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The preclinical foundation is strong, particularly for BPC-157 and thymosin beta-4, but the gap between animal evidence and clinical application can only be bridged through rigorous controlled studies in human fracture patients

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In order to prevent mitochondrial malfunction and sustain metabolic function/energy generation (ATP), NAD+ supplementation may counterbalance the age-related degradation of NAD+ and its precursor nicotinamide mononucleotide by NADases, particularly CD38.7 NAD+ replenishment, however, appears to support a number of other metabolic pathways via NAD+-dependent enzymes in research involving human and animal models (as well as samples and cell lines) (1,2,3)

Xue S, Chen S, Ge Y, Guan T, Han Y

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