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vx 765  (MedChemExpress)


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    Structured Review

    MedChemExpress vx 765
    Vx 765, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 237 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/vx+765/Belnacasan/pm42571819-80-29-31
    Average 97 stars, based on 237 article reviews
    vx 765 - by Bioz Stars, 2026-11
    97/100 stars

    Images

    Related Articles

    Magnetic Beads:

    Article Title: African swine fever virus pEP364R acts as an important inflammatory-inducing factor to activate NLRP3 inflammasome-mediated pyroptosis by regulating DDX3X.
    Article Snippet: All the cells are cultured with RPMI 1640 or DMEM (Gibco, USA) with 10% fetal bovine serum (FBS) (Aoqing Biotechnology Co.,LTD, Beijing, China). .. Lipopolysaccharide (LPS), nigericin, MCC950, VX-765, DSS Crosslinker, and Protein A/G Magnetic Beads were purchased from MCE. .. RK-33 was purchased from TargetMol.

    Staining:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Activity Assay:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Lactate Dehydrogenase Assay:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Serine synergizes with lipopolysaccharide to induce macrophage pyroptosis through extracellular Hsp90α and early skin immune microenvironment disruption in diabetic foot.
    Article Snippet: Background: The pathogenesis of early-stage skin lesions in diabetic foot (DF) remains poorly understood, and cannot be fully explained by conventional theories.. Skin microbiota dysbiosis has recently emerged as a critical factor, but the underlying mechanisms remain unclear.. Methods: In this study, we integrated metabolomics and metagenomics analyses of skin samples to investigate metabolic dysregulation driven by microbial dysbiosis.

    Infection:

    Article Title: Integrated transcriptomic and proteomic analysis reveals inflammatory activation and blood-brain barrier disruption during meningitis-associated extraintestinal pathogenic Escherichia coli infection
    Article Snippet: Cytotoxicity was assessed by measuring lactate dehydrogenase (LDH) release using the LDH Cytotoxicity Assay Kit (Beyotime, China) according to the manufacturer’s instructions. .. For inhibitor experiments, hCMEC/D3 cells were pretreated for 1 h with BAPTA-AM (10 μM), Necrostatin-1 (10 μM), VX-765 (10 μM), or Z-DEVD-FMK (20 μM) (all from MedChemExpress, USA) prior to RS218 infection. ..

    In Vitro:


    other:

    Article Title: IL-17RA Promotes Cigarette Smoke-Induced Alveolar Epithelial Cell Pyroptosis in COPD via Dual Activation of the NLRP3/Caspase1/GSDMD and NF-κB/GSDME Pathways
    Article Snippet: MCC950 (Item No. HY-12815), VX-765 (Item No. HY-13205), IL-17A (Item No. HY- P70527 ) were all procured from MCE Corporation in New Jersey, USA.



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    Ability of inhibitors of the NLRP3 inflammasome <t>or</t> <t>caspase-1</t> to inhibit BzATP-induced IL-1β and IL-18 release from LPS-primed hMDM. Human monocyte-derived microglia (hMDM) cultures were preincubated for 1 h in the absence (vehicle) or presence of the NLRP3 inflammasome inhibitor MCC950 ( A and B ) or the caspase-1 <t>inhibitor</t> <t>VX-765</t> ( C and D ) prior to priming with LPS (100 ng/ml; 2 h), followed by stimulation with BzATP (100 μM) for 4 h. ( A and D ) Three circles to the left ( left y -axis; mean ± SEM) display IL-1β or IL-18 levels in the cell culture supernatants and curve fits (iterative curve fit according to a four-parameter logistic equation) of the impact of the MCC950 or VX-765 upon percentage release relative to the LPS + BzATP response (open circles; 100 µM BzATP). Data are expressed as the mean ± standard error of the mean from five independent donors. Significance was determined using a one-way ANOVA with Dunnett’s post hoc test for comparison of picograms per millilitre BzATP-induced IL-1β or IL-18 release compared with either LPS or vehicle control ( left y -axis), or for comparison of the percentage IL-1β or IL-18 release at each concentration of inhibitor to their relative vehicle control (set to 100%; right y -axis). Significant difference between indicated data: *** P < 0.001. Significant difference from LPS + BzATP: ++ P < 0.01 and +++ P < 0.001. BzATP = 2′(3′)- O -(4-benzoylbenzoyl) ATP; IL = interleukin; LPS = lipopolysaccharide.
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    Ability of inhibitors of the NLRP3 inflammasome <t>or</t> <t>caspase-1</t> to inhibit BzATP-induced IL-1β and IL-18 release from LPS-primed hMDM. Human monocyte-derived microglia (hMDM) cultures were preincubated for 1 h in the absence (vehicle) or presence of the NLRP3 inflammasome inhibitor MCC950 ( A and B ) or the caspase-1 <t>inhibitor</t> <t>VX-765</t> ( C and D ) prior to priming with LPS (100 ng/ml; 2 h), followed by stimulation with BzATP (100 μM) for 4 h. ( A and D ) Three circles to the left ( left y -axis; mean ± SEM) display IL-1β or IL-18 levels in the cell culture supernatants and curve fits (iterative curve fit according to a four-parameter logistic equation) of the impact of the MCC950 or VX-765 upon percentage release relative to the LPS + BzATP response (open circles; 100 µM BzATP). Data are expressed as the mean ± standard error of the mean from five independent donors. Significance was determined using a one-way ANOVA with Dunnett’s post hoc test for comparison of picograms per millilitre BzATP-induced IL-1β or IL-18 release compared with either LPS or vehicle control ( left y -axis), or for comparison of the percentage IL-1β or IL-18 release at each concentration of inhibitor to their relative vehicle control (set to 100%; right y -axis). Significant difference between indicated data: *** P < 0.001. Significant difference from LPS + BzATP: ++ P < 0.01 and +++ P < 0.001. BzATP = 2′(3′)- O -(4-benzoylbenzoyl) ATP; IL = interleukin; LPS = lipopolysaccharide.
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    MedChemExpress inhibitors vx 765
    ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with <t>VX-765,</t> Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.
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    InvivoGen small molecule caspase 1 4 inhibitor vx 765
    ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with <t>VX-765,</t> Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.
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    MedChemExpress caspase 1 inhibitor vx 765
    ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with <t>VX-765,</t> Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.
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    MedChemExpress belnacasan vx 765
    In vivo anti-tumor efficacy and immune evaluation (A) Schematic illustration of the in vivo treatment procedure. (B) Average tumor growth curves of each group. (C) H&E and Ki-67 staining of tumor sections (scale bar: H&E, 200 μm; Ki-67, 100 μm). (D) Immunofluorescence staining of NLRP3, C-Cas-1, and GSDMD-N in tumor sections (scale bar: 100 μm). (E) Schematic illustration of the immune evaluation procedure. (F–M) Flow cytometry analysis of CD80 + CD86 + DCs in CD11c + cells (F), CD8 + CD3 + T cells in CD45 + cells (G), CD4 + CD3 + T cells in CD45 + cells (H), IFN-γ + CD8 + T cells in CD3 + CD45 + cells (I), CD49b + NK cells in CD3 − CD45 + cells (J), the ratio of M1 to M2 macrophages (K), Foxp3 + CD4 + Tregs in CD3 + CD45 + cells (L), and Gr-1 + CD11b + MDSCs in CD45 + cells (M). (N) ELISA assay for the detection of the cytokines TNF-α, IL-1β, IFN-γ, and IL-12p70 within the tumor. (O) Schematic illustration of the treatment and evaluation procedure in combination with <t>VX-765.</t> (P) Average tumor growth curves of each group. (Q–V) Flow cytometry analysis of DCs (Q), CD8 + T cells (R), CD4 + T cells (S), NK cells (T), MDSCs (U), and Arg-1 + MDSCs (V). (W) Schematic illustration of the treatment procedure in combination with αLy6G/Ly6C (Gr-1). (X) Average tumor growth curves of each group. (Y) Immunofluorescence staining of CD8 and CD4 in tumor sections (scale bar: 100 μm). The data were presented as mean ± SD from n = 5. Statistical significance was calculated by two-way ANOVA comparison test in (B) by day 10 and in (P) and (X), one-way ANOVA with Dunnett’s comparison test in (F)–(M), and with Tukey’s comparison test in (Q)–(V).
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    InvivoGen vx765
    In vivo anti-tumor efficacy and immune evaluation (A) Schematic illustration of the in vivo treatment procedure. (B) Average tumor growth curves of each group. (C) H&E and Ki-67 staining of tumor sections (scale bar: H&E, 200 μm; Ki-67, 100 μm). (D) Immunofluorescence staining of NLRP3, C-Cas-1, and GSDMD-N in tumor sections (scale bar: 100 μm). (E) Schematic illustration of the immune evaluation procedure. (F–M) Flow cytometry analysis of CD80 + CD86 + DCs in CD11c + cells (F), CD8 + CD3 + T cells in CD45 + cells (G), CD4 + CD3 + T cells in CD45 + cells (H), IFN-γ + CD8 + T cells in CD3 + CD45 + cells (I), CD49b + NK cells in CD3 − CD45 + cells (J), the ratio of M1 to M2 macrophages (K), Foxp3 + CD4 + Tregs in CD3 + CD45 + cells (L), and Gr-1 + CD11b + MDSCs in CD45 + cells (M). (N) ELISA assay for the detection of the cytokines TNF-α, IL-1β, IFN-γ, and IL-12p70 within the tumor. (O) Schematic illustration of the treatment and evaluation procedure in combination with <t>VX-765.</t> (P) Average tumor growth curves of each group. (Q–V) Flow cytometry analysis of DCs (Q), CD8 + T cells (R), CD4 + T cells (S), NK cells (T), MDSCs (U), and Arg-1 + MDSCs (V). (W) Schematic illustration of the treatment procedure in combination with αLy6G/Ly6C (Gr-1). (X) Average tumor growth curves of each group. (Y) Immunofluorescence staining of CD8 and CD4 in tumor sections (scale bar: 100 μm). The data were presented as mean ± SD from n = 5. Statistical significance was calculated by two-way ANOVA comparison test in (B) by day 10 and in (P) and (X), one-way ANOVA with Dunnett’s comparison test in (F)–(M), and with Tukey’s comparison test in (Q)–(V).
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    Image Search Results


    Ability of inhibitors of the NLRP3 inflammasome or caspase-1 to inhibit BzATP-induced IL-1β and IL-18 release from LPS-primed hMDM. Human monocyte-derived microglia (hMDM) cultures were preincubated for 1 h in the absence (vehicle) or presence of the NLRP3 inflammasome inhibitor MCC950 ( A and B ) or the caspase-1 inhibitor VX-765 ( C and D ) prior to priming with LPS (100 ng/ml; 2 h), followed by stimulation with BzATP (100 μM) for 4 h. ( A and D ) Three circles to the left ( left y -axis; mean ± SEM) display IL-1β or IL-18 levels in the cell culture supernatants and curve fits (iterative curve fit according to a four-parameter logistic equation) of the impact of the MCC950 or VX-765 upon percentage release relative to the LPS + BzATP response (open circles; 100 µM BzATP). Data are expressed as the mean ± standard error of the mean from five independent donors. Significance was determined using a one-way ANOVA with Dunnett’s post hoc test for comparison of picograms per millilitre BzATP-induced IL-1β or IL-18 release compared with either LPS or vehicle control ( left y -axis), or for comparison of the percentage IL-1β or IL-18 release at each concentration of inhibitor to their relative vehicle control (set to 100%; right y -axis). Significant difference between indicated data: *** P < 0.001. Significant difference from LPS + BzATP: ++ P < 0.01 and +++ P < 0.001. BzATP = 2′(3′)- O -(4-benzoylbenzoyl) ATP; IL = interleukin; LPS = lipopolysaccharide.

    Journal: Brain

    Article Title: P2X7 receptor-mediated IL-1β release by human brain tissue: the impact of CNS-penetrant potential therapeutics

    doi: 10.1093/brain/awag068

    Figure Lengend Snippet: Ability of inhibitors of the NLRP3 inflammasome or caspase-1 to inhibit BzATP-induced IL-1β and IL-18 release from LPS-primed hMDM. Human monocyte-derived microglia (hMDM) cultures were preincubated for 1 h in the absence (vehicle) or presence of the NLRP3 inflammasome inhibitor MCC950 ( A and B ) or the caspase-1 inhibitor VX-765 ( C and D ) prior to priming with LPS (100 ng/ml; 2 h), followed by stimulation with BzATP (100 μM) for 4 h. ( A and D ) Three circles to the left ( left y -axis; mean ± SEM) display IL-1β or IL-18 levels in the cell culture supernatants and curve fits (iterative curve fit according to a four-parameter logistic equation) of the impact of the MCC950 or VX-765 upon percentage release relative to the LPS + BzATP response (open circles; 100 µM BzATP). Data are expressed as the mean ± standard error of the mean from five independent donors. Significance was determined using a one-way ANOVA with Dunnett’s post hoc test for comparison of picograms per millilitre BzATP-induced IL-1β or IL-18 release compared with either LPS or vehicle control ( left y -axis), or for comparison of the percentage IL-1β or IL-18 release at each concentration of inhibitor to their relative vehicle control (set to 100%; right y -axis). Significant difference between indicated data: *** P < 0.001. Significant difference from LPS + BzATP: ++ P < 0.01 and +++ P < 0.001. BzATP = 2′(3′)- O -(4-benzoylbenzoyl) ATP; IL = interleukin; LPS = lipopolysaccharide.

    Article Snippet: For experiments investigating inflammasome pathway modulation, hMDM were preincubated with the selective inflammasome inhibitor MCC950 (Selleck Chemicals) or the selective caspase-1 inhibitor VX-765 (InvivoGen) or relevant vehicle (water/DMSO; 0.03%) for 1 h prior to priming with LPS (100 ng/ml), for 2 h, followed by stimulation with BzATP for 4 h.

    Techniques: Derivative Assay, Cell Culture, Comparison, Control, Concentration Assay

    ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with VX-765, Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.

    Journal: Science Advances

    Article Title: Chemo-metallo nanodrivers for spatiotemporally controlled in situ vaccination

    doi: 10.1126/sciadv.aee4577

    Figure Lengend Snippet: ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with VX-765, Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.

    Article Snippet: The pharmacological inhibitors VX-765, Ac-DEVD-CHO, and Nec-1 were purchased from MedChemExpress (USA).

    Techniques: Control, Staining, Fluorescence, Microscopy, Flow Cytometry, Immunofluorescence, Western Blot, Analysis, Activity Assay, Expressing, Immune Cell, Two Tailed Test

    In vivo anti-tumor efficacy and immune evaluation (A) Schematic illustration of the in vivo treatment procedure. (B) Average tumor growth curves of each group. (C) H&E and Ki-67 staining of tumor sections (scale bar: H&E, 200 μm; Ki-67, 100 μm). (D) Immunofluorescence staining of NLRP3, C-Cas-1, and GSDMD-N in tumor sections (scale bar: 100 μm). (E) Schematic illustration of the immune evaluation procedure. (F–M) Flow cytometry analysis of CD80 + CD86 + DCs in CD11c + cells (F), CD8 + CD3 + T cells in CD45 + cells (G), CD4 + CD3 + T cells in CD45 + cells (H), IFN-γ + CD8 + T cells in CD3 + CD45 + cells (I), CD49b + NK cells in CD3 − CD45 + cells (J), the ratio of M1 to M2 macrophages (K), Foxp3 + CD4 + Tregs in CD3 + CD45 + cells (L), and Gr-1 + CD11b + MDSCs in CD45 + cells (M). (N) ELISA assay for the detection of the cytokines TNF-α, IL-1β, IFN-γ, and IL-12p70 within the tumor. (O) Schematic illustration of the treatment and evaluation procedure in combination with VX-765. (P) Average tumor growth curves of each group. (Q–V) Flow cytometry analysis of DCs (Q), CD8 + T cells (R), CD4 + T cells (S), NK cells (T), MDSCs (U), and Arg-1 + MDSCs (V). (W) Schematic illustration of the treatment procedure in combination with αLy6G/Ly6C (Gr-1). (X) Average tumor growth curves of each group. (Y) Immunofluorescence staining of CD8 and CD4 in tumor sections (scale bar: 100 μm). The data were presented as mean ± SD from n = 5. Statistical significance was calculated by two-way ANOVA comparison test in (B) by day 10 and in (P) and (X), one-way ANOVA with Dunnett’s comparison test in (F)–(M), and with Tukey’s comparison test in (Q)–(V).

    Journal: Cell Reports Medicine

    Article Title: STAT3 interference-driven nanomodulators reverse lipid metabolism-associated chemoresistance and potentiate metalloimmunotherapy in breast cancer

    doi: 10.1016/j.xcrm.2026.102844

    Figure Lengend Snippet: In vivo anti-tumor efficacy and immune evaluation (A) Schematic illustration of the in vivo treatment procedure. (B) Average tumor growth curves of each group. (C) H&E and Ki-67 staining of tumor sections (scale bar: H&E, 200 μm; Ki-67, 100 μm). (D) Immunofluorescence staining of NLRP3, C-Cas-1, and GSDMD-N in tumor sections (scale bar: 100 μm). (E) Schematic illustration of the immune evaluation procedure. (F–M) Flow cytometry analysis of CD80 + CD86 + DCs in CD11c + cells (F), CD8 + CD3 + T cells in CD45 + cells (G), CD4 + CD3 + T cells in CD45 + cells (H), IFN-γ + CD8 + T cells in CD3 + CD45 + cells (I), CD49b + NK cells in CD3 − CD45 + cells (J), the ratio of M1 to M2 macrophages (K), Foxp3 + CD4 + Tregs in CD3 + CD45 + cells (L), and Gr-1 + CD11b + MDSCs in CD45 + cells (M). (N) ELISA assay for the detection of the cytokines TNF-α, IL-1β, IFN-γ, and IL-12p70 within the tumor. (O) Schematic illustration of the treatment and evaluation procedure in combination with VX-765. (P) Average tumor growth curves of each group. (Q–V) Flow cytometry analysis of DCs (Q), CD8 + T cells (R), CD4 + T cells (S), NK cells (T), MDSCs (U), and Arg-1 + MDSCs (V). (W) Schematic illustration of the treatment procedure in combination with αLy6G/Ly6C (Gr-1). (X) Average tumor growth curves of each group. (Y) Immunofluorescence staining of CD8 and CD4 in tumor sections (scale bar: 100 μm). The data were presented as mean ± SD from n = 5. Statistical significance was calculated by two-way ANOVA comparison test in (B) by day 10 and in (P) and (X), one-way ANOVA with Dunnett’s comparison test in (F)–(M), and with Tukey’s comparison test in (Q)–(V).

    Article Snippet: Belnacasan (VX-765) , MCE , Cat# HY-13205.

    Techniques: In Vivo, Staining, Immunofluorescence, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Comparison