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epigenetic inhibitors  (TargetMol)


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    TargetMol epigenetic inhibitors
    Epigenetic Inhibitors, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/epigenetic+modifications/Histone+Modification+Compound+Library/pm41713838-53-7-15
    Average 94 stars, based on 19 article reviews
    epigenetic inhibitors - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Screening:

    Article Title: BRD4-mediated histone H4K12 lactylation drives ovarian cancer progression by activating the Ube2v1-DDX3X ubiquitination axis.
    Article Snippet: .. 212 Screening for potential inhibitors that reduce H4K12la levels 213 The Histone Modification Compound Library (TargetMol, L3500) contained 444 types of 214 inhibitor or compound target proteins related to histone modification. ..

    Modification:

    Article Title: BRD4-mediated histone H4K12 lactylation drives ovarian cancer progression by activating the Ube2v1-DDX3X ubiquitination axis.
    Article Snippet: .. 212 Screening for potential inhibitors that reduce H4K12la levels 213 The Histone Modification Compound Library (TargetMol, L3500) contained 444 types of 214 inhibitor or compound target proteins related to histone modification. ..

    Drug discovery:

    Article Title: BRD4-mediated histone H4K12 lactylation drives ovarian cancer progression by activating the Ube2v1-DDX3X ubiquitination axis.
    Article Snippet: .. 212 Screening for potential inhibitors that reduce H4K12la levels 213 The Histone Modification Compound Library (TargetMol, L3500) contained 444 types of 214 inhibitor or compound target proteins related to histone modification. ..

    Article Title: Targeting SIRT6 epigenetically restrains neutrophil hyperplasia and enhances chemotherapeutic efficacy
    Article Snippet: .. The Epigenetics Compound Library (#L3500, TargetMol, Shanghai, China. ..

    Article Title: Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesis via inhibiting exosome oversecretion from tubular cells
    Article Snippet: Data were performed with GraphPad Prism 8.0. .. Epigenetic targeting now is the leading strategy in drug discovery27, therefore, epigenetic compound library (TargetMol) was utilized for screen. ..

    other:

    Article Title: Acquired resistance to the PRMT5 inhibitor confers collateral sensitivity to MEK inhibition in MTAP-null non-small cell lung cancer
    Article Snippet: A high-throughput drug screen was performed using a compound library consisting of 619 compounds, including 59 SGC epigenetic compounds, 380 TargetMol epigenetic inhibitors and 180 FDA-approved oncology drugs.



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    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC <t>epigenetic</t> compounds, FDA-approved oncology drugs, and TargetMol epigenetic <t>inhibitors.</t> (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.
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    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC <t>epigenetic</t> compounds, FDA-approved oncology drugs, and TargetMol epigenetic <t>inhibitors.</t> (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.
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    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including <t>SGC</t> <t>epigenetic</t> compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.
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    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including <t>SGC</t> <t>epigenetic</t> compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.
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    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including <t>SGC</t> <t>epigenetic</t> compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.
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    Image Search Results


    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

    Journal: bioRxiv

    Article Title: Acquired resistance to the PRMT5 inhibitor confers collateral sensitivity to MEK inhibition in MTAP-null non-small cell lung cancer

    doi: 10.64898/2026.04.16.719008

    Figure Lengend Snippet: High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

    Article Snippet: The screening library comprised 619 compounds, including SGC epigenetic compounds, TargetMol epigenetic inhibitors, and FDA-approved oncology drugs ( ).

    Techniques: High Throughput Screening Assay, Drug discovery, Control

    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

    Journal: bioRxiv

    Article Title: Acquired resistance to the PRMT5 inhibitor confers collateral sensitivity to MEK inhibition in MTAP-null non-small cell lung cancer

    doi: 10.64898/2026.04.16.719008

    Figure Lengend Snippet: High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

    Article Snippet: A high-throughput drug screen was performed using a compound library consisting of 619 compounds, including 59 SGC epigenetic compounds, 380 TargetMol epigenetic inhibitors and 180 FDA-approved oncology drugs.

    Techniques: High Throughput Screening Assay, Drug discovery, Control

    High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

    Journal: bioRxiv

    Article Title: Acquired resistance to the PRMT5 inhibitor confers collateral sensitivity to MEK inhibition in MTAP-null non-small cell lung cancer

    doi: 10.64898/2026.04.16.719008

    Figure Lengend Snippet: High-throughput drug screen and MEK inhibitor sensitivity in MRTX1719-resistant NSCLC cells. (A) Composition of the compound library used for drug screen, including SGC epigenetic compounds, FDA-approved oncology drugs, and TargetMol epigenetic inhibitors. (B) IC50 values of MRTX1719 and anisomycin in DMSO and MRTXR cells. Anisomycin was included as a nonselective control in the drug screen. (C) Dose-response curves of DMSO and MRTXR cells treated with the MEK inhibitor selumetinib. Data are presented as mean ± SD. (D) Synergy heatmaps of MRTX1719 and selumetinib in DMSO and MRTXR cells. Synergy mean scores were calculated using the Bliss model with the SynergyFinder+ tool.

    Article Snippet: A high-throughput drug screen was performed using a compound library consisting of 619 compounds, including 59 SGC epigenetic compounds, 380 TargetMol epigenetic inhibitors and 180 FDA-approved oncology drugs.

    Techniques: High Throughput Screening Assay, Drug discovery, Control