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[2] Investigations have extended observations across hepatic, pancreatic, cardiac, and endothelial injury paradigms, with comparative data suggesting that BPC157 activity may involve engagement with broader regulatory networks coordinating vascular and organ-level repair responses

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and (ii) off-target resistance caused by the activation of bypass signal transduction resulting from the amplification of the ERBB family of receptor tyrosine kinase genes, BRAF amplification, KRAS amplification, and KRAS mutations [148]

doi: 10.1136/pn-2022-003631