Tesofensine (400 mcg, 60 units)
GHK-Cu Copper Peptide (100MG)
This batch of GHK-Cu has been third party lab tested and verified for quality.
TESTED FOR:
purity
weight
TFA FREE
sterility
endotoxins(lps)
$49.99
| Quantity | Price | |
|---|---|---|
| 0% | 1 - 4 | $49.99 |
| 10% | 5 - 9 | $44.99 |
| 20% | 10 - 19 | $39.99 |
| 30% | 20 + | $34.99 |
This product comes as lyophilized powder and is not reconstituted. All products and materials sold on this site are for Research Use Only and not for human use; subject to our Terms and Conditions.
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| Peptide vial specifications | Results | |
|---|---|---|
Not reconstituted | ||
Bottle type: | Vial - sealed - flip top | |
Form: | Powder (lyophilized) | |
Vial size: | 3ML | |
GHK-Cu Certificate of Analysis (COA) Test Result
| Date Tested: | |
|---|---|
| Purity: | 99.910% |
| Weight: | 97.91mg |
| Endotoxins (LPS): | Pass |
| Sterility: | Pass |
| TFA: | Not detected |
| Batch #: | GHK072615100O |
| Testing Lab: | Janoshik |
| COA Verified Link: | Purity Report Endotoxin Report |
| Testing Methods: | HPLC, LAL, TAMC/YAMC USP <71> |
GHK-Cu Specifications: Molecular Weight, CAS Number & Sequence
GHK-Cu (CAS 89030-95-5) is a copper peptide complex with the molecular formula C14H22CuN6O4 and a molecular weight of 401.9 g/mol.
| Form: | Powder (lyophilized) |
|---|---|
| Weight: | 100mg |
| Appearance: | Blue to light blue lyophilized powder |
| CAS Number: | 89030-95-5 |
| Molecular Formula: | C14H22CuN6O4 |
| Molecular Weight: | 401.9 g/mol |
| PubChem CID: | 165429100 |
| Sequence: | Gly-His-Lys(Cu2+) |
| Other Names: | GHK-Cu, GHKCu, Copper Peptide, Copper Tripeptide-1 |
| Terms: | Subject to our Terms and Conditions. This material is sold for laboratory research use only. Not for human consumption, animal, or medical use. |
GHK-Cu Molecular Structure
GHK-Cu Amino Acid Sequence
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What is GHK-Cu?
GHK-Cu (glycyl-L-histidyl-L-lysine bound to copper) is a naturally occurring copper-binding tripeptide known for its regenerative, antioxidant, and anti-inflammatory functions. It supports angiogenesis, tissue repair, and the modulation of transforming growth factor beta 1 (TGFβ1) signaling. Recent research has expanded beyond its well-known wound healing and skin regeneration properties to explore its neuroprotective potential in Alzheimer's Disease models, where it demonstrates the ability to reduce amyloid plaque formation and improve cognitive function through multiple biological pathways.
GHK-Cu Research Studies
Peer-reviewed scientific research findings
📚 Peer-Reviewed Study
GHK-Cu in Mice: Improved Cognition and Fewer Amyloid Plaques
Overview of the GHK-Cu Study
This study explored the GHK-Cu copper peptide for its neuroprotective properties against Alzheimer's Disease (AD). Researchers investigated whether intranasal delivery of GHK-Cu could enhance cognition and reduce hallmark neuropathological changes in 5xFAD transgenic mice, a well-established model of early-onset AD.
Over a 12-week period, male and female mice received intranasal GHK-Cu three times per week. Results demonstrated that GHK-Cu treatment improved memory performance, reduced amyloid plaque burden, and decreased neuroinflammatory activity compared with saline-treated controls. These outcomes position GHK-Cu peptide as a promising candidate for further preclinical evaluation in neurodegenerative research.
Why GHK-Cu Is Being Studied for Alzheimer's
The GHK-Cu peptide (glycyl-L-histidyl-L-lysine bound to copper) is a naturally occurring complex known for its regenerative, antioxidant, and anti-inflammatory functions. It supports angiogenesis, tissue repair, and the modulation of transforming growth factor beta 1 (TGFβ1) signaling—a pathway linked to amyloid plaque formation and tau pathology.
Prior GHK-Cu studies showed it improves cognitive function in aged animals and counteracts oxidative stress relevant to AD pathogenesis. Because GHK-Cu copper peptide can be delivered intranasally, bypassing the restrictive blood-brain barrier, this route was selected as an efficient and non-invasive way to achieve central nervous system exposure.
Experimental Design and Methodology
The study used both male and female 5xFAD transgenic mice, aged four months at the onset of testing. Mice were divided into GHK-Cu–treated and saline-treated groups, along with wild-type controls. The GHK-Cu peptide was administered intranasally at a dose of 15 mg/kg three times weekly for three months.
Cognitive function was measured using the Y-Maze spontaneous alternation test, a reliable indicator of working memory. Neuropathological assessments included Congo red staining for amyloid plaques and MCP-1 immunohistochemistry to evaluate neuroinflammation.
GHK-Cu Key Findings — Behavioral Improvements
Treatment with intranasal GHK-Cu significantly enhanced performance in the Y-Maze test. Female mice exhibited notable gains in spontaneous alternation scores at weeks 8 and 12, while males showed earlier improvement beginning at week 4. By the end of the study, the GHK-Cu–treated mice performed nearly at the level of wild-type controls, suggesting substantial restoration of working memory and executive function.
These behavioral outcomes align with prior GHK-Cu studies demonstrating improved cognition following peptide exposure.
GHK-Cu effects Y-maze alternation test
Reduction of Amyloid Plaques
Congo red staining revealed that GHK-Cu–treated transgenic mice displayed markedly fewer amyloid plaques in the frontal cortex, hippocampus, and thalamus compared with saline-treated counterparts. The plaques that did form were smaller, less dense, and less numerous.
These reductions indicate that intranasal GHK-Cu copper peptide not only mitigates amyloid accumulation but also potentially slows early neurodegenerative processes characteristic of AD pathology.
Decreased Neuroinflammation via MCP-1 Suppression
MCP-1 (monocyte chemoattractant protein-1) staining intensity—a biomarker of neuroinflammation—was significantly reduced in the frontal cortex and hippocampus of GHK-Cu–treated mice. Digital quantification confirmed lower optical density levels compared with saline-treated controls.
This indicates that GHK-Cu peptide effectively downregulated chemokine-related immune activation, supporting a more stable neuroinflammatory environment. The findings reinforce GHK-Cu's multifaceted mechanism, including modulation of inflammatory and oxidative pathways.
The Role of Intranasal Administration
Intranasal delivery allowed direct access to the brain through the olfactory and trigeminal pathways, bypassing the blood-brain barrier. This method increased peptide uptake efficiency while maintaining low systemic copper levels, minimizing toxicity risks.
Researchers emphasized that this non-invasive route could serve as a model for other neuroactive synthetic peptides, providing a foundation for future translational studies on neurodegenerative conditions.
GHK-Cu Discussion and Implications
This GHK-Cu latest research underscores a broad therapeutic potential via three mechanisms: antioxidant protection, anti-inflammatory regulation, and amyloid plaque reduction. By attenuating multiple pathological pathways simultaneously, GHK-Cu contrasts with traditional single-target AD drugs.
The study's outcomes suggest that GHK-Cu copper peptide could hold translational value as a neuroprotective therapy, though further testing in aged or tau-based models is warranted. The authors also highlight the safety of repeated intranasal use and encourage long-term studies assessing neurodegeneration and synaptic health.
Conclusion
Intranasal GHK-Cu copper peptide treatment improved cognitive performance, reduced amyloid plaque deposition, and decreased MCP-1–mediated neuroinflammation in 5xFAD mice over a 12-week study. The evidence supports its viability as a neuroprotective and cognitive-enhancing agent for Alzheimer's research.
This GHK-Cu latest research demonstrates that bypassing the blood-brain barrier through intranasal delivery may represent a promising strategy for peptide-based therapies aimed at neurodegeneration.
Frequently Asked Questions (FAQ)
Does GHK Cu help with brain health or cognition?
In recent animal research, GHK-Cu peptide improved memory and cognitive function in mice with Alzheimer's-like pathology. Treated animals showed enhanced performance in behavioral tests, such as the Y-maze, indicating improved working memory and restored neural function. These effects are attributed to GHK-Cu's antioxidant, anti-inflammatory, and neuroprotective properties.
What are the results of the newest GHK Cu studies?
The GHK-Cu latest research in 5xFAD transgenic mice demonstrated that intranasal GHK-Cu significantly reduced amyloid plaque formation, lowered neuroinflammation markers, and improved cognitive outcomes. The findings suggest that GHK-Cu acts through multiple biological pathways to counteract Alzheimer's-related degeneration.
How is GHK-Cu administered in animal trials?
In this study, researchers delivered GHK-Cu copper peptide intranasally at a dose of 15 mg/kg, three times per week for 12 weeks. The intranasal route was chosen for its ability to bypass the blood-brain barrier, allowing the peptide to reach brain tissue more effectively while minimizing systemic copper exposure.
What are the anti-inflammatory effects of GHK-Cu in Alzheimer's models?
GHK-Cu reduced inflammation in the brain by decreasing MCP-1 (monocyte chemoattractant protein-1) staining intensity in the frontal cortex and hippocampus. This reduction indicates lower immune activation and diminished neuroinflammatory stress, which are critical in slowing Alzheimer's progression.
What is the GHK-Cu peptide and how does it work?
The GHK-Cu peptide is a naturally occurring copper-binding tripeptide (glycyl-L-histidyl-L-lysine). In animal brains, it supports cellular repair, combats oxidative stress, and regulates inflammatory signaling pathways. Its copper-bound form (GHK-Cu) activates protective genes and suppresses those involved in tissue damage and neuroinflammation.
How does intranasal administration improve peptide delivery?
Intranasal administration enables direct access to the brain via the olfactory and trigeminal neural pathways, effectively bypassing the blood-brain barrier. This approach improves GHK-Cu peptide bioavailability in the central nervous system and avoids potential toxicity associated with systemic copper overload.
What were the key behavioral outcomes in the Y-maze test?
Mice treated with GHK-Cu copper peptide exhibited significantly higher spontaneous alternation percentages in the Y-maze, a measure of working memory. Males improved as early as week 4, while females showed strong gains by week 8, with both groups nearing the performance levels of healthy wild-type controls.
Can GHK-Cu reduce amyloid plaque accumulation?
Congo red staining revealed that GHK-Cu–treated mice had substantially fewer amyloid plaques across the frontal cortex, hippocampus, and thalamus. The plaques were smaller, less dense, and less numerous than in untreated mice, demonstrating the peptide's potential to mitigate amyloid-related toxicity.
How is GHK-Cu copper peptide different from topical cosmetic formulations?
Topical GHK-Cu formulations are designed for skin regeneration and anti-aging, acting locally to stimulate collagen production and wound repair. In contrast, the GHK-Cu peptide used in neuroscience research is administered systemically at controlled doses to influence brain pathways and cognitive function—representing a completely different therapeutic application.
Study Reference
Tucker M, Liao GY, Park JY, et al. Behavioral and neuropathological features of Alzheimer's disease are attenuated in 5xFAD mice treated with intranasal GHK peptide. Preprint. bioRxiv. 2023;2023.11.20.567908. Published 2023 Nov 21. doi:10.1101/2023.11.20.567908
https://pubmed.ncbi.nlm.nih.gov/38045355/