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    Home > Active Ingredient News > Immunology News > ACC: Evidence of QT interval prolongation in COVID-19 patients treated with hydroxychloroquine

    ACC: Evidence of QT interval prolongation in COVID-19 patients treated with hydroxychloroquine

    • Last Update: 2022-04-24
    • Source: Internet
    • Author: User
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    Background: The outbreak of coronavirus disease 2019 (COVID-19), an acute respiratory infectious disease caused by a new type of coronavirus infection, still lacks effective therapeutic drugs.
    Among the candidate drugs for the treatment of new coronary pneumonia, old drugs are newly used.
    is the mainstream strategy
    .
    At one time, experts and scholars recommended hydroxychloroquine (HCQ) as an emergency treatment option for COVID-19


    .


    background:

    Hydroxychloroquine has been used as a traditional antimalarial and antirheumatic drug for about 70 years.
    Studies have found that this drug has broad-spectrum antiviral activity, especially against severe acute respiratory syndrome coronavirus (SARS-CoV).
    The infection has a potential preventive effect, and it has been confirmed to have anti-SARSCoV activity in vitro, and the new coronary pneumonia is caused by severe acute respiratory syndrome coronavirus
    2 (SARS-CoV-2), suggesting that hydroxyl Chloroquine has the advantages of both prevention and treatment for this type of coronavirus infection
    .

    Hydroxychloroquine has been used as a traditional antimalarial and antirheumatic drug for about 70 years.
    Studies have found that this drug has broad-spectrum antiviral activity, especially against severe acute respiratory syndrome coronavirus (SARS-CoV).


    The infection has a potential preventive effect, and it has been confirmed to have anti-SARSCoV activity in vitro, and the new coronary pneumonia is caused by severe acute respiratory syndrome coronavirus


    QT prolongation is achieved by disrupting the human ether-a-go-go-related gene hERG +


    Methods: HEK293 cell line stably expressing hERG-WT channel ( hERG-HEK transiently expressing hERG-p.
    Y652A or hERG-p.
    F656A mutant) and HEK293 cells were treated with HCQ


    .



    Results: hERG hERG hERG reduction


    Conclusions: We conclude that HCQ induces QTc prolongation by reducing mature hERG channel expression and IhERG by enhancing channel degradation
    .
    HCQ also interacts with the canonical hERG binding site involving residues Tyr652 and Phe656


    .


    Conclusion: We conclude that HCQ reduces mature hERG channel expression and IhERG
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