targetmol epigenetic inhibitors  (TargetMol)

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

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

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

Journal: Experimental & Molecular Medicine

Article Title: DNA methyltransferase inhibition is a therapeutic vulnerability in VHL-deficient renal cell carcinoma cells

doi: 10.1038/s12276-026-01663-w

Figure Lengend Snippet: a Stable overexpression of VHL-HA plasmid in 786-O cells (a VHL mutated RCC cell). Western blotting detected the protein level of VHL, HA tag and its downstream target genes HIF-2α in this VHL-isogenic 786-O cell pair. Data are shown as the mean ± s.d., n = 3. b A schematic diagram of synthetic lethal drug screen using VHL-isogenic 786-O cell pair on the Epigenetics Compound Library. c Selectivity index (fold-difference in IC 50 values between VHL −/− and wtVHL OE cells) plot to identify top five synthetic lethal drug candidates. d–g Dose–response curve of 786-O VHL-isogenic cell pair ( d ) and VHL non-isogenic cell pair ( f ) treated with decitabine for 72 h. Data are shown as the mean ± s.d., n = 3. The representative images of cell density with the indicated concentration of decitabine for wtVHL OE and VHL −/− ( e ) and Caki-1 and 769-p ( g ) cells. h , i Azacitidine effect on cell viability in 786-O VHL-isogenic cell pair ( h ) and VHL non-isogenic cell pair ( i ). Data are shown as the mean ± s.d., n = 3. ** P < 0.01, *** P < 0.001 between two indicated groups, Student’s t -test. j , k Dose–response curve of 786-O VHL-isogenic cell pair treated with RC-3117 ( j ) and SGI-1027 ( k ). Data are shown as the mean ± s.d., n = 3. l Chemical structures of DNMT inhibitors used in this study. m–p Western blotting detected the protein level of VHL in H1975 ( m ) and PLC/PRF/5 cells ( o ) and decitabine effect on cell viability of VHL-depleted H1975 cells ( n ) and PLC/PRF/5 ( p ). Data are shown as the mean ± s.d., n = 3. ** P < 0.01, **** P < 0.001 between two indicated groups, Student’s t -test.

Article Snippet: Epigenetics compounds library contains 138 small molecules which was purchased from Selleck Chemicals.

Techniques: Over Expression, Plasmid Preparation, Western Blot, Drug discovery, Concentration Assay