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423 The research further demonstrated that this anti-inflammatory effect was not mediated by GLP-1R in the blood or endothelial cells but required the GLP-1R in the CNS

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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

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