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GHK-Cu has been directly shown to suppress SASP in stressed fibroblast models: Reduced secretion of IL-6, IL-8, MMP-3, IGFBP-7 in HO-induced and replicative senescent fibroblasts Downregulation of p21 (CDKN1A) and p16 (CDKN2A) mRNA in some model systems Restoration of proliferative capacity markers (Ki-67 positivity, S-phase entry by BrdU) in stressed cultures Reduced SA--galactosidase activity (senescence staining) in aged fibroblast populations Epitalon reduces markers of replicative senescence primarily via telomere maintenance (preventing the telomere shortening that triggers p53/p21 senescence checkpoints) rather than through direct SASP suppression