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dipyridamole  (MedChemExpress)


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    MedChemExpress dipyridamole
    A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., <t>dipyridamole)</t> and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).
    Dipyridamole, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 51 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "hENT Inhibition Prevents Pyrimidine-Driven Resistance to DHODH Inhibition in Malignant Rhabdoid Tumors"

    Article Title: hENT Inhibition Prevents Pyrimidine-Driven Resistance to DHODH Inhibition in Malignant Rhabdoid Tumors

    Journal: bioRxiv

    doi: 10.64898/2026.01.25.701565

    A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., dipyridamole) and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).
    Figure Legend Snippet: A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., dipyridamole) and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).

    Techniques Used: Synthesized, Inhibition, Concentration Assay, Generated, Software, Standard Deviation, Control, Labeling, Incubation, Isotopic Labeling, Comparison

    A) Bar graph depicting the average viability (%) of ecMRT tumoroids cultured in KOM supplemented with 30 μM uridine following 120-hour treatment with various concentrations of dipyridamole. Data represent the mean ± SD of n = 3 independent experiments, each consisting of technical triplicates. Viability values were normalized to the DMSO vehicle control (100%). B) Dose-response curves for ecMRT tumoroid models 60T and 78T treated with GTX-196 for 120 hours in Plasmax™ medium, with or without the hENT1/2 inhibitor dipyridamole (500 nM). ecMRT tumoroids treated with GTX-196 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid models 60T treated with BAY-2402234 (panel C ) and 103T treated with GTX-196 (panel D) for 120 hours in KOM supplemented with 3 μM uridine, with or without different concentrations of hENT1/2 inhibitor dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for BAY-2402234 combined with dipyridamole (panel E ) and GTX-196 combined with dipyridamole (panel F ) (corresponding to figure panels C and D ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G , I) Dose-response curves for ecMRT tumoroid model 103T treated with GTX-196 for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of hENT inhibitors draflazine (panel G ) or nitrobenzylthioinosine (NBMPR; panel I). Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). H , J ) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for GTX-196 combined with draflazine (panel H ) and GTX-196 combined with NBMPR (panel J ) (corresponding to figure panels G and I ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . K) Isotopic labeling pattern of extracellular uridine levels measured in the medium of BME (no cells) and two different ecMRT tumoroids following 24-hour incubation with 3⍰μM or 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. All conditions were statistically compared to the BME (no cells) reference group. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).
    Figure Legend Snippet: A) Bar graph depicting the average viability (%) of ecMRT tumoroids cultured in KOM supplemented with 30 μM uridine following 120-hour treatment with various concentrations of dipyridamole. Data represent the mean ± SD of n = 3 independent experiments, each consisting of technical triplicates. Viability values were normalized to the DMSO vehicle control (100%). B) Dose-response curves for ecMRT tumoroid models 60T and 78T treated with GTX-196 for 120 hours in Plasmax™ medium, with or without the hENT1/2 inhibitor dipyridamole (500 nM). ecMRT tumoroids treated with GTX-196 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid models 60T treated with BAY-2402234 (panel C ) and 103T treated with GTX-196 (panel D) for 120 hours in KOM supplemented with 3 μM uridine, with or without different concentrations of hENT1/2 inhibitor dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for BAY-2402234 combined with dipyridamole (panel E ) and GTX-196 combined with dipyridamole (panel F ) (corresponding to figure panels C and D ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G , I) Dose-response curves for ecMRT tumoroid model 103T treated with GTX-196 for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of hENT inhibitors draflazine (panel G ) or nitrobenzylthioinosine (NBMPR; panel I). Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). H , J ) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for GTX-196 combined with draflazine (panel H ) and GTX-196 combined with NBMPR (panel J ) (corresponding to figure panels G and I ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . K) Isotopic labeling pattern of extracellular uridine levels measured in the medium of BME (no cells) and two different ecMRT tumoroids following 24-hour incubation with 3⍰μM or 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. All conditions were statistically compared to the BME (no cells) reference group. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).

    Techniques Used: Cell Culture, Control, Concentration Assay, Generated, Software, Isotopic Labeling, Incubation



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    A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., <t>dipyridamole)</t> and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).
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    A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., <t>dipyridamole)</t> and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).
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    A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., <t>dipyridamole)</t> and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).
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    A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., dipyridamole) and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).

    Journal: bioRxiv

    Article Title: hENT Inhibition Prevents Pyrimidine-Driven Resistance to DHODH Inhibition in Malignant Rhabdoid Tumors

    doi: 10.64898/2026.01.25.701565

    Figure Lengend Snippet: A) Schematic overview of de novo nucleotide biosynthesis and nucleotide salvage pathways. Nucleosides and nucleobases are imported into the cell via hENT 1 and 2 and subsequently phosphorylated to their corresponding nucleotide monophosphates (NMPs). In parallel, nucleotides can be synthesized de novo from metabolic precursors, resulting in the formation of NMPs. Key enzymes involved in these pathways, including uridine-cytidine kinase (UCK), DHODH, and carbamoyl-phosphate synthetase 2/ aspartate transcarbamylase/ dihydroorotase (CAD), are highlighted. Both pathways can be subjected to pharmacological inhibition by agents targeting hENT1/2 (e.g., dipyridamole) and DHODH (e.g., BAY-2402234 and GTX-196). B) Dose-response curves for ecMRT tumoroid models 60T and 103T treated with BAY-2402234 for 120 hours in Plasmax™ medium, with or without dipyridamole (500 nM). ecMRT tumoroids treated with BAY-2402234 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid model 103T treated with BAY-2402234 (panel C ) or GTX-196 (panel D) for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) ZIP synergy landscapes for BAY-2402234 + dipyridamole (E) and GTX-196 + dipyridamole (F) , corresponding to panels C–D. ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G) Bar graph depicting the average cell viability (%) of ecMRT tumoroid models following 120-hour treatment with 5 nM GTX-196, 10 μM dipyridamole, or their combination, in the presence or absence of nucleoside supplementation. Data represent the mean ± standard deviation (SD) of n = 3 independent experiments, each performed in technical triplicates. Viability values were normalized to the DMSO vehicle control without nucleoside supplementation (set to 100%). H) Relative isotopologue distribution (fractional labeling) of CTP and UTP in two ecMRT models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle or 10 μM DP, in the presence or absence of 30⍰μM uridine. Statistical testing was performed within each uridine condition. I) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with [U- 13 C 6 ]-glucose upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof, in the presence or absence of 30⍰μM uridine. DMSO and GTX-196 reference data originate from the same [U- 13 C 6 ]-glucose tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl within each uridine condition. J) Isotopic labeling pattern of CTP and UTP in two ecMRT tumoroid models following 24-hour incubation with 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. DMSO and GTX-196 reference data originate from the same [ 13 C 9 - 15 N 2 ]-uridine tracing experiment as previously presented in , but are shown again to provide direct comparison across all treatment conditions. Unless specified otherwise, all conditions were statistically compared to the DMSO ctrl. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).

    Article Snippet: BAY-2402234 (MedChemExpress, HY-112645), GTX-196 (Genase Therapeutics), AG-636 (MedChemExpress, HY-137463), ASLAN003/Farudodstat (MedChemExpress, HY-129239), PTC299 (MedChemExpress, HY-124593), Dipyridamole (MedChemExpress, HY-B0312), Nitrobenzylthioinosine (NBMPR; MedChemExpress, HY-W010936), and Draflazine (MedChemExpress, HY-106841) were tested at final concentrations ranging between 0.01 nM and 10 μM.

    Techniques: Synthesized, Inhibition, Concentration Assay, Generated, Software, Standard Deviation, Control, Labeling, Incubation, Isotopic Labeling, Comparison

    A) Bar graph depicting the average viability (%) of ecMRT tumoroids cultured in KOM supplemented with 30 μM uridine following 120-hour treatment with various concentrations of dipyridamole. Data represent the mean ± SD of n = 3 independent experiments, each consisting of technical triplicates. Viability values were normalized to the DMSO vehicle control (100%). B) Dose-response curves for ecMRT tumoroid models 60T and 78T treated with GTX-196 for 120 hours in Plasmax™ medium, with or without the hENT1/2 inhibitor dipyridamole (500 nM). ecMRT tumoroids treated with GTX-196 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid models 60T treated with BAY-2402234 (panel C ) and 103T treated with GTX-196 (panel D) for 120 hours in KOM supplemented with 3 μM uridine, with or without different concentrations of hENT1/2 inhibitor dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for BAY-2402234 combined with dipyridamole (panel E ) and GTX-196 combined with dipyridamole (panel F ) (corresponding to figure panels C and D ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G , I) Dose-response curves for ecMRT tumoroid model 103T treated with GTX-196 for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of hENT inhibitors draflazine (panel G ) or nitrobenzylthioinosine (NBMPR; panel I). Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). H , J ) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for GTX-196 combined with draflazine (panel H ) and GTX-196 combined with NBMPR (panel J ) (corresponding to figure panels G and I ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . K) Isotopic labeling pattern of extracellular uridine levels measured in the medium of BME (no cells) and two different ecMRT tumoroids following 24-hour incubation with 3⍰μM or 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. All conditions were statistically compared to the BME (no cells) reference group. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).

    Journal: bioRxiv

    Article Title: hENT Inhibition Prevents Pyrimidine-Driven Resistance to DHODH Inhibition in Malignant Rhabdoid Tumors

    doi: 10.64898/2026.01.25.701565

    Figure Lengend Snippet: A) Bar graph depicting the average viability (%) of ecMRT tumoroids cultured in KOM supplemented with 30 μM uridine following 120-hour treatment with various concentrations of dipyridamole. Data represent the mean ± SD of n = 3 independent experiments, each consisting of technical triplicates. Viability values were normalized to the DMSO vehicle control (100%). B) Dose-response curves for ecMRT tumoroid models 60T and 78T treated with GTX-196 for 120 hours in Plasmax™ medium, with or without the hENT1/2 inhibitor dipyridamole (500 nM). ecMRT tumoroids treated with GTX-196 in KOM medium served as a reference. Data represent mean ± SD from three independent experiments, each performed with technical duplicates. Data are normalized to DMSO vehicle in KOM (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). C-D) Dose-response curves for ecMRT tumoroid models 60T treated with BAY-2402234 (panel C ) and 103T treated with GTX-196 (panel D) for 120 hours in KOM supplemented with 3 μM uridine, with or without different concentrations of hENT1/2 inhibitor dipyridamole. Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). E-F) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for BAY-2402234 combined with dipyridamole (panel E ) and GTX-196 combined with dipyridamole (panel F ) (corresponding to figure panels C and D ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . G , I) Dose-response curves for ecMRT tumoroid model 103T treated with GTX-196 for 120 hours in KOM supplemented with 30 μM uridine, with or without different concentrations of hENT inhibitors draflazine (panel G ) or nitrobenzylthioinosine (NBMPR; panel I). Data represent mean ± SD from three independent drug matrix experiments. Data are normalized to DMSO vehicle (100%). The grey dotted horizontal line represents a viability of 50% (IC 50 ). H , J ) Two-dimensional (2D) synergy landscapes visualized as contour plots, displaying ZIP (Zero Interaction Potency) synergy scores across concentration matrices for GTX-196 combined with draflazine (panel H ) and GTX-196 combined with NBMPR (panel J ) (corresponding to figure panels G and I ). ZIP scores >10 indicate synergistic interactions, scores between -10 and 10 represent additive effects, and scores <–10 indicate antagonism. Regions outlined in white represent the most synergistic concentration combinations. Synergy landscapes were generated using SynergyFinder software . K) Isotopic labeling pattern of extracellular uridine levels measured in the medium of BME (no cells) and two different ecMRT tumoroids following 24-hour incubation with 3⍰μM or 30⍰μM [ 13 C 9 - 15 N 2 ]-uridine upon 48-hour treatment with DMSO vehicle, 5 nM GTX-196, 10 μM DP, or the combination thereof. All conditions were statistically compared to the BME (no cells) reference group. (*, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001).

    Article Snippet: BAY-2402234 (MedChemExpress, HY-112645), GTX-196 (Genase Therapeutics), AG-636 (MedChemExpress, HY-137463), ASLAN003/Farudodstat (MedChemExpress, HY-129239), PTC299 (MedChemExpress, HY-124593), Dipyridamole (MedChemExpress, HY-B0312), Nitrobenzylthioinosine (NBMPR; MedChemExpress, HY-W010936), and Draflazine (MedChemExpress, HY-106841) were tested at final concentrations ranging between 0.01 nM and 10 μM.

    Techniques: Cell Culture, Control, Concentration Assay, Generated, Software, Isotopic Labeling, Incubation