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Pharmacokinetic (PK) profiling in both species revealed linear doseexposure relationships, with [H] BPC157 rapidly metabolized into small peptides and ultimately tritium-labeled proline for normal amino acid catabolism/excretion [11]

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GHK further inhibited TGF-1, p-Smad2, p-Smad3, and IGF-1 expression, indicating its potential as a subject of further research in pulmonary fibrosis by targeting the TGF-1/Smad 2/3 and IGF-1 pathways

As a naturally occurring peptide fragment, BPC-157 also lacks strong patent protection, which has likely reduced commercial incentive to fund the trials needed for FDA approval