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In the LPS-induced acutelung injury mouse model, treatment of GHK-Cu also significantly suppressed TNF-α and IL-6 expression with a significant decrease of both NF-κB p65 and p38 MAPK signaling, suggesting that GHK-Cu is useful for the development of novel anti-inflammatory therapies [22]

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Neither mechanism has been demonstrated in a treated human, and TB-500's belongs to the 43-residue parent protein rather than the seven-residue fragment