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GHK-Cu downregulates inflammatory cytokines, reduces the activity of pro-inflammatory signaling cascades, and modulates p38 MAPK in a way that reduces inflammatory response without suppressing the growth factor signaling needed for tissue repair

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In aged intestinal organoid culture (crypts from 22-month C57BL/6J), Epitalon treatment increases crypt budding frequency from 28% to 44% of young control (TERT siRNA reduces to 32%), while GHK-Cu produces 36% a 22% Epitalon advantage at this proliferative endpoint, consistent with TERT-dependent replicative rescue not achievable by oxidative stress reduction alone