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Its foundational mechanismscentered on VEGFR2 activation and systemic cytoprotectionprovide a compelling scientific basis for its observed benefits in both gastrointestinal healing and central nervous system stabilization

Critically, when we introduced mutations into the Fc that reduce FcRIIIa bindingwhile retaining the cysteine at position 330and co-expressed this construct with the cysteine-mutated FcRIIIa soluble domain, we failed to produce the complex despite robust expression of both components, indicating that the native interaction is essential for guiding and stabilizing the intermolecular disulfide (Supplementary Fig

Elastin: The main component of elastic fibers, provides stretch, recoil, and elasticity to the skin