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Its main mechanism of action is based on increasing the expression of BDNF (Brain-Derived Neurotrophic Factor) and its TrkB receptors in the hippocampus and prefrontal cortex, promoting synaptic plasticity, long-term potentiation (LTP), and memory consolidation (Dolotov et al., Neuroscience 2006)

Proposed Mechanism BPC-157 appears to work through multiple pathways: Maintaining vesicular integrity (affecting VMATs and dopamine transporters) Possibly occupying its own vesicular storage sites Competing for dopamine receptor binding Functionally substituting when dopaminergic neurons are lost This last property, essentially filling in for missing dopamine function, would explain why the peptide counteracts both receptor agonists (apomorphine) and antagonists (haloperidol, fluphenazine, clozapine, sulpiride) with equal effectiveness