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Metabolic reprogramming and CRC metastasis: mechanistic insights and therapeutic implications Beyond its established role in therapy resistance, metabolic reprogramming is increasingly recognized as a critical driver of CRC metastasis, a major cause of poor patient prognosis [92, 93]

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Consequently, the GSH deprotonation step was considered non-rate-determining and thermodynamically favoured, leading us to use the GSH-thiolate as the starting point to compute the reaction mechanism for the conversion of flav-3-on-4-ol ( 7 ) into cyanidin ( 8-B4 ) in the wild-type enzyme and the C13S variant (Extended Data Fig

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