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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

Moreover, certain regulators of ferroptosis in HSCs, including p53, ELAV-like protein 1 (ELAVL1), and zinc finger protein 36 (ZFP36), have been reported as promising targets in preventing liver fibrosis [84, 85]