To enhance service speed and avoid tariff delays, we've opened a US warehouse. All US orders ship directly from our US facility.
| Cas No.: | 1638750-96-5 |
| Chemical Name: | Adenosine, [P(R)]-5'-O-[(R)-hydroxymercaptophosphinyl]-P-thioadenylyl-(2'→5')-, cyclic nucleotide, ammonium salt (1:2) |
| Synonyms: | STING-Inducer-1 ammonium salt |
| SMILES: | OC1([H])[C@](O[P@](S)(OC[C@](O[C@@H](N2C3=NC=NC(N)=C3N=C2)[C@@H]4O)([H])[C@@]4([H])O5)=O)([H])[C@H](N6C7=NC=NC(N)=C7N=C6)O[C@]1([H])CO[P@]5(S)=O.N.N |
| Formula: | C20H30N12O10P2S2 |
| M.Wt: | 724.604124 |
| Purity: | >98% |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | ADU-S100 ammonium salt is an activator of stimulator of interferon genes (STING). |
| Target: | STING[1] |
| In Vivo: | ADU-S100 shows higher anti-tumor control than the endogenous ML cGAMP. A dose response of the ADU-S100 compound is performed in B16 tumor-bearing mice, which identifies an optimal antitumor dose level that also elicites maximum tumor antigen-specific CD8+ T cell responses, and improves long-term survival to 50%[1]. |
| In Vitro: | ADU-S100 shows enhanced type I IFN production over CDA in THP-1 human monocytes. In contrast, the dithio, mixed-linkage cyclic dinucleotide (CDN) derivatives (ML RR-CDA, ML RR-S2 CDG, and ML RR-S2 cGAMP) potently activate all five hSTING alleles, including the refractory hSTINGREF and hSTINGQ alleles. ADU-S100 induces the highest expression of IFN-β and the pro-inflammatory cytokines TNF-α, IL-6, and MCP-1 on a molar equivalent basis, as compared to endogenous ML cGAMP and the TLR3 agonist poly I:C. ADU-S100 is also found to induce aggregation of STING and induce phosphorylation of TBK1 and IRF3 in mouse bone marrow macrophage (BMM). ADU-S100 induces significantly higher levels of IFN-α when compared to ML cGAMP[1]. |
| Cell Assay: | Cryopreserved hPBMCs are thawed and 1×106 cells per well are plated in a 96 well plate in RPMI media supplemented with 10% FBS, 1% non-essential amino acids, 1% penicillin/streptomycin, L-glutamine, 10 mM HEPES buffer, 1 mM Sodium Pyruvate, 0.055 mM β-ME at 37°C with 5% CO2. Cells are stimulated with 10 μM ADU-S100 or ML cGAMP for 6 hours and supernatants are harvested. Supernatants are diluted 1:2 and assayed for IFN-α protein using Cytometric Bead Array (CBA) Human Flex Set. Data is collected using a FACSVerse cytometer and analyzed by FCAP Array Software[1]. |
| Animal Administration: | Mice[1] WT C57BL/6 mice are inoculated with 5×104 B16.F10 cells in the left flank (n=8). When tumor volumes are 100 mm3 mice receive three IT doses of either ML RR-S2 CDG (25 μg), ADU-S100 (50 μg), or HBSS as control. WT C57BL/6 mice are inoculated with 5×104 B16.F10 cells in the left flank (n=5). When tumor volumes are 100 mm3 they received three IT doses of ADU-S100 at 5, 25, 50 or 100 μg or HBSS as control. WT C57BL/6 mice are inoculated with 5×104 B16.F10 cells in the left flank (n=8). When tumor volumes are 100 mm3 they receive three IT doses of 100 μg ADU-S100 or HBSS as control. Treatments are administered on days 13, 17 and 20 and tumor measurements are taken twice weekly. Results are shown as percent survival by Log-rank (Mantel-Cox) test (A and C). |
| References: | [1]. Corrales L, et al. Direct Activation of STING in the Tumor Microenvironment Leads to Potent and Systemic Tumor Regression and Immunity. Cell Rep. 2015 May 19;11(7):1018-30. |
MSDS
COA
| LOT NO. | DOWNLOAD |
|
|
|
| 2018-0101 |
|
| 2018-0101 |
|