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tng908  (MedChemExpress)


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    Structured Review

    MedChemExpress tng908
    MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, <t>TNG908</t> and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)
    Tng908, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tng908/product/MedChemExpress
    Average 93 stars, based on 3 article reviews
    tng908 - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "MTA-Cooperative PRMT5 Inhibitors Are Efficacious in MTAP-Deleted Malignant Peripheral Nerve Sheath Tumor Models"

    Article Title: MTA-Cooperative PRMT5 Inhibitors Are Efficacious in MTAP-Deleted Malignant Peripheral Nerve Sheath Tumor Models

    Journal: Clinical Cancer Research

    doi: 10.1158/1078-0432.CCR-24-3610

    MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, TNG908 and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)
    Figure Legend Snippet: MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, TNG908 and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)

    Techniques Used: Inhibition, In-Cell ELISA, Activity Assay, Viability Assay

    MTA-cooperative PRMT5 inhibitors are efficacious and selective in MTAP -null MPNST cell lines. A, MTAP and PRMT5 protein levels were determined by WES western analysis in human MPNST cell lines. B, Densitometry for MTAP and PRMT5 protein levels in MPNST cell lines, normalized to vinculin loading control. C and D, MTAP WT MPNST cells (JH-2-009 and JH-2-031) and MTAP -null MPNST (JH-2-079, JH-2-002, and WU-356) cells were treated with the indicated doses of MTA-cooperative PRMT5 inhibitors, ( C ) TNG908 or ( D ) TNG462, for 7 to 14 days. Cell viability was examined by CTG assay, and assay length was determined by the doubling time of each cell line. Data are presented as the mean ± SEM.
    Figure Legend Snippet: MTA-cooperative PRMT5 inhibitors are efficacious and selective in MTAP -null MPNST cell lines. A, MTAP and PRMT5 protein levels were determined by WES western analysis in human MPNST cell lines. B, Densitometry for MTAP and PRMT5 protein levels in MPNST cell lines, normalized to vinculin loading control. C and D, MTAP WT MPNST cells (JH-2-009 and JH-2-031) and MTAP -null MPNST (JH-2-079, JH-2-002, and WU-356) cells were treated with the indicated doses of MTA-cooperative PRMT5 inhibitors, ( C ) TNG908 or ( D ) TNG462, for 7 to 14 days. Cell viability was examined by CTG assay, and assay length was determined by the doubling time of each cell line. Data are presented as the mean ± SEM.

    Techniques Used: Western Blot, Control, CTG Assay

    MTA-cooperative PRMT5 inhibitors induce cell death in MPNST cell lines. A–C, MTAP WT (JH-2-009 and JH-2-031) and MTAP -null (JH-2-079, JH-2-002, and WU-356) MPNST cells were treated with the indicated doses of PRMT5 inhibitors, TNG908 or TNG462, for 7 days. A and B, Cell death was determined by IncuCyte assay using YOYO-1 dye. Data are presented as the mean ± SEM. *, P < 0.05 versus vehicle control. C, Apoptotic protein levels, total or cleaved (Cl) PARP-1 or caspase (Casp) 3, were determined by WES western analysis.
    Figure Legend Snippet: MTA-cooperative PRMT5 inhibitors induce cell death in MPNST cell lines. A–C, MTAP WT (JH-2-009 and JH-2-031) and MTAP -null (JH-2-079, JH-2-002, and WU-356) MPNST cells were treated with the indicated doses of PRMT5 inhibitors, TNG908 or TNG462, for 7 days. A and B, Cell death was determined by IncuCyte assay using YOYO-1 dye. Data are presented as the mean ± SEM. *, P < 0.05 versus vehicle control. C, Apoptotic protein levels, total or cleaved (Cl) PARP-1 or caspase (Casp) 3, were determined by WES western analysis.

    Techniques Used: Control, Western Blot

    MTA-cooperative PRMT5 inhibitors, TNG908 and TNG462, dramatically reduce tumor growth in two MPNST PDX mouse models. Mice bearing ( A–C ) WU-356 or ( D–F ) WU-386 PDX tumors (both NF1 -mutated and MTAP -null) were treated with ( A and D ) TNG908 or ( B, C, E, and F ) TNG462 for 5–6 weeks at the indicated doses. A, B, D, and E, Tumor growth curves of different treatment groups are shown as the mean ± SEM. C and F, Waterfall plots of the percent change in tumor volume, with tumor volume at the end of drug treatment normalized to the baseline tumor volume. All treatments were well tolerated. G and H, Immunoblots performed on terminal mouse tumors treated as indicated and collected from either WU-386 16 hours after the last dose ( G ) or WU-356 8 hours after the last dose ( H ). KP4 MTAP-isogenic pancreatic cancer xenograft samples are included as controls for MTAP and SDMA-modified protein levels. KP4 + empty vector (EV) is MTAP -null and KP4 + MTAP exogenously expresses MTAP cDNA. BID, twice per day.
    Figure Legend Snippet: MTA-cooperative PRMT5 inhibitors, TNG908 and TNG462, dramatically reduce tumor growth in two MPNST PDX mouse models. Mice bearing ( A–C ) WU-356 or ( D–F ) WU-386 PDX tumors (both NF1 -mutated and MTAP -null) were treated with ( A and D ) TNG908 or ( B, C, E, and F ) TNG462 for 5–6 weeks at the indicated doses. A, B, D, and E, Tumor growth curves of different treatment groups are shown as the mean ± SEM. C and F, Waterfall plots of the percent change in tumor volume, with tumor volume at the end of drug treatment normalized to the baseline tumor volume. All treatments were well tolerated. G and H, Immunoblots performed on terminal mouse tumors treated as indicated and collected from either WU-386 16 hours after the last dose ( G ) or WU-356 8 hours after the last dose ( H ). KP4 MTAP-isogenic pancreatic cancer xenograft samples are included as controls for MTAP and SDMA-modified protein levels. KP4 + empty vector (EV) is MTAP -null and KP4 + MTAP exogenously expresses MTAP cDNA. BID, twice per day.

    Techniques Used: Western Blot, Modification, Plasmid Preparation



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    MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, <t>TNG908</t> and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)
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    MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, <t>TNG908</t> and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)
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    MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, <t>TNG908</t> and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)
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    Image Search Results


    MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, TNG908 and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)

    Journal: Clinical Cancer Research

    Article Title: MTA-Cooperative PRMT5 Inhibitors Are Efficacious in MTAP-Deleted Malignant Peripheral Nerve Sheath Tumor Models

    doi: 10.1158/1078-0432.CCR-24-3610

    Figure Lengend Snippet: MTA-cooperative PRMT5 inhibitors target cells with MTAP deletion. A, Diagram of MPNST PDX mouse model propagation and drug treatments. B, Schema demonstrating the enhanced PRMT5 dependence of MTAP -null cancers and the rationale for MTA-cooperative PRMT5 inhibitors. C and D, Chemical structure of the PRMT5 inhibitor compounds, TNG908 and TNG462. E, PRMT5 inhibition determined by SDMA in-cell western (ICW) assay (left) and antiproliferative activity determined by CTG in a 7-day viability assay (right) in the HAP1 MTAP -isogenic cell lines. Data are presented as the mean ± SD. ( A and B , Created in BioRender. Hirbe, A. [2025] https://BioRender.com/w31j902 and https://BioRender.com/r41e580 .)

    Article Snippet: On day 1, TNG908 , TNG462 (WO2022026892; ref. ), or GSK3326595 (either from custom synthesis ( ) or MedChemExpress HY-101563) were dosed using a Tecan D300e and normalized to highest class volume with DMSO (the final DMSO percentage was 0.2%).

    Techniques: Inhibition, In-Cell ELISA, Activity Assay, Viability Assay

    MTA-cooperative PRMT5 inhibitors are efficacious and selective in MTAP -null MPNST cell lines. A, MTAP and PRMT5 protein levels were determined by WES western analysis in human MPNST cell lines. B, Densitometry for MTAP and PRMT5 protein levels in MPNST cell lines, normalized to vinculin loading control. C and D, MTAP WT MPNST cells (JH-2-009 and JH-2-031) and MTAP -null MPNST (JH-2-079, JH-2-002, and WU-356) cells were treated with the indicated doses of MTA-cooperative PRMT5 inhibitors, ( C ) TNG908 or ( D ) TNG462, for 7 to 14 days. Cell viability was examined by CTG assay, and assay length was determined by the doubling time of each cell line. Data are presented as the mean ± SEM.

    Journal: Clinical Cancer Research

    Article Title: MTA-Cooperative PRMT5 Inhibitors Are Efficacious in MTAP-Deleted Malignant Peripheral Nerve Sheath Tumor Models

    doi: 10.1158/1078-0432.CCR-24-3610

    Figure Lengend Snippet: MTA-cooperative PRMT5 inhibitors are efficacious and selective in MTAP -null MPNST cell lines. A, MTAP and PRMT5 protein levels were determined by WES western analysis in human MPNST cell lines. B, Densitometry for MTAP and PRMT5 protein levels in MPNST cell lines, normalized to vinculin loading control. C and D, MTAP WT MPNST cells (JH-2-009 and JH-2-031) and MTAP -null MPNST (JH-2-079, JH-2-002, and WU-356) cells were treated with the indicated doses of MTA-cooperative PRMT5 inhibitors, ( C ) TNG908 or ( D ) TNG462, for 7 to 14 days. Cell viability was examined by CTG assay, and assay length was determined by the doubling time of each cell line. Data are presented as the mean ± SEM.

    Article Snippet: On day 1, TNG908 , TNG462 (WO2022026892; ref. ), or GSK3326595 (either from custom synthesis ( ) or MedChemExpress HY-101563) were dosed using a Tecan D300e and normalized to highest class volume with DMSO (the final DMSO percentage was 0.2%).

    Techniques: Western Blot, Control, CTG Assay

    MTA-cooperative PRMT5 inhibitors induce cell death in MPNST cell lines. A–C, MTAP WT (JH-2-009 and JH-2-031) and MTAP -null (JH-2-079, JH-2-002, and WU-356) MPNST cells were treated with the indicated doses of PRMT5 inhibitors, TNG908 or TNG462, for 7 days. A and B, Cell death was determined by IncuCyte assay using YOYO-1 dye. Data are presented as the mean ± SEM. *, P < 0.05 versus vehicle control. C, Apoptotic protein levels, total or cleaved (Cl) PARP-1 or caspase (Casp) 3, were determined by WES western analysis.

    Journal: Clinical Cancer Research

    Article Title: MTA-Cooperative PRMT5 Inhibitors Are Efficacious in MTAP-Deleted Malignant Peripheral Nerve Sheath Tumor Models

    doi: 10.1158/1078-0432.CCR-24-3610

    Figure Lengend Snippet: MTA-cooperative PRMT5 inhibitors induce cell death in MPNST cell lines. A–C, MTAP WT (JH-2-009 and JH-2-031) and MTAP -null (JH-2-079, JH-2-002, and WU-356) MPNST cells were treated with the indicated doses of PRMT5 inhibitors, TNG908 or TNG462, for 7 days. A and B, Cell death was determined by IncuCyte assay using YOYO-1 dye. Data are presented as the mean ± SEM. *, P < 0.05 versus vehicle control. C, Apoptotic protein levels, total or cleaved (Cl) PARP-1 or caspase (Casp) 3, were determined by WES western analysis.

    Article Snippet: On day 1, TNG908 , TNG462 (WO2022026892; ref. ), or GSK3326595 (either from custom synthesis ( ) or MedChemExpress HY-101563) were dosed using a Tecan D300e and normalized to highest class volume with DMSO (the final DMSO percentage was 0.2%).

    Techniques: Control, Western Blot

    MTA-cooperative PRMT5 inhibitors, TNG908 and TNG462, dramatically reduce tumor growth in two MPNST PDX mouse models. Mice bearing ( A–C ) WU-356 or ( D–F ) WU-386 PDX tumors (both NF1 -mutated and MTAP -null) were treated with ( A and D ) TNG908 or ( B, C, E, and F ) TNG462 for 5–6 weeks at the indicated doses. A, B, D, and E, Tumor growth curves of different treatment groups are shown as the mean ± SEM. C and F, Waterfall plots of the percent change in tumor volume, with tumor volume at the end of drug treatment normalized to the baseline tumor volume. All treatments were well tolerated. G and H, Immunoblots performed on terminal mouse tumors treated as indicated and collected from either WU-386 16 hours after the last dose ( G ) or WU-356 8 hours after the last dose ( H ). KP4 MTAP-isogenic pancreatic cancer xenograft samples are included as controls for MTAP and SDMA-modified protein levels. KP4 + empty vector (EV) is MTAP -null and KP4 + MTAP exogenously expresses MTAP cDNA. BID, twice per day.

    Journal: Clinical Cancer Research

    Article Title: MTA-Cooperative PRMT5 Inhibitors Are Efficacious in MTAP-Deleted Malignant Peripheral Nerve Sheath Tumor Models

    doi: 10.1158/1078-0432.CCR-24-3610

    Figure Lengend Snippet: MTA-cooperative PRMT5 inhibitors, TNG908 and TNG462, dramatically reduce tumor growth in two MPNST PDX mouse models. Mice bearing ( A–C ) WU-356 or ( D–F ) WU-386 PDX tumors (both NF1 -mutated and MTAP -null) were treated with ( A and D ) TNG908 or ( B, C, E, and F ) TNG462 for 5–6 weeks at the indicated doses. A, B, D, and E, Tumor growth curves of different treatment groups are shown as the mean ± SEM. C and F, Waterfall plots of the percent change in tumor volume, with tumor volume at the end of drug treatment normalized to the baseline tumor volume. All treatments were well tolerated. G and H, Immunoblots performed on terminal mouse tumors treated as indicated and collected from either WU-386 16 hours after the last dose ( G ) or WU-356 8 hours after the last dose ( H ). KP4 MTAP-isogenic pancreatic cancer xenograft samples are included as controls for MTAP and SDMA-modified protein levels. KP4 + empty vector (EV) is MTAP -null and KP4 + MTAP exogenously expresses MTAP cDNA. BID, twice per day.

    Article Snippet: On day 1, TNG908 , TNG462 (WO2022026892; ref. ), or GSK3326595 (either from custom synthesis ( ) or MedChemExpress HY-101563) were dosed using a Tecan D300e and normalized to highest class volume with DMSO (the final DMSO percentage was 0.2%).

    Techniques: Western Blot, Modification, Plasmid Preparation