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In the context of therapeutic response and resistance, accumulating evidence indicates that ROS contribute to the maintenance and reinforcement of resistance to platinum-based chemotherapy through adaptive mechanisms such as activation of the DNA damage response (ATR-Chk1), remodeling of ROS-regulated phosphorylation networks (e.g., CAMK2G-ITPKB), alterations in mitochondrial dynamics, and loss of MAPK regulators such as MKP3

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(8) A lesser-known but extremely beneficial effect of GHK-Cu is its suppression of fibrinogen, which is a molecule that forms blood clots in vessels of the body