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Its working mechanism is allosteric facilitation of HGF/c-Met signaling: Dihexa binds HGF with high affinity (reported K d ~65 pM in the original work) and is proposed to potentiate HGF dimerization and c-Met phosphorylation at subthreshold endogenous HGF concentrations

Increased GLUT4 transporter expression means more glucose can move from the bloodstream into muscle cells, where it can be used for energy or stored as glycogen

The endotoxin fragments persist

Finally, the long-term, whole-body effects of administering a peptide that is normally restricted to the stomach remain completely unknown

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