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molecule inhibitor ac2 26  (TargetMol)


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    Structured Review

    TargetMol molecule inhibitor ac2 26
    Schematic overview of the experimental workflow for generating ANXA1-knockdown CHO cell lines <t>and</t> <t>AC2-26</t> inhibitor treatment. (A) Generation and validation of ANXA1-knockdown cell lines for rADM antibody production. (B) AC2-26 inhibitor treatment in low-producer CHO cells (ADM-14) and subsequent rADM expression analysis.
    Molecule Inhibitor Ac2 26, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/molecule inhibitor ac2 26/product/TargetMol
    Average 94 stars, based on 2 article reviews
    molecule inhibitor ac2 26 - by Bioz Stars, 2026-05
    94/100 stars

    Images

    1) Product Images from "Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach"

    Article Title: Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach

    Journal: Synthetic and Systems Biotechnology

    doi: 10.1016/j.synbio.2025.12.001

    Schematic overview of the experimental workflow for generating ANXA1-knockdown CHO cell lines and AC2-26 inhibitor treatment. (A) Generation and validation of ANXA1-knockdown cell lines for rADM antibody production. (B) AC2-26 inhibitor treatment in low-producer CHO cells (ADM-14) and subsequent rADM expression analysis.
    Figure Legend Snippet: Schematic overview of the experimental workflow for generating ANXA1-knockdown CHO cell lines and AC2-26 inhibitor treatment. (A) Generation and validation of ANXA1-knockdown cell lines for rADM antibody production. (B) AC2-26 inhibitor treatment in low-producer CHO cells (ADM-14) and subsequent rADM expression analysis.

    Techniques Used: Knockdown, Biomarker Discovery, Expressing

    AC2-26 effect on ADM-14 CHO cells. (A) Cell density/viability under AC2-26 treatment (n = 3). (B) rADM expression by Western blot with quantification (n = 3). (C) ANXA1 mRNA/protein comparison (n = 3). Quantification was performed using ImageJ (for Western blot densitometry) and GraphPad Prism 10 (for statistical analysis). (∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). n: represents independent biological replicates.
    Figure Legend Snippet: AC2-26 effect on ADM-14 CHO cells. (A) Cell density/viability under AC2-26 treatment (n = 3). (B) rADM expression by Western blot with quantification (n = 3). (C) ANXA1 mRNA/protein comparison (n = 3). Quantification was performed using ImageJ (for Western blot densitometry) and GraphPad Prism 10 (for statistical analysis). (∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). n: represents independent biological replicates.

    Techniques Used: Expressing, Western Blot, Comparison



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    Image Search Results


    Schematic overview of the experimental workflow for generating ANXA1-knockdown CHO cell lines and AC2-26 inhibitor treatment. (A) Generation and validation of ANXA1-knockdown cell lines for rADM antibody production. (B) AC2-26 inhibitor treatment in low-producer CHO cells (ADM-14) and subsequent rADM expression analysis.

    Journal: Synthetic and Systems Biotechnology

    Article Title: Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach

    doi: 10.1016/j.synbio.2025.12.001

    Figure Lengend Snippet: Schematic overview of the experimental workflow for generating ANXA1-knockdown CHO cell lines and AC2-26 inhibitor treatment. (A) Generation and validation of ANXA1-knockdown cell lines for rADM antibody production. (B) AC2-26 inhibitor treatment in low-producer CHO cells (ADM-14) and subsequent rADM expression analysis.

    Article Snippet: On day 3 of suspension culture, the small molecule inhibitor AC2-26 (Topscience Co., Ltd., China) was added [ ], using DMSO (Solarbio Life Sciences, China) as the solvent control.

    Techniques: Knockdown, Biomarker Discovery, Expressing

    AC2-26 effect on ADM-14 CHO cells. (A) Cell density/viability under AC2-26 treatment (n = 3). (B) rADM expression by Western blot with quantification (n = 3). (C) ANXA1 mRNA/protein comparison (n = 3). Quantification was performed using ImageJ (for Western blot densitometry) and GraphPad Prism 10 (for statistical analysis). (∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). n: represents independent biological replicates.

    Journal: Synthetic and Systems Biotechnology

    Article Title: Leveraging ANXA1 to enhance recombinant protein yields in CHO cells: A UPR-Mediated bioprocessing approach

    doi: 10.1016/j.synbio.2025.12.001

    Figure Lengend Snippet: AC2-26 effect on ADM-14 CHO cells. (A) Cell density/viability under AC2-26 treatment (n = 3). (B) rADM expression by Western blot with quantification (n = 3). (C) ANXA1 mRNA/protein comparison (n = 3). Quantification was performed using ImageJ (for Western blot densitometry) and GraphPad Prism 10 (for statistical analysis). (∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001). n: represents independent biological replicates.

    Article Snippet: On day 3 of suspension culture, the small molecule inhibitor AC2-26 (Topscience Co., Ltd., China) was added [ ], using DMSO (Solarbio Life Sciences, China) as the solvent control.

    Techniques: Expressing, Western Blot, Comparison

    Cytotoxicity of EK1, antibodies, and M pro inhibitors on Caco-2 and RD cells. ( A–G ) Cytotoxicity of EK1, PF-07321332, RAY1216, S-217622, G7, bn03, and control on Caco-2 cells. ( H–L ) Cytotoxicity of EK1, PF-07321332, RAY1216, S-217622, and control on RD cells. Data represent mean ± SD from three independent experiments ( n = 3).

    Journal: Journal of Virology

    Article Title: Potent in vitro synergistic antiviral effects of the pan-coronavirus fusion inhibitor EK1 in combination with RBD-specific antibodies or M pro inhibitors

    doi: 10.1128/jvi.00076-26

    Figure Lengend Snippet: Cytotoxicity of EK1, antibodies, and M pro inhibitors on Caco-2 and RD cells. ( A–G ) Cytotoxicity of EK1, PF-07321332, RAY1216, S-217622, G7, bn03, and control on Caco-2 cells. ( H–L ) Cytotoxicity of EK1, PF-07321332, RAY1216, S-217622, and control on RD cells. Data represent mean ± SD from three independent experiments ( n = 3).

    Article Snippet: The small-molecule M pro inhibitors nirmatrelvir (PF-07321332), RAY1216, and ensitrelvir (S-217622) were purchased from MedChemExpress (Shanghai, China).

    Techniques: Control

    Synergistic inhibition of authentic SARS-CoV-2 BA.2 and HCoV-OC43 by dual antiviral combinations. ( A ) Crystal structure of the M pro active site (PDB ID: 7CAM ). The protease is shown as a semi-transparent surface in gray, with the inhibitor-binding cleft highlighted in green. ( B ) Binding sites of M pro with PF-07321332 (PDB ID: 7VH8) in green, RAY1216 (PDB ID: 8IGN ) in yellow, and S-217622 (PDB ID: 8HEF ) in orange. ( C–H ) Dose-response analyses of the fusion inhibitor EK1 in combination with three distinct M pro inhibitors against authentic SARS-CoV-2 BA.2 ( C–E ) and HCoV-OC43 ( F–H ). In each panel, EK1 and the respective M pro inhibitor were tested both individually and as fixed-ratio combinations (molar ratios: PF-07321332, 20:3 for BA.2 and 25:4 for OC43; RAY1216, 4:1 for BA.2 and 25:1 for OC43; S-217622, 4:1 for BA.2 and 25:1 for OC43). Viral inhibition was quantified by fluorescent plaque assay (BA.2), and cell viability was assessed using the cell counting kit-8 (CCK-8) assay (OC43) at 48 h post-infection. Data represent mean ± SD from three independent experiments ( n = 3).

    Journal: Journal of Virology

    Article Title: Potent in vitro synergistic antiviral effects of the pan-coronavirus fusion inhibitor EK1 in combination with RBD-specific antibodies or M pro inhibitors

    doi: 10.1128/jvi.00076-26

    Figure Lengend Snippet: Synergistic inhibition of authentic SARS-CoV-2 BA.2 and HCoV-OC43 by dual antiviral combinations. ( A ) Crystal structure of the M pro active site (PDB ID: 7CAM ). The protease is shown as a semi-transparent surface in gray, with the inhibitor-binding cleft highlighted in green. ( B ) Binding sites of M pro with PF-07321332 (PDB ID: 7VH8) in green, RAY1216 (PDB ID: 8IGN ) in yellow, and S-217622 (PDB ID: 8HEF ) in orange. ( C–H ) Dose-response analyses of the fusion inhibitor EK1 in combination with three distinct M pro inhibitors against authentic SARS-CoV-2 BA.2 ( C–E ) and HCoV-OC43 ( F–H ). In each panel, EK1 and the respective M pro inhibitor were tested both individually and as fixed-ratio combinations (molar ratios: PF-07321332, 20:3 for BA.2 and 25:4 for OC43; RAY1216, 4:1 for BA.2 and 25:1 for OC43; S-217622, 4:1 for BA.2 and 25:1 for OC43). Viral inhibition was quantified by fluorescent plaque assay (BA.2), and cell viability was assessed using the cell counting kit-8 (CCK-8) assay (OC43) at 48 h post-infection. Data represent mean ± SD from three independent experiments ( n = 3).

    Article Snippet: The small-molecule M pro inhibitors nirmatrelvir (PF-07321332), RAY1216, and ensitrelvir (S-217622) were purchased from MedChemExpress (Shanghai, China).

    Techniques: Inhibition, Binding Assay, Plaque Assay, Cell Counting, CCK-8 Assay, Infection

    Conceptual framework for combinatorial antiviral trident therapy. Schematic overview illustrating the underlying rationale and mechanistic logic of multi-agent intervention against coronavirus infection. By simultaneously targeting discrete stages of the viral life cycle, including membrane fusion (EK1, PDB ID: 7C53 ), receptor engagement (neutralizing antibodies G7 (PDB ID: 8YWE) and nanobodies bn03 (PDB ID: 7WHJ) against RBD), and viral replication (M pro inhibitors: PF-07321332 [PDB ID: 7VH8 ]; RAY1216 [PDB ID: 8IGN ]; S-217622 [PDB ID: 8HEF ]), this approach achieves potent, synergistic inhibition of viral entry, genome replication, and progeny virion production. Dual- or triple-agent combinations permit dose reduction of individual compounds, thereby minimizing toxicity and cost, while curtailing the emergence of resistant variants through multifaceted blockade. Trident therapy defines a modular platform for rapid deployment of broad-spectrum antivirals against SARS-CoV-2 and future zoonotic coronaviruses.

    Journal: Journal of Virology

    Article Title: Potent in vitro synergistic antiviral effects of the pan-coronavirus fusion inhibitor EK1 in combination with RBD-specific antibodies or M pro inhibitors

    doi: 10.1128/jvi.00076-26

    Figure Lengend Snippet: Conceptual framework for combinatorial antiviral trident therapy. Schematic overview illustrating the underlying rationale and mechanistic logic of multi-agent intervention against coronavirus infection. By simultaneously targeting discrete stages of the viral life cycle, including membrane fusion (EK1, PDB ID: 7C53 ), receptor engagement (neutralizing antibodies G7 (PDB ID: 8YWE) and nanobodies bn03 (PDB ID: 7WHJ) against RBD), and viral replication (M pro inhibitors: PF-07321332 [PDB ID: 7VH8 ]; RAY1216 [PDB ID: 8IGN ]; S-217622 [PDB ID: 8HEF ]), this approach achieves potent, synergistic inhibition of viral entry, genome replication, and progeny virion production. Dual- or triple-agent combinations permit dose reduction of individual compounds, thereby minimizing toxicity and cost, while curtailing the emergence of resistant variants through multifaceted blockade. Trident therapy defines a modular platform for rapid deployment of broad-spectrum antivirals against SARS-CoV-2 and future zoonotic coronaviruses.

    Article Snippet: The small-molecule M pro inhibitors nirmatrelvir (PF-07321332), RAY1216, and ensitrelvir (S-217622) were purchased from MedChemExpress (Shanghai, China).

    Techniques: Infection, Membrane, Inhibition