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These observations strongly support the current hypothesis that reactive metabolite formation and protein binding especially in mitochondria are the key initiating events in the toxicity, which is then the trigger for a moderate mitochondrial oxidant stress with release of superoxide by complex III towards the cytosol without compromise of mitochondrial respiration [33]

They are unlikely to be as low as the MSF calculates because biosimilars are much more expensive to develop than generic medicines

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