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With the shortage resolved, the regulatory framework simply returns to its usual conditions: compounding justified by individual clinical need, with a prescription and a clear reason why the standard commercial product does not work for that patient

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found that these two vectors were highly expressed in myocardial mitochondria and showed that inhibition of DIC and OGC increased mitochondrial ROS and GSH depletion, exacerbating ferroptosis in the myocardium [60]