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Single intraperitoneal administration of NaBPC157 in the form of a pre-treatment resulted in prevention of electrocardiographically demonstrated ischemia and histological myocardial damage during the immobilization stress test

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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