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Frataxin-knockout mouse myoblasts, heart, and skin fibroblasts all showed characteristics of ferroptosis, and Nrf2 was downregulated in Friedreichs Ataxia patients and frataxin-knockout mice, while Nrf2 activators EPI-743 or sulforaphane regulated redox imbalances and rescued ferroptosis in frataxin knockout cells

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None of that is fully replicated in a telehealth subscription model that ships compounds without an in-person evaluation

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This is possible because these medications act through different mechanisms

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