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Another recent research from Emmert and coworkers has demonstrated that nuclear GSH is independently regulated during proliferation, with levels increasing during the early S phase and then stabilizing during the G2 phase, while whole-cell GSH levels remain relatively constant throughout the cell cycle [11]

In the absence of the cluster, such monothiol glutaredoxins can still be glutathionylated 26,27,29 and might (slowly) transfer the glutathione moiety to reduced cysteine residues as suggested for the AtGrxS15-dependent oxidation of reduced roGFP2 by GSSG

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How they work together Glutathione directly supports cellular antioxidant defenses, while vitamin C helps recycle glutathione back to its reduced, active state

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The takeaway from that table is the whole point of an honest comparison: the two rows with real strength each describe only one drug, the direct cagrilintide-vs-retatrutide row is empty, and the only cross-drug row is explicitly weak