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Proposed HGF/c-Met Receptor Potentiation The central mechanistic hypothesis is that Dihexa binds directly to HGF with high affinity, inhibits HGF self-dimerization, and acts synergistically with HGF to enhance c-Met receptor tyrosine kinase signaling, including downstream effects on cell scattering, motility, and proliferation in non-neuronal assays, and on dendritic spinogenesis and synaptogenesis in hippocampal neurons

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We can't stress this enough: a multi-pronged approach is often more effective than a single one

Everything else, semaglutide, mazdutide , survodutide , tirzepatide, retatrutide, works through some combination of incretin receptors