      Product Title: GLOW Blend (GHK-Cu, BPC-157, TB-500) X 70mg

      URL handle: glow-blend-ghk-cu-bpc-157-tb-500-70mg-biolongevity-labs

      SKU: BPC-TB5-GHK-70MG

      Brand: Biolongevity Labs

      Current URL: https://fmihealth.com/products/glow-blend-ghk-cu-bpc-157-tb-500-70mg-biolongevity-labs

      Meta Title: GLOW Blend (GHK-Cu, BPC-157, TB-500) X 70mg

      Meta Description: Description--The GLOW blend is a research‑grade peptide formulation combining GHK‑Cu, BPC‑157, and TB‑500 into a single vial for laboratory investigation. This synergistic blend is designed to support studies on tissue repair, vascular formation, and cellular signaling in vitro and ex vivo models. Each peptide contribu

      Health Conditions: N/A



      Description HTML:

      <p>Description--The GLOW blend is a research‑grade peptide formulation combining GHK‑Cu, BPC‑157, and TB‑500 into a single vial for laboratory investigation. This synergistic blend is designed to support studies on tissue repair, vascular formation, and cellular signaling in vitro and ex vivo models. Each peptide contributes distinct regenerative mechanisms, offering complementary pathways for wound healing and recovery research.</p>
<p> </p>
<p><strong>Mechanistic Claims</strong></p>
<ul>
<li>
<strong>GHK‑Cu (50 mg):</strong>
<ul>
<li>Up‑regulates wound healing processes.</li>
<li>Stimulates collagen and elastin production.</li>
<li>Enhances angiogenic growth‑factor expression.</li>
</ul>
</li>
<li>
<strong>BPC‑157 (10 mg):</strong>
<ul>
<li>Exhibits gastro‑protective and soft‑tissue repair properties.</li>
<li>Modulates nitric oxide signaling and growth‑factor receptor activity.</li>
<li>Balances cytokine responses to reduce inflammation.</li>
</ul>
</li>
<li>
<strong>TB‑500 (10 mg):</strong>
<ul>
<li>Synthetic fragment of Thymosin Beta‑4.</li>
<li>Promotes cell migration and angiogenesis.</li>
<li>Functions via actin‑sequestering and integrin‑linked pathways.</li>
</ul>
</li>
</ul>
<p> </p>
<p><strong>Synergistic Potential:</strong></p>
<ul>
<li>Copper‑mediated extracellular matrix activation (GHK‑Cu).</li>
<li>Cytoprotective signaling and anti‑inflammatory effects (BPC‑157).</li>
<li>Actin‑dependent cell motility and vascular formation (TB‑500).</li>
<li>Together, these mechanisms may enhance collagen deposition, angiogenic indices, and recovery metrics in controlled tissue injury models.</li>
</ul>
<p> </p>
<p><strong>Research Applications</strong></p>
<ul>
<li>Tissue repair and wound healing studies</li>
<li>Angiogenesis and vascular biology investigations</li>
<li>Cellular signaling and extracellular matrix activation models</li>
<li>In vitro and ex vivo recovery assays</li>
<li>Exploratory regenerative medicine research</li>
</ul>
<p> </p>
<p><strong>GLOW Blend Research Insights</strong></p>
<ul>
<li>Combines three regenerative peptides into a single lyophilized formulation.</li>
<li>Designed for complementary activity across matrix activation, cytoprotection, and cell motility pathways.</li>
<li>Evidence remains preclinical and exploratory, with promising activity in tissue repair and angiogenesis models.</li>
<li>Supplied in freeze‑dried, filler‑free form to maximize stability and preserve chemical integrity.</li>
<li>Recommended storage: reconstitute with sterile solvent prior to use; store aliquots at ≤ –20 °C to avoid repeated freeze–thaw cycles.</li>
</ul>
<p> </p>
<p><!--EndFragment --></p>
<p><strong>Research: GHK-Cu, BPC-157, and TB-500 (Thymosin Beta 4)</strong></p>
<p>Laboratory investigations of the GLOW peptide combination reveal synergistic mechanisms for cellular repair, vascular formation, and inflammatory modulation—valuable tools for in vitro research applications.</p>
<p> </p>
<p><em><strong>Angiogenesis and Vascular Formation</strong></em></p>
<p>BPC-157 demonstrates a unique mechanism by upregulating VEGFR2 expression without affecting VEGF-A levels. This unusual pathway activates the VEGFR2-Akt-eNOS signaling cascade in vascular endothelial cell cultures[1].</p>
<p>GHK-Cu increased VEGF and bFGF expression by 230% in irradiated human dermal fibroblasts at nanomolar concentration[2]. Liposomal delivery systems showed 33.1% increased HUVEC proliferation rates with enhanced expression of cell cycle proteins[3].</p>
<p>TB-500 acts as a potent endothelial cell chemoattractant, stimulating 4-6-fold increases in HUVEC migration[4]. The peptide’s seven amino acid sequence LKKTET shows activity at approximately 50 nanomolar concentration.</p>
<p> </p>
<p><em><strong>Tissue Repair and Regeneration</strong></em></p>
<p>The actions of the GHK-Cu peptide include modulating 31.2% of human genes (4,192 genes) with ≥50% expression changes[5]. The peptide binds to integrin-linked kinase on cell membranes, activating ILK-related pathways.</p>
<p>BPC-157 promotes tissue regeneration through FAK-paxillin pathway activation. This mechanism dramatically increases phosphorylation of focal adhesion kinase and paxillin proteins without changing total protein amounts[6].</p>
<p>TB-500’s regenerative effects stem from G-actin sequestration activity—binding monomeric G-actin in a 1:1 ratio. Rat wound healing models demonstrated 42-61% increased reepithelialization with enhanced collagen deposition[7].</p>
<p> </p>
<p><em><strong>Collagen Synthesis and Extracellular Matrix</strong></em></p>
<p>GHK-Cu stimulates collagen synthesis at picomolar to nanomolar concentrations[8]. The peptide increased decorin production by 302% and stimulated glycosaminoglycan accumulation in skin fibroblasts.</p>
<p>BPC-157 enhances collagen formation across multiple tissue types in animal models. Studies show significantly increased collagen, reticulin, and blood vessel formation[9].</p>
<p>TB-500 demonstrates anti-fibrotic properties while promoting organized collagen deposition. Treated wounds show tightly organized mature collagen fibers with reduced myofibroblast formation[10].</p>
<p> </p>
<p><em><strong>Inflammatory Modulation</strong></em></p>
<p>GHK-Cu works to reduce inflammation by inhibiting NF-κB p65 and p38 MAPK pathways. The peptide decreased ROS levels and reduced production of pro-inflammatory cytokines TNF-α and IL-6 in macrophage cell cultures[2].</p>
<p>BPC-157 decreased TNF-α, IL-6, and IL-1β levels in tissue samples. The peptide reduced COX-2 gene expression and myeloperoxidase activity in various inflammation models[11].</p>
<p>TB-500 exhibits biphasic regulation of the inflammatory response. The peptide downregulates TNF-α (6.2-fold reduction) and IL-6 (4.1-fold reduction) while upregulating anti-inflammatory IL-10 (8.1-fold increase)[12].</p>
<p> </p>
<p><em><strong>Neuroprotection and Neural Mechanisms</strong></em></p>
<p>GHK-Cu increases production of nerve growth factor and neurotrophins NT-3 and NT-4[13]. Delivery showed enhanced spatial memory and learning navigation in aging models.</p>
<p>BPC-157 demonstrates complex neurotransmitter system modulation[14]. The peptide interacts with dopaminergic systems without directly binding to dopamine receptors.</p>
<p>TB-500 provides neuroprotection through anti-apoptotic effects via caspase-3 inhibition. The peptide promotes oligodendrocyte progenitor cell proliferation and differentiation through p38 MAPK upregulation[15].</p>
<p> </p>
<p><em><strong>Cellular Migration and Proliferation</strong></em></p>
<p>TB-500’s G-actin sequestration represents the primary mechanism for cellular migration[7]. Local photorelease of caged TB-500 causes directional cell turning in locomoting keratocytes.</p>
<p>GHK-Cu acts as a potent chemoattractant for macrophages, mast cells, and capillary endothelial cells[16]. Irradiated fibroblasts treated with GHK showed growth dynamics similar to non-irradiated control cells.</p>
<p>BPC-157 regulates cellular migration through ERK1/2 phosphorylation[17]. Downstream transcription factors showed dramatic upregulation: c-Fos by 4.99-fold, c-Jun by 7.05-fold, and Egr-1 by 3.70-fold.</p>
<p> </p>
<p><em><strong>Wound Healing Mechanisms</strong></em></p>
<p>BPC-157 demonstrates route-independent efficacy. The peptide accelerates cellular repair phases including inflammation, collagen deposition, angiogenesis, and epithelial repair[9].</p>
<p>GHK-Cu enhances wound healing through systemic effects and local tissue remodeling. Collagen dressing with incorporated GHK resulted in faster wound contraction and higher glutathione and ascorbic acid levels[5].</p>
<p>TB-500 promotes organized wound repair with anti-scarring properties. The peptide enhanced wound contraction by 11% and increased reepithelialization by 42-61% in full-thickness wound models[10].</p>
<p> </p>
<p><em><strong>Oxidative Stress Response</strong></em></p>
<p>GHK-Cu demonstrates potent ROS reduction in cell cultures[18]. The peptide increased superoxide dismutase activity and quenched hydroxyl and peroxyl radicals.</p>
<p>TB-500 provides targeted upregulation of antioxidant enzymes[11]. Pretreatment reduced intracellular ROS levels and upregulated Cu/Zn-SOD and catalase.</p>
<p>BPC-157 functions as a free radical scavenger. The peptide normalizes nitric oxide and malondialdehyde levels while increasing expression of antioxidant enzymes heme oxygenase-1 and NOS-3[11].</p>
<p><em>These peptides are intended for in vitro laboratory research purposes only and are not intended for human consumption or therapeutic use.</em></p>
<p> </p>
<p><strong>References</strong></p>
<ol>
<li>M.-J. Hsieh <em>et al.</em>, “Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation,” Springer Science and Business Media LLC, Nov. 2016. doi: 10.1007/s00109-016-1488-y. Available:<span> </span><a href="https://doi.org/10.1007/s00109-016-1488-y" rel="noopener" target="_blank">https://doi.org/10.1007/s00109-016-1488-y</a>
</li>
<li>Y. Dou, A. Lee, L. Zhu, J. Morton, and W. Ladiges, “The potential of GHK as an anti-aging peptide,” Ant Publishing, Mar. 2020. doi: 10.31491/apt.2020.03.014. Available: <a href="https://doi.org/10.31491/apt.2020.03.014" rel="noopener" target="_blank">https://doi.org/10.31491/apt.2020.03.014</a>
</li>
<li>X. Wang <em>et al.</em>, “GHK‐Cu‐liposomes accelerate scald wound healing in mice by promoting cell proliferation and angiogenesis,” Wiley, Apr. 2017. doi: 10.1111/wrr.12520. Available:<span> </span><a href="https://doi.org/10.1111/wrr.12520" rel="noopener" target="_blank">https://doi.org/10.1111/wrr.12520</a>
</li>
<li>K. M. Malinda, A. L. Goldstein, and H. K. Kueinman, “Thymosin β            4            stimulates directional migration of human umbilical vein endothelial cells,” Wiley, May 1997. doi: 10.1096/fasebj.11.6.9194528. Available:<span> </span><a href="https://doi.org/10.1096/fasebj.11.6.9194528" rel="noopener" target="_blank">https://doi.org/10.1096/fasebj.11.6.9194528</a>
</li>
<li>L. Pickart and A. Margolina, “Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data,” MDPI AG, Jul. 2018. doi: 10.3390/ijms19071987. Available: <a href="https://doi.org/10.3390/ijms19071987" rel="noopener" target="_blank">https://doi.org/10.3390/ijms19071987</a>
</li>
<li>C.-H. Chang, W.-C. Tsai, M.-S. Lin, Y.-H. Hsu, and J.-H. S. Pang, “The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration,” American Physiological Society, Mar. 2011. doi: 10.1152/japplphysiol.00945.2010. Available: <a href="https://doi.org/10.1152/japplphysiol.00945.2010" rel="noopener" target="_blank">https://doi.org/10.1152/japplphysiol.00945.2010</a>
</li>
<li>B. Xue, C. Leyrat, J. M. Grimes, and R. C. Robinson, “Structural basis of thymosin-β4/profilin exchange leading to actin filament polymerization,” Proceedings of the National Academy of Sciences, Oct. 2014. doi: 10.1073/pnas.1412271111. Available: <a href="https://doi.org/10.1073/pnas.1412271111" rel="noopener" target="_blank">https://doi.org/10.1073/pnas.1412271111</a>
</li>
<li>F.-X. Maquart, L. Pickart, M. Laurent, P. Gillery, J.-C. Monboisse, and J.-P. Borel, “Stimulation of collagen synthesis in fibroblast cultures by the tripeptide‐copper complex glycyl‐L‐histidyl‐L‐lysine‐Cu2+,” Wiley, Oct. 1988. doi: 10.1016/0014-5793(88)80509-x. Available: <a href="https://doi.org/10.1016/0014-5793(88)80509-x" rel="noopener" target="_blank">https://doi.org/10.1016/0014-5793(88)80509-x</a>
</li>
<li>S. Seiwerth <em>et al.</em>, “Stable Gastric Pentadecapeptide BPC 157 and Wound Healing,” Frontiers Media SA, Jun. 2021. doi: 10.3389/fphar.2021.627533. Available:<span> </span><a href="https://doi.org/10.3389/fphar.2021.627533" rel="noopener" target="_blank">https://doi.org/10.3389/fphar.2021.627533</a>
</li>
<li>K. M. Malinda <em>et al.</em>, “Thymosin beta4 accelerates wound healing.,”<span> </span><em>Journal of Investigative Dermatology</em>, vol. 113 3, pp. 364–8, 1999.</li>
<li>H. Demirtaş, A. Özer, A. K. Yıldırım, A. D. Dursun, Ş. C. Sezen, and M. Arslan, “Protective Effects of BPC 157 on Liver, Kidney, and Lung Distant Organ Damage in Rats with Experimental Lower-Extremity Ischemia–Reperfusion Injury,” MDPI AG, Feb. 2025. doi: 10.3390/medicina61020291. Available: <a href="https://doi.org/10.3390/medicina61020291" rel="noopener" target="_blank">https://doi.org/10.3390/medicina61020291</a>
</li>
<li>M. A. Evans <em>et al.</em>, “Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing,” Springer Science and Business Media LLC, Jul. 2013. doi: 10.1038/ncomms3081. Available:<span> </span><a href="https://doi.org/10.1038/ncomms3081" rel="noopener" target="_blank">https://doi.org/10.1038/ncomms3081</a>
</li>
<li>L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “The Human Tripeptide GHK-Cu in Prevention of Oxidative Stress and Degenerative Conditions of Aging: Implications for Cognitive Health,” Hindawi Limited, 2012. doi: 10.1155/2012/324832. Available: <a href="https://doi.org/10.1155/2012/324832" rel="noopener" target="_blank">https://doi.org/10.1155/2012/324832</a>
</li>
<li>J. Vukojevic <em>et al.</em>, “Pentadecapeptide BPC 157 and the central nervous system,” Medknow, 2022. doi: 10.4103/1673-5374.320969. Available:<span> </span><a href="https://doi.org/10.4103/1673-5374.320969" rel="noopener" target="_blank">https://doi.org/10.4103/1673-5374.320969</a>
</li>
<li>S. Kim, J. Choi, and J. Kwon, “Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106–126) via Neurotrophic Factor Signaling,” MDPI AG, May 2023. doi: 10.3390/molecules28093920. Available:<span> </span><a href="https://doi.org/10.3390/molecules28093920" rel="noopener" target="_blank">https://doi.org/10.3390/molecules28093920</a>
</li>
<li>L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration,” Wiley, 2015. doi: 10.1155/2015/648108. Available:<span> </span><a href="https://doi.org/10.1155/2015/648108" rel="noopener" target="_blank">https://doi.org/10.1155/2015/648108</a>
</li>
<li>T. Huang <em>et al.</em>, “Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro,” Informa UK Limited, Apr. 2015. doi: 10.2147/dddt.s82030. Available:<span> </span><a href="https://doi.org/10.2147/dddt.s82030" rel="noopener" target="_blank">https://doi.org/10.2147/dddt.s82030</a>
</li>
<li>S. Sharma, M. F. Anwar, A. Dinda, M. Singhal, and A. Malik, “In Vitro and in Vivo Studies of pH-Sensitive GHK-Cu-Incorporated Polyaspartic and Polyacrylic Acid Superabsorbent Polymer,” American Chemical Society (ACS), Nov. 2019. doi: 10.1021/acsomega.9b00655. Available: <a href="https://doi.org/10.1021/acsomega.9b00655" rel="noopener" target="_blank">https://doi.org/10.1021/acsomega.9b00655</a>
</li>
</ol>
<p><br><br><br>Label--<strong>Peptide Information</strong></p>
<table>
<thead>
<tr>
<th><strong>Property</strong></th>
<th><strong>GHK-Cu</strong></th>
<th><strong>BPC-157</strong></th>
<th><strong>TB-500</strong></th>
</tr>
</thead>
<tbody>
<tr>
<td><strong>Sequence</strong></td>
<td> Gly-His-Lys.Cu.xHAc</td>
<td>Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val</td>
<td>Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr-Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser</td>
</tr>
<tr>
<td><strong>Molecular Formula</strong></td>
<td>C₁₄H₂₃CuN₆O₄</td>
<td>C₆₂H₉₈N₁₆O₂₂</td>
<td>C₂₁₂H₃₅₀N₅₆O₇₈S</td>
</tr>
<tr>
<td><strong>Molecular Weight</strong></td>
<td>401.91 g/mol</td>
<td>1419.5 g/mol</td>
<td>4963.55 g/mol</td>
</tr>
<tr>
<td><strong>PubChem CID</strong></td>
<td>73587</td>
<td>9941957</td>
<td>16132341</td>
</tr>
<tr>
<td><strong>CAS Number</strong></td>
<td>89030-95-5</td>
<td>137525-51-0</td>
<td>77591-33-4</td>
</tr>
<tr>
<td><strong>Synonyms</strong></td>
<td>Copper peptide GHK, Cu-GHK, NSC 661251</td>
<td>PL-14736, Body-Protection Compound-157, Bepecin</td>
<td>Thymosin-β4 fragment 17-23, TB-500 acetate, Ac-LKKTETQ</td>
</tr>
</tbody>
</table>
<p> </p>
<p>Dosage--<strong>This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY.</strong><span> This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only.  This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabeled as a drug, food or cosmetic.</span></p>
    

      
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GLOW Blend (GHK-Cu, BPC-157, TB-500) X 70mg

Biolongevity Labs

Rs. 30,658

Unit price: per

100% Authentic

Made in USA

Authorised distributor

1-5 Days delivery

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GLOW Blend (GHK-Cu, BPC-157, TB-500) X 70mg

Rs. 30,658

Unit price: per

No Reviews

Rs. 30,658

Unit price: per

Price includes all duties and taxes

SKU: BPC-TB5-GHK-70MG FMI's Choice

About the Product

GLOW Peptide Research Blend: A 70 mg lyophilized laboratory formulation uniting three extensively studied regenerative peptides to investigate coordinated tissue-repair and cellular signaling pathways in vitro and ex vivo models.
Multi-Pathway Tissue Repair Signaling: GHK-Cu (50 mg) supports extracellular matrix activation and collagen, elastin, and angiogenic growth-factor expression; BPC-157 (10 mg) is examined for cytoprotective and nitric-oxide–mediated signaling balance; TB-500 (10 mg) enhances actin-dependent cell migration and angiogenic processes.
Vascular & Matrix Remodeling Research Applications: Designed for controlled studies evaluating collagen deposition dynamics, angiogenic indices, epithelial recovery metrics, and integrin-linked repair mechanisms following induced tissue stress.
Complementary Mechanistic Synergy: Enables investigation into copper-mediated matrix remodeling (GHK-Cu), growth-factor receptor and cytokine modulation (BPC-157), and cytoskeletal reorganization via actin sequestration pathways (TB-500).
Lyophilized, Filler-Free Stability: Supplied as a freeze-dried blend without excipients to preserve structural integrity and experimental consistency; reconstitute with sterile solvent prior to use and store aliquots at ≤ –20 °C to maintain peptide stability.

The GLOW blend is a research‑grade peptide formulation combining GHK‑Cu, BPC‑157, and TB‑500 into a single vial for laboratory investigation. This synergistic blend is designed to support studies on tissue repair, vascular formation, and cellular signaling in vitro and ex vivo models. Each peptide contributes distinct regenerative mechanisms, offering complementary pathways for wound healing and recovery research.

Mechanistic Claims

GHK‑Cu (50 mg):
- Up‑regulates wound healing processes.
- Stimulates collagen and elastin production.
- Enhances angiogenic growth‑factor expression.
BPC‑157 (10 mg):
- Exhibits gastro‑protective and soft‑tissue repair properties.
- Modulates nitric oxide signaling and growth‑factor receptor activity.
- Balances cytokine responses to reduce inflammation.
TB‑500 (10 mg):
- Synthetic fragment of Thymosin Beta‑4.
- Promotes cell migration and angiogenesis.
- Functions via actin‑sequestering and integrin‑linked pathways.

Synergistic Potential:

Copper‑mediated extracellular matrix activation (GHK‑Cu).
Cytoprotective signaling and anti‑inflammatory effects (BPC‑157).
Actin‑dependent cell motility and vascular formation (TB‑500).
Together, these mechanisms may enhance collagen deposition, angiogenic indices, and recovery metrics in controlled tissue injury models.

Research Applications

Tissue repair and wound healing studies
Angiogenesis and vascular biology investigations
Cellular signaling and extracellular matrix activation models
In vitro and ex vivo recovery assays
Exploratory regenerative medicine research

GLOW Blend Research Insights

Combines three regenerative peptides into a single lyophilized formulation.
Designed for complementary activity across matrix activation, cytoprotection, and cell motility pathways.
Evidence remains preclinical and exploratory, with promising activity in tissue repair and angiogenesis models.
Supplied in freeze‑dried, filler‑free form to maximize stability and preserve chemical integrity.
Recommended storage: reconstitute with sterile solvent prior to use; store aliquots at ≤ –20 °C to avoid repeated freeze–thaw cycles.

Research: GHK-Cu, BPC-157, and TB-500 (Thymosin Beta 4)

Laboratory investigations of the GLOW peptide combination reveal synergistic mechanisms for cellular repair, vascular formation, and inflammatory modulation—valuable tools for in vitro research applications.

Angiogenesis and Vascular Formation

BPC-157 demonstrates a unique mechanism by upregulating VEGFR2 expression without affecting VEGF-A levels. This unusual pathway activates the VEGFR2-Akt-eNOS signaling cascade in vascular endothelial cell cultures[1].

GHK-Cu increased VEGF and bFGF expression by 230% in irradiated human dermal fibroblasts at nanomolar concentration[2]. Liposomal delivery systems showed 33.1% increased HUVEC proliferation rates with enhanced expression of cell cycle proteins[3].

TB-500 acts as a potent endothelial cell chemoattractant, stimulating 4-6-fold increases in HUVEC migration[4]. The peptide’s seven amino acid sequence LKKTET shows activity at approximately 50 nanomolar concentration.

Tissue Repair and Regeneration

The actions of the GHK-Cu peptide include modulating 31.2% of human genes (4,192 genes) with ≥50% expression changes[5]. The peptide binds to integrin-linked kinase on cell membranes, activating ILK-related pathways.

BPC-157 promotes tissue regeneration through FAK-paxillin pathway activation. This mechanism dramatically increases phosphorylation of focal adhesion kinase and paxillin proteins without changing total protein amounts[6].

TB-500’s regenerative effects stem from G-actin sequestration activity—binding monomeric G-actin in a 1:1 ratio. Rat wound healing models demonstrated 42-61% increased reepithelialization with enhanced collagen deposition[7].

Collagen Synthesis and Extracellular Matrix

GHK-Cu stimulates collagen synthesis at picomolar to nanomolar concentrations[8]. The peptide increased decorin production by 302% and stimulated glycosaminoglycan accumulation in skin fibroblasts.

BPC-157 enhances collagen formation across multiple tissue types in animal models. Studies show significantly increased collagen, reticulin, and blood vessel formation[9].

TB-500 demonstrates anti-fibrotic properties while promoting organized collagen deposition. Treated wounds show tightly organized mature collagen fibers with reduced myofibroblast formation[10].

Inflammatory Modulation

GHK-Cu works to reduce inflammation by inhibiting NF-κB p65 and p38 MAPK pathways. The peptide decreased ROS levels and reduced production of pro-inflammatory cytokines TNF-α and IL-6 in macrophage cell cultures[2].

BPC-157 decreased TNF-α, IL-6, and IL-1β levels in tissue samples. The peptide reduced COX-2 gene expression and myeloperoxidase activity in various inflammation models[11].

TB-500 exhibits biphasic regulation of the inflammatory response. The peptide downregulates TNF-α (6.2-fold reduction) and IL-6 (4.1-fold reduction) while upregulating anti-inflammatory IL-10 (8.1-fold increase)[12].

Neuroprotection and Neural Mechanisms

GHK-Cu increases production of nerve growth factor and neurotrophins NT-3 and NT-4[13]. Delivery showed enhanced spatial memory and learning navigation in aging models.

BPC-157 demonstrates complex neurotransmitter system modulation[14]. The peptide interacts with dopaminergic systems without directly binding to dopamine receptors.

TB-500 provides neuroprotection through anti-apoptotic effects via caspase-3 inhibition. The peptide promotes oligodendrocyte progenitor cell proliferation and differentiation through p38 MAPK upregulation[15].

Cellular Migration and Proliferation

TB-500’s G-actin sequestration represents the primary mechanism for cellular migration[7]. Local photorelease of caged TB-500 causes directional cell turning in locomoting keratocytes.

GHK-Cu acts as a potent chemoattractant for macrophages, mast cells, and capillary endothelial cells[16]. Irradiated fibroblasts treated with GHK showed growth dynamics similar to non-irradiated control cells.

BPC-157 regulates cellular migration through ERK1/2 phosphorylation[17]. Downstream transcription factors showed dramatic upregulation: c-Fos by 4.99-fold, c-Jun by 7.05-fold, and Egr-1 by 3.70-fold.

Wound Healing Mechanisms

BPC-157 demonstrates route-independent efficacy. The peptide accelerates cellular repair phases including inflammation, collagen deposition, angiogenesis, and epithelial repair[9].

GHK-Cu enhances wound healing through systemic effects and local tissue remodeling. Collagen dressing with incorporated GHK resulted in faster wound contraction and higher glutathione and ascorbic acid levels[5].

TB-500 promotes organized wound repair with anti-scarring properties. The peptide enhanced wound contraction by 11% and increased reepithelialization by 42-61% in full-thickness wound models[10].

Oxidative Stress Response

GHK-Cu demonstrates potent ROS reduction in cell cultures[18]. The peptide increased superoxide dismutase activity and quenched hydroxyl and peroxyl radicals.

TB-500 provides targeted upregulation of antioxidant enzymes[11]. Pretreatment reduced intracellular ROS levels and upregulated Cu/Zn-SOD and catalase.

BPC-157 functions as a free radical scavenger. The peptide normalizes nitric oxide and malondialdehyde levels while increasing expression of antioxidant enzymes heme oxygenase-1 and NOS-3[11].

These peptides are intended for in vitro laboratory research purposes only and are not intended for human consumption or therapeutic use.

References

M.-J. Hsieh et al., “Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation,” Springer Science and Business Media LLC, Nov. 2016. doi: 10.1007/s00109-016-1488-y. Available: https://doi.org/10.1007/s00109-016-1488-y
Y. Dou, A. Lee, L. Zhu, J. Morton, and W. Ladiges, “The potential of GHK as an anti-aging peptide,” Ant Publishing, Mar. 2020. doi: 10.31491/apt.2020.03.014. Available: https://doi.org/10.31491/apt.2020.03.014
X. Wang et al., “GHK‐Cu‐liposomes accelerate scald wound healing in mice by promoting cell proliferation and angiogenesis,” Wiley, Apr. 2017. doi: 10.1111/wrr.12520. Available: https://doi.org/10.1111/wrr.12520
K. M. Malinda, A. L. Goldstein, and H. K. Kueinman, “Thymosin β 4 stimulates directional migration of human umbilical vein endothelial cells,” Wiley, May 1997. doi: 10.1096/fasebj.11.6.9194528. Available: https://doi.org/10.1096/fasebj.11.6.9194528
L. Pickart and A. Margolina, “Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data,” MDPI AG, Jul. 2018. doi: 10.3390/ijms19071987. Available: https://doi.org/10.3390/ijms19071987
C.-H. Chang, W.-C. Tsai, M.-S. Lin, Y.-H. Hsu, and J.-H. S. Pang, “The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration,” American Physiological Society, Mar. 2011. doi: 10.1152/japplphysiol.00945.2010. Available: https://doi.org/10.1152/japplphysiol.00945.2010
B. Xue, C. Leyrat, J. M. Grimes, and R. C. Robinson, “Structural basis of thymosin-β4/profilin exchange leading to actin filament polymerization,” Proceedings of the National Academy of Sciences, Oct. 2014. doi: 10.1073/pnas.1412271111. Available: https://doi.org/10.1073/pnas.1412271111
F.-X. Maquart, L. Pickart, M. Laurent, P. Gillery, J.-C. Monboisse, and J.-P. Borel, “Stimulation of collagen synthesis in fibroblast cultures by the tripeptide‐copper complex glycyl‐L‐histidyl‐L‐lysine‐Cu2+,” Wiley, Oct. 1988. doi: 10.1016/0014-5793(88)80509-x. Available: https://doi.org/10.1016/0014-5793(88)80509-x
S. Seiwerth et al., “Stable Gastric Pentadecapeptide BPC 157 and Wound Healing,” Frontiers Media SA, Jun. 2021. doi: 10.3389/fphar.2021.627533. Available: https://doi.org/10.3389/fphar.2021.627533
K. M. Malinda et al., “Thymosin beta4 accelerates wound healing.,” Journal of Investigative Dermatology, vol. 113 3, pp. 364–8, 1999.
H. Demirtaş, A. Özer, A. K. Yıldırım, A. D. Dursun, Ş. C. Sezen, and M. Arslan, “Protective Effects of BPC 157 on Liver, Kidney, and Lung Distant Organ Damage in Rats with Experimental Lower-Extremity Ischemia–Reperfusion Injury,” MDPI AG, Feb. 2025. doi: 10.3390/medicina61020291. Available: https://doi.org/10.3390/medicina61020291
M. A. Evans et al., “Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing,” Springer Science and Business Media LLC, Jul. 2013. doi: 10.1038/ncomms3081. Available: https://doi.org/10.1038/ncomms3081
L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “The Human Tripeptide GHK-Cu in Prevention of Oxidative Stress and Degenerative Conditions of Aging: Implications for Cognitive Health,” Hindawi Limited, 2012. doi: 10.1155/2012/324832. Available: https://doi.org/10.1155/2012/324832
J. Vukojevic et al., “Pentadecapeptide BPC 157 and the central nervous system,” Medknow, 2022. doi: 10.4103/1673-5374.320969. Available: https://doi.org/10.4103/1673-5374.320969
S. Kim, J. Choi, and J. Kwon, “Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106–126) via Neurotrophic Factor Signaling,” MDPI AG, May 2023. doi: 10.3390/molecules28093920. Available: https://doi.org/10.3390/molecules28093920
L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration,” Wiley, 2015. doi: 10.1155/2015/648108. Available: https://doi.org/10.1155/2015/648108
T. Huang et al., “Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro,” Informa UK Limited, Apr. 2015. doi: 10.2147/dddt.s82030. Available: https://doi.org/10.2147/dddt.s82030
S. Sharma, M. F. Anwar, A. Dinda, M. Singhal, and A. Malik, “In Vitro and in Vivo Studies of pH-Sensitive GHK-Cu-Incorporated Polyaspartic and Polyacrylic Acid Superabsorbent Polymer,” American Chemical Society (ACS), Nov. 2019. doi: 10.1021/acsomega.9b00655. Available: https://doi.org/10.1021/acsomega.9b00655

Label--Peptide Information

Property	GHK-Cu	BPC-157	TB-500
Sequence	Gly-His-Lys.Cu.xHAc	Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val	Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr-Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser
Molecular Formula	C₁₄H₂₃CuN₆O₄	C₆₂H₉₈N₁₆O₂₂	C₂₁₂H₃₅₀N₅₆O₇₈S
Molecular Weight	401.91 g/mol	1419.5 g/mol	4963.55 g/mol
PubChem CID	73587	9941957	16132341
CAS Number	89030-95-5	137525-51-0	77591-33-4
Synonyms	Copper peptide GHK, Cu-GHK, NSC 661251	PL-14736, Body-Protection Compound-157, Bepecin	Thymosin-β4 fragment 17-23, TB-500 acetate, Ac-LKKTETQ

Dosage--This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabeled as a drug, food or cosmetic.

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: Not a diet substitute. Seek Medical guidance if unsure before use.

Product Information Sheet

Mechanistic Claims

GHK‑Cu (50 mg):
- Up‑regulates wound healing processes.
- Stimulates collagen and elastin production.
- Enhances angiogenic growth‑factor expression.
BPC‑157 (10 mg):
- Exhibits gastro‑protective and soft‑tissue repair properties.
- Modulates nitric oxide signaling and growth‑factor receptor activity.
- Balances cytokine responses to reduce inflammation.
TB‑500 (10 mg):
- Synthetic fragment of Thymosin Beta‑4.
- Promotes cell migration and angiogenesis.
- Functions via actin‑sequestering and integrin‑linked pathways.

Synergistic Potential:

Copper‑mediated extracellular matrix activation (GHK‑Cu).
Cytoprotective signaling and anti‑inflammatory effects (BPC‑157).
Actin‑dependent cell motility and vascular formation (TB‑500).
Together, these mechanisms may enhance collagen deposition, angiogenic indices, and recovery metrics in controlled tissue injury models.

Research Applications

Tissue repair and wound healing studies
Angiogenesis and vascular biology investigations
Cellular signaling and extracellular matrix activation models
In vitro and ex vivo recovery assays
Exploratory regenerative medicine research

GLOW Blend Research Insights

Combines three regenerative peptides into a single lyophilized formulation.
Designed for complementary activity across matrix activation, cytoprotection, and cell motility pathways.
Evidence remains preclinical and exploratory, with promising activity in tissue repair and angiogenesis models.
Supplied in freeze‑dried, filler‑free form to maximize stability and preserve chemical integrity.
Recommended storage: reconstitute with sterile solvent prior to use; store aliquots at ≤ –20 °C to avoid repeated freeze–thaw cycles.

Research: GHK-Cu, BPC-157, and TB-500 (Thymosin Beta 4)

Angiogenesis and Vascular Formation

Tissue Repair and Regeneration

Collagen Synthesis and Extracellular Matrix

GHK-Cu stimulates collagen synthesis at picomolar to nanomolar concentrations[8]. The peptide increased decorin production by 302% and stimulated glycosaminoglycan accumulation in skin fibroblasts.

BPC-157 enhances collagen formation across multiple tissue types in animal models. Studies show significantly increased collagen, reticulin, and blood vessel formation[9].

TB-500 demonstrates anti-fibrotic properties while promoting organized collagen deposition. Treated wounds show tightly organized mature collagen fibers with reduced myofibroblast formation[10].

Inflammatory Modulation

BPC-157 decreased TNF-α, IL-6, and IL-1β levels in tissue samples. The peptide reduced COX-2 gene expression and myeloperoxidase activity in various inflammation models[11].

Neuroprotection and Neural Mechanisms

GHK-Cu increases production of nerve growth factor and neurotrophins NT-3 and NT-4[13]. Delivery showed enhanced spatial memory and learning navigation in aging models.

BPC-157 demonstrates complex neurotransmitter system modulation[14]. The peptide interacts with dopaminergic systems without directly binding to dopamine receptors.

Cellular Migration and Proliferation

TB-500’s G-actin sequestration represents the primary mechanism for cellular migration[7]. Local photorelease of caged TB-500 causes directional cell turning in locomoting keratocytes.

BPC-157 regulates cellular migration through ERK1/2 phosphorylation[17]. Downstream transcription factors showed dramatic upregulation: c-Fos by 4.99-fold, c-Jun by 7.05-fold, and Egr-1 by 3.70-fold.

Wound Healing Mechanisms

BPC-157 demonstrates route-independent efficacy. The peptide accelerates cellular repair phases including inflammation, collagen deposition, angiogenesis, and epithelial repair[9].

TB-500 promotes organized wound repair with anti-scarring properties. The peptide enhanced wound contraction by 11% and increased reepithelialization by 42-61% in full-thickness wound models[10].

Oxidative Stress Response

GHK-Cu demonstrates potent ROS reduction in cell cultures[18]. The peptide increased superoxide dismutase activity and quenched hydroxyl and peroxyl radicals.

TB-500 provides targeted upregulation of antioxidant enzymes[11]. Pretreatment reduced intracellular ROS levels and upregulated Cu/Zn-SOD and catalase.

BPC-157 functions as a free radical scavenger. The peptide normalizes nitric oxide and malondialdehyde levels while increasing expression of antioxidant enzymes heme oxygenase-1 and NOS-3[11].

These peptides are intended for in vitro laboratory research purposes only and are not intended for human consumption or therapeutic use.

References

M.-J. Hsieh et al., “Therapeutic potential of pro-angiogenic BPC157 is associated with VEGFR2 activation and up-regulation,” Springer Science and Business Media LLC, Nov. 2016. doi: 10.1007/s00109-016-1488-y. Available: https://doi.org/10.1007/s00109-016-1488-y
Y. Dou, A. Lee, L. Zhu, J. Morton, and W. Ladiges, “The potential of GHK as an anti-aging peptide,” Ant Publishing, Mar. 2020. doi: 10.31491/apt.2020.03.014. Available: https://doi.org/10.31491/apt.2020.03.014
X. Wang et al., “GHK‐Cu‐liposomes accelerate scald wound healing in mice by promoting cell proliferation and angiogenesis,” Wiley, Apr. 2017. doi: 10.1111/wrr.12520. Available: https://doi.org/10.1111/wrr.12520
K. M. Malinda, A. L. Goldstein, and H. K. Kueinman, “Thymosin β 4 stimulates directional migration of human umbilical vein endothelial cells,” Wiley, May 1997. doi: 10.1096/fasebj.11.6.9194528. Available: https://doi.org/10.1096/fasebj.11.6.9194528
L. Pickart and A. Margolina, “Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data,” MDPI AG, Jul. 2018. doi: 10.3390/ijms19071987. Available: https://doi.org/10.3390/ijms19071987
C.-H. Chang, W.-C. Tsai, M.-S. Lin, Y.-H. Hsu, and J.-H. S. Pang, “The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration,” American Physiological Society, Mar. 2011. doi: 10.1152/japplphysiol.00945.2010. Available: https://doi.org/10.1152/japplphysiol.00945.2010
B. Xue, C. Leyrat, J. M. Grimes, and R. C. Robinson, “Structural basis of thymosin-β4/profilin exchange leading to actin filament polymerization,” Proceedings of the National Academy of Sciences, Oct. 2014. doi: 10.1073/pnas.1412271111. Available: https://doi.org/10.1073/pnas.1412271111
F.-X. Maquart, L. Pickart, M. Laurent, P. Gillery, J.-C. Monboisse, and J.-P. Borel, “Stimulation of collagen synthesis in fibroblast cultures by the tripeptide‐copper complex glycyl‐L‐histidyl‐L‐lysine‐Cu2+,” Wiley, Oct. 1988. doi: 10.1016/0014-5793(88)80509-x. Available: https://doi.org/10.1016/0014-5793(88)80509-x
S. Seiwerth et al., “Stable Gastric Pentadecapeptide BPC 157 and Wound Healing,” Frontiers Media SA, Jun. 2021. doi: 10.3389/fphar.2021.627533. Available: https://doi.org/10.3389/fphar.2021.627533
K. M. Malinda et al., “Thymosin beta4 accelerates wound healing.,” Journal of Investigative Dermatology, vol. 113 3, pp. 364–8, 1999.
H. Demirtaş, A. Özer, A. K. Yıldırım, A. D. Dursun, Ş. C. Sezen, and M. Arslan, “Protective Effects of BPC 157 on Liver, Kidney, and Lung Distant Organ Damage in Rats with Experimental Lower-Extremity Ischemia–Reperfusion Injury,” MDPI AG, Feb. 2025. doi: 10.3390/medicina61020291. Available: https://doi.org/10.3390/medicina61020291
M. A. Evans et al., “Thymosin β4-sulfoxide attenuates inflammatory cell infiltration and promotes cardiac wound healing,” Springer Science and Business Media LLC, Jul. 2013. doi: 10.1038/ncomms3081. Available: https://doi.org/10.1038/ncomms3081
L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “The Human Tripeptide GHK-Cu in Prevention of Oxidative Stress and Degenerative Conditions of Aging: Implications for Cognitive Health,” Hindawi Limited, 2012. doi: 10.1155/2012/324832. Available: https://doi.org/10.1155/2012/324832
J. Vukojevic et al., “Pentadecapeptide BPC 157 and the central nervous system,” Medknow, 2022. doi: 10.4103/1673-5374.320969. Available: https://doi.org/10.4103/1673-5374.320969
S. Kim, J. Choi, and J. Kwon, “Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106–126) via Neurotrophic Factor Signaling,” MDPI AG, May 2023. doi: 10.3390/molecules28093920. Available: https://doi.org/10.3390/molecules28093920
L. Pickart, J. M. Vasquez-Soltero, and A. Margolina, “GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration,” Wiley, 2015. doi: 10.1155/2015/648108. Available: https://doi.org/10.1155/2015/648108
T. Huang et al., “Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro,” Informa UK Limited, Apr. 2015. doi: 10.2147/dddt.s82030. Available: https://doi.org/10.2147/dddt.s82030
S. Sharma, M. F. Anwar, A. Dinda, M. Singhal, and A. Malik, “In Vitro and in Vivo Studies of pH-Sensitive GHK-Cu-Incorporated Polyaspartic and Polyacrylic Acid Superabsorbent Polymer,” American Chemical Society (ACS), Nov. 2019. doi: 10.1021/acsomega.9b00655. Available: https://doi.org/10.1021/acsomega.9b00655

Peptide Information

Property	GHK-Cu	BPC-157	TB-500
Sequence	Gly-His-Lys.Cu.xHAc	Gly-Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val	Ac-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr-Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser
Molecular Formula	C₁₄H₂₃CuN₆O₄	C₆₂H₉₈N₁₆O₂₂	C₂₁₂H₃₅₀N₅₆O₇₈S
Molecular Weight	401.91 g/mol	1419.5 g/mol	4963.55 g/mol
PubChem CID	73587	9941957	16132341
CAS Number	89030-95-5	137525-51-0	77591-33-4
Synonyms	Copper peptide GHK, Cu-GHK, NSC 661251	PL-14736, Body-Protection Compound-157, Bepecin	Thymosin-β4 fragment 17-23, TB-500 acetate, Ac-LKKTETQ

This PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. All product information available on this website is for educational purposes only. This product should only be handled by licensed, qualified professionals. This product is not a drug, food, or cosmetic and may not be misbranded, misused or mislabeled as a drug, food or cosmetic.