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Targeting glutamine metabolism shows promise as an anticancer therapy

In endothelial cell models, BPC-157 significantly enhanced ERK1/2 phosphorylation in a dose-dependent manner, leading to increased cellular proliferation, migration, and vascular tube formation mediated through downstream activation of transcription factors c-Fos, c-Jun, and EGR-1

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BPC-157 related signaling has been associated with nitric oxide mediated cascades involving Src, Cav-1, and eNOS signaling components [1]