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Last source check: 2026-07-21

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GHK-Cu treatment reduced reactive oxygen species (ROS) production, increased superoxide dismutase (SOD) activity, and decreased TNF- and IL-6 production by inhibiting NF-B p65 and p38 MAPK signaling in LPS-induced macrophages and ALI models

Mechanistic studies using proteomics analysis revealed that this compound mediates these effects through the aryl hydrocarbon receptor-nuclear factor erythroid 2-related factor 2 (AhR-Nrf2) pathway [2]

Treatment-induced tumor dormancy through YAP-mediated transcriptional reprogramming of the apoptotic pathway

doi: 10.1007/s00432-024-05917-w