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showed that GSH is required for cancer initiation partially because of the upregulated activation of the thioredoxin (TXN) antioxidant pathway and inhibition of both GSH and TXN pathway activation, synergistically inhibiting tumor growth 26

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The protective Aib8 substitution in the unlipidated semaglutide control extended its half-life to 5.4 h ( Table 1 and Supplementary Table 2 ), whereas all aza-modified analogues remained intact beyond 24 h, with no measurable loss after 48 h

Editing by Christopher Cushing and Clarence Fernandez)