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TB-500 (thymosin 4) drives systemic cell migration and angiogenesis, accelerating endothelial migration several-fold in preclinical research[2]

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In chronic or biofilm-associated infections, however, microbial persistence and metabolic cues from the wound microbiome can skew phagocyte polarization toward a dysfunctional state either sustaining a prolonged M1-like inflammatory profile that damages tissue or inducing an immunosuppressed M2-like state that allows microbial survival [42]