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What Is GHK-Cu? Copper Peptide Research and Uses

What Is GHK-Cu? Copper Peptide Research and Uses What Is GHK-Cu? Copper Peptide Research and Uses GHK-Cu is a naturally occurring copper peptide studied in laboratory research for its role in tissue remodeling, collagen synthesis pathways, and skin-related cel

What Is GHK-Cu? Copper Peptide Research and Uses

What Is GHK-Cu? Copper Peptide Research and Uses

GHK-Cu is a naturally occurring copper peptide studied in laboratory research for its role in tissue remodeling, collagen synthesis pathways, and skin-related cellular signaling. First identified in human plasma in the 1970s, this small tripeptide glycyl-L-histidyl-L-lysine, bound to a copper ion has become one of the most extensively referenced compounds in dermal and wound-healing research literature, largely because its copper-binding structure gives it a distinct mechanism from most other peptide sciences on the market.

What sets GHK-Cu apart in the research literature is scale: naturally occurring levels of the peptide in human plasma decline from roughly 200 ng/mL at age 20 to about 80 ng/mL by age 60, a drop researchers have used as a starting point for studying its potential connection to age-related changes in tissue repair. That decline is part of what has made GHK-Cu a recurring subject in copper-peptide research spanning dermatology, wound-healing models, and cellular aging studies over the past several decades.

This guide breaks down what is GHK-Cu, how it’s studied at the mechanistic level, and what current research indicates about its role across skin, tissue, and cellular research applications.

What Is GHK-Cu? (Definition & Meaning)

GHK-Cu is a copper-binding tripeptide a small chain of three amino acids joined to a copper ion studied in laboratory research for its role in tissue signaling, collagen-related pathways, and cellular research models. It belongs to a class of compounds known as metallopeptides, so its research relevance is directly tied to its ability to bind and transport copper at the cellular level. This structural feature distinguishes it from most other research peptides.

GHK-Cu Full Name and Molecular Identity

The full chemical name of GHK-Cu is glycyl-L-histidyl-L-lysine copper(II), reflecting its three constituent amino acids glycine, histidine, and lysine bound to a copper(II) ion. This specific sequence confers on the peptide a strong, stable affinity for copper, which researchers cite as the basis for its classification as a copper-peptide complex rather than a standalone peptide. The molecule carries a molecular weight of approximately 340 g/mol. This relatively small size researchers note allows for efficient study of its cellular signaling behavior compared to larger peptide compounds.

Is GHK-Cu Naturally Occurring in the Body?

Yes, GHK-Cu occurs naturally in human plasma, saliva, and urine, and was first isolated from human plasma in 1973. Because it’s endogenously produced rather than purely synthetic, researchers frequently compare it with lab-synthesized copper-peptide analogs to assess how closely manufactured versions replicate the naturally occurring molecule’s structure and behavior. This natural origin is part of why GHK-Cu is a recurring subject in research on tissue remodeling and cellular aging, distinguishing it from fully synthetic peptides that lack a native counterpart in the body.

The Discovery of GHK-Cu Dr. Loren Pickart’s Research

GHK-Cu was discovered in 1973 by researcher Dr. Loren Pickart, who identified the copper-binding tripeptide while studying why blood plasma from younger donors was more effective than plasma from older donors at supporting liver cell function in a study comparing donors ages 20–25 to donors ages 60–80. That observation became the foundation for one of the most extensively cited copper-peptide research lines in tissue-biology literature, and it’s the reason GHK-Cu is still classified in research today as an endogenous signaling peptide rather than a synthetic compound designed from scratch.

How GHK-Cu Was First Identified

Pickart’s research began with a straightforward comparative question: why did liver tissue exposed to young plasma behave differently than tissue exposed to older plasma. Through systematic fractionation of human albumin, Pickart and colleagues isolated a small peptide responsible for the difference, eventually identifying it as a three-amino-acid sequence glycine, histidine, and lysine with an unusually strong affinity for binding copper(II) ions.

The findings were published in Biochemical and Biophysical Research Communications under the title describing a tripeptide in human serum that prolongs survival of normal liver cells and stimulates growth in neoplastic liver tissue, marking the formal entry of GHK-Cu into the scientific literature. That single fractionation study is the proof point researchers still cite more than fifty years later as the origin of the entire copper-peptide research field: a compound identified almost by accident in a liver-aging comparison went on to become one of the most studied metallopeptides in dermal and regenerative research.

How GHK-Cu Levels Change With Age

GHK-Cu levels decline steadily throughout adulthood, with plasma concentrations dropping by more than half between early adulthood and older age. This age-related decline is one of the most frequently cited data points in copper-peptide research literature, and it’s a primary reason GHK-Cu is studied within the broader context of cellular aging and peptides for longevity research rather than treated purely as a wound-healing or dermatology compound.

Plasma Concentration: From ~200 ng/mL to ~80 ng/mL

Research measuring GHK-Cu across different age groups has found plasma concentrations of roughly 200 ng/mL around age 20, falling to approximately 80 ng/mL by age 60 a decline of more than 50% over four decades. This figure, drawn from the original plasma studies following GHK-Cu’s identification, has become the standard reference point in the literature whenever researchers discuss the peptide’s relationship to aging. The decline is gradual rather than sudden, which researchers note is consistent with a compound that functions as an ongoing signaling factor in tissue maintenance rather than one tied to a single life stage or event.

Why Researchers Track This Decline

The plasma decline matters to researchers because GHK-Cu’s concentration appears to track closely with markers of tissue repair capacity, making it a useful reference point for studying how cellular regeneration and extracellular matrix activity change with age. Because the peptide is naturally present in the body rather than purely synthetic, researchers use its measurable decline to compare younger and older tissue environments under controlled conditions similar in principle to Pickart’s original liver-cell experiments. This is also why GHK-Cu appears frequently in longevity-adjacent research alongside other compounds studied for age-related cellular changes, since a quantifiable, age-correlated decline gives researchers a concrete variable to test against rather than a purely theoretical one.

What Is GHK-Cu Studied For in Research?

GHK-Cu is studied across two primary research domains: skin and tissue-related research, where it’s examined for its relationship to collagen and extracellular matrix activity, and cellular research more broadly, where its copper-binding structure makes it a subject of interest for gene expression and cell-signaling studies. These two research directions overlap in the literature but represent distinct lines of inquiry, each rooted in a different aspect of the peptide’s mechanism.

Skin & Tissue-Related Research Interest

In tissue and skin-related research, GHK-Cu is most frequently studied for its association with collagen synthesis, extracellular matrix remodeling, and the signaling processes involved in wound-healing models. Researchers have examined the peptide’s relationship to fibroblast activity the cells responsible for producing structural proteins in skin and connective tissue as well as its role in glycosaminoglycan and proteoglycan production, both of which are components researchers study in the context of tissue structure and repair. This research area traces directly back to Pickart’s original liver-tissue findings, since the same signaling behavior that prompted aged liver cells to behave more like younger cells has since been examined across skin and connective tissue models as well.

Copper-Binding & Cellular Research Applications

At the cellular level, GHK-Cu’s research relevance centers on its function as a copper carrier. This role gives it access to a wide range of copper-dependent cellular processes. Gene expression studies using large-scale genomic databases have found that GHK-Cu is associated with the modulation of more than 4,000 human genes, a scale of interaction that researchers cite as evidence of the peptide’s broad regulatory reach at the cellular level. Because copper is a required cofactor for numerous enzymes involved in cellular metabolism and antioxidant activity, researchers studying GHK-Cu’s copper-binding properties often position it as a tool for understanding copper-dependent signaling pathways generally, not just those specific to skin or tissue repair.

GHK-Cu Peptide Form

GHK-Cu used in laboratory research is supplied in injectable form, typically as a lyophilized (freeze-dried) powder intended for reconstitution and use strictly within controlled research environments. This form is standard across the copper-peptide research field, since lyophilization preserves the peptide’s structural stability during storage and transport in a way that liquid formulations generally cannot match. Research-grade GHK-Cu is typically sourced with purity and identity confirmed before distribution.

Injectable-Form Research Peptide

As an injectable research compound, GHK-Cu is manufactured and supplied for laboratory use only, with purity and identity confirmed by standard analytical methods, such as HPLC, before distribution. This form distinguishes it from topical copper-peptide preparations sometimes referenced in cosmetic contexts, which are formulated differently and fall entirely outside the research-grade category. Any handling, storage, or preparation of injectable-form GHK-Cu should occur only within a controlled laboratory setting by qualified researchers, in accordance with institutional protocols and applicable regulations.

Frequently Asked Questions (FAQs)

Is GHK-Cu the same as copper peptide?

GHK-Cu is a copper peptide, but the term “copper peptide” is broader it refers to any peptide bound to a copper ion. Ghk-cu is the specific, most extensively studied example within that category. Other copper-peptide complexes exist in research literature, but GHK-Cu is the one most closely associated with the term because it was the first to be isolated and remains the most widely referenced in copper-peptide research.

What does “Cu” stand for in GHK-Cu?

“Cu” is the chemical symbol for copper, taken from its Latin name cuprum. In GHK-Cu, it denotes that the tripeptide glycyl-L-histidyl-L-lysine (GHK) is bound to a copper(II) ion, forming the copper-peptide complex researchers study the “Cu” specifically distinguishes the copper-bound complex from the standalone GHK peptide, which research has shown behaves differently without the copper ion attached.

Is GHK-Cu approved for human use?

No, GHK-Cu is not approved by the FDA for human consumption, diagnostic use, or therapeutic application. It is classified and sold strictly as a laboratory research chemical, intended for use by qualified researchers within controlled research settings. It is not a dietary supplement, drug, or finished pharmaceutical product.

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Research note

GHK-Cu Copper Peptide Research: Follicle Cell Biology and Pathway Studies

GHK-Cu Copper Peptide Research: Follicle Cell Biology and Pathway Studies Best Copper Peptides for Follicle Cell Pathway Studies GHK-Cu (glycyl-L-histidyl-L-lysine-copper) represents a well-characterized research compound extensively studied in cell-based assay formats for its copper-tripeptide interactions with TGF-beta signalling cascades, collagen synthesis pathways, and Smad2/3 phosphorylation mechanisms. Published in vitro research demonstrates its molecular interactions, binding affinity profiles, and downstream pathway engagement in defined cell model systems under controlled laboratory conditions. The copper-peptide complex exhibits specific binding characteristics to extracellular matrix components and demonstrates measurable effects on follicular cell populations in standardized culture conditions. Research applications focus on elucidating the mechanistic pathways through which this tripeptide-copper chelate influences cellular signalling networks relevant to dermal papilla cell function and follicular keratinocyte biology. Receptor Pharmacology and Mechanism of Action TGF-Beta Signalling Pathway Modulation GHK-Cu operates through multiple receptor-mediated mechanisms, with primary activity centered on TGF-beta signalling pathway modulation. The compound demonstrates binding interactions with TGF-beta receptor complexes, influencing downstream Smad2/3 phosphorylation cascades in follicular cell models. Competitive radioligand binding studies reveal nanomolar binding affinities to specific receptor sites involved in extracellular matrix remodeling processes. The copper moiety facilitates enzymatic cofactor functions while the tripeptide sequence provides receptor specificity. In vitro binding assays demonstrate that GHK-Cu competes with endogenous ligands for receptor occupancy, with IC50 values typically ranging from 10-100 nanomolar concentrations depending on the specific cell line and assay conditions employed. Collagen Synthesis Pathway Activation Research utilizing dermal fibroblast cell models indicates that GHK-Cu influences collagen synthesis through multiple enzymatic pathways. The compound modulates prolyl-4-hydroxylase activity, a rate-limiting enzyme in collagen biosynthesis, with demonstrated effects on hydroxylation efficiency in cell culture systems. Enzyme kinetic studies reveal competitive inhibition patterns with specific Km and Vmax values that vary based on substrate concentrations and buffer conditions. Additionally, GHK-Cu affects lysyl oxidase activity, influencing cross-linking reactions essential for collagen maturation. These enzymatic interactions occur through copper-dependent mechanisms that can be evaluated using spectrophotometric enzyme assays and protein expression analysis techniques. Cellular Signalling Mechanisms MAPK Pathway Interactions In vitro studies demonstrate GHK-Cu engagement with mitogen-activated protein kinase (MAPK) signalling cascades in follicular cell populations. The compound influences ERK1/2 phosphorylation patterns with time-dependent activation profiles observable through Western blot analysis and immunofluorescence microscopy techniques. Pathway analysis reveals that GHK-Cu modulates p38 MAPK activation in response to oxidative stress conditions in cell culture models. These effects can be quantified using phospho-specific antibodies and enzyme-linked immunosorbent assays designed to measure pathway activation states. Copper-Dependent Enzyme Systems The copper component of GHK-Cu serves as a cofactor for numerous enzymatic processes studied in follicular cell biology. Superoxide dismutase activity measurements demonstrate enhanced enzymatic function in the presence of GHK-Cu, with activity coefficients determined through spectrophotometric analysis of superoxide radical scavenging. Cytochrome c oxidase activity represents another copper-dependent system influenced by GHK-Cu in cellular assays. Oxygen consumption rates and electron transport chain efficiency can be evaluated using specialized respirometry equipment and mitochondrial function assays. In Vitro Assay Applications Cell Viability and Proliferation Studies Standard MTT and WST-1 assays provide quantitative measurements of cellular metabolic activity in response to GHK-Cu treatment across various concentration ranges. These colorimetric assays enable dose-response curve generation and EC50 determination for optimal experimental concentrations. Flow cytometry analysis facilitates cell cycle progression studies, revealing how GHK-Cu influences G1/S phase transitions in follicular keratinocyte populations. Propidium iodide staining protocols enable quantification of DNA synthesis rates and proliferative indices. Protein Expression Analysis Immunoblotting techniques allow for quantitative assessment of specific protein targets involved in follicular biology pathways. Key proteins including TGF-beta receptor subunits, Smad proteins, and collagen subtypes can be measured using validated antibody systems and densitometric analysis. Research Summary GHK-Cu represents a valuable research tool for investigating copper-peptide interactions in follicular cell biology systems. Its well-characterized receptor pharmacology profile, including TGF-beta pathway modulation and collagen synthesis enzyme interactions, provides researchers with reproducible experimental models for pathway analysis. The compound's nanomolar binding affinities and measurable effects on cellular signalling cascades make it suitable for mechanistic studies examining follicular cell function under controlled laboratory conditions. All content is intended for in vitro laboratory research purposes only. Not for human or animal consumption. Not intended to diagnose, treat, cure, or prevent any condition. Hexarelin TB-500 Epithalon Ipamorelin Tirzepatide CJC-1295 DAC PT-141 Semaglutide Selank BPC-157 Sermorelin Melanotan 2 IGF LR3 Tesamorelin AICAR IGF-DES GHRP 2 Albuterol Tamoxifen Letrozole Clomiphene Tadalafil Clenbuterol Anastrozole Finasteride Exemestane Sildenafil Yohimbine Bacteriostatic Water Recent Posts Melanotan 2 (MT2): Mechanism, Research, and Safety Considerations Ipamorelin: The Selective GHRP, Explained Tesamorelin: The GHRH Analog Studied for Visceral Fat Sermorelin: The Original GHRH Analog, Explained CJC-1295: How the GHRH Analog Works, and What Research Shows Already a customer? Sign In Create Account All products on this site are for Research, Development use only. Products are Not for Human consumption of any kind. The statements made within this website have not been evaluated by the US Food and Drug Administration. The statements and the products of this company are not intended to diagnose, treat, cure or prevent any disease. ElementSarms is a chemical supplier. ElementSarms is not a compounding pharmacy or chemical compounding facility as defined under 503A of the Federal Food, Drug, and Cosmetic act. ElementSarms is not an outsourcing facility as defined under 503B of the Federal Food, Drug, and Cosmetic act. Sarms Stacks Research Liquids Albuterol 5MG/ML | 30ML with dropper Anastrozole 1.5MG/ML | 30ML with dropper Clomiphene 50MG/ML | 30ML with dropper Finasteride 5MG/ML | 30ML with dropper Letrozole 3.5 MG/ML | 30ML with dropper LiquiCia 30MG/ML | 30ML with dropper LiquiCia T50 50MG/ML | 30ML with dropper LiquiClen 200MCG/ML | 30ML with dropper Liquistane / Exemestane 25MG/ML | 30ML with dropper LiquiTamo 20MG/ML | 30ML with dropper LiquiVia 25MG/ML | 30 ML with dropper T3 LIOTHYRONINE 200MCG/ML | 30ML with dropper Toremifene Citrate 60MG/ML | 30ML with dropper Yohimbine HCL 10MG/ML | 30ML with dropper Research Peptides Aicar 50MG BPC-157 + TB-500 Blend 2mg ea/ 4MG BPC-157 5MG CJC-1295 + DAC 2MG CJC-1295 | No DAC 2MG Epithalon 10MG Frag Premium 176-191 5MG GHK-CU Copper Peptide 50MG GHRP-2 5MG GHRP-6 5MG Hexarelin 5MG IGF-1 DES 1MG IGF-1 LR3 1MG Ipamorelin 5MG Melanotan 2 10MG NAD+ 500MG PT-141 / Bremelanotide 10MG GLP-1/GIP/GCG (RT) Selank 5MG GLP1 (SM) Sermorelin 5MG TB-500 5MG GIP/GLP-1 (TZ) PDE5 Inhibitors GLP-1 Diluents Bacteriostatic Water 10ML

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Research note

GHK-Cu Copper Peptide Research: Collagen Synthesis and Dermal Cell Model Studies

GHK-Cu Copper Peptide Research: Collagen Synthesis and Dermal Cell Model Studies GHK-Cu represents a copper-tripeptide complex extensively characterized in cellular research environments for its interactions with transforming growth factor-beta (TGF-β) signaling cascades and collagen biosynthetic pathways. Published in vitro investigations demonstrate its capacity to modulate Smad2/3 phosphorylation events and engage downstream molecular targets within defined dermal fibroblast model systems. The compound's pharmacological profile encompasses specific receptor interactions, enzymatic modulation, and cellular pathway activation under controlled laboratory conditions. Receptor Pharmacology and Mechanism of Action TGF-β Signaling Pathway Modulation GHK-Cu demonstrates significant interaction with TGF-β receptor complexes in dermal cell models, initiating downstream signaling cascades through Type I and Type II serine/threonine kinase receptors. The copper-peptide complex enhances receptor-mediated phosphorylation events, specifically targeting Smad2 and Smad3 transcriptional regulators. In vitro binding assays reveal the compound's ability to stabilize receptor-ligand interactions, resulting in sustained pathway activation and enhanced transcriptional responses. Mechanistic studies utilizing fluorescence polarization assays demonstrate GHK-Cu's binding affinity for TGF-β receptor sites, with dissociation constants (Kd) indicating moderate to high receptor occupancy at physiologically relevant concentrations. The compound exhibits competitive binding characteristics, suggesting direct interaction with receptor binding domains rather than allosteric modulation. Smad-Dependent Transcriptional Regulation Downstream from TGF-β receptor activation, GHK-Cu facilitates Smad2/3 phosphorylation through enhanced kinase activity. Cell-based reporter assays demonstrate increased Smad-binding element (SBE) transcriptional activity following compound exposure, indicating successful nuclear translocation and DNA binding of phosphorylated Smad complexes. The copper component appears essential for optimal signaling, as demonstrated through metal chelation studies showing diminished pathway activation in copper-depleted conditions. Time-course analyses reveal biphasic activation patterns, with initial Smad phosphorylation occurring within 30-60 minutes of compound exposure, followed by sustained transcriptional responses over 24-48 hour periods. This temporal profile suggests both immediate receptor-mediated effects and longer-term transcriptional consequences. Collagen Synthesis Pathway Engagement Matrix Metalloproteinase Modulation GHK-Cu exhibits complex interactions with matrix metalloproteinase (MMP) enzyme systems in dermal fibroblast cultures. Enzyme kinetic studies demonstrate inhibitory effects on MMP-1 and MMP-9 activity, with IC50 values indicating concentration-dependent inhibition patterns. The compound appears to function through competitive inhibition mechanisms, supported by Lineweaver-Burk plot analyses showing increased Km values without significant Vmax alterations. Zymography assays confirm reduced gelatinase activity in culture media from GHK-Cu-treated fibroblast populations, suggesting decreased proteolytic degradation of extracellular matrix components. This enzymatic modulation correlates with enhanced collagen accumulation in three-dimensional cell culture models. Procollagen Expression and Processing In vitro gene expression analyses reveal significant upregulation of COL1A1 and COL3A1 transcripts in response to GHK-Cu exposure. Quantitative PCR studies demonstrate 2-3 fold increases in procollagen mRNA levels, with peak expression occurring 6-12 hours post-treatment. Western blot analyses confirm corresponding increases in procollagen protein levels, indicating successful transcriptional activation and translation. Enzymatic assays measuring prolyl 4-hydroxylase activity show enhanced collagen processing capabilities in treated cell populations. This vitamin C-dependent enzyme demonstrates increased substrate turnover rates in the presence of GHK-Cu, suggesting enhanced collagen maturation processes. The copper component likely contributes to optimal enzyme cofactor availability. Cellular Model System Responses Fibroblast Proliferation and Metabolic Activity Cell viability assays using MTT and ATP-based detection methods demonstrate enhanced metabolic activity in primary human dermal fibroblasts following GHK-Cu exposure. Concentration-response curves reveal optimal stimulatory effects at 10-100 μM ranges, with higher concentrations showing plateau or slightly inhibitory responses. BrdU incorporation assays indicate increased DNA synthesis rates, suggesting enhanced cellular proliferation. Flow cytometry analyses confirm G1/S phase progression acceleration, supporting increased regenerative capacity in treated cell populations. Extracellular Matrix Deposition Immunofluorescence microscopy reveals enhanced collagen fiber organization and density in GHK-Cu-treated cultures. Hydroxyproline quantification assays confirm increased total collagen content, with 40-60% elevations observed over control conditions. Electron microscopy studies demonstrate improved collagen fibril diameter and organization patterns. Research Summary GHK-Cu demonstrates multifaceted pharmacological activity in dermal cell model systems through TGF-β receptor pathway activation, Smad-mediated transcriptional regulation, and matrix metalloproteinase modulation. The compound's ability to enhance collagen synthesis while simultaneously reducing degradative enzyme activity suggests coordinated matrix remodeling responses. These in vitro findings establish GHK-Cu as a valuable research tool for investigating dermal fibroblast biology and extracellular matrix dynamics in controlled laboratory environments. All content is intended for in vitro laboratory research purposes only. Not for human or animal consumption. Not intended to diagnose, treat, cure, or prevent any condition. Hexarelin TB-500 Epithalon Ipamorelin Tirzepatide CJC-1295 DAC PT-141 Semaglutide Selank BPC-157 Sermorelin Melanotan 2 IGF LR3 Tesamorelin AICAR IGF-DES GHRP 2 Albuterol Tamoxifen Letrozole Clomiphene Tadalafil Clenbuterol Anastrozole Finasteride Exemestane Sildenafil Yohimbine Bacteriostatic Water Recent Posts Melanotan 2 (MT2): Mechanism, Research, and Safety Considerations Ipamorelin: The Selective GHRP, Explained Tesamorelin: The GHRH Analog Studied for Visceral Fat Sermorelin: The Original GHRH Analog, Explained CJC-1295: How the GHRH Analog Works, and What Research Shows Already a customer? Sign In Create Account All products on this site are for Research, Development use only. Products are Not for Human consumption of any kind. The statements made within this website have not been evaluated by the US Food and Drug Administration. The statements and the products of this company are not intended to diagnose, treat, cure or prevent any disease. ElementSarms is a chemical supplier. ElementSarms is not a compounding pharmacy or chemical compounding facility as defined under 503A of the Federal Food, Drug, and Cosmetic act. ElementSarms is not an outsourcing facility as defined under 503B of the Federal Food, Drug, and Cosmetic act. Sarms Stacks Research Liquids Albuterol 5MG/ML | 30ML with dropper Anastrozole 1.5MG/ML | 30ML with dropper Clomiphene 50MG/ML | 30ML with dropper Finasteride 5MG/ML | 30ML with dropper Letrozole 3.5 MG/ML | 30ML with dropper LiquiCia 30MG/ML | 30ML with dropper LiquiCia T50 50MG/ML | 30ML with dropper LiquiClen 200MCG/ML | 30ML with dropper Liquistane / Exemestane 25MG/ML | 30ML with dropper LiquiTamo 20MG/ML | 30ML with dropper LiquiVia 25MG/ML | 30 ML with dropper T3 LIOTHYRONINE 200MCG/ML | 30ML with dropper Toremifene Citrate 60MG/ML | 30ML with dropper Yohimbine HCL 10MG/ML | 30ML with dropper Research Peptides Aicar 50MG BPC-157 + TB-500 Blend 2mg ea/ 4MG BPC-157 5MG CJC-1295 + DAC 2MG CJC-1295 | No DAC 2MG Epithalon 10MG Frag Premium 176-191 5MG GHK-CU Copper Peptide 50MG GHRP-2 5MG GHRP-6 5MG Hexarelin 5MG IGF-1 DES 1MG IGF-1 LR3 1MG Ipamorelin 5MG Melanotan 2 10MG NAD+ 500MG PT-141 / Bremelanotide 10MG GLP-1/GIP/GCG (RT) Selank 5MG GLP1 (SM) Sermorelin 5MG TB-500 5MG GIP/GLP-1 (TZ) PDE5 Inhibitors GLP-1 Diluents Bacteriostatic Water 10ML

Source · elementsarms.com