gartisertib (MedChemExpress)

MedChemExpress gartisertib
Gartisertib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/gartisertib/product/MedChemExpress
Average 93 stars, based on 1 article reviews

gartisertib - by Bioz Stars, 2026-03

93/100 stars

Buy from Supplier

gartisertib (m4344) (Merck & Co)

Merck & Co gartisertib (m4344)

( A ) Dose-response of <t>gartisertib</t> treated glioblastoma cell lines (median IC50 = 0.56 μM). ( B ) Dose response of an astrocyte cell line treated with gartisertib (IC50 = 7.22 μM). Data points represent the mean ± SEM cell viability (%) of biological triplicates undertaken in three independent experiments. ( C ) Heatmap depicting gartisertib sensitivity, MGMT methylation status and baseline DDR gene mutation in the 12 glioblastoma cell lines. A trend is apparent where more gartisertib sensitive cell lines have higher amounts of DDR mutations and are MGMT unmethylated. See Supplementary Table 1 for specific SNVs and zygosity of such genes within each cell line. ( D ) Pearson correlation of the frequency of identified baseline mutations in DDR-related genes vs. log10 gartisertib IC50, showing a correlation of higher DDR mutations with lower gartisertib IC50 (r = −0.62, p = 0.03) ( E ) Pearson correlation of gartisertib log10 IC50 vs. CHEK2 gene expression (log2 TPM) within the 12 glioblastoma cell lines, in which higher expression of CHEK2 correlated with gartisertib sensitivity (r = −0.72, p = 0.007). Baseline RNA-seq expression for each cell line published by Stringer et al. was used for correlation analysis. P < 0.05 was considered significant.

Gartisertib (M4344), supplied by Merck & Co, 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/gartisertib (m4344)/product/Merck & Co
Average 90 stars, based on 1 article reviews

gartisertib (m4344) - by Bioz Stars, 2026-03

90/100 stars

Buy from Supplier

gartisertib (Merck KGaA)

Merck KGaA gartisertib

O ptimizing activation and inhibition of ATR . A , U-2 OS cells were incubated with thymidine (2 mM) for 24 h and released for 3 h at which point nocodazole (100 ng/ml) was added for a further 12 h. Cells were released from nocodazole into fresh medium for the times indicated. Cells were fixed, stained with propidium iodide (PI) and analysed by FACS. B , U-2 OS cells synchronized in S-phase (11 h after release from nocodazole) were pre-incubated for 1 h with the indicated concentrations of berzosertib or <t>gartisertib</t> before addition of HU (1 mM) for 1 h. Cells were lysed, and extracts were subjected to Western blotting with the antibodies indicated. C , same as ( B ) except that S-phase cells were pre-incubated with berzosertib or gartisertib (1 μM for 1 h) before addition of HU (1 mM) for the times indicated. D , optimized cell treatment workflow.

Gartisertib, supplied by Merck KGaA, 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/gartisertib/product/Merck KGaA
Average 90 stars, based on 1 article reviews

gartisertib - by Bioz Stars, 2026-03

90/100 stars

Buy from Supplier

gartisertib (Vertex Pharmaceuticals)

Vertex Pharmaceuticals gartisertib

Gartisertib, supplied by Vertex Pharmaceuticals, 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/gartisertib/product/Vertex Pharmaceuticals
Average 90 stars, based on 1 article reviews

gartisertib - by Bioz Stars, 2026-03

90/100 stars

Buy from Supplier

Image Search Results

( A ) Dose-response of gartisertib treated glioblastoma cell lines (median IC50 = 0.56 μM). ( B ) Dose response of an astrocyte cell line treated with gartisertib (IC50 = 7.22 μM). Data points represent the mean ± SEM cell viability (%) of biological triplicates undertaken in three independent experiments. ( C ) Heatmap depicting gartisertib sensitivity, MGMT methylation status and baseline DDR gene mutation in the 12 glioblastoma cell lines. A trend is apparent where more gartisertib sensitive cell lines have higher amounts of DDR mutations and are MGMT unmethylated. See Supplementary Table 1 for specific SNVs and zygosity of such genes within each cell line. ( D ) Pearson correlation of the frequency of identified baseline mutations in DDR-related genes vs. log10 gartisertib IC50, showing a correlation of higher DDR mutations with lower gartisertib IC50 (r = −0.62, p = 0.03) ( E ) Pearson correlation of gartisertib log10 IC50 vs. CHEK2 gene expression (log2 TPM) within the 12 glioblastoma cell lines, in which higher expression of CHEK2 correlated with gartisertib sensitivity (r = −0.72, p = 0.007). Baseline RNA-seq expression for each cell line published by Stringer et al. was used for correlation analysis. P < 0.05 was considered significant.

Journal: Oncotarget

Article Title: ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

doi: 10.18632/oncotarget.28551

Figure Lengend Snippet: ( A ) Dose-response of gartisertib treated glioblastoma cell lines (median IC50 = 0.56 μM). ( B ) Dose response of an astrocyte cell line treated with gartisertib (IC50 = 7.22 μM). Data points represent the mean ± SEM cell viability (%) of biological triplicates undertaken in three independent experiments. ( C ) Heatmap depicting gartisertib sensitivity, MGMT methylation status and baseline DDR gene mutation in the 12 glioblastoma cell lines. A trend is apparent where more gartisertib sensitive cell lines have higher amounts of DDR mutations and are MGMT unmethylated. See Supplementary Table 1 for specific SNVs and zygosity of such genes within each cell line. ( D ) Pearson correlation of the frequency of identified baseline mutations in DDR-related genes vs. log10 gartisertib IC50, showing a correlation of higher DDR mutations with lower gartisertib IC50 (r = −0.62, p = 0.03) ( E ) Pearson correlation of gartisertib log10 IC50 vs. CHEK2 gene expression (log2 TPM) within the 12 glioblastoma cell lines, in which higher expression of CHEK2 correlated with gartisertib sensitivity (r = −0.72, p = 0.007). Baseline RNA-seq expression for each cell line published by Stringer et al. was used for correlation analysis. P < 0.05 was considered significant.

Article Snippet: ATR inhibitors (ATRi) have been developed including gartisertib (M4344), tuvusertib (M1774), and berzosertib (M6620) (Merck), ceralasertib (AZD6738) (AstraZeneca, Cambridge, United Kingdom), and elimusertib (BAY-1895344) (Bayer, Leverkusen, Germany), and are in multiple clinical trials for treatment of solid tumours.

Techniques: Methylation, Mutagenesis, Expressing, RNA Sequencing Assay

Average cell confluence across glioblastoma cell lines ( n = 12) within a 7-day post-treatment incubation is shown ( A ). Data points represent the mean ± SEM at 24 hr increments. Average (± SEM) cell confluence ( B ), apoptosis ( C ) and cell death ( D ) was calculated across all 12 glioblastoma cell lines at the 7-day assay endpoint. Data points represent the average confluence, apoptosis and cell death for each individual cell line calculated from three independent experiments. Statistical analysis was performed using a one-way ANOVA used for the following comparisons (using collated replicate data across all cell lines): DMSO vs. TMZ+RT, DMSO vs. gartisertib+TMZ+RT, gartisertib vs. TMZ+RT, TMZ+RT vs. gartisertib+TMZ+RT, gartisertib vs. gartisertib+TMZ, gartisertib vs. gartisertib+RT, gartisertib vs. gartisertib+TMZ+RT, gartisertib+TMZ vs. gartisertib+TMZ+RT, gartisertib+RT vs. gartisertib+TMZ+RT ( * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). The combination of gartisertib+TMZ+RT significantly reduced cell confluence and increased apoptosis/cell death compared to single agent gartisertib and TMZ+RT. The SB2b cell line is depicted in ( E – H ) in which phase contrast images were taken using 10x objective on day 7 after treatment with DMSO (E), TMZ+ RT (F), gartisertib (G), and gartisertib+ TMZ+ RT (H). Green - Cytotox Green Reagent; Red - Annexin V Red Dye.

Journal: Oncotarget

Article Title: ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

doi: 10.18632/oncotarget.28551

Figure Lengend Snippet: Average cell confluence across glioblastoma cell lines ( n = 12) within a 7-day post-treatment incubation is shown ( A ). Data points represent the mean ± SEM at 24 hr increments. Average (± SEM) cell confluence ( B ), apoptosis ( C ) and cell death ( D ) was calculated across all 12 glioblastoma cell lines at the 7-day assay endpoint. Data points represent the average confluence, apoptosis and cell death for each individual cell line calculated from three independent experiments. Statistical analysis was performed using a one-way ANOVA used for the following comparisons (using collated replicate data across all cell lines): DMSO vs. TMZ+RT, DMSO vs. gartisertib+TMZ+RT, gartisertib vs. TMZ+RT, TMZ+RT vs. gartisertib+TMZ+RT, gartisertib vs. gartisertib+TMZ, gartisertib vs. gartisertib+RT, gartisertib vs. gartisertib+TMZ+RT, gartisertib+TMZ vs. gartisertib+TMZ+RT, gartisertib+RT vs. gartisertib+TMZ+RT ( * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001). The combination of gartisertib+TMZ+RT significantly reduced cell confluence and increased apoptosis/cell death compared to single agent gartisertib and TMZ+RT. The SB2b cell line is depicted in ( E – H ) in which phase contrast images were taken using 10x objective on day 7 after treatment with DMSO (E), TMZ+ RT (F), gartisertib (G), and gartisertib+ TMZ+ RT (H). Green - Cytotox Green Reagent; Red - Annexin V Red Dye.

Techniques: Incubation

Cell confluence ( A ), and cell death ( B ) of treated SB2b cells was observed across a 7-day time course using the Incucyte ® S3 Live-Cell Analysis System (mean ± SEM). The combination of gartisertib with TMZ+RT reduced cell growth and enhanced cell death in SB2b cells significantly greater than TMZ+RT alone. Western blot analysis ( C ) confirmed the inhibition of ATR after 24 hr and 96 hr, while an increase in DNA damage (γ-H2AX levels) was consistent with cell confluence reduction and increased cell death after 96 hr. See Supplementary Figure 8 for original blots and Supplementary Figure 9 for quantification of expression for SB2b, FPW1 and MN1 treated cell lines.

Journal: Oncotarget

Article Title: ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

doi: 10.18632/oncotarget.28551

Figure Lengend Snippet: Cell confluence ( A ), and cell death ( B ) of treated SB2b cells was observed across a 7-day time course using the Incucyte ® S3 Live-Cell Analysis System (mean ± SEM). The combination of gartisertib with TMZ+RT reduced cell growth and enhanced cell death in SB2b cells significantly greater than TMZ+RT alone. Western blot analysis ( C ) confirmed the inhibition of ATR after 24 hr and 96 hr, while an increase in DNA damage (γ-H2AX levels) was consistent with cell confluence reduction and increased cell death after 96 hr. See Supplementary Figure 8 for original blots and Supplementary Figure 9 for quantification of expression for SB2b, FPW1 and MN1 treated cell lines.

Techniques: Western Blot, Inhibition, Expressing

( A ) ZIP synergy scores were calculated for each combination as an average across all concentrations tested, with each data point representing one cell line. Combinations of gartisertib with TMZ and/or RT had significantly higher synergy scores than TMZ+RT ( **** p < 0.0001, *** p < 0.001, ** p < 0.01). ( B ) ZIP synergy scores are shown across the various concentrations of gartisertib tested when combined with the clinically relevant doses of RT (2 Gy) and TMZ (33 μM). Asterisks denote statistically significant synergy scores compared to TMZ+RT from a one-way ANOVA ( ** p < 0.01, * p < 0.05). Overall, gartisertib was significantly more synergistic than a clinically relevant dose of TMZ+RT when combined with TMZ and/or RT at lower gartisertib concentrations (0.039–0.156 μM). ( C – E ) Cell viability (mean + SEM) of all glioblastoma cell lines treated with gartisertib alone (blue) and in combination with clinically relevant doses of TMZ (33 μM) (C), RT (2 Gy) (D) or TMZ (33 μM) + RT (2 Gy) (E) (red) are depicted for each concentration of gartisertib tested. The average cell viability for single agent treatment of TMZ, RT and TMZ+RT (green) is also shown. Data points represent the mean ± SEM of synergy scores and cell viability of combined data across all 12 glioblastoma cell lines. This shows that low doses of gartisertib achieve favourable reduction in cell viability with TMZ and/or RT, while at higher doses (>2.5 μM) there is less change compared to gartisertib alone.

Journal: Oncotarget

Article Title: ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

doi: 10.18632/oncotarget.28551

Figure Lengend Snippet: ( A ) ZIP synergy scores were calculated for each combination as an average across all concentrations tested, with each data point representing one cell line. Combinations of gartisertib with TMZ and/or RT had significantly higher synergy scores than TMZ+RT ( **** p < 0.0001, *** p < 0.001, ** p < 0.01). ( B ) ZIP synergy scores are shown across the various concentrations of gartisertib tested when combined with the clinically relevant doses of RT (2 Gy) and TMZ (33 μM). Asterisks denote statistically significant synergy scores compared to TMZ+RT from a one-way ANOVA ( ** p < 0.01, * p < 0.05). Overall, gartisertib was significantly more synergistic than a clinically relevant dose of TMZ+RT when combined with TMZ and/or RT at lower gartisertib concentrations (0.039–0.156 μM). ( C – E ) Cell viability (mean + SEM) of all glioblastoma cell lines treated with gartisertib alone (blue) and in combination with clinically relevant doses of TMZ (33 μM) (C), RT (2 Gy) (D) or TMZ (33 μM) + RT (2 Gy) (E) (red) are depicted for each concentration of gartisertib tested. The average cell viability for single agent treatment of TMZ, RT and TMZ+RT (green) is also shown. Data points represent the mean ± SEM of synergy scores and cell viability of combined data across all 12 glioblastoma cell lines. This shows that low doses of gartisertib achieve favourable reduction in cell viability with TMZ and/or RT, while at higher doses (>2.5 μM) there is less change compared to gartisertib alone.

Techniques: Concentration Assay

( A ) Genes involved in DDR and immune function were examined for difference in log2 TPM expression across all 12 glioblastoma cell lines through a paired t -test across comparisons for the effect of TMZ+RT, gartisertib and gartisertib+TMZ+RT treatments. Significant differences ( p < 0.05) are shown in red (up-regulated) or blue (down-regulated). TMZ+RT treatment induced an upregulation of multiple DDR genes, while most DDR pathways were downregulated following ATR inhibition using gartisertib. ( B ) Core analysis using IPA was performed on significantly upregulated or downregulated genes ( padj < 0.05, fold change ≥1.5) identified in prior DESeq2 analysis of all 12 glioblastoma cell lines treated with gartisertib+TMZ+RT against DMSO control cells. The top 20 canonical pathways are shown (z-score ≥2 or ≤−2). Significantly enriched IPA pathways were determined with a −log10 B-H p -value > 1.3 (above dotted line) (red = upregulated, blue = downregulated). ( C ) Through this comparison, a mechanistic network is shown representing the connection of canonical pathways, diseases, and molecules. Upregulated (orange) and downregulated (blue) components are shown. Legends for network shapes and arrows are depicted from https://qiagen.secure.force.com/KnowledgeBase/articles/Knowledge/Legend . Overall, ATR inhibition using gartisertib significantly induced the upregulation of pro-inflammatory pathways.

Journal: Oncotarget

Article Title: ATR inhibition using gartisertib enhances cell death and synergises with temozolomide and radiation in patient-derived glioblastoma cell lines

doi: 10.18632/oncotarget.28551

Figure Lengend Snippet: ( A ) Genes involved in DDR and immune function were examined for difference in log2 TPM expression across all 12 glioblastoma cell lines through a paired t -test across comparisons for the effect of TMZ+RT, gartisertib and gartisertib+TMZ+RT treatments. Significant differences ( p < 0.05) are shown in red (up-regulated) or blue (down-regulated). TMZ+RT treatment induced an upregulation of multiple DDR genes, while most DDR pathways were downregulated following ATR inhibition using gartisertib. ( B ) Core analysis using IPA was performed on significantly upregulated or downregulated genes ( padj < 0.05, fold change ≥1.5) identified in prior DESeq2 analysis of all 12 glioblastoma cell lines treated with gartisertib+TMZ+RT against DMSO control cells. The top 20 canonical pathways are shown (z-score ≥2 or ≤−2). Significantly enriched IPA pathways were determined with a −log10 B-H p -value > 1.3 (above dotted line) (red = upregulated, blue = downregulated). ( C ) Through this comparison, a mechanistic network is shown representing the connection of canonical pathways, diseases, and molecules. Upregulated (orange) and downregulated (blue) components are shown. Legends for network shapes and arrows are depicted from https://qiagen.secure.force.com/KnowledgeBase/articles/Knowledge/Legend . Overall, ATR inhibition using gartisertib significantly induced the upregulation of pro-inflammatory pathways.

Techniques: Expressing, Inhibition, Comparison

Journal: Molecular & Cellular Proteomics : MCP

Article Title: Chemo-Phosphoproteomic Profiling with ATR Inhibitors Berzosertib and Gartisertib Uncovers New Biomarkers and DNA Damage Response Regulators

doi: 10.1016/j.mcpro.2024.100802

Figure Lengend Snippet: O ptimizing activation and inhibition of ATR . A , U-2 OS cells were incubated with thymidine (2 mM) for 24 h and released for 3 h at which point nocodazole (100 ng/ml) was added for a further 12 h. Cells were released from nocodazole into fresh medium for the times indicated. Cells were fixed, stained with propidium iodide (PI) and analysed by FACS. B , U-2 OS cells synchronized in S-phase (11 h after release from nocodazole) were pre-incubated for 1 h with the indicated concentrations of berzosertib or gartisertib before addition of HU (1 mM) for 1 h. Cells were lysed, and extracts were subjected to Western blotting with the antibodies indicated. C , same as ( B ) except that S-phase cells were pre-incubated with berzosertib or gartisertib (1 μM for 1 h) before addition of HU (1 mM) for the times indicated. D , optimized cell treatment workflow.

Article Snippet: This work was supported by the 10.13039/501100000265 Medical Research Council (grant number MC_UU_12016/1 ; M. G., P. L., F. L., I. M., J. R.) and by the healthcare business of 10.13039/100009945 Merck KGaA , Darmstadt, Germany (CrossRef Funder ID: 10.13039/100009945 ) who provided berzosertib and gartisertib free of charge.

Techniques: Activation Assay, Inhibition, Incubation, Staining, Western Blot

Phosphoproteomic screening of phosphorylation sites sensitive to berzosertib or gartisertib . A and B , Volcano plot showing phosphorylation sites affected by berzosertib ( A ) or gartisertib ( B ). The horizontal cut-off lines represent an adjusted p -value of 0.05. Phosphopeptides lower in abundance after inhibitor treatment are in the negative logFC region of the plots. The mass spectrometry proteomics raw data for this figure have been deposited to the ProteomeXchange Consortium via the jPOSTrepo partner repository with the dataset identifier PXD040469 . Data analysis scripts and annotated spectra are available via Zenodo under https://doi.org/10.5281/zenodo.10581948 . C , overlap of proteins and phosphorylation sites affected by berzosertib or gartisertib. D and E , Phosphomotif analysis for berzosertib ( D ) and gartisertib ( E ). F , the five proteins whose phosphorylation is most strongly affected by berzosertib (“Class 1” hits). The phosphorylated residue is highlighted in red in the “Motif” column. Fold change refers to the difference between HU±ATRi. G , schematic diagram showing the location of the ATR-dependent phosphorylation sites in the DNA helicase FANCJ and the protein kinase TLK2.

Journal: Molecular & Cellular Proteomics : MCP

Article Title: Chemo-Phosphoproteomic Profiling with ATR Inhibitors Berzosertib and Gartisertib Uncovers New Biomarkers and DNA Damage Response Regulators

doi: 10.1016/j.mcpro.2024.100802

Figure Lengend Snippet: Phosphoproteomic screening of phosphorylation sites sensitive to berzosertib or gartisertib . A and B , Volcano plot showing phosphorylation sites affected by berzosertib ( A ) or gartisertib ( B ). The horizontal cut-off lines represent an adjusted p -value of 0.05. Phosphopeptides lower in abundance after inhibitor treatment are in the negative logFC region of the plots. The mass spectrometry proteomics raw data for this figure have been deposited to the ProteomeXchange Consortium via the jPOSTrepo partner repository with the dataset identifier PXD040469 . Data analysis scripts and annotated spectra are available via Zenodo under https://doi.org/10.5281/zenodo.10581948 . C , overlap of proteins and phosphorylation sites affected by berzosertib or gartisertib. D and E , Phosphomotif analysis for berzosertib ( D ) and gartisertib ( E ). F , the five proteins whose phosphorylation is most strongly affected by berzosertib (“Class 1” hits). The phosphorylated residue is highlighted in red in the “Motif” column. Fold change refers to the difference between HU±ATRi. G , schematic diagram showing the location of the ATR-dependent phosphorylation sites in the DNA helicase FANCJ and the protein kinase TLK2.

Techniques: Phospho-proteomics, Mass Spectrometry, Residue

gartisertib Search Results

Image Search Results