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    Home > Active Ingredient News > Antitumor Therapy > Clin Cancer Res: SHP2 inhibitor TNO155 enhances the efficacy of a variety of targeted drugs by blocking RTK signals.

    Clin Cancer Res: SHP2 inhibitor TNO155 enhances the efficacy of a variety of targeted drugs by blocking RTK signals.

    • Last Update: 2020-10-20
    • Source: Internet
    • Author: User
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    RTK signaling paths are carcinogenic drivers of a variety of tumors or are often activated by feedback during targeted treatments, including RTKi and MAPKi.
    SHP2 inhibitors provide an attractive new method for inhibiting RTK signal transducing.
    study aims to assess the efficacy and synergetic mechanisms used in collaboration with the new SHP2 inhibitor TNO155 to understand its clinical progress.
    the efficacy of TNO155 in combined use with EGFRi, BRAFi, KRASG12Ci, CDK4/6i, or anti-PD-1 antibodies, as well as the effects on downstream signals, in appropriate tumor models both in vivo and in vivo.
    in the EGFR mutant lung cancer model, TNO155 was used in association with EGFRi (nazartinib) to have a certain effect, consistent with the effect of continuous inhibition of ERK.
    in colorectal cancer models with BRAF V600E mutations, TNO155 worked in synergy with BRAF-MEK inhibitors by blocking the activation of ERK feedback by different RTKs.
    in cancer cells with KRAS G12C mutations, TNO155 can effectively block the feedback activation of KRASG12Ci-induced wild-type KRAS or other RAS sub-types, greatly improving the efficacy.
    addition, TNO155 and CDK4/6 inhibitors Rebosini showed combined benefits in a large number of heterogeneous transplant models for lung and colorectal cancer patients, including models carrying KRAS mutations.
    , TNO155 effectively inhibits the activation of RAS by CSF1R (CSF1R is essential for the maturation of immunosuppressive tumor-related macrophages) and exhibits joint activity with anti-PD-1 antibodies.
    , the results show that TNO155 can effectively block RTK signals with tumor promotion and immunosuppressive effects in RTK and MAPK-driven cancers and their tumor micro-environments, providing a basis for clinical evaluation of these joint programs.
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