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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

No human clinical trial data quantifies the precise acceleration rate in humans, and the direct translation of the 30% to 50% figure from rodent models to human tendon repair remains unconfirmed by controlled clinical research