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BPC-157 and TB-500 have each been extensively studied for wound healing promotion and with BPC-157 accelerating wound closure through fibroblast migration, angiogenesis, and cytoprotective effects on epithelial cells, and TB-500 promoting wound healing through PI3K/Akt-mediated keratinocyte and fibroblast migration, actin cytoskeletal dynamics that drive cell motility into wound beds, and anti-inflammatory modulation of the wound healing microenvironment

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This study demonstrates how epigenetic mechanisms used by oxidative stress can result in the creation of amyloid beta (A) plaques and suggests promising therapeutic avenues for this pathway