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camostat  (BPS Bioscience)


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    BPS Bioscience camostat
    Camostat, supplied by BPS Bioscience, used in various techniques. Bioz Stars score: 94/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 17 article reviews
    camostat - by Bioz Stars, 2026-06
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    camostat  (MedChemExpress)
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    Susceptibility of the nine different SARS-CoV-2 strains to inhibitors of TMPRSS2-mediated fusion and cathepsin-mediated endocytosis. SARS-CoV-2 European wild-type (B.1.1), variant-of-concern (VOC) Alpha (B1.1.7 Q27*K68*, B.1.1.7 Q27*), Delta (AY.33), and Omicron (BA.1.17.2, BA.1.1, BA.2.9, BE.1.1, BA.5.1) were propagated in four human cell lines (Calu-3, Caco-2, A549 hACE2+/TMPRSS2+ , HEK293T) in the presence of increasing concentrations (0.024-100 µM) of <t>camostat,</t> an inhibitor of TMPRSS2-mediated viral direct fusion with cellular membrane (green <t>curve),</t> <t>aloxistatin,</t> an inhibitor of cathepsin-mediated viral endocytic uptake (pink curve), and a 1:1 mixture of both inhibitors (black curve). Viral load was determined in cell culture supernatants 48h p.i. using RT-qPCR and are presented as log 10 RNA copies/ml. Controls included cells infected with SARS-CoV-2 in the absence of inhibitors (“virus control”, VC), and cells fixed with 4% paraformaldehyde and exposed to SARS-CoV-2 (“background control”, BG), shown as dashed horizontal lines. Data show mean and standard error of three independent experiments.
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    The flipGFP-based reporter system could be optimized for high-throughput screening of compounds targeting 3C protease. ( A ) Schematic representation of the flipGFP-based reporter system optimized for 96-well format. The fluorescence signal from flipGFP was quantified by the plate reader (GloMax Discover System, Promega). The inhibitory efficacy of each compound was calculated using the indicated formula. ( B ) HEK293T cells co-transfected with the expression vector of flipGFP (3B/3C) or flipGFP (VP2/VP3) and 3C protease were treated with rupintrivir. The inhibitory efficacy of the compound was calculated 24 h post-transfection using the detected fluorescent intensity. The cell viability of the HEK293T cells treated with the rupintrivir for 24 h was determined by CellTiter-Glo (Promega). ( C ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with rupintrivir, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( D ) HEK293T cells were treated with DC07090, GC376, Ebselen, Ensitrelvir, Luteoloside, Nimatrelvir, or Camostat Mesilate for 24 h, and cell viability was determined by CellTiter-Glo (Promega). ( E ) HEK293T cells transfected with the expression vector of 3C protease and flipGFP (3B/3C) were treated with DC07090, GC376, Ebselen, Ensitrelvir, Luteoloside, Nimatrelvir, or Camostat Mesilate at concentrations of 3, 10, or 30 µM. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( F ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with DC07090, GC376, Ebselen, or Ensitrelvir at concentrations of 3, 10, or 30 µM, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( G ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with Ebselen at concentrations of 30 µM, and incubated for 24 h at 33°C. The fluorescence signals were monitored using fluorescence microscopy. ( H ) HEK293T cells stably expressing SCARB2 were infected with EV-A71-mGL at an MOI of 1.0, treated with Ebselen at concentrations of 3, 10, or 30 µM, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( I ) HEK293T cells co-transfected with the expression vector of flipGFP (3B/3C) and 3C protease were treated with Ebselen. The inhibitory efficacy of the compound was calculated 24 h post-transfection using the detected fluorescent intensity. The cell viability of the HEK293T cells treated with Ebselen for 24 h was determined by CellTiter-Glo (Promega). ( J ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with Ebselen, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( K ) RD-S cells were infected with EV-A71 (strain SK-EV006) at an MOI of 0.1, treated with Ebselen at concentrations of 30 µM, and incubated for 24 h at 37°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (left). RD-S cells were infected with EV-A71 (strain SK-EV006) at an MOI of 0.001, treated with Ebselen at concentrations of 30 µM, and incubated for 48 h at 37°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (right). ( L ) RD-A cells were infected with EV-D68 (strain Fermon) at an MOI of 0.1, treated with Ebselen at concentrations of 30 µM, and incubated for 48 h at 33°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (left). RD-A cells were infected with EV-D68 (US/IL/14-18952) at an MOI of 0.1, treated with Ebselen at concentrations of 30 µM, and incubated for 24 h at 33°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (right). Data in panels B to J are representative of two independent experiments; data presented in panels K and L are mean ± S.D. of two independent experiments. For the experiment presented in K and L, significance was determined using Student’s t -test ( n = 4) (* P ≤ 0.05; ** P ≤ 0.01; **** P ≤ 0.0001).

    Journal: Journal of Virology

    Article Title: Establishment of a green fluorescent protein (GFP)-based reporter for picornaviral 3C proteases

    doi: 10.1128/jvi.01936-25

    Figure Lengend Snippet: The flipGFP-based reporter system could be optimized for high-throughput screening of compounds targeting 3C protease. ( A ) Schematic representation of the flipGFP-based reporter system optimized for 96-well format. The fluorescence signal from flipGFP was quantified by the plate reader (GloMax Discover System, Promega). The inhibitory efficacy of each compound was calculated using the indicated formula. ( B ) HEK293T cells co-transfected with the expression vector of flipGFP (3B/3C) or flipGFP (VP2/VP3) and 3C protease were treated with rupintrivir. The inhibitory efficacy of the compound was calculated 24 h post-transfection using the detected fluorescent intensity. The cell viability of the HEK293T cells treated with the rupintrivir for 24 h was determined by CellTiter-Glo (Promega). ( C ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with rupintrivir, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( D ) HEK293T cells were treated with DC07090, GC376, Ebselen, Ensitrelvir, Luteoloside, Nimatrelvir, or Camostat Mesilate for 24 h, and cell viability was determined by CellTiter-Glo (Promega). ( E ) HEK293T cells transfected with the expression vector of 3C protease and flipGFP (3B/3C) were treated with DC07090, GC376, Ebselen, Ensitrelvir, Luteoloside, Nimatrelvir, or Camostat Mesilate at concentrations of 3, 10, or 30 µM. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( F ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with DC07090, GC376, Ebselen, or Ensitrelvir at concentrations of 3, 10, or 30 µM, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( G ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with Ebselen at concentrations of 30 µM, and incubated for 24 h at 33°C. The fluorescence signals were monitored using fluorescence microscopy. ( H ) HEK293T cells stably expressing SCARB2 were infected with EV-A71-mGL at an MOI of 1.0, treated with Ebselen at concentrations of 3, 10, or 30 µM, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( I ) HEK293T cells co-transfected with the expression vector of flipGFP (3B/3C) and 3C protease were treated with Ebselen. The inhibitory efficacy of the compound was calculated 24 h post-transfection using the detected fluorescent intensity. The cell viability of the HEK293T cells treated with Ebselen for 24 h was determined by CellTiter-Glo (Promega). ( J ) RD-S cells were infected with EV-A71-mGL at an MOI of 1.0, treated with Ebselen, and incubated for 24 h at 33°C. The inhibitory efficacy of the compound was calculated using the detected fluorescent intensity. ( K ) RD-S cells were infected with EV-A71 (strain SK-EV006) at an MOI of 0.1, treated with Ebselen at concentrations of 30 µM, and incubated for 24 h at 37°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (left). RD-S cells were infected with EV-A71 (strain SK-EV006) at an MOI of 0.001, treated with Ebselen at concentrations of 30 µM, and incubated for 48 h at 37°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (right). ( L ) RD-A cells were infected with EV-D68 (strain Fermon) at an MOI of 0.1, treated with Ebselen at concentrations of 30 µM, and incubated for 48 h at 33°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (left). RD-A cells were infected with EV-D68 (US/IL/14-18952) at an MOI of 0.1, treated with Ebselen at concentrations of 30 µM, and incubated for 24 h at 33°C. Infectious titers in the culture supernatants were determined using a plaque-forming assay (right). Data in panels B to J are representative of two independent experiments; data presented in panels K and L are mean ± S.D. of two independent experiments. For the experiment presented in K and L, significance was determined using Student’s t -test ( n = 4) (* P ≤ 0.05; ** P ≤ 0.01; **** P ≤ 0.0001).

    Article Snippet: The following antibodies and reagents were used in this study: Enterovirus 71 VP1 antibody (GT185) (GTX633390; GeneTex), Enterovirus 71 2C antibody (GTX132354; GeneTex), Enterovirus 71 3C antibody (GTX132357; GeneTex), Enterovirus 71 3CD antibody (GTX132355; GeneTex), anti-FLAG M2-Peroxidase (HRP) monoclonal antibody produced in mouse (A8592; Merck), Anti-Strep-tag II mAb (M211-3; MBL), Anti-DDDDK-tag mAb-Alexa Fluor 594 (M185-A59, MBL), anti-β-Actin monoclonal antibody produced in mouse (A2228; Merck), Peroxidase AffiniPure Goat anti-mouse IgG (H+L) (115-035-003; Jackson Immuno Research Laboratories, Inc.), Peroxidase AffiniPure Goat anti-Rabbit IgG (H+L) (111-035-003; Jackson Immuno Research Laboratories, Inc.), Rupintrivir ( T16809 ; TargetMol), DC07090 dihydrochloride (HY-123517; MedChemExpress), GC376 (S0475; Selleck Chemicals), Ebselen (E0946; TOKYO CHEMICAL INDUSTRY CO., LTD.), Ensitrelvir (HY-143216; MedChemExpress), Luteoloside (S9018; Selleck Chemicals), Nirmatrelvir (HY-138687; MedChemExpress), and Camostat Mesilate (HY-13512; MedChemExpress).

    Techniques: High Throughput Screening Assay, Fluorescence, Transfection, Expressing, Plasmid Preparation, Infection, Incubation, Microscopy, Stable Transfection

    Susceptibility of the nine different SARS-CoV-2 strains to inhibitors of TMPRSS2-mediated fusion and cathepsin-mediated endocytosis. SARS-CoV-2 European wild-type (B.1.1), variant-of-concern (VOC) Alpha (B1.1.7 Q27*K68*, B.1.1.7 Q27*), Delta (AY.33), and Omicron (BA.1.17.2, BA.1.1, BA.2.9, BE.1.1, BA.5.1) were propagated in four human cell lines (Calu-3, Caco-2, A549 hACE2+/TMPRSS2+ , HEK293T) in the presence of increasing concentrations (0.024-100 µM) of camostat, an inhibitor of TMPRSS2-mediated viral direct fusion with cellular membrane (green curve), aloxistatin, an inhibitor of cathepsin-mediated viral endocytic uptake (pink curve), and a 1:1 mixture of both inhibitors (black curve). Viral load was determined in cell culture supernatants 48h p.i. using RT-qPCR and are presented as log 10 RNA copies/ml. Controls included cells infected with SARS-CoV-2 in the absence of inhibitors (“virus control”, VC), and cells fixed with 4% paraformaldehyde and exposed to SARS-CoV-2 (“background control”, BG), shown as dashed horizontal lines. Data show mean and standard error of three independent experiments.

    Journal: Frontiers in Immunology

    Article Title: SARS-CoV-2 evolution enhances endocytic uptake while preserving TMPRSS2-dependent fusion

    doi: 10.3389/fimmu.2025.1736891

    Figure Lengend Snippet: Susceptibility of the nine different SARS-CoV-2 strains to inhibitors of TMPRSS2-mediated fusion and cathepsin-mediated endocytosis. SARS-CoV-2 European wild-type (B.1.1), variant-of-concern (VOC) Alpha (B1.1.7 Q27*K68*, B.1.1.7 Q27*), Delta (AY.33), and Omicron (BA.1.17.2, BA.1.1, BA.2.9, BE.1.1, BA.5.1) were propagated in four human cell lines (Calu-3, Caco-2, A549 hACE2+/TMPRSS2+ , HEK293T) in the presence of increasing concentrations (0.024-100 µM) of camostat, an inhibitor of TMPRSS2-mediated viral direct fusion with cellular membrane (green curve), aloxistatin, an inhibitor of cathepsin-mediated viral endocytic uptake (pink curve), and a 1:1 mixture of both inhibitors (black curve). Viral load was determined in cell culture supernatants 48h p.i. using RT-qPCR and are presented as log 10 RNA copies/ml. Controls included cells infected with SARS-CoV-2 in the absence of inhibitors (“virus control”, VC), and cells fixed with 4% paraformaldehyde and exposed to SARS-CoV-2 (“background control”, BG), shown as dashed horizontal lines. Data show mean and standard error of three independent experiments.

    Article Snippet: Aloxistatin and camostat (both MedChemExpress, Monmouth Junction, NJ) were used at concentrations of 0.024-100 μM to inhibit SARS-CoV-2 endocytic uptake and direct TMPRSS2-mediated fusion on the cell surface, respectively.

    Techniques: Variant Assay, Membrane, Cell Culture, Quantitative RT-PCR, Infection, Virus, Control

    Degree of direct TMRPSS2-mediated fusion and cathepsin-mediated endocytic uptake of the nine different SARS-CoV-2 strains in four different cell lines. Calculation of the reduction in viral load induced by aloxistatin (pink columns) and camostat (green columns) at the non-toxic concentration of 25 µM as % inhibition induced by the mixture of the two inhibitors for Calu-3 cells (A) , HEK293T cells (B) , Caco-2 cells (C) and A549 hACE2+/TMPRSS2+ cells (D) . A higher percentage indicates a stronger role of the respective mode of entry for the respective virus strain. In A549 hACE2+/TMPRSS2+ cells, strains BA.1.17.2 and BA.1.1 were non-replicative (n.r.). In HEK293T cells, virus replication was observed for strains BE.1.1 and BA.5.1 only. Statistics was performed using two-way ANOVA with Šidák’s correction to account for multiple comparisons. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

    Journal: Frontiers in Immunology

    Article Title: SARS-CoV-2 evolution enhances endocytic uptake while preserving TMPRSS2-dependent fusion

    doi: 10.3389/fimmu.2025.1736891

    Figure Lengend Snippet: Degree of direct TMRPSS2-mediated fusion and cathepsin-mediated endocytic uptake of the nine different SARS-CoV-2 strains in four different cell lines. Calculation of the reduction in viral load induced by aloxistatin (pink columns) and camostat (green columns) at the non-toxic concentration of 25 µM as % inhibition induced by the mixture of the two inhibitors for Calu-3 cells (A) , HEK293T cells (B) , Caco-2 cells (C) and A549 hACE2+/TMPRSS2+ cells (D) . A higher percentage indicates a stronger role of the respective mode of entry for the respective virus strain. In A549 hACE2+/TMPRSS2+ cells, strains BA.1.17.2 and BA.1.1 were non-replicative (n.r.). In HEK293T cells, virus replication was observed for strains BE.1.1 and BA.5.1 only. Statistics was performed using two-way ANOVA with Šidák’s correction to account for multiple comparisons. *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

    Article Snippet: Aloxistatin and camostat (both MedChemExpress, Monmouth Junction, NJ) were used at concentrations of 0.024-100 μM to inhibit SARS-CoV-2 endocytic uptake and direct TMPRSS2-mediated fusion on the cell surface, respectively.

    Techniques: Concentration Assay, Inhibition, Virus