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In a diabetic mouse model, it reduced oxidative stress-induced neuropathy by triggering antioxidative defense signals (Agca et al

Inhibition by coenzyme Q of ethanol- and carbon tetrachloride-stimulated lipid peroxidation in vivo and catalyzed by microsomal and mitochondrial systems

This PK-PD disconnect is compatible with a peptide whose mechanism triggers downstream signalling cascades (VEGFR2 activation, fibroblast migration, angiogenesis) that persist well beyond direct peptide presence

In comparison, highly proliferating RAW cells can more easily succumb to mechanical stress associated with their high phagocytic capacity