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sting agonist adu s100  (InvivoGen)


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    Structured Review

    InvivoGen sting agonist adu s100
    Sting Agonist Adu S100, supplied by InvivoGen, used in various techniques. Bioz Stars score: 95/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sting+agonist+adu+s100/2%E2%80%993%E2%80%99-c-di-AM(PS)2/pmc13175861-110-1-13
    Average 95 stars, based on 39 article reviews
    sting agonist adu s100 - by Bioz Stars, 2026-11
    95/100 stars

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    other:

    Article Title: Antigen-presenting cancer-associated fibroblasts in murine pancreatic tumors differentially control regulatory T cell phenotype and function via CXCL9 and CCL22
    Article Snippet: C57BL/6J (JAX #000664), B6.Cg-Tg(TcraTcrb)425Cbn/J (JAX #004194), C57BL/6-Tg(Pdgfra-cre)1Clc/J (JAX #013148), and B6.129X1-H2-Ab1tm1Koni/J (JAX #013181) were purchased from The Jackson Laboratory.

    Article Title: A Chlamydia trachomatis CPAF-STING agonist conjugate vaccine administered intramuscularly and intradermally is immunogenic in the pig model
    Article Snippet: The STING agonist ADU-S100 (2’3’-c-di-AM(PS)2 (Rp,RP)) was prepared according to the manufacturer’s instructions (InvivoGen, San Diego, CA).



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    Dynamics of immune cell subsets in response to agonist stimulation. A Schematic of the experimental workflow. Immune profiling by flow cytometry was performed 48 h after a single intratumoral injection of PRR agonists. B Percentage of CD45 + leukocytes among live cells following intratumoral administration of different agonists: TLR3 agonist poly IC (25 µg/tumor), TLR7 agonist imiquimod hydrochloride (25 µg/tumor), TLR8 agonist TL8-506 (10 µg/tumor), TLR9 agonist CpG ODN 2395 (50 µg/tumor), STING <t>agonist</t> <t>ADU-S100</t> ammonium salt (25 µg/tumor), NOD1 agonist Tri-DAP (10 µg/tumor), and NOD2 agonist murabutide (5 µg/tumor). C Proportion of cDCs within the CD45 + population. D Percentage of ZsGreen + cells among DCs. E Proportion of macrophages within the CD45 + population. F Percentage of ZsGreen + cells among macrophages. G Proportion of CD8 + T cells within the CD45 + compartment. H Proportion of cCD4 + T cells within the CD45 + compartment. I Proportion of Tregs within the CD45 + compartment, pooled from two independent experiments. J Ratio of cCD4 + T cells to Tregs. (K) Ratio of CD8 + T cells to Tregs. Data represent the mean ± SEM ( n = 8 mice per group). Statistical comparisons were performed using one-way ANOVA. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001
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    Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations <t>of</t> <t>ADU-S100</t> and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Image Search Results


    Dynamics of immune cell subsets in response to agonist stimulation. A Schematic of the experimental workflow. Immune profiling by flow cytometry was performed 48 h after a single intratumoral injection of PRR agonists. B Percentage of CD45 + leukocytes among live cells following intratumoral administration of different agonists: TLR3 agonist poly IC (25 µg/tumor), TLR7 agonist imiquimod hydrochloride (25 µg/tumor), TLR8 agonist TL8-506 (10 µg/tumor), TLR9 agonist CpG ODN 2395 (50 µg/tumor), STING agonist ADU-S100 ammonium salt (25 µg/tumor), NOD1 agonist Tri-DAP (10 µg/tumor), and NOD2 agonist murabutide (5 µg/tumor). C Proportion of cDCs within the CD45 + population. D Percentage of ZsGreen + cells among DCs. E Proportion of macrophages within the CD45 + population. F Percentage of ZsGreen + cells among macrophages. G Proportion of CD8 + T cells within the CD45 + compartment. H Proportion of cCD4 + T cells within the CD45 + compartment. I Proportion of Tregs within the CD45 + compartment, pooled from two independent experiments. J Ratio of cCD4 + T cells to Tregs. (K) Ratio of CD8 + T cells to Tregs. Data represent the mean ± SEM ( n = 8 mice per group). Statistical comparisons were performed using one-way ANOVA. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: TLR8 agonists remodel the tumor immune microenvironment through PF4-dependent T cell recruitment and ancillary mechanisms

    doi: 10.1007/s00262-026-04329-8

    Figure Lengend Snippet: Dynamics of immune cell subsets in response to agonist stimulation. A Schematic of the experimental workflow. Immune profiling by flow cytometry was performed 48 h after a single intratumoral injection of PRR agonists. B Percentage of CD45 + leukocytes among live cells following intratumoral administration of different agonists: TLR3 agonist poly IC (25 µg/tumor), TLR7 agonist imiquimod hydrochloride (25 µg/tumor), TLR8 agonist TL8-506 (10 µg/tumor), TLR9 agonist CpG ODN 2395 (50 µg/tumor), STING agonist ADU-S100 ammonium salt (25 µg/tumor), NOD1 agonist Tri-DAP (10 µg/tumor), and NOD2 agonist murabutide (5 µg/tumor). C Proportion of cDCs within the CD45 + population. D Percentage of ZsGreen + cells among DCs. E Proportion of macrophages within the CD45 + population. F Percentage of ZsGreen + cells among macrophages. G Proportion of CD8 + T cells within the CD45 + compartment. H Proportion of cCD4 + T cells within the CD45 + compartment. I Proportion of Tregs within the CD45 + compartment, pooled from two independent experiments. J Ratio of cCD4 + T cells to Tregs. (K) Ratio of CD8 + T cells to Tregs. Data represent the mean ± SEM ( n = 8 mice per group). Statistical comparisons were performed using one-way ANOVA. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

    Article Snippet: When tumors reached approximately 200 mm 3 , PRR agonists were administered via intratumoral injection at the following doses: TLR3 agonist poly(I:C) (Sigma-Aldrich, #42,424–50-0; 25 μg/tumor); TLR7 agonist imiquimod hydrochloride (MedChemExpress, #HY-B0180A; 25 μg/tumor); TLR8 agonist TL8-506 (InvivoGen, #tlrl-tl8506; 10 μg/tumor); TLR8 agonist motolimod (MedChemExpress, #HY-13773; 50 μg/tumor); TLR9 agonist CpG ODN 2395 (Class C) (InvivoGen, #tlrl-2395–1; 50 μg/tumor); STING agonist ADU-S100 ammonium salt (MedChemExpress, #HY-12885B; 25 μg/tumor); NOD1 agonist Tri-DAP (InvivoGen, #tlrl-tdap; 10 μg/tumor); and NOD2 agonist murabutide (InvivoGen, #tlrl-mbt; 5 μg/tumor).

    Techniques: Flow Cytometry, Injection

    Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations of ADU-S100 and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: Journal of Innate Immunity

    Article Title: Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of Mycobacterium tuberculosis in Human Macrophages

    doi: 10.1159/000550530

    Figure Lengend Snippet: Activation of the cGAS-STING pathway enhances Mtb phagocytosis and intracellular clearance. a Effects of different concentrations of ADU-S100 and HCQ on THP-1 cell viability, assessed by CCK-8 assay after 24 h of treatment. b Quantification of Mtb CFU counts at 2 h post-infection to assess bacterial uptake. Both HCQ and si-cGAS significantly reduced uptake compared to control (* p < 0.05; *** p < 0.001). c Time-course analysis of intracellular Mtb survival at 24 and 48 h post-infection. ADU-S100 treatment significantly reduced intracellular bacterial load over time, while HCQ and si-cGAS treatments favored bacterial survival. Data are presented as mean ± SD from three independent experiments ( n = 3). Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: The cGAS-STING signaling pathway agonists ADU-S100 (HY-12885A) and autophagy inhibitor hydroxychloroquine (HCQ) (HY-B1370) were obtained from MCE (China).

    Techniques: Activation Assay, CCK-8 Assay, Infection, Control

    Activation of the STING signaling pathway enhances autophagy in Mtb-infected macrophages. a Western blot analysis of LC3-I to LC3-II conversion in THP-1 cells treated with 4 µ m ADU-S100, 20 µ m HCQ, or si-cGAS for 24 h during Mtb infection. β-actin was used as a loading control. b Densitometric analysis of the LC3-II/β-actin ratio from three independent experiments ( n = 3). ADU-S100 significantly increased LC3-II levels (* p < 0.05). c Representative confocal microscopy images showing the colocalization of Mtb-EGFP (green) and LysoTracker Red-stained lysosomes (red). Nuclei were stained with DAPI (blue). Scale bar = 10 µm. Quantitative analysis is provided in online suppl. Fig. 2. Data in ( b ) are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; *** p < 0.001.

    Journal: Journal of Innate Immunity

    Article Title: Pharmacological Stimulator of Interferon Genes Activation Enhances Autophagy-Mediated Clearance of Mycobacterium tuberculosis in Human Macrophages

    doi: 10.1159/000550530

    Figure Lengend Snippet: Activation of the STING signaling pathway enhances autophagy in Mtb-infected macrophages. a Western blot analysis of LC3-I to LC3-II conversion in THP-1 cells treated with 4 µ m ADU-S100, 20 µ m HCQ, or si-cGAS for 24 h during Mtb infection. β-actin was used as a loading control. b Densitometric analysis of the LC3-II/β-actin ratio from three independent experiments ( n = 3). ADU-S100 significantly increased LC3-II levels (* p < 0.05). c Representative confocal microscopy images showing the colocalization of Mtb-EGFP (green) and LysoTracker Red-stained lysosomes (red). Nuclei were stained with DAPI (blue). Scale bar = 10 µm. Quantitative analysis is provided in online suppl. Fig. 2. Data in ( b ) are presented as mean ± SD. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. * p < 0.05; *** p < 0.001.

    Article Snippet: The cGAS-STING signaling pathway agonists ADU-S100 (HY-12885A) and autophagy inhibitor hydroxychloroquine (HCQ) (HY-B1370) were obtained from MCE (China).

    Techniques: Activation Assay, Infection, Western Blot, Control, Confocal Microscopy, Staining