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The anti-hepatitis C agent nitazoxanide induces phosphorylation of eukaryotic initiation factor 2alpha via protein kinase activated by double-stranded RNA activation

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However, in this case, the double bond is formed between C-2 and C-3, rather than between C-1 and C-2

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At the same time, elevated tumor GSH can be exploited as a conditional trigger for prodrug activation, nanomedicine-based delivery, or metal-driven cytotoxicity, thereby converting a classical resistance factor into a therapeutically actionable vulnerability