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The classic mechanism of acetaminophen hepatotoxicity is that its reactive metabolite, N-acetyl-p-benzoquinoneimine (NAPQI), depletes GSH and then covalently binds to proteins

Very low doses required due to extreme potency

BPC-157 activates endothelial nitric oxide synthase (eNOS), an enzyme responsible for producing NO in endothelial cells

Stable protein-protein interactions are easiest to isolate by physical methods like pull-down assays because the protein complex does not disassemble over time