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It is derived from the C-terminal end of alpha-melanocyte-stimulating hormone, and it retains the parent molecule anti-inflammatory properties without the melanogenic (skin-darkening) effects

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[1] According to the researchers TGF-beta1 induction of angiogenesis requires a rapid and transient apoptotic effect mediated by VEGF/VEGFR2. AHK-Cu, by enhancing levels of the Vascular Endothelial Growth Factor, may possibly activate fibroblasts and endothelial cells

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