HY-141591 Search Results


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MedChemExpress datopotamab deruxtecan
Models of acquired resistance to TROP2 ADC can be overcome with TROP2 CARs. A, PC9 with KO of TROP2 were reconstituted with either WT TROP2 or the T256R mutation, which has been previously described to have developed in acquired resistance to TROP2 ADC. Mean fluorescence intensity after TROP2 staining by flow cytometry on viable (DAPI-negative) cells is shown. B, In vitro viability of constructs described in ( A ) after generation of spheroids and treatment in an ultralow attachment 96-well plate with <t>datopotamab</t> <t>deruxtecan.</t> Cells were incubated with ADC for 6 days, followed by viability assessment by luciferase assay. Viability was normalized to vehicle (0 µg/mL) for each construct. Data are representative of two different experiments with technical triplicates, with error bars showing SD. C, In vitro viability of either WT TROP2 or T256R TROP2 with TROP2 CARs at a 1:1 E:T ratio. Assay after 24 hours of incubation. Data are representative of two different experiments with different donors and technical triplicates, with error bars showing SD. D, In vitro viability of either WT TOP1 or E418K TOP1 with TROP2 CARs after 24 hours of incubation, with technical triplicates, with error bars showing SD. E, Model of resistance to TROP2 ADC by TROP2 T256R mutation or TOP1 mutation and how TROP2 CARs are able to maintain cytolytic activity, created with Biorender. P values are reported as follows compared with control: *, P ≤ 0.05; **, P ≤ 0.01; ****, P ≤ 0.0001. dsDNA, double-stranded DNA; GzmB, granzyme B.
Datopotamab Deruxtecan, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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CYT296 is a target chromatin de-condensation compound. CYT296 can improve the induction of induced pluripotent stem cell (iPSCs) mediated by defined factors (OSKM) and induce an open chromatin state in Mouse Embryonic Fibroblast (MEFs) to
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Models of acquired resistance to TROP2 ADC can be overcome with TROP2 CARs. A, PC9 with KO of TROP2 were reconstituted with either WT TROP2 or the T256R mutation, which has been previously described to have developed in acquired resistance to TROP2 ADC. Mean fluorescence intensity after TROP2 staining by flow cytometry on viable (DAPI-negative) cells is shown. B, In vitro viability of constructs described in ( A ) after generation of spheroids and treatment in an ultralow attachment 96-well plate with datopotamab deruxtecan. Cells were incubated with ADC for 6 days, followed by viability assessment by luciferase assay. Viability was normalized to vehicle (0 µg/mL) for each construct. Data are representative of two different experiments with technical triplicates, with error bars showing SD. C, In vitro viability of either WT TROP2 or T256R TROP2 with TROP2 CARs at a 1:1 E:T ratio. Assay after 24 hours of incubation. Data are representative of two different experiments with different donors and technical triplicates, with error bars showing SD. D, In vitro viability of either WT TOP1 or E418K TOP1 with TROP2 CARs after 24 hours of incubation, with technical triplicates, with error bars showing SD. E, Model of resistance to TROP2 ADC by TROP2 T256R mutation or TOP1 mutation and how TROP2 CARs are able to maintain cytolytic activity, created with Biorender. P values are reported as follows compared with control: *, P ≤ 0.05; **, P ≤ 0.01; ****, P ≤ 0.0001. dsDNA, double-stranded DNA; GzmB, granzyme B.

Journal: Cancer Immunology Research

Article Title: Systematic Engineering of TROP2-Targeted CAR T-Cell Therapy Overcomes Resistance Pathways in Solid Tumors

doi: 10.1158/2326-6066.CIR-25-0527

Figure Lengend Snippet: Models of acquired resistance to TROP2 ADC can be overcome with TROP2 CARs. A, PC9 with KO of TROP2 were reconstituted with either WT TROP2 or the T256R mutation, which has been previously described to have developed in acquired resistance to TROP2 ADC. Mean fluorescence intensity after TROP2 staining by flow cytometry on viable (DAPI-negative) cells is shown. B, In vitro viability of constructs described in ( A ) after generation of spheroids and treatment in an ultralow attachment 96-well plate with datopotamab deruxtecan. Cells were incubated with ADC for 6 days, followed by viability assessment by luciferase assay. Viability was normalized to vehicle (0 µg/mL) for each construct. Data are representative of two different experiments with technical triplicates, with error bars showing SD. C, In vitro viability of either WT TROP2 or T256R TROP2 with TROP2 CARs at a 1:1 E:T ratio. Assay after 24 hours of incubation. Data are representative of two different experiments with different donors and technical triplicates, with error bars showing SD. D, In vitro viability of either WT TOP1 or E418K TOP1 with TROP2 CARs after 24 hours of incubation, with technical triplicates, with error bars showing SD. E, Model of resistance to TROP2 ADC by TROP2 T256R mutation or TOP1 mutation and how TROP2 CARs are able to maintain cytolytic activity, created with Biorender. P values are reported as follows compared with control: *, P ≤ 0.05; **, P ≤ 0.01; ****, P ≤ 0.0001. dsDNA, double-stranded DNA; GzmB, granzyme B.

Article Snippet: Datopotamab deruxtecan was obtained from MedChemExpress (cat. # HY-141598).

Techniques: Mutagenesis, Fluorescence, Staining, Flow Cytometry, In Vitro, Construct, Incubation, Luciferase, Activity Assay, Control