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Along with resistance to treatment in some patients with glioblastoma, the inability to cross the bloodbrain barrier (BBB) is deemed another flaw of such methods of treatment [30]

BPC-157s primary signalling mechanisms are well-characterised: it activates VEGFR2, drives downstream ERK1/2 phosphorylation, and stimulates nitric oxide synthesis via the Akt-eNOS axis producing pro-angiogenic, fibroblast-activating, and extracellular matrix-stabilising effects in experimental models

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This results in reduced food intake, delayed gastric emptying, and improved satiety