Review



eht1864  (Tocris)


Bioz Verified Symbol Tocris is a verified supplier
Bioz Manufacturer Symbol Tocris manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 95
      Buy from Supplier

    Structured Review

    Tocris eht1864
    Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM <t>EHT1864</t> (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.
    Eht1864, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 114 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/eht1864/product/Tocris
    Average 95 stars, based on 114 article reviews
    eht1864 - by Bioz Stars, 2026-03
    95/100 stars

    Images

    1) Product Images from "Cardiomyocytes, cardiac endothelial cells and fibroblasts contribute to anthracycline-induced cardiac injury through RAS-homologous small GTPases RAC1 and CDC42."

    Article Title: Cardiomyocytes, cardiac endothelial cells and fibroblasts contribute to anthracycline-induced cardiac injury through RAS-homologous small GTPases RAC1 and CDC42.

    Journal: Pharmacological research

    doi: 10.1016/j.phrs.2024.107165

    Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM EHT1864 (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.
    Figure Legend Snippet: Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM EHT1864 (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.

    Techniques Used: Staining, Marker, Control, Immunocytochemistry, Incubation

    Fig. 6. Effect of RAC1 inhibition on DOX-induced cytotoxicity in primary cardiac cells. a-c Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by treatment with increasing concentrations of DOX for 48 h in the absence of EHT. AlamarBlue™ assay was performed to assess the DOX-induced loss of cell viability following RAC1 inhibition. Data shown are the mean + SD from n=3–12 independent experiments each performed in biological triplicates. *p≤0.05 (vs. corresponding Con); one-way ANOVA, Bonferroni’s post-hoc test. d Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by 1 μM DOX treatment for 48 h in the absence of EHT. Immunocytochemical TUNEL assay was performed to quantify the percentage of apoptotic cells. Data shown are the mean + SD from n=3–8 independent experiments. *p≤0.05 (vs. Con), ns, not significant; one-way ANOVA, Bonferroni’s post-hoc test. The lower panel shows repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), TUNEL (green), DAPI (blue); 20x objective. TUNEL positive cells are exemplarily indicated by yellow arrows.
    Figure Legend Snippet: Fig. 6. Effect of RAC1 inhibition on DOX-induced cytotoxicity in primary cardiac cells. a-c Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by treatment with increasing concentrations of DOX for 48 h in the absence of EHT. AlamarBlue™ assay was performed to assess the DOX-induced loss of cell viability following RAC1 inhibition. Data shown are the mean + SD from n=3–12 independent experiments each performed in biological triplicates. *p≤0.05 (vs. corresponding Con); one-way ANOVA, Bonferroni’s post-hoc test. d Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by 1 μM DOX treatment for 48 h in the absence of EHT. Immunocytochemical TUNEL assay was performed to quantify the percentage of apoptotic cells. Data shown are the mean + SD from n=3–8 independent experiments. *p≤0.05 (vs. Con), ns, not significant; one-way ANOVA, Bonferroni’s post-hoc test. The lower panel shows repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), TUNEL (green), DAPI (blue); 20x objective. TUNEL positive cells are exemplarily indicated by yellow arrows.

    Techniques Used: Inhibition, Alamar Blue Assay, TUNEL Assay, Staining, Marker



    Similar Products

    eht1864  (Tocris)
    95
    Tocris eht1864
    Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM <t>EHT1864</t> (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.
    Eht1864, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/eht1864/product/Tocris
    Average 95 stars, based on 1 article reviews
    eht1864 - by Bioz Stars, 2026-03
    95/100 stars
    		  Buy from Supplier
    eht1864 3872  (Tocris)
    90
    Tocris eht1864 3872
    Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM <t>EHT1864</t> (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.
    Eht1864 3872, supplied by Tocris, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/eht1864 3872/product/Tocris
    Average 90 stars, based on 1 article reviews
    eht1864 3872 - by Bioz Stars, 2026-03
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM EHT1864 (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.

    Journal: Pharmacological research

    Article Title: Cardiomyocytes, cardiac endothelial cells and fibroblasts contribute to anthracycline-induced cardiac injury through RAS-homologous small GTPases RAC1 and CDC42.

    doi: 10.1016/j.phrs.2024.107165

    Figure Lengend Snippet: Fig. 4. Effect of RHO GTPase inhibitors on DOX-induced DSB formation and repair in primary cardiac cells. a-c Primary cardiac cell types were pre-treated with different RHO GTPase inhibitors (Supplementary Table 1) (30 μM EHT1864 (EHT), 100 μM ML141 (ML) , 10 μM Aza1, 100 μM rhosin for 3 h or with 20 μM lovastatin (Lova), overnight), followed by 1 μM DOX co-treatment for 2 h. The number of DOX-induced γH2AX foci in the presence or absence of RHO GTPase inhibitors was quantified. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. Con), +p≤0.05 (vs. DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show representative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective. Control pictures of mono-treatment with RHO GTPase inhibitors treated cells are shown in Supplementary Fig. 6. d-f Primary cardiac cells were pre-treated with 30 μM EHT for 3 h, followed by 1 μM DOX co-treatment for 2 h. To evaluate DSB induction and repair, the number of nuclear γH2AX foci was quantified by immunocytochemistry immediately after the DOX pulse-treatment (0 h) or after post-incubation (24 h), respectively, in the absence of EHT and DOX. Data shown are the mean + SD from n=3–11 independent experiments with >50 nuclei per condition being analyzed. *p≤0.05 (vs. corresponding Con), +p≤0.05 (vs. corresponding DOX); one-way ANOVA, Bonferroni’s post-hoc test. The lower panels show repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), γH2AX (green), DAPI (blue); 100x objective.

    Article Snippet: For the inhibition of RHO GTPases, cells were pre-treated with following inhibitors: EHT1864 (30 μM), NSC23766 (100 μM), rhosin (100 μM) (Tocris, Wiesbaden-Nordenstadt, Germany), EHop-016 (10 μM), ML141 (100 μM), Y-27632 (10 μM) (Sigma Aldrich, Darmstadt, Germany), Aza1 (10 μM) (MedChemExpress, Monmouth Junction, NJ, USA) for 3 h; lovastatin (20 μM) overnight, prior to DOX treatment for 2 h. Specificity and mode of action of RHO GTPase inhibitors are shown in Supplementary Table 1.

    Techniques: Staining, Marker, Control, Immunocytochemistry, Incubation

    Fig. 6. Effect of RAC1 inhibition on DOX-induced cytotoxicity in primary cardiac cells. a-c Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by treatment with increasing concentrations of DOX for 48 h in the absence of EHT. AlamarBlue™ assay was performed to assess the DOX-induced loss of cell viability following RAC1 inhibition. Data shown are the mean + SD from n=3–12 independent experiments each performed in biological triplicates. *p≤0.05 (vs. corresponding Con); one-way ANOVA, Bonferroni’s post-hoc test. d Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by 1 μM DOX treatment for 48 h in the absence of EHT. Immunocytochemical TUNEL assay was performed to quantify the percentage of apoptotic cells. Data shown are the mean + SD from n=3–8 independent experiments. *p≤0.05 (vs. Con), ns, not significant; one-way ANOVA, Bonferroni’s post-hoc test. The lower panel shows repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), TUNEL (green), DAPI (blue); 20x objective. TUNEL positive cells are exemplarily indicated by yellow arrows.

    Journal: Pharmacological research

    Article Title: Cardiomyocytes, cardiac endothelial cells and fibroblasts contribute to anthracycline-induced cardiac injury through RAS-homologous small GTPases RAC1 and CDC42.

    doi: 10.1016/j.phrs.2024.107165

    Figure Lengend Snippet: Fig. 6. Effect of RAC1 inhibition on DOX-induced cytotoxicity in primary cardiac cells. a-c Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by treatment with increasing concentrations of DOX for 48 h in the absence of EHT. AlamarBlue™ assay was performed to assess the DOX-induced loss of cell viability following RAC1 inhibition. Data shown are the mean + SD from n=3–12 independent experiments each performed in biological triplicates. *p≤0.05 (vs. corresponding Con); one-way ANOVA, Bonferroni’s post-hoc test. d Primary cardiac cells were treated with 30 μM EHT1864 (EHT) for 3 h, followed by 1 μM DOX treatment for 48 h in the absence of EHT. Immunocytochemical TUNEL assay was performed to quantify the percentage of apoptotic cells. Data shown are the mean + SD from n=3–8 independent experiments. *p≤0.05 (vs. Con), ns, not significant; one-way ANOVA, Bonferroni’s post-hoc test. The lower panel shows repre sentative pictures of each cell type stained with the corresponding cell type-specific marker (red), TUNEL (green), DAPI (blue); 20x objective. TUNEL positive cells are exemplarily indicated by yellow arrows.

    Article Snippet: For the inhibition of RHO GTPases, cells were pre-treated with following inhibitors: EHT1864 (30 μM), NSC23766 (100 μM), rhosin (100 μM) (Tocris, Wiesbaden-Nordenstadt, Germany), EHop-016 (10 μM), ML141 (100 μM), Y-27632 (10 μM) (Sigma Aldrich, Darmstadt, Germany), Aza1 (10 μM) (MedChemExpress, Monmouth Junction, NJ, USA) for 3 h; lovastatin (20 μM) overnight, prior to DOX treatment for 2 h. Specificity and mode of action of RHO GTPase inhibitors are shown in Supplementary Table 1.

    Techniques: Inhibition, Alamar Blue Assay, TUNEL Assay, Staining, Marker