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Lactic acidosis portends a poor prognosis (by Kings College Hospital (KCH) criteria), and the mechanism of lactic acidemia is two-fold: NAPQI being present in excess and causing mitochondrial dysregulation, followed in subsequent hours by tissue hypoxia and decreased hepatic metabolism and clearance of lactate, leading to a two-hit effect on worsening of the lactic acidosis condition

This is followed by multiple immune abnormalities: marked impairment of the immunosuppressive function of myeloid-derived suppressor cells (MDSCs), pro-inflammatory polarization of Kupffer cells, T-cell differentiation imbalance, and B-cell hyperactivation that induces antimitochondrial antibody (AMA)-mediated cytotoxicity

BPC-157 promotes local tissue repair by increasing blood vessel formation at the injury site

The reconstitution table is a measurement tool, not a dosing recommendation, and the confidence its precision inspires should attach only to the arithmetic, never to the numbers plugged into it