by 1μg/mL LPS for 24h. After treatment, mitochondrial superoxide was measured by MitoSOX Red staining, STING/TBK1/NF-κB signaling by Western blot (STING, p-TBK1/TBK1, p-NF-κB/NF-κB), microglia polarization by Western blot (MHCII as M1 marker, CD206 as M2 marker), and IL-1β by Western blot. |
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Reaction Conditions |
20μM; 24h co-treatment with 1μg/mL LPS |
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Applications |
C-176 did not change mitochondrial superoxide levels or total STING protein levels in LPS-stimulated GMI-R1 cells. C-176 reduced LPS-induced phosphorylation of TBK1 and NF-κB in GMI-R1 cells. C-176 reduced LPS-induced MHCII protein levels in GMI-R1 cells. C-176 increased CD206 protein levels in LPS-stimulated GMI-R1 cells. C-176 reduced LPS-induced IL-1β protein levels in GMI-R1 cells. |
| Animal experiment [2]: | |
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Animal models |
6-8-week-old male C57BL/6J mice (whole-thorax irradiation-induced radiation-induced lung injury model) |
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Preparation Method |
Mice were irradiated with a single dose of 20Gy whole-thorax irradiation (60Co-γ, 1Gy/min). 1mg/mL C-176 was administered by intraperitoneal injection at 24h before irradiation, 2h after irradiation, and 24h after irradiation (200μL per injection). Mice were sacrificed at 7 days (early inflammation), 8 weeks and 16 weeks (late fibrosis) for H&E and Masson staining, lung coefficient measurement, Western blot of STING/cGAS/p-TBK1/p-IRF3, and serum ELISA (TGF-β1, ET-1, IFN-γ, TNF-α, IL-1, IL-4, IL-13). |
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Dosage form |
1mg/mL; i.p.; 3 injections (24h pre-IR, 2h post-IR, 24h post-IR) |
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Applications |
C-176 reduced lung tissue STING and cGAS protein levels. C-176 reduced phosphorylated TBK1 and phosphorylated IRF3 levels in lung tissue. C-176 ameliorated radiation-induced alveolar wall thickening, alveolar collapse, inflammatory cell infiltration and extracellular matrix deposition. C-176 reduced lung coefficient (lung weight/body weight). C-176 reduced Masson's trichrome collagen deposition at 8 and 16 weeks. C-176 reduced serum TGF-β1 and ET-1 levels. C-176 reduced serum IFN-γ, TNF-α and IL-1 levels at early stage. C-176 reduced serum IL-4 and IL-13 levels at 8 weeks. |
References: [1] Zhang X, Li X, Wang W, et al. STING Contributes to Cancer-Induced Bone Pain by Promoting M1 Polarization of Microglia in the Medial Prefrontal Cortex. Cancers. 2022 Oct 22;14(21):5188. [2] Zhao X, Du L, Ma N, et al. The role of cGAS-STING pathway in the development of radiation-induced lung injury. J Cancer Res Clin Oncol. 2025;151:48. | |
| Cas No. | 314054-00-7 | SDF | |
| Canonical SMILES | O=C(C1=CC=C([N+]([O-])=O)O1)NC2=CC=C(I)C=C2 | ||
| Formula | C11H7IN2O4 | M.Wt | 358.09 |
| Solubility | DMSO : 150 mg/mL (418.89 mM) | Storage | Store at -20°C |
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7926 mL | 13.963 mL | 27.9259 mL |
| 5 mM | 558.5 μL | 2.7926 mL | 5.5852 mL |
| 10 mM | 279.3 μL | 1.3963 mL | 2.7926 mL |
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- Purity: >98.00% Appearance: A solid
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Average Rating: 5 (Based on Reviews and 8 reference(s) in Google Scholar.)