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Unlike TB-500 (Thymosin Beta-4 fragment), which acts primarily via G-actin sequestration and endothelial progenitor cell mobilization, BPC-157 exerts its action via an NO-dependent pathway and VEGFR2 modulation — two distinct but potentially complementary mechanisms, which is why research protocols sometimes combine both peptides (synergy documented in animal tendon repair models)

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These results showed that variant-induced changes in RT-deletion were consistent with changes in berberine binding