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Proposed Mechanisms of Action Research suggests BPC-157 may influence tissue repair through several pathways: Angiogenesis Promotion: Upregulation of vascular endothelial growth factor (VEGF) expression in preclinical studies Enhanced blood vessel formation in wound healing models Improved blood flow to injured tissues, potentially supporting nutrient delivery Interaction with the nitric oxide (NO) pathway affecting vasodilation Growth Factor Modulation: Potential influence on fibroblast growth factor (FGF) signaling Modulation of growth hormone receptor expression in some studies Effects on collagen synthesis and extracellular matrix remodeling Anti-inflammatory Properties: Observed reduction in inflammatory markers in animal models Potential modulation of cytokine profiles Effects on neutrophil and macrophage activity in tissue injury models Mechanistically, these effects are thought to converge on the vascular and connective-tissue repair response

Most current OA animal models, such as the DMM model or chemically induced models, can simulate cartilage damage in the short term but struggle to fully replicate the long-term cumulative multifactorial pathological changes of human chronic OA

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