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Immunotherapy · Journal article
International Journal of Pharmaceutics: X · July 2, 2026
Encouraging direction, but not yet definitive.
A biomimetic erythrocyte membrane-camouflaged nanoplatform co-delivering Vismodegib and BMS-1 (E-V/B@NM) significantly accumulated in tumors and controllably released drugs in response to the acidic tumor microenvironment. The platform inhibited Hedgehog pathway activation, suppressed cancer-associated fibroblast ECM secretion, repolarized tumor-associated macrophages, enhanced dendritic cell maturation, boosted CD8+ T cell infiltration, and suppressed primary tumor progression and metastasis in TNBC murine models when combined with PD-1/PD-L1 inhibition.
Preclinical in vitro and in vivo study. TNBC murine models. Intervention: Erythrocyte membrane-camouflaged biomimetic nanoplatform co-delivering Vismodegib and BMS-1 (E-V/B@NM).
E-V/B@NM significantly accumulated in tumors and controllably released drugs in response to the acidic tumor microenvironment The therapeutic agents effectively inhibited Hedgehog pathway activation, suppressed ECM component secretion by CAFs, and repolarized M2-like TAMs toward M1 phenotype Synergizing with PD-1/PD-L1 inhibition, the strategy significantly enhanced dendritic cell maturation and antigen-presenting function
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This preclinical work identifies a potential strategy to overcome immunosuppression in triple-negative breast cancer by simultaneously targeting cancer-associated fibroblasts and tumor-associated macrophages. Clinical translation requires human safety and efficacy studies.
Preclinical murine model study demonstrates nanoplatform remodels tumor microenvironment and enhances immune checkpoint blockade efficacy in triple-negative breast cancer.
As stated by the source record.
This preclinical work identifies a potential strategy to overcome immunosuppression in triple-negative breast cancer by simultaneously targeting cancer-associated fibroblasts and tumor-associated macrophages. Clinical translation requires human safety and efficacy studies.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Immune checkpoint blockade (ICB) has emerged as a cornerstone therapy for triple-negative breast cancer (TNBC); however, its clinical efficacy remains suboptimal due to the immunosuppressive tumor microenvironment (TME). TNBC is characterized by persistent activation of cancer-associated fibroblasts (CAFs) and infiltration of immunosuppressive cells, particularly tumor-associated macrophages (TAMs). Notably, the Hedgehog (Hh) signaling pathway plays a crucial role in both CAF activation and TAM polarization. To address these limitations, we developed an erythrocyte membrane-camouflaged biomimetic co-delivery nanoplatform encapsulating Vismodegib and BMS-1 (designated as E-V/B@NM). In vitro and in vivo studies demonstrated that the fabricated E-V/B@NM significantly accumulated in tumors and controllably released drugs in response to the acidic TME. The therapeutic agents effectively inhibited Hh pathway activation, which consequently suppressed the secretion of extracellular matrix (ECM) components by CAFs, and repolarized M2-like TAMs toward immunostimulatory M1 phenotype. Synergizing with PD-1/PD-L1 inhibition, this strategy significantly enhanced dendritic cells (DCs) maturation and antigen-presenting function, boosted CD8+ T cell infiltration and immune response, and effectively suppressed primary tumor progression and metastasis in TNBC murine models. Our findings highlight that the biomimetic nanoplatform based on E-V/B@NM remodels the TME by reprogramming both CAFs and TAMs, thereby overcoming immunosuppression and improving ICB efficacy in TNBC.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.