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The mechanism of this combined effect appears to be sequential: TB-500 mobilizes and migrates repair cells to the injury site (via actin regulation and chemotactic signaling), while BPC-157 creates the optimal local microenvironment (via angiogenesis, growth factor expression, and NO modulation) for those cells to perform effective repair once they arrive

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The standard redox potential of cysteinecystine from the thioldisulphide exchange reaction with glutathione and lipoic acid

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With studies characterising reduced infarct size, improved cardiac function, promotion of cardiac progenitor cell migration, cardiomyocyte survival through PI3K/Akt anti-apoptotic signalling, and stimulation of new vessel formation in infarcted myocardium