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Dinitrochlorobenzene can bind to tissue proteins eliciting a cell-mediated immune response with signiflcantly higher levels of CD4+ CD29+ cells.[] Moreover, this model can be also used as an excellent apoptosis model in IBD possibly in experiments on regeneration capacity of different compounds

This distinction is reinforced by the data of Jin X

Where BPC-157 and TB-500 act primarily through actin/cytoskeletal and growth-factor pathways, GHK-Cu's mechanism is dominated by transcriptional reprogramming via copper-dependent gene regulation, making it a complementary research tool when investigators wish to dissect transcription-driven from structural-protein-driven repair phenotypes