epigenetic compound library  (TargetMol)

Journal: Acta Pharmaceutica Sinica. B

Article Title: Targeting NAT10 with Remodelin reshapes the pro-fibrotic microenvironment in renal fibrogenesis via inhibiting exosome oversecretion from tubular cells

doi: 10.1016/j.apsb.2026.05.020

Figure Lengend Snippet: Targeting acetyltransferase NAT10 with Remodelin breaks the TEC-fibroblast pro-fibrotic chain (A) The graph indicating the selection strategy of screen based on in vitro model of TEC-fibroblast communication with epigenetic inhibitor compounds. (B) The heatmap of viability of NRK-49F cells incubated with CM from HK-2 cells with indicated treatments respectively (left panel). The dots indicated the average fold of viability of NRK-49F cells incubated with CM from HK-2 cells treated with TGF- β and epigenetic inhibitors, in relative to the NRK-49F cells incubated with CM from HK-2 cells treated with TGF- β and DMSO (right panel). The red dots indicated the selected inhibitors for further screen. (C) The heatmap of viability of NRK-49F cells incubated with CM from HK-2 cells with indicated treatments, respectively. (D) The heatmap (left) and table (right) demonstrating the details of 13 effective epigenetic inhibitors. (E) The immunoblot analysis of NAT10 in kidneys from sham mice ( n = 5) and UUO mice ( n = 5). (F) The dot blot analysis of ac4C in kidneys from sham mice ( n = 2) and UUO mice ( n = 2). (G) The immunohistochemistry staining of NAT10 in kidneys from sham mice and UUO mice. (H) The immunofluorescence staining of NAT10 in kidneys from sham mice and UUO mice. LTL was used as marker of proximal tubular cells. (I) The immunoblot analysis of NAT10 in kidneys from CKD patients ( n = 18) and non-CKD control ( n = 5). (J) The dot blot analysis of ac4C in kidneys from CKD patients ( n = 18) and non-CKD control ( n = 5). Data are presented as mean ± SD. Student's t test was used for comparison between two groups and one-way ANOVA was used for comparison between multiple groups; ∗ P < 0.05; ∗∗ P < 0.01; ∗∗∗ P < 0.001.

Article Snippet: HK-2 cells were seeded in 96-well plates at the density of 10,000 cells per well, and then treated with TGF- β (5 ng/mL) in the presence of each inhibitor (1 or 5 μmol/L) of Epigenetic Compound Library (TargetMol, MA, USA).

Techniques: Selection, In Vitro, Incubation, Western Blot, Analysis, Dot Blot, Immunohistochemistry, Staining, Immunofluorescence, Marker, Control, Comparison

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