Function
While GHK-Cu acts as a tissue-remodeling and wound-healing signal, enhancing skin regeneration, angiogenesis, and repair while reducing inflammation and oxidative damage in experimental models31383, Thymosin Beta-4 promotes wound healing, angiogenesis, and tissue regeneration in preclinical models via effects on cytoskeleton dynamics, cell migration, and anti-apoptotic pathways25579.
Mechanism
While GHK-Cu works as an endogenous tripeptide, Gly-His-Lys, that chelates Cu²⁺ and modulates gene expression, stimulating collagen, elastin, proteoglycan, and glycosaminoglycan synthesis while exerting antioxidant and anti-inflammatory effects31383, Thymosin Beta-4 is an endogenous 43-amino-acid actin-sequestering peptide that maintains a pool of G-actin monomers and regulates actin polymerization, thereby influencing cell migration, proliferation, and differentiation25579.