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    Home > Active Ingredient News > Antitumor Therapy > The antimalarial drug 芴 to treat GBM that resists radiotherapy and tymoamine

    The antimalarial drug 芴 to treat GBM that resists radiotherapy and tymoamine

    • Last Update: 2021-01-03
    • Source: Internet
    • Author: User
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    Glioblastoma (GBM) is a highly invasive malignant brain tumor, and there is no effective treatment.
    resistance to radiotherapy and tymoamine (radio/TMZ) is a major factor in GBM recurrence and treatment failure.
    THE mechanism by which GBM resists radiotherapy and thymosamine may be thermoshock protein (HSPs) that reshapes and transforms the exosome-interstate (EMT) by regulating the extracellular substation (ECM).
    Yetirajam Rajesh of the School of Medical Science and Technology of the Indian University of Science and Technology in Bangladesh, India, etc., reviewed the literature to review the antimalarial drug benzeneol to reverse GBM's resistance to radiotherapy and tymoamine.
    article was published in PNAS in June 2020.
    results of the study, it has been reported that the Friend Leukemia Integration 1 (Fli-1) signal network is involved in the process of GBM's evil change and has become a hot topic of research on new treatments.
    Fli-1 was associated with tumor transformation, and was raised in GBM against radiotherapy and tymoamine, and transcription regulated HSPB1.
    researchers screened drugs using multiple transcription targets and a variety of natural drug products, market drugs, and existing and new therapeutic agents to find that an FDA-approved aromatic amino alcohol antimalarial drug, lumefantrine, may be a Fli-1 inhibitor.
    confirms that lufantrine binds and interacts directly with the Fli-1 protein by docking and isothermal heat titration.
    Insotrophic, lumefantrine inhibits Fli-1/HSPB1, MMP-2/-9 and EMT; inhibits GBM growth and time dependence against radiotherapy and tymoamine induces apoptosis; and inhibits tumor growth without toxicity in GBM's U87MG cell family, as well as in in-place tumor models that resist radiotherapy and timoamine GBM.
    Conclusion This study review shows that HSPB1 and Fli-1 play an important role in regulating GBM against radiotherapy/thymosamine, and in-body and animal model experiments, it is shown that lubefantine targets EMT and ECM reshaping signaling axis mediated by Fli-1/HSPB1, providing a new treatment that can be used to treat glioblastoma of anti-radiation therapy/tymoamine.
    but further research is needed on the effects of these new anti-glioblastoma drugs through the blood-brain barrier, as well as the therapeutic effects of combinations with other drugs.
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