GHK-Cu Research: 50 Years of Copper Peptide Science

In 1973, a biochemist named Loren Pickart noticed something unexpected. When he exposed liver cells from older donors to blood plasma from younger people, those aged cells started behaving like young ones again. The factor responsible turned out to be a tiny molecule — just three amino acids bound to a copper ion — called GHK-Cu.

That discovery launched more than five decades of research into one of the most studied peptides in regenerative science. From wound healing and skin rejuvenation to gene expression reprogramming and potential cancer applications, GHK-Cu has generated a body of work that spans hundreds of published studies across dozens of research institutions.

This article traces that research arc — from Pickart's original isolation of the peptide through today's genomic studies — and examines the key findings that have shaped our understanding of what this copper tripeptide can do.

The Discovery: 1973-1980
What GHK-Cu Actually Is
Wound Healing Research: The 1980s Foundation
Skin Rejuvenation Studies
The Gene Expression Revolution: 2010-2020
Lung Disease and Tissue Remodeling
Anti-Cancer Gene Patterns
Neuroprotection and Cognitive Decline
Stem Cell and Regenerative Effects
The Age-Related Decline Problem
Current Limitations and Open Questions
GHK-Cu Research Timeline
FAQ
The Bottom Line
References

The Discovery: 1973-1980

The GHK-Cu story begins with a straightforward observation about aging blood. Working at the University of California, San Francisco, Loren Pickart was studying why older tissue loses its regenerative capacity. He separated components of human blood plasma and found that a fraction from younger donors could make liver cells from older donors produce proteins at rates typical of younger tissue [1].

By 1977, Pickart had identified the active compound as a tripeptide: glycyl-L-histidyl-L-lysine, or GHK. The peptide had a strong natural affinity for copper(II) ions, and it was this copper-bound form — GHK-Cu — that showed the most biological activity.

A key 1980 paper published in Nature proposed that this growth-modulating tripeptide "may function by facilitating copper uptake into cells" [2]. That insight — that GHK acts partly as a copper delivery vehicle — has held up remarkably well over the decades.

Pickart also determined that GHK isn't just floating freely in plasma. The peptide sequence appears within a larger protein called SPARC (also known as osteonectin or BM-40), a glycoprotein heavily expressed in embryonic tissues and at sites of tissue injury. When SPARC breaks down after an injury, it releases GHK fragments — positioning the peptide as what researchers have called an "emergency response molecule" released from the extracellular matrix at sites of damage [3].

What GHK-Cu Actually Is

GHK-Cu is a naturally occurring tripeptide-copper complex found in human plasma, saliva, and urine. Here are the basics:

Property	Detail
Full name	Glycyl-L-histidyl-L-lysine copper(II)
Molecular weight	403.9 Da (with copper)
Source	Released from SPARC protein during tissue breakdown
Plasma level (age 20)	~200 ng/mL
Plasma level (age 60)	~80 ng/mL
Active concentration	Picomolar to nanomolar range
Copper binding	High affinity for Cu(II) ions

The copper component isn't just along for the ride. Copper acts as a cofactor for enzymes like lysyl oxidase and lysyl hydroxylase, which are needed for proper collagen cross-linking and stability. Studies comparing GHK alone versus GHK-Cu found that only the copper-bound form exhibited the full range of wound healing and skin remodeling properties [4].

Wound Healing Research: The 1980s Foundation

The first major application of GHK-Cu research was wound healing, and results in the 1980s were striking enough to attract serious attention.

Key Early Findings

At picomolar to nanomolar concentrations — remarkably low doses — GHK-Cu stimulated collagen synthesis in skin fibroblasts and increased accumulation of total proteins, glycosaminoglycans, and DNA in dermal wounds in rats [5]. By 1983, Pickart had established that GHK-Cu:

Accelerated wound healing and wound contraction
Improved transplanted skin graft survival
Reduced inflammation at wound sites
Attracted macrophages and mast cells to clear damaged tissue

How It Works in Wounds

GHK-Cu doesn't just do one thing during healing — it participates across all three phases:

Inflammatory phase: The peptide is a powerful attractant for capillary cells, macrophages, and mast cells. These immune cells remove damaged cellular debris and secrete proteins needed for wound contraction [5].

Proliferative phase: At just 1 nM concentration, GHK-Cu increases expression of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in irradiated human dermal fibroblasts. Both factors drive new blood vessel formation and blood flow into damaged tissue [3].

Remodeling phase: GHK-Cu stimulates the production of collagen, dermatan sulfate, chondroitin sulfate, and the small proteoglycan decorin. It also modulates matrix metalloproteinases (MMPs) — the enzymes responsible for breaking down and rebuilding the extracellular matrix — balancing beneficial remodeling against excessive tissue degradation [4].

Antioxidant Properties in Wounds

One of Pickart's important findings was that GHK-Cu inhibits lipid peroxidation when the iron source is ferritin. The proposed mechanism: GHK-Cu binds to channels of ferritin involved in iron release, physically preventing the release of Fe(II) — the form of iron that drives oxidative damage in wounds. This antioxidant function helps protect damaged tissue from inflammation and infection [1].

For more on how peptides support tissue repair, see our guide on the best peptides for wound healing.

Skin Rejuvenation Studies

If wound healing was GHK-Cu's first act, skin rejuvenation became its most commercially visible chapter. Multiple clinical studies have tested topical GHK-Cu formulations — and the results have been consistently positive.

The 12-Week Collagen Study

In one of the most-cited clinical comparisons, GHK-Cu was applied to thigh skin of women for 12 weeks and compared against two gold-standard anti-aging ingredients. The results [6]:

Treatment	Women Showing Improved Collagen
GHK-Cu cream	70%
Vitamin C cream	50%
Retinoic acid	40%

GHK-Cu outperformed both vitamin C and retinoic acid — two of the most widely recommended topical treatments in dermatology.

Facial Photoaging Trials

A trial of 71 women with mild to advanced signs of photoaging applied a facial cream containing GHK-Cu daily for three months. Results showed increased skin density and thickness, reduced sagging, and visible improvement in fine lines and wrinkles [6].

A separate eye-area trial enrolled 41 women with mild to advanced photodamage. After three months of GHK-Cu eye cream application, participants showed reduced lines and wrinkles, improved skin density, and increased skin thickness — outperforming both placebo and vitamin K cream [6].

Ultrasound-Measured Results

A clinical study led by Wayne Carey, MD, Professor of Dermatology at McGill University, used ultra-high resolution ultrasound imaging to measure actual changes in facial skin structure. After 3 months of GHK-Cu use [7]:

Average increase in subdermal echogenic density (correlating with collagen/elastin): 28%
Top quartile of participants: 51% improvement in collagen density
67% reduction in wrinkle volume measured by profilometry

These ultrasound-verified results are notable because they go beyond subjective appearance ratings and measure actual structural changes in the skin.

Why It Works for Skin

GHK-Cu's skin benefits come from multiple mechanisms working together:

Collagen production: Up to 70% increase in laboratory studies, affecting both Type I (structural) and Type III (flexibility and repair) collagen [6]
Elastin synthesis: Supports elastic fiber formation alongside collagen
MMP regulation: Balances matrix metalloproteinase activity to promote healthy remodeling without excessive breakdown
Keratinocyte proliferation: Strongly stimulates dermal keratinocyte growth [6]
Decorin synthesis: Stimulates this small proteoglycan that regulates collagen fibril assembly

For a broader look at peptides that support skin health, see our guide on the best peptides for skin anti-aging and our complete copper peptides skincare guide.

The Gene Expression Revolution: 2010-2020

For decades, researchers knew GHK-Cu did many beneficial things but couldn't fully explain how a single small molecule could have such wide-ranging effects. That changed around 2010, when a powerful new tool became available.

The Connectivity Map

The Broad Institute of MIT and Harvard created the Connectivity Map (cMap) — a publicly available database containing more than 7,000 gene expression profiles of five human cell lines treated with 1,309 distinct small molecules. Three GHK profiles were included in this database, created using the GeneChip HT Human Genome U133A Array [8].

When researchers analyzed the cMap data, the scope of GHK's activity became clear for the first time.

The Numbers

Out of the 22,277 probe sets in the Broad data — representing 13,424 genes — GHK increased or decreased gene expression by 50% or more in 32.1% of human genes. That translates to roughly 4,000+ genes affected at a meaningful threshold [8].

Here's how those gene changes broke down across key categories:

Gene Category	Genes Stimulated (UP)	Genes Suppressed (DOWN)
DNA repair	47	5
Antioxidant	14	2 (prooxidant)
Ubiquitin/proteasome system	41	1
Caspases (cell death)	6 of 12	—
Cancer-related genes	—	70% of 54 overexpressed in cancer

What This Means

The gene expression data offered an explanation for GHK's seemingly diverse effects. Rather than acting through a single pathway, GHK appears to function as a broad gene regulator — resetting gene expression patterns from diseased or aged states toward healthier profiles [8].

As the researchers put it: "Even though numerous and diverse beneficial effects of GHK have been known for decades, it was not clear how one simple molecule could accomplish so much. The use of gene expression data greatly extends our understanding."

Lung Disease and Tissue Remodeling

One of the most compelling applications of GHK-Cu gene expression research has been in lung disease, particularly COPD (chronic obstructive pulmonary disease) and pulmonary fibrosis.

The COPD Gene Signature Study

A landmark study published in Genome Medicine mapped the gene expression patterns of emphysematous lung destruction. Genes increasing with progressive destruction were tied to inflammation (including B-cell receptor signaling), while genes decreasing were involved in tissue repair — particularly the TGF-beta pathway, actin organization, and integrin signaling [9].

When the researchers searched the Connectivity Map for compounds that could reverse this destructive gene signature, GHK emerged as the top candidate out of 1,309 bioactive molecules tested.

Here's what happened in follow-up experiments:

Treatment of human fibroblasts with GHK recapitulated TGF-beta-induced gene expression patterns
GHK organized the actin cytoskeleton and elevated integrin beta-1 expression
Adding GHK or TGF-beta restored collagen I contraction and remodeling by fibroblasts derived from COPD patients [9]

In other words, GHK reversed the gene expression pattern associated with lung destruction and restored normal tissue remodeling function in cells from actual COPD patients.

Pulmonary Fibrosis Mouse Model

A separate study tested GHK in a bleomycin-induced pulmonary fibrosis mouse model. The peptide, administered at three different doses [10]:

Reduced inflammatory cell infiltration and interstitial thickness
Improved collagen deposition and MMP-9/TIMP-1 balance
Reduced TNF-alpha and IL-6 in bronchoalveolar lavage fluid
Reversed bleomycin-induced increases in TGF-beta1, p-Smad2, p-Smad3, and IGF-1

The researchers concluded that GHK inhibits fibrosis progression and the inflammatory response through the TGF-beta1/Smad 2/3 and IGF-1 pathway.

Cigarette Smoke Emphysema Model

A Frontiers in Molecular Biosciences study exposed mice to cigarette smoke for 12 weeks and tested GHK-Cu at three doses (0.2, 2, and 20 micrograms/g/day). GHK-Cu treatment [11]:

Attenuated emphysematous changes
Partially reversed MMP-9/TIMP-1 imbalance
Reversed NF-kappa-B activation induced by cigarette smoke
Increased Nrf2 levels as an antioxidant defense

In cell experiments, GHK-Cu also inhibited oxidative stress in human alveolar epithelial cells exposed to cigarette smoke extract by upregulating the Nrf2/Keap1 pathway.

Anti-Cancer Gene Patterns

GHK-Cu's potential anti-cancer activity is one of its most intriguing — and most cautionary — research areas.

The Metastatic Colon Cancer Discovery

In a study that used genome-wide profiling to identify genetic biomarkers for metastasis-prone colorectal cancer, Hong et al. searched 1,309 bioactive compounds in the Connectivity Map for substances that could downregulate the expression of "metastatic" genes. Only two compounds proved effective: GHK and the plant alkaloid securinine [12].

GHK suppressed RNA production in 70% of 54 human genes overexpressed in patients with aggressive metastatic colon cancer. It did so at a low, non-toxic 1 micromolar concentration (securinine required 18 micromolar). The suppressed genes included "node molecules" YWHAB, MAP3K5, LMNA, APP, GNAQ, F3, NFATC2, and TGM2 — all involved in regulating multiple biological functions through complex molecular networks [12].

Cell Line Studies

When three lines of human cancer cells were incubated with 1 to 10 nanomolar GHK, the programmed cell death system (apoptosis) was reactivated and cell growth was inhibited [8]:

SH-SY5Y neuroblastoma cells
U937 histolytic cells
Breast cancer cells

Separate research examined GHK-Cu's gene effects on MCF7 breast cancer cells and PC3 prostate cancer cells, finding patterns consistent with tumor suppression [13].

The Mouse Study

An earlier study (1983), using a method developed by Linus Pauling's group, tested GHK-Cu combined with ascorbic acid against sarcoma-180 in mice. The combination produced strong tumor suppression without evident distress to the animals. These results remained unpublished until 2014, when gene expression data provided supporting context [1].

An Important Caveat

GHK-Cu promotes angiogenesis — the formation of new blood vessels. While this is beneficial for wound healing and tissue repair, new blood vessel growth can also support tumor growth. Because of this dual nature, researchers have noted that people with active or suspected cancer should be cautious. The anti-cancer gene data is promising but preliminary, and no clinical trials have tested GHK-Cu as a cancer treatment in humans [8].

Neuroprotection and Cognitive Decline

More recent GHK-Cu research has moved into brain health and cognitive function — an area with significant unmet need given that over 99% of investigational Alzheimer's drugs have failed in clinical trials [14].

Gene Expression in Nervous System Genes

Analysis of the Connectivity Map data showed that GHK modulates expression of multiple genes critical for neuronal development and function. The peptide's antioxidant and anti-inflammatory properties are relevant here because oxidative stress, disrupted copper homeostasis, and neuroinflammation are considered leading factors in age-related neurodegeneration [14].

The Intranasal Mouse Study (2023)

A key 2023 study tested intranasal GHK-Cu in aging mice. Male and female C57BL/6 mice, 20 months old (equivalent to roughly 60-70 human years), received intranasal GHK-Cu at 15 mg/kg daily for two months [15]. Results:

Improved cognitive performance in spatial memory and learning navigation tasks
Decreased neuroinflammatory markers — specifically MCP-1, a marker for brain inflammation
Reduced axonal damage markers
Interestingly, the anti-inflammatory effects were more pronounced in female mice, while cognitive improvements were stronger in males

Follow-Up Research (2025)

A University of Washington thesis built on these findings, using immunohistochemistry and RNA sequencing on hippocampal tissue from the treated mice. Mice that received GHK-Cu showed [16]:

Lower expression of potentially harmful reactive astrocytes
Upregulation and downregulation of gene pathways supporting healthy brain aging
Sex-dependent differences in affected pathways

Alzheimer's Connection

A peptidomimetic inhibitor (P6) based on the GHK structure has been shown to interact with amyloid-beta peptide and its aggregates — the hallmark protein clumps of Alzheimer's disease. P6 prevented formation of toxic amyloid-beta oligomeric species, fibrillar aggregates, and DNA damage [14].

All of this research remains preclinical. No human clinical trials have tested GHK-Cu for cognitive decline or neurodegeneration. But the direction is promising enough to warrant further investigation.

For more on peptides that may support longevity and brain health, see our guide on the best peptides for anti-aging and longevity.

Stem Cell and Regenerative Effects

GHK-Cu's relationship with stem cells adds another dimension to its regenerative profile.

Mesenchymal Stem Cell Trophic Factor Secretion

A 2014 study published in Acta Biomaterialia by Jose et al. tested GHK's effects on mesenchymal stem cells (MSCs). Key findings [17]:

GHK showed no cytotoxic effects on MSCs across a wide concentration range
Researchers detected a dose-dependent increase in VEGF secretion by GHK-treated MSCs
This increased VEGF boosted endothelial cell proliferation, migration, and tubule formation
When MSCs were embedded in GHK-modified alginate hydrogels, they secreted increased VEGF and basic fibroblast growth factor
When pretreated with antibodies blocking integrins alpha-1 and beta-1, the VEGF increase was abolished — confirming that GHK's effects on MSC trophic factor secretion work through integrin signaling pathways

Osteogenic Differentiation

Umbilical cord blood MSCs encapsulated in GHK-modified alginate hydrogels showed significantly improved osteogenic (bone-forming) differentiation compared to control hydrogels [17]. This suggests potential applications in bone healing and regeneration.

Broader Stemness Effects

The Broad Institute gene data showed that GHK increases cellular "stemness" — the stem-cell-like properties of treated cells — alongside its effects on trophic factor secretion [3]. The practical significance: GHK may help maintain the regenerative capacity that naturally declines with age.

A recurring theme across GHK-Cu research is the peptide's natural decline with age — and how that decline maps onto the body's decreasing regenerative capacity.

Age	Plasma GHK Level	Relative Regenerative Capacity
20	~200 ng/mL	High
40	~150 ng/mL (estimated)	Moderate
60	~80 ng/mL	Reduced

That 60% drop between ages 20 and 60 correlates with visible and measurable declines in wound healing speed, skin elasticity, collagen density, and tissue repair capacity [1]. The question that drives much of current GHK-Cu research: can restoring youthful GHK levels reverse some of these age-related declines?

The gene expression data suggests the answer may be yes — at least at the cellular level. GHK appears to reset gene expression patterns of aged or diseased cells toward profiles more characteristic of younger, healthier tissue [8]. Whether that translates reliably to clinical outcomes in humans is still being tested.

Current Limitations and Open Questions

For all its promise, GHK-Cu research has real gaps:

Limited human clinical data beyond topical applications. Most clinical trials have focused on skin creams and wound dressings. The gene expression, cancer, lung, and brain studies are primarily in vitro (cell culture) or in animal models.

Delivery challenges. As a small peptide, GHK-Cu is readily broken down by enzymes in the body. Effective systemic delivery (beyond topical application) remains an engineering problem.

Regulatory status. In 2023, the FDA restricted commercial compounding of injectable GHK-Cu. This limits access to the peptide in forms other than topical skincare products [3].

The angiogenesis question. GHK-Cu's ability to promote new blood vessel growth is beneficial for wounds but theoretically problematic for anyone with existing cancerous tumors. The balance between pro-repair and potentially pro-tumor effects needs more study.

Reproducibility. As with many peptide research areas, synthesis methods and characterization standards vary across laboratories. Standardization would strengthen the field.

GHK-Cu Research Timeline

Year	Milestone
1973	Pickart isolates GHK from human plasma albumin
1977	Tripeptide identified as glycyl-L-histidyl-L-lysine
1980	Nature paper proposes copper uptake mechanism
1983	Wound healing and anti-inflammatory effects established; early anti-cancer mouse study
Late 1980s	Collagen synthesis, tissue remodeling effects demonstrated
2000	mRNA analysis confirms stimulation of collagen, dermatan sulfate, decorin
~2002	Clinical trials show skin density, thickness, and wrinkle improvements
~2010	Broad Institute Connectivity Map reveals GHK affects 4,000+ genes
2012	Emphysema/COPD gene signature reversal study published
2014	Comprehensive gene expression papers: anti-cancer, DNA repair, genome resetting
2017	Pulmonary fibrosis mouse model shows anti-fibrotic effects
2022	Cigarette smoke emphysema model demonstrates protection
2023	Intranasal GHK-Cu improves cognition in aged mice; FDA restricts injectable compounding
2025	University of Washington brain research deepens neuroprotection findings

FAQ

How was GHK-Cu discovered?

Loren Pickart discovered GHK-Cu in 1973 while studying why tissue from older donors lost regenerative capacity. He found that a fraction of younger human blood plasma could make aged liver cells produce proteins at rates typical of younger tissue. The active compound was identified as a copper-binding tripeptide.

How many genes does GHK-Cu affect?

Based on Broad Institute Connectivity Map data, GHK-Cu increases or decreases gene expression by 50% or more in approximately 32% of human genes — roughly 4,000+ genes out of 13,424 analyzed. These include genes involved in DNA repair, antioxidant defense, collagen production, inflammation, and cell death.

Is GHK-Cu safe?

Topical GHK-Cu has been used in skincare products for decades without reported adverse effects. Clinical wound healing studies have also shown strong safety. However, injectable forms are currently restricted by the FDA for commercial compounding as of 2023.

What's the difference between GHK and GHK-Cu?

GHK is the tripeptide alone. GHK-Cu is GHK bound to a copper(II) ion. Studies have shown that only GHK-Cu — not GHK without copper — exhibits the full range of wound healing and skin remodeling properties. The copper component is needed for key enzyme functions like collagen cross-linking.

Does GHK-Cu work for hair growth?

GHK-Cu has shown effects on hair follicle stimulation in some research, and it is included in some hair growth products. For a detailed look, see our guide on the best peptides for hair growth.

Can GHK-Cu treat cancer?

No clinical trials have tested GHK-Cu as a cancer treatment. Gene expression studies show it suppresses cancer-promoting genes and reactivates cell death pathways in lab settings. However, because GHK-Cu also promotes angiogenesis (new blood vessel growth), which could theoretically support tumor growth, this area requires much more research before any clinical applications.

Why do GHK-Cu levels drop with age?

Plasma GHK-Cu drops from about 200 ng/mL at age 20 to about 80 ng/mL by age 60. The exact reason isn't fully understood, but it may relate to decreased SPARC protein turnover and changes in copper metabolism with aging.

The Bottom Line

GHK-Cu is one of the most thoroughly researched peptides in regenerative science, with a publication record stretching back more than 50 years. The evidence is strongest for topical skin applications — multiple clinical trials show measurable improvements in collagen density, skin thickness, and wrinkle reduction, often outperforming established ingredients like vitamin C and retinoids.

The Broad Institute gene expression data opened up a new chapter, revealing that this small molecule influences thousands of human genes in patterns that shift diseased and aged cells toward healthier states. The lung disease, anti-cancer, and neuroprotection research is genuinely exciting but remains largely preclinical.

What makes GHK-Cu unusual in the peptide world is the sheer breadth of documented effects from a single, naturally occurring molecule. It isn't a pharmaceutical designed for one target. It's a molecule your own body produces — and produces less of as you age.

The gap between what GHK-Cu does in cell culture and gene expression studies versus what's been proven in human clinical trials is real, and it's worth being honest about. Topical skincare and wound healing applications rest on solid clinical ground. Everything else — cancer, COPD, brain health, systemic anti-aging — is still working through the translational pipeline. The next chapter of GHK-Cu research will likely focus on closing that gap.

For more on how GHK-Cu relates to other regenerative peptides, see our peptide stacking guide and our overview of the best peptides for anti-aging and longevity.

References

Pickart, L., & Margolina, A. (2018). Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data. International Journal of Molecular Sciences, 19(7), 1987. PMC6073405
Pickart, L., & Thaler, M.M. (1980). Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells. Nature, 288, 715-717.
Pickart, L., & Margolina, A. (2015). GHK peptide as a natural modulator of multiple cellular pathways in skin regeneration. BioMed Research International, 2015, 648108. PMC4508379
Maquart, F.X., et al. (2000). In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. Journal of Clinical Investigation, 92(5), 2368-2376.
Pickart, L. (2008). The human tri-peptide GHK and tissue remodeling. Journal of Biomaterials Science, Polymer Edition, 19(8), 969-988.
Leyden, J., et al. (2002). Effects of GHK-Cu on MMP and TIMP expression, collagen and elastin production and facial wrinkle parameters. Journal of Aging Science, 1(1), 1-7.
Carey, W. (2015). Epigenetic mechanisms activated by GHK-Cu increase skin collagen density in clinical trial. McGill University Dermatology Department.
Pickart, L., Vasquez-Soltero, J.M., & Margolina, A. (2014). GHK and DNA: Resetting the human genome to health. BioMed Research International, 2014, 151479. PMC4180391
Campbell, J.D., et al. (2012). A gene expression signature of emphysema-related lung destruction and its reversal by the tripeptide GHK. Genome Medicine, 4(67). PMC4064320
Zhou, X.M., et al. (2017). GHK peptide inhibits bleomycin-induced pulmonary fibrosis in mice by suppressing TGF-beta1/Smad-mediated epithelial-to-mesenchymal transition. Frontiers in Pharmacology, 8, 904. PMC5733019
Zhang, J., et al. (2022). Glycyl-L-histidyl-L-lysine-Cu2+ attenuates cigarette smoke-induced pulmonary emphysema and inflammation by reducing oxidative stress pathway. Frontiers in Molecular Biosciences, 9, 925700.
Pickart, L., Vasquez-Soltero, J.M., & Margolina, A. (2014). GHK, the human skin remodeling peptide, induces anti-cancer expression of numerous caspase, growth regulatory, and DNA repair genes. Journal of Analytical Oncology, 3, 79-87.
Pickart, L., & Margolina, A. (2021). Modulation of gene expression in human breast cancer MCF7 and prostate cancer PC3 cells by the human copper-binding peptide GHK-Cu. OBM Genetics, 5(2), 128.
Pickart, L., Vasquez-Soltero, J.M., & Margolina, A. (2017). The effect of the human peptide GHK on gene expression relevant to nervous system function and cognitive decline. Brain Sciences, 7(2), 20. PMC5332963
Tucker, L.B., et al. (2023). Intranasal GHK peptide enhances resilience to cognitive decline in aging mice. GeroScience. PMC10680828
University of Washington Digital Collections (2025). Investigation of cellular and molecular targets in the brain of mice given intranasal GHK peptide to treat age-related cognitive decline.
Jose, S., et al. (2014). Enhanced trophic factor secretion by mesenchymal stem/stromal cells with Glycine-Histidine-Lysine (GHK)-modified alginate hydrogels. Acta Biomaterialia, 10(5), 1955-1964. PMC3976757

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