◇ Compound Reference
Copper Peptide · 10mg
Tripeptide-copper complex. Drives extracellular matrix reorganization, dermal regeneration, and anti-inflammatory signaling.
Copper Peptide · 10mg per vial · dispensed after a physician review.
Every 100 units are drawn from one lot and tested once. The certificate below is the one that applies to this batch - when it closes, the next opens with a new lot and a new certificate.
GHK-Cu is a tripeptide-copper complex (Glycyl-L-Histidyl-L-Lysine bound to copper) naturally found in human plasma. Plasma levels decline significantly with age, correlating with reduced regenerative capacity.
GHK-Cu is one of the most extensively studied regenerative peptides in dermatology.
Drives extracellular matrix reorganization, increases collagen and elastin synthesis, modulates inflammatory cascade, and stimulates dermal stem cell proliferation. Genome-level analysis shows GHK-Cu modulates expression of over 4,000 genes toward a more youthful expression profile.
Dermatological - GHK-Cu, V-06
These protocols support skin elasticity, clarity, and dermal repair. Assessment here leans on dermatological evaluation and imaging more than bloodwork, with inflammation tracked as a supporting signal.
Incremental approach. Conservative, often topical or low-dose protocols assessed visually and by imaging over a defined window before extending.
Educational only - not medical advice or a dosing instruction. Your physician orders the tests, sets your dose, interprets results, and decides if a protocol is right for you. See the Informed Consent & Disclaimer for full terms.
| Class | Copper-binding tripeptide (Gly-His-Lys : Cu) |
| Studied mechanism | Copper delivery; collagen/ECM remodelling and fibroblast signalling - well-described in dermatological literature |
| Human pharmacokinetics | Endogenous peptide; plasma GHK declines with age. Topical/systemic PK context-dependent |
| Evidence base | Moderate - dermatological research relatively well-developed; systemic use less characterised |
| Form | Lyophilized powder, reconstituted under clinical protocol |
| Regulatory status | Not an approved systemic therapy; physician-supervised use only |
GHK-Cu carries the most developed clinical and mechanistic evidence base of any peptide in Vivre’s catalog.
Randomized, controlled, multi-center trial in patients with chronic non-healing diabetic foot ulcers. Topical GHK-Cu hydrogel achieved 87.5–88% complete wound closure compared with 30–34% in the standard-care control arm. Median time to complete closure was approximately 6.2 weeks for the GHK-Cu group versus more than 11 weeks for control. Localized infection rates were also significantly reduced. This remains one of the strongest human RCT data points for any peptide in the regenerative category.
View on publisher ↗Landmark in vitro study in human dermal fibroblast cultures. Demonstrated that micromolar GHK-Cu drives dose-dependent synthesis of Type I and Type III collagen, elastin, and glycosaminoglycans, and balances matrix metalloproteinase (MMP) and TIMP activity to favour clean tissue remodelling over fibrotic scarring. The mechanistic basis for GHK-Cu’s use in dermal-architecture protocols.
View on publisher ↗Broad Institute Connectivity Map (cMap) computational analysis quantified that GHK-Cu modulates expression of approximately 4,192 human genes, shifting tissue toward a younger homeostatic profile. Upregulates antioxidant systems, neurotrophic factors, and metabolic clearance pathways; downregulates pro-inflammatory networks. The genomic-systems basis for why GHK-Cu has effects across multiple tissue beds.
View on publisher ↗Review of the GHK-Cu literature including gene-expression profiling work showing modulation of multiple tissue-repair-related genes, with effects on collagen synthesis, matrix metalloproteinase regulation, and inflammatory signalling. Strongest evidence is in dermal/topical applications; systemic use is less characterised in controlled trials.
View on publisher ↗In vitro and ex vivo dermal study (human keratinocytes). Demonstrated that GHK-Cu maintains the stemness of basal keratinocytes and integrin expressions, mobilising intrinsic progenitor cell lines to migrate toward sites of acute structural degradation. Provides the cellular basis for GHK-Cu’s role in dermal renewal beyond fibroblast-mediated matrix synthesis.
View on publisher ↗Mechanistic review documenting GHK’s role as a non-toxic copper chaperone delivering Cu(II) into cells without triggering radical-induced lipid peroxidation. Cytochrome c Oxidase (Complex IV) of the mitochondrial electron transport chain requires copper at its catalytic centres, so adequate copper delivery is upstream of ATP synthesis. Genomic profiling confirmed upregulation of PGC-1α pathway genes (mitochondrial biogenesis). The often-quoted "67% ATP increase" originates from localised in vitro stress-condition data and should be framed as "restoration of defective ATP production under cellular stress" rather than a baseline boost - Vivre presents it this way honestly.
View on publisher ↗Preclinical · Animal Models. In rat coronary-ligation experiments, pre-treatment with GHK-Cu reduced infarct size and preserved cardiac function via upregulation of bFGF and VEGF (angiogenesis). In rodent diabetic nephropathy models, GHK-Cu downregulated TGF-β (the primary fibrosis driver), reducing mesangial expansion, basement membrane thickening, and extracellular matrix accumulation in the renal filtering apparatus. Note: these are animal-model data and have not been translated to human cardiology or nephrology RCTs - Vivre cites them as mechanistic support for the tissue-remodelling case, not as human clinical efficacy.
View on publisher ↗Preclinical · Rodent and In Vitro. Genomic data verify that GHK-Cu downregulates the amyloid precursor protein (APP) gene and upregulates neurotrophic pathways (NGF and BDNF). Animal-model evidence indicates blood-brain-barrier permeability and neuroprotective effects against beta-amyloid and oxidative-stress insults. The frequently-quoted "300% NGF increase" originates from rodent / in-vitro data and is presented here as preclinical signal, not as human cognitive-clinical evidence - which does not yet exist in controlled RCT form for GHK-Cu.
View on publisher ↗Preclinical · In Vitro + Mouse Alopecia Model. The novel contribution of the paper is a bio-based ionic liquid microemulsion (CaT-ME, made from L-carnitine and tartaric acid) as a topical delivery vehicle - not GHK-Cu efficacy per se. Loaded with GHK-Cu, the system improved porcine-skin permeation 3.18× vs PBS in vitro, and in a C57BL/6 mouse alopecia model, GHK-Cu/CaT-ME entered the anagen (growth) phase at day 6 versus day 9 for 5% topical minoxidil - a head-to-head win against the FDA-approved comparator in a mouse model. Mechanism work documented upregulation of VEGF and HGF (follicular angiogenic factors), CD31 (vascular endothelium), Ki67 (proliferation), β-catenin and p-GSK3β (Wnt pathway activation), and Ldha (hair follicle stem cell activation enzyme). The paper reinforces three mechanisms that anchor GHK-Cu's hair-growth thesis: fibroblast-stimulated VEGF, TGF-β suppression preventing premature anagen→catagen, and dermal papilla cell proliferation. Important methodology framing: preclinical (mouse + ex vivo porcine skin) only - no human RCT. The route tested is topical microemulsion, not the injectable route Vivre offers - the shared element is the GHK-Cu mechanism, not the delivery vehicle. Two co-author affiliations (Shenzhen Shinehigh Innovation Technology, Harbin Voolga Technology) have commercial interests in the technology, and the GHK-Cu raw material was supplied by a related Shenzhen entity. The authors declare no conflict of interest per ICMJE rules, but the originating-group + commercial-affiliation pattern is flagged here per Vivre's standard discipline (same approach applied to Epithalon and other single-group preclinical work).
View on publisher ↗GHK-Cu is verified and lot-tested, dispensed following a Biological Audit. The Audit is complimentary for the Batch 001 cohort.
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