| 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 | MRC-5 cells |
Preparation Method | 0.1, 1, 10 μM diABZI, or RDV, or DMSO as a control was added to the basolateral chamber of the ALI, followed by apical challenge with SARS-CoV-2 (Beta CoV/France/IDF0571/2020 strain) challenge apically.The viral RNA collected from apical washes at 48 h and 72 h hpi was quantified, and disruption of the epithelial layer was measured as TEER. |
Reaction Conditions | 0.1, 1, 10 μM, at 48 h and 72 h |
Applications | diABZI in all tested concentration range potently decreased the level of SARS-CoV-2 viral RNA in a dose-dependent manner. Treatment with diABZI at the concentration as low as 0.1 μM fully protected the integrity of the epithelial layer in the ALI model from SARS-CoV-2 challenge. |
Animal models | Female C57BL/6Rj mice |
Preparation Method | STING agonist diABZI (0.01, 0.1, or 1 μg, i.t.) DMSO (0.25%) vehicle or saline were administered daily in WT mice for 3 consecutive days and parameters were analyzed on day 4. Concentration of CXCL1/KC in the bronchoalveolar lavage fluid (BALF) determined by ELISA. |
Dosage form | 0.01, 0.1, or 1 μg, i.t. |
Applications | Endotracheal administration of diABZI for 3 consecutive days induced a strong airway inflammation within 24 h. CXCL1 was released in the bronchoalveolar space after 0.1–1 μg diABZI administration |
| 产品描述 | diABZI STING agonist-1 trihydrochloride, as a STING agonist, is internalized into the cytoplasm through unknown receptor and induce the activation and dimerization of STING followed by TBK1/IRF3 phosporylation leading to type I IFN response.[2] diABZI STING agonist-1 trihydrochloride can activate STING and has an effictively effect in limiting SARS-CoV-2 replication in cells and animals.[1] In vitro, diABZI dose dependently protected the cells from CPEs with an EC50 value of 3 nM, suggesting the significant anti-HCoV-229E activity comparable to that of Remdesivir (RDV, EC50 = 26 nM). Furthermore, the half maximal cytotoxic concentration value (CC50) of diABZI was greater than 100 μM in MRC-5 cells, indicating that the observed antiviral effects were not related to nonspecific cytotoxicity.[3] In vitro, treatment with 0.1 μM diABZI-4 in CD14+ human monocytes it shown that diABZI-4 (STING agonist) induced oligomerization of STING, transcription of IFNB1, TNF, CXCL10 and IL6 and the secretion of TNF-α and IFN-βin primary human CD14+ monocytes. In the meanwhile, 0.1 μM of diABZI-4 also inhibits SARS-CoV-2 replication in lung epithelial cells.[1]In vitro efficacy test, treatment with 1 μM DiABZI induced the release of IFNα, IFNβ, CXCL10, IL-6, TNFα, CXCL1, and IL-10 at 16 h. Treatment with 1–10 μM DiABZI induced the expression of IFNβ, IL-1β, and IL-8. In addition, DiABZI at 0.3–1 μM induced the phosphorylation of STING and downstream TBK1 kinase, together with STAT1 phosphorylation, similar to cGAMP.[2] In vivo experiment it indicated that after endotracheal administration of 0.1–1 μg diABZI, STING overexpression and activation visible by increased STING dimers in immunoblots of lung tissue. References: |
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