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In biological systems, this lack of binding affinity prevents rapid clearance, resulting in a half-life approximately 120 times longer than endogenous IGF-1

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These pre-clinical studies attributed the recovery in symptom profile to modulation of glucose transport, over-expression of mitochondrial genes, bypassing defective pathways of ETC (electron transport chain), and improvement in mitochondrial biosynthesis, modulation of microbiota, regulation of brain neuronal networks, and promoting synthesis of white matter in the brain [168]

doi:10.1172/jci.insight.93751 349