Klow 80mg: Mechanism of Action

Mechanism of Action — Per Component

GHK-Cu (50 mg) — Copper Delivery & Gene Modulation

GHK-Cu (Gly-His-Lys-Cu²⁺, ~401.9 Da) is a redox-silenced copper-tripeptide complex that delivers Cu(II) intracellularly without driving Fenton-reaction toxicity, supplying copper to enzymes such as lysyl oxidase (collagen crosslinking) and Cu/Zn-SOD (antioxidant defense).[1] Connectivity Map analysis links GHK-Cu to >50% expression changes in ~31% of human genes, biasing toward ECM synthesis (collagen I/III, elastin, decorin, GAGs), Nrf2/Keap1-driven HO-1 transcription, and suppression of NF-κB p65 / p38-MAPK phosphorylation.[2][10] Collagen-synthesis dose response is biphasic, peaking at ~10⁻⁹ M.

BPC-157 (10 mg) — Angiogenic / Cytoprotective Pentadecapeptide

BPC-157 (sequence GEPPPGKPADDAGLV, 1419 Da) is a partial sequence of a gastric body-protective compound, exceptionally stable in human gastric juice (>24 h) and active across oral, parenteral and topical routes in preclinical models.[3] Reported mechanisms include VEGFR2 internalization and Src-Caveolin-1-eNOS coupling driving NO release and angiogenesis; FAK-paxillin activation supporting fibroblast migration; homeostatic buffering of the L-NAME / L-arginine NO axis; and modulation of dopaminergic and serotonergic systems without direct receptor binding.[6][11] Tissue coverage in animal models spans tendon-to-bone reattachment, GI mucosal repair, and CNS injury.

TB-500 (10 mg) — Thymosin β4 Actin-Binding Fragment

TB-500 (Ac-LKKTETQ, ~889 Da) is a synthetic acetylated heptapeptide corresponding to the actin-binding region (residues 17–23) of full-length Thymosin β4. It interacts with G-actin sequestration and cytoskeletal dynamics that underlie cell migration, re-epithelialization and angiogenesis, with hair-follicle and corneal/dermal wound-healing read-outs in preclinical literature.[7][8] Recent metabolite work (Rahaman et al., 2024) suggests the in-vitro wound-healing signal may be carried by the metabolite Ac-LKKTE rather than the parent peptide, an important caveat when interpreting blend-level data.[12]

KPV (10 mg) — α-MSH(11–13) NF-κB Suppressor

KPV (Lys-Pro-Val, 342.4 Da) is the C-terminal tripeptide of α-MSH and operates through a melanocortin-receptor-independent pathway. It is taken up by the proton-coupled PepT1 (SLC15A1) oligopeptide transporter (Kₘ ~160 µM in Caco2-BBE intestinal epithelia), then binds Importin-α3 at armadillo domains 7–8, physically blocking nuclear import of NF-κB p65/RelA while stabilizing IκBα.[4][9] KPV additionally inhibits ERK1/2, JNK and p38 MAP kinases and has shown activity at concentrations as low as 10 nM, with antimicrobial activity against S. aureus and C. albicans across picomolar–micromolar ranges.[13]