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Syndax Inc entinostat

<t>Entinostat</t> enhances the efficacy of DNA-damaging and DDR-targeting agents in PDAC. ( A and B ) Representative Western blots ( A ) and quantification ( B ) showing increased γH2A.X (normalized to H2A.X) in FC1245 cells after 6 h of Ent treatment (1 µM) combined with cisplatin (Cis, 1 µM) or oxaliplatin (Oxa, 5 µM). ( C – F ) Representative plots and maximum scores (highest single agent model) from synergy analysis on viability of human and mouse PDAC cells under graded co-treatments of Ent with Cis ( C and D ) or Oxa ( E and F ). ( G and H ) Representative Western blots ( G ) and quantifications ( H ) showing increased γH2A.X in FC1245 after 6 h combined treatments of Ent (1 µM) with mitomycin C (MMC, 0.5 µM) or niraparib, (Nir, 2 µM). ( I – L ) Synergy plots and maximum scores from co-treatments of Ent and MMC ( I and J ) or Nir ( K and L ) in PDAC cells. Western blotting, n = 2 independent experiments; synergy analysis, n = 3 cell sample replicates. ( M ) Tumor weights from orthotopic transplantation models (FC1245) treated for two weeks with Ent (20 mg/kg, daily) and/or Cis (0.5 mg/kg, q3d). n = 7 (Veh), 6 (Ent, Cis), or 5 (Ent+Cis) mice. ( N and O ) Representative IHC images and quantifications of γH2A.X in tumors across treatment groups. n = 5 (Veh, Ent+Cis) or 4 (Ent, Cis) tumors. Scale bar, 50 µm. Data are presented as mean values ± SEM ( M and O ). **, p < 0.01; ****, p < 0.0001. One-way ANOVA.

Entinostat, supplied by Syndax Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/entinostat/product/Syndax Inc
Average 86 stars, based on 1 article reviews

entinostat - by Bioz Stars, 2026-06

86/100 stars

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1) Product Images from "HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery"

Article Title: HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery

Journal: bioRxiv

doi: 10.64898/2026.05.18.726071

Entinostat enhances the efficacy of DNA-damaging and DDR-targeting agents in PDAC. ( A and B ) Representative Western blots ( A ) and quantification ( B ) showing increased γH2A.X (normalized to H2A.X) in FC1245 cells after 6 h of Ent treatment (1 µM) combined with cisplatin (Cis, 1 µM) or oxaliplatin (Oxa, 5 µM). ( C – F ) Representative plots and maximum scores (highest single agent model) from synergy analysis on viability of human and mouse PDAC cells under graded co-treatments of Ent with Cis ( C and D ) or Oxa ( E and F ). ( G and H ) Representative Western blots ( G ) and quantifications ( H ) showing increased γH2A.X in FC1245 after 6 h combined treatments of Ent (1 µM) with mitomycin C (MMC, 0.5 µM) or niraparib, (Nir, 2 µM). ( I – L ) Synergy plots and maximum scores from co-treatments of Ent and MMC ( I and J ) or Nir ( K and L ) in PDAC cells. Western blotting, n = 2 independent experiments; synergy analysis, n = 3 cell sample replicates. ( M ) Tumor weights from orthotopic transplantation models (FC1245) treated for two weeks with Ent (20 mg/kg, daily) and/or Cis (0.5 mg/kg, q3d). n = 7 (Veh), 6 (Ent, Cis), or 5 (Ent+Cis) mice. ( N and O ) Representative IHC images and quantifications of γH2A.X in tumors across treatment groups. n = 5 (Veh, Ent+Cis) or 4 (Ent, Cis) tumors. Scale bar, 50 µm. Data are presented as mean values ± SEM ( M and O ). **, p < 0.01; ****, p < 0.0001. One-way ANOVA.

Figure Legend Snippet: Entinostat enhances the efficacy of DNA-damaging and DDR-targeting agents in PDAC. ( A and B ) Representative Western blots ( A ) and quantification ( B ) showing increased γH2A.X (normalized to H2A.X) in FC1245 cells after 6 h of Ent treatment (1 µM) combined with cisplatin (Cis, 1 µM) or oxaliplatin (Oxa, 5 µM). ( C – F ) Representative plots and maximum scores (highest single agent model) from synergy analysis on viability of human and mouse PDAC cells under graded co-treatments of Ent with Cis ( C and D ) or Oxa ( E and F ). ( G and H ) Representative Western blots ( G ) and quantifications ( H ) showing increased γH2A.X in FC1245 after 6 h combined treatments of Ent (1 µM) with mitomycin C (MMC, 0.5 µM) or niraparib, (Nir, 2 µM). ( I – L ) Synergy plots and maximum scores from co-treatments of Ent and MMC ( I and J ) or Nir ( K and L ) in PDAC cells. Western blotting, n = 2 independent experiments; synergy analysis, n = 3 cell sample replicates. ( M ) Tumor weights from orthotopic transplantation models (FC1245) treated for two weeks with Ent (20 mg/kg, daily) and/or Cis (0.5 mg/kg, q3d). n = 7 (Veh), 6 (Ent, Cis), or 5 (Ent+Cis) mice. ( N and O ) Representative IHC images and quantifications of γH2A.X in tumors across treatment groups. n = 5 (Veh, Ent+Cis) or 4 (Ent, Cis) tumors. Scale bar, 50 µm. Data are presented as mean values ± SEM ( M and O ). **, p < 0.01; ****, p < 0.0001. One-way ANOVA.

Techniques Used: Western Blot, Transplantation Assay

Entinostat treatment suppresses DDR pathways and induces DNA damage in PDAC. ( A and B ) Volcano plots showing RNA-seq results of differentially expressed genes between entinostat (Ent, 5 µM, 24 h) and vehicle (Veh) treatment in human MIA PaCa2 ( A ) and mouse FC1245 ( B ) PDAC cells. 3602 (MIA PaCa2) and 3543 (FC1245) genes are significantly upregulated, and 3478 (MIA PaCa2) and 3158 (FC1245) genes downregulated with representative DDR-related genes highlighted. FC, fold change. n = 2 independent cell samples. ( C ) GSEA enrichment plot showing DNA repair hallmark enriched in Ent-downregulated genes in FC1245. NES, normalized enrichment score; FDR, false discovery rate; Up, upregulation; Down, downregulation. ( D ) DDR-related gene ontology (GO) terms enriched in Ent-downregulated genes from GSEA. GG-NER, global genome nucleotide excision repair; PCNA, proliferating cell nuclear antigen. ( E and F ) Representative Western blots ( E ) and quantifications ( F ) showing increased γH2A.X and H3ac (normalized to histone H2A.X and H3, respectively) under graded Ent treatments. n = 2 independent experiments. ( G ) 4 gene clusters with downregulation trends (D1–D4) identified by temporal expression analysis in FC1245 cells with 0–24 h treatment of Ent (5 µM). n = 3 independent cell samples. ( H ) Enrichment of selected GO terms in downregulated clusters.

Figure Legend Snippet: Entinostat treatment suppresses DDR pathways and induces DNA damage in PDAC. ( A and B ) Volcano plots showing RNA-seq results of differentially expressed genes between entinostat (Ent, 5 µM, 24 h) and vehicle (Veh) treatment in human MIA PaCa2 ( A ) and mouse FC1245 ( B ) PDAC cells. 3602 (MIA PaCa2) and 3543 (FC1245) genes are significantly upregulated, and 3478 (MIA PaCa2) and 3158 (FC1245) genes downregulated with representative DDR-related genes highlighted. FC, fold change. n = 2 independent cell samples. ( C ) GSEA enrichment plot showing DNA repair hallmark enriched in Ent-downregulated genes in FC1245. NES, normalized enrichment score; FDR, false discovery rate; Up, upregulation; Down, downregulation. ( D ) DDR-related gene ontology (GO) terms enriched in Ent-downregulated genes from GSEA. GG-NER, global genome nucleotide excision repair; PCNA, proliferating cell nuclear antigen. ( E and F ) Representative Western blots ( E ) and quantifications ( F ) showing increased γH2A.X and H3ac (normalized to histone H2A.X and H3, respectively) under graded Ent treatments. n = 2 independent experiments. ( G ) 4 gene clusters with downregulation trends (D1–D4) identified by temporal expression analysis in FC1245 cells with 0–24 h treatment of Ent (5 µM). n = 3 independent cell samples. ( H ) Enrichment of selected GO terms in downregulated clusters.

Techniques Used: RNA Sequencing, Western Blot, Expressing

Entinostat preferentially increases intergenic H3K27ac, diverting BRD4 and Pol II from DDR gene promoters. ( A ) Numbers and percentages of annotated H3K27ac, BRD4, and RPB1 peaks in FC1245 cells treated with Veh or Ent (5 µM, 6h or 24h) by CUT&RUN. ( B ) Venn diagrams showing H3K27ac, BRD4, and RPB1 peak distributions across treatments. ( C – H ) Heatmaps and average profiles of H3K27ac ( C and D ), BRD4 ( E and F ), and RPB1 ( G and H ) occupancy across treatments at baseline H3K27ac peaks (Veh). ( I ) Genome browser tracks of representative DDR gene loci illustrating Ent-induced changes of H3K27ac, BRD4, and RPB1 at promoters (yellow) and in selected adjacent intergenic/genic regions (blue) along with RNA changes. NT, no treatment. Scale bar, 5 kb.

Figure Legend Snippet: Entinostat preferentially increases intergenic H3K27ac, diverting BRD4 and Pol II from DDR gene promoters. ( A ) Numbers and percentages of annotated H3K27ac, BRD4, and RPB1 peaks in FC1245 cells treated with Veh or Ent (5 µM, 6h or 24h) by CUT&RUN. ( B ) Venn diagrams showing H3K27ac, BRD4, and RPB1 peak distributions across treatments. ( C – H ) Heatmaps and average profiles of H3K27ac ( C and D ), BRD4 ( E and F ), and RPB1 ( G and H ) occupancy across treatments at baseline H3K27ac peaks (Veh). ( I ) Genome browser tracks of representative DDR gene loci illustrating Ent-induced changes of H3K27ac, BRD4, and RPB1 at promoters (yellow) and in selected adjacent intergenic/genic regions (blue) along with RNA changes. NT, no treatment. Scale bar, 5 kb.

Techniques Used:

Image Search Results

Journal: bioRxiv

Article Title: HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery

doi: 10.64898/2026.05.18.726071

Figure Lengend Snippet: Entinostat enhances the efficacy of DNA-damaging and DDR-targeting agents in PDAC. ( A and B ) Representative Western blots ( A ) and quantification ( B ) showing increased γH2A.X (normalized to H2A.X) in FC1245 cells after 6 h of Ent treatment (1 µM) combined with cisplatin (Cis, 1 µM) or oxaliplatin (Oxa, 5 µM). ( C – F ) Representative plots and maximum scores (highest single agent model) from synergy analysis on viability of human and mouse PDAC cells under graded co-treatments of Ent with Cis ( C and D ) or Oxa ( E and F ). ( G and H ) Representative Western blots ( G ) and quantifications ( H ) showing increased γH2A.X in FC1245 after 6 h combined treatments of Ent (1 µM) with mitomycin C (MMC, 0.5 µM) or niraparib, (Nir, 2 µM). ( I – L ) Synergy plots and maximum scores from co-treatments of Ent and MMC ( I and J ) or Nir ( K and L ) in PDAC cells. Western blotting, n = 2 independent experiments; synergy analysis, n = 3 cell sample replicates. ( M ) Tumor weights from orthotopic transplantation models (FC1245) treated for two weeks with Ent (20 mg/kg, daily) and/or Cis (0.5 mg/kg, q3d). n = 7 (Veh), 6 (Ent, Cis), or 5 (Ent+Cis) mice. ( N and O ) Representative IHC images and quantifications of γH2A.X in tumors across treatment groups. n = 5 (Veh, Ent+Cis) or 4 (Ent, Cis) tumors. Scale bar, 50 µm. Data are presented as mean values ± SEM ( M and O ). **, p < 0.01; ****, p < 0.0001. One-way ANOVA.

Article Snippet: R.M.E. and M.D. are co-founders of Syndax, which holds the rights to entinostat.

Techniques: Western Blot, Transplantation Assay

Journal: bioRxiv

Article Title: HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery

doi: 10.64898/2026.05.18.726071

Figure Lengend Snippet: Entinostat treatment suppresses DDR pathways and induces DNA damage in PDAC. ( A and B ) Volcano plots showing RNA-seq results of differentially expressed genes between entinostat (Ent, 5 µM, 24 h) and vehicle (Veh) treatment in human MIA PaCa2 ( A ) and mouse FC1245 ( B ) PDAC cells. 3602 (MIA PaCa2) and 3543 (FC1245) genes are significantly upregulated, and 3478 (MIA PaCa2) and 3158 (FC1245) genes downregulated with representative DDR-related genes highlighted. FC, fold change. n = 2 independent cell samples. ( C ) GSEA enrichment plot showing DNA repair hallmark enriched in Ent-downregulated genes in FC1245. NES, normalized enrichment score; FDR, false discovery rate; Up, upregulation; Down, downregulation. ( D ) DDR-related gene ontology (GO) terms enriched in Ent-downregulated genes from GSEA. GG-NER, global genome nucleotide excision repair; PCNA, proliferating cell nuclear antigen. ( E and F ) Representative Western blots ( E ) and quantifications ( F ) showing increased γH2A.X and H3ac (normalized to histone H2A.X and H3, respectively) under graded Ent treatments. n = 2 independent experiments. ( G ) 4 gene clusters with downregulation trends (D1–D4) identified by temporal expression analysis in FC1245 cells with 0–24 h treatment of Ent (5 µM). n = 3 independent cell samples. ( H ) Enrichment of selected GO terms in downregulated clusters.

Article Snippet: R.M.E. and M.D. are co-founders of Syndax, which holds the rights to entinostat.

Techniques: RNA Sequencing, Western Blot, Expressing

Journal: bioRxiv

Article Title: HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery

doi: 10.64898/2026.05.18.726071

Figure Lengend Snippet: Entinostat preferentially increases intergenic H3K27ac, diverting BRD4 and Pol II from DDR gene promoters. ( A ) Numbers and percentages of annotated H3K27ac, BRD4, and RPB1 peaks in FC1245 cells treated with Veh or Ent (5 µM, 6h or 24h) by CUT&RUN. ( B ) Venn diagrams showing H3K27ac, BRD4, and RPB1 peak distributions across treatments. ( C – H ) Heatmaps and average profiles of H3K27ac ( C and D ), BRD4 ( E and F ), and RPB1 ( G and H ) occupancy across treatments at baseline H3K27ac peaks (Veh). ( I ) Genome browser tracks of representative DDR gene loci illustrating Ent-induced changes of H3K27ac, BRD4, and RPB1 at promoters (yellow) and in selected adjacent intergenic/genic regions (blue) along with RNA changes. NT, no treatment. Scale bar, 5 kb.

Article Snippet: R.M.E. and M.D. are co-founders of Syndax, which holds the rights to entinostat.

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1) Product Images from "HDAC Inhibition Sensitizes Pancreatic Tumors to DNA Damage by Global Redistribution of the Transcriptional Machinery"

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