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The combined effect of classical and non-classical pathways led to an increase in intracellular lipid reactive oxide species, triggering ferroptosis and enhancing the expression of BH3 interacting domain death agonist (BID), apoptosis-inducing factor (AIF), and endonuclease G proteins (EndoG)

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These safety differences stem from AOD-9604s mechanism as a C-terminal fragment lacking affinity for the traditional growth hormone receptor