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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

tPA and proteolysis in the neurovascular unit

An overarching theme in this exploration is that therapeutic agents that downregulate PKC, and particularly PRKCG, appear to have benefit in reducing neuropsychiatric symptom expression

Research interest centers on the compound's proposed capacity to potentiate HGF activity at the MET receptor, with particular attention to downstream effects on synaptic density and cognitive function-related signalling in neurological research models