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The published research base, predominantly preclinical with growing clinical extension, identifies several mechanisms of action
Structural analysis demonstrates how FOXO4-DRI exploits the unique architecture of senescent cells, where FOXO4 latches onto p53 and prevents it from executing its normal pro-apoptotic function
Broad Connectivity Map analysis has shown that GHK-Cu can suppress genes associated with metastasis, tissue destruction, and inflammation while activating genes associated with stem cell maintenance and DNA repair [3]
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