GHK vs KPV

Cosmetic

Immune

Research Only

Research Only

GHK is a high-affinity ligand for copper(II), forming the GHK-Cu complex that mediates most of its documented biology. Via the copper-bound form, GHK is proposed to modulate expression of a large number of human genes (microarray and Broad Institute Connectivity Map analyses from Pickart's group), including pathways related to extracellular matrix remodeling, antioxidant response element induction, angiogenesis, and DNA repair. Reported in vitro and preclinical effects include stimulation of fibroblast collagen and glycosaminoglycan synthesis and acceleration of wound healing. The bare (non-copper) peptide is typically weaker than GHK-Cu in these assays and is generally assumed to acquire copper in serum-containing environments.

KPV enters cells (in part via the di/tripeptide transporter PepT1 in intestinal epithelium and immune cells) and acts intracellularly to inhibit NF-kB activation, reducing pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β). Unlike full-length alpha-MSH, KPV does not meaningfully activate MC1R and does not cause skin pigmentation, differentiating it from melanocortin agonists such as MT-I and MT-II.

50–200 ppm topical (~0.005–0.02%)

200–500 mcg (SubQ); 500 mcg–1 mg (oral)

Topical

Oral, SubQ, or Topical