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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
This variability complicates efforts to standardize treatment and calls for a more personalized approach rather than blanket recommendations [48, 49]
Ultimately, the effectiveness of oral glutathione depends almost entirely on how it is formulated for absorption
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