| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
Cell lines | Hcc-1806 cell line |
Preparation Method | Cells were treated in C-176 (STING inhibitor 1) for 8 hours at the indicated concentration, |
Reaction Conditions | 10 μM C-176 (STING inhibitor 1) for 8hs |
Applications | C-176 (STING inhibitor 1) induced apoptosis in HCC-1806 cells, C-176 (STING inhibitor 1) induced CHOP expression in HCC-1806 cells. |
Animal models | Trex1 - / - mice(2-5 weeks of age) |
Preparation Method | For toxicology studies, 8-week-old mice were injected daily with 562.5 nmol of C-176 for 2 weeks. At day 14, blood samples were collected in lithium-heparin-coated tubes. |
Dosage form | 562.5 nmol of C-176 (STING inhibitor 1) for 2 weeks |
Applications | Treatment of Trex1-/- mice with C-176 (STING inhibitor 1) resulted in a significant reduction in serum levels of type I IFNs and in a strong suppression of inflammatory parameters in the heart.We next conducted a three-month trial with C-176 (STING inhibitor 1) in Trex1-/- mice, which demonstrated marked amelioration of various signs of systemic inflammation. Thus, C-176 (STING inhibitor 1) attenuates STING-associated autoinflammatory disease in mice. |
| 产品描述 | C-176 (STING inhibitor 1) strongly reduces STING-mediated, but not RIG-I- or TBK1-mediated, IFNβ reporter activity. It directly targets mouse STING (mmSTING) but not human STING (hsSTING)[1]. Cytotoxicity against human HCC1806 cells assessed as reduction in cell viability incubated for 3 days by cell-titer-Glo reagent based assay, IC50 = 6.2 μM. C-176 (STING inhibitor 1) induced apoptosis in HCC-1806 cells, C-176 (STING inhibitor 1) induced CHOP expression in HCC-1806 cells[2].STING was mainly distributed in microglia, and microglial STING expression was significantly increased after SAH. Administration of C-176 (STING inhibitor 1) substantially attenuated SAH-induced brain edema and neuronal injury. More importantly, C-176 (STING inhibitor 1) significantly alleviated both short-term and persistent neurological dysfunction after SAH[3].Inhibition of mmSTING by C-176 (STING inhibitor 1) enhanced type H vessels' formation, implying osteogenesis promotion in bone healing (higher bone volume density and more OCN-positive cells). STING inhibition accelerates the bone healing process while enhancing type H vessel formation[7]. C-176 (STING inhibitor 1) covalently binds to Cys91 of STING preventing activation via blockade of palmitoylation at Cys91. Treatment of Trex-/- mice with C-176 (STING inhibitor 1) resulted in a significant reduction in serum levels of Type I Interferons and amelioration of systemic inflammation[1]. When explored the molecular mechanisms of STING in regulating lipopolysaccharide (LPS)-induced lung injury. Mice were pretreated with a STING inhibitor C-176 (STING inhibitor 1) (15, 30 mg/kg) before LPS inhalation to induce ALI. LPS inhalation significantly increased STING expression in the lung tissues, whereas C-176 (STING inhibitor 1) pretreatment dose-dependently suppressed the expression of STING, decreased the production of inflammatory cytokines including TNF-α, IL-6, IL-12, and IL-1β, and restrained the expression of chemokines and adhesion molecule vascular cell adhesion protein-1 (VCAM-1) in the lung tissues[4].Genetic deletion of Sting in Apoe-/- mice reduced atherosclerotic lesions in the aortic arch, lipid, and macrophage accumulation in plaques, and inflammatory molecule expression in the aorta. Pharmacological blockade of STING using a specific inhibitor, C-176 (STING inhibitor 1), ameliorated atherogenesis in Apoe-/- mice[5]. Treatment with the STING inhibitor, C-176, suppressed EBV-induced transformation in peripheral blood mononuclear cells. In an EBV-LPD mouse model, C-176 (STING inhibitor 1) treatment also inhibited tumor formation and prolonged survival[6]. References: |
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