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sting agonist 1a  (MedChemExpress)


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    MedChemExpress sting agonist 1a
    Schematic illustration of the design and mechanism of MD1a NP for synergistic cancer immunotherapy. (A) The HOCl-responsive methylene blue (MB)–doxorubicin (DOX) dimer prodrug co-assembles with the stimulator of interferon genes <t>(STING)</t> agonist <t>1a</t> to form a tumor-activatable nanoplatform (MD1a NP). HOCl stimulation activates and triggers the release of MB and DOX, which in turn promotes nanoparticle disassembly and facilitates the subsequent liberation of 1a. (B) Following intravenous administration, elevated intratumoral HOCl triggers the activation and the subsequent release of MB and DOX, enabling synergistic photochemotherapy under near-infrared (NIR) laser irradiation. This process induces robust immunogenic cell death (ICD) while minimizing systemic off-target effects. Concurrently, HOCl-triggered nanoparticle disassembly accelerates 1a release, activating the STING pathway and establishing an immune-promoting tumor microenvironment (TME). In orthotopic 4T1 breast cancer mouse models, MD1a NP-mediated in situ tumor vaccination (ISTV) elicited strong antitumor immunity, effectively inhibiting both primary and distant tumor growth, preventing lung metastasis, and prolonging overall survival. PDT, photodynamic therapy; DAMPs, damage-associated molecular patterns; DC, dendritic cell.
    Sting Agonist 1a, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sting agonist 1a/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    sting agonist 1a - by Bioz Stars, 2026-03
    94/100 stars

    Images

    1) Product Images from "Hypochlorous Acid-Responsive Prodrug Nanoplatform for Synergistic Cancer Immunotherapy"

    Article Title: Hypochlorous Acid-Responsive Prodrug Nanoplatform for Synergistic Cancer Immunotherapy

    Journal: Biomaterials Research

    doi: 10.34133/bmr.0300

    Schematic illustration of the design and mechanism of MD1a NP for synergistic cancer immunotherapy. (A) The HOCl-responsive methylene blue (MB)–doxorubicin (DOX) dimer prodrug co-assembles with the stimulator of interferon genes (STING) agonist 1a to form a tumor-activatable nanoplatform (MD1a NP). HOCl stimulation activates and triggers the release of MB and DOX, which in turn promotes nanoparticle disassembly and facilitates the subsequent liberation of 1a. (B) Following intravenous administration, elevated intratumoral HOCl triggers the activation and the subsequent release of MB and DOX, enabling synergistic photochemotherapy under near-infrared (NIR) laser irradiation. This process induces robust immunogenic cell death (ICD) while minimizing systemic off-target effects. Concurrently, HOCl-triggered nanoparticle disassembly accelerates 1a release, activating the STING pathway and establishing an immune-promoting tumor microenvironment (TME). In orthotopic 4T1 breast cancer mouse models, MD1a NP-mediated in situ tumor vaccination (ISTV) elicited strong antitumor immunity, effectively inhibiting both primary and distant tumor growth, preventing lung metastasis, and prolonging overall survival. PDT, photodynamic therapy; DAMPs, damage-associated molecular patterns; DC, dendritic cell.
    Figure Legend Snippet: Schematic illustration of the design and mechanism of MD1a NP for synergistic cancer immunotherapy. (A) The HOCl-responsive methylene blue (MB)–doxorubicin (DOX) dimer prodrug co-assembles with the stimulator of interferon genes (STING) agonist 1a to form a tumor-activatable nanoplatform (MD1a NP). HOCl stimulation activates and triggers the release of MB and DOX, which in turn promotes nanoparticle disassembly and facilitates the subsequent liberation of 1a. (B) Following intravenous administration, elevated intratumoral HOCl triggers the activation and the subsequent release of MB and DOX, enabling synergistic photochemotherapy under near-infrared (NIR) laser irradiation. This process induces robust immunogenic cell death (ICD) while minimizing systemic off-target effects. Concurrently, HOCl-triggered nanoparticle disassembly accelerates 1a release, activating the STING pathway and establishing an immune-promoting tumor microenvironment (TME). In orthotopic 4T1 breast cancer mouse models, MD1a NP-mediated in situ tumor vaccination (ISTV) elicited strong antitumor immunity, effectively inhibiting both primary and distant tumor growth, preventing lung metastasis, and prolonging overall survival. PDT, photodynamic therapy; DAMPs, damage-associated molecular patterns; DC, dendritic cell.

    Techniques Used: Activation Assay, Irradiation, In Situ



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    sting agonist 1a  (MedChemExpress)
    94
    MedChemExpress sting agonist 1a
    Schematic illustration of the design and mechanism of MD1a NP for synergistic cancer immunotherapy. (A) The HOCl-responsive methylene blue (MB)–doxorubicin (DOX) dimer prodrug co-assembles with the stimulator of interferon genes <t>(STING)</t> agonist <t>1a</t> to form a tumor-activatable nanoplatform (MD1a NP). HOCl stimulation activates and triggers the release of MB and DOX, which in turn promotes nanoparticle disassembly and facilitates the subsequent liberation of 1a. (B) Following intravenous administration, elevated intratumoral HOCl triggers the activation and the subsequent release of MB and DOX, enabling synergistic photochemotherapy under near-infrared (NIR) laser irradiation. This process induces robust immunogenic cell death (ICD) while minimizing systemic off-target effects. Concurrently, HOCl-triggered nanoparticle disassembly accelerates 1a release, activating the STING pathway and establishing an immune-promoting tumor microenvironment (TME). In orthotopic 4T1 breast cancer mouse models, MD1a NP-mediated in situ tumor vaccination (ISTV) elicited strong antitumor immunity, effectively inhibiting both primary and distant tumor growth, preventing lung metastasis, and prolonging overall survival. PDT, photodynamic therapy; DAMPs, damage-associated molecular patterns; DC, dendritic cell.
    Sting Agonist 1a, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/sting agonist 1a/product/MedChemExpress
    Average 94 stars, based on 1 article reviews
    sting agonist 1a - by Bioz Stars, 2026-03
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    Schematic illustration of the design and mechanism of MD1a NP for synergistic cancer immunotherapy. (A) The HOCl-responsive methylene blue (MB)–doxorubicin (DOX) dimer prodrug co-assembles with the stimulator of interferon genes (STING) agonist 1a to form a tumor-activatable nanoplatform (MD1a NP). HOCl stimulation activates and triggers the release of MB and DOX, which in turn promotes nanoparticle disassembly and facilitates the subsequent liberation of 1a. (B) Following intravenous administration, elevated intratumoral HOCl triggers the activation and the subsequent release of MB and DOX, enabling synergistic photochemotherapy under near-infrared (NIR) laser irradiation. This process induces robust immunogenic cell death (ICD) while minimizing systemic off-target effects. Concurrently, HOCl-triggered nanoparticle disassembly accelerates 1a release, activating the STING pathway and establishing an immune-promoting tumor microenvironment (TME). In orthotopic 4T1 breast cancer mouse models, MD1a NP-mediated in situ tumor vaccination (ISTV) elicited strong antitumor immunity, effectively inhibiting both primary and distant tumor growth, preventing lung metastasis, and prolonging overall survival. PDT, photodynamic therapy; DAMPs, damage-associated molecular patterns; DC, dendritic cell.

    Journal: Biomaterials Research

    Article Title: Hypochlorous Acid-Responsive Prodrug Nanoplatform for Synergistic Cancer Immunotherapy

    doi: 10.34133/bmr.0300

    Figure Lengend Snippet: Schematic illustration of the design and mechanism of MD1a NP for synergistic cancer immunotherapy. (A) The HOCl-responsive methylene blue (MB)–doxorubicin (DOX) dimer prodrug co-assembles with the stimulator of interferon genes (STING) agonist 1a to form a tumor-activatable nanoplatform (MD1a NP). HOCl stimulation activates and triggers the release of MB and DOX, which in turn promotes nanoparticle disassembly and facilitates the subsequent liberation of 1a. (B) Following intravenous administration, elevated intratumoral HOCl triggers the activation and the subsequent release of MB and DOX, enabling synergistic photochemotherapy under near-infrared (NIR) laser irradiation. This process induces robust immunogenic cell death (ICD) while minimizing systemic off-target effects. Concurrently, HOCl-triggered nanoparticle disassembly accelerates 1a release, activating the STING pathway and establishing an immune-promoting tumor microenvironment (TME). In orthotopic 4T1 breast cancer mouse models, MD1a NP-mediated in situ tumor vaccination (ISTV) elicited strong antitumor immunity, effectively inhibiting both primary and distant tumor growth, preventing lung metastasis, and prolonging overall survival. PDT, photodynamic therapy; DAMPs, damage-associated molecular patterns; DC, dendritic cell.

    Article Snippet: All solvents were obtained from Sinopharm Chemical Reagent Co., Ltd. STING agonist 1a (HY-131994) and Cell Counting Kit-8 (CCK-8) were purchased from MedChemExpress, China.

    Techniques: Activation Assay, Irradiation, In Situ