This product is a box of 10 vials.
What Is KLOW ?
The BPC157, TB500 (43 amino acid Thymosin Beta-4), KPV, and GHK-Cu quad blend combines four well-studied peptides that work through different but complementary pathways. BPC157 has been researched for supporting faster tissue healing, new blood vessel growth, and protection of the stomach and gut lining. TB500, the full 43-amino-acid Thymosin Beta-4 peptide, helps regulate actin, a key protein for cell movement and repair, and plays an important role in wound healing and tissue regeneration. KPV, a short fragment of alpha-MSH, is known for its anti-inflammatory and antimicrobial effects, mainly by reducing overactive immune signaling. GHK-Cu is a natural copper-binding peptide that stimulates collagen production, skin and hair regeneration, and cellular repair. Together, these four peptides may act synergistically—BPC157 and Thymosin Beta-4 strengthen repair and blood flow, KPV calms inflammation, and GHK-Cu drives tissue remodeling and renewal—making this blend a broad research platform for studying healing and regeneration.
Chemical Diagrams:
Compound 1: TB-500
Sequence: 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: C212H350N56O78S
Molar Mass: 4963.4408
CAS number: 77591-33-4
PubChem: CID 16132341
Compound 2: BPC-157
Sequence: Gly- Glu-Pro-Pro-Pro-Gly-Lys-Pro-Ala-Asp-Asp-Ala-Gly-Leu-Val
Molecular Formula: C62H98N16O22
Molecular Weight: 1419.556 g/mol
PubChem CID: 108101
Compound 3: KPV
Amino Acid Sequence: Lys-Pro-Val
Molecular Formula: C17H32N6O4
Molecular Weight: 384.48 g/mol
PubChem CID: 125672
CAS Number: 112965-21-6
Synonyms: MSH (11-13), ACTH(11-13), alpha-MSH(11-13)
Compound 4: GHK-Cu
Sequence: Gly-His-Lys.Cu.xHAc
Molecular Formula: C14H23CuN6O4
Molecular Weight: 401.91 g/mol
PubChem CID: 73587
CAS Number: 89030-95-5
Biochemistry
TB500 is a synthetic peptide derived from thymosin beta-4 (TB-4), a naturally occurring protein in the human body known for its anti-inflammatory and tissue-repairing properties. Like TB-4, TB500 binds to actin and plays a role in gene regulation. It has shown benefits across various systems, including cardiovascular health, muscle regeneration, immune modulation, and central nervous system function. TB500 has even been linked to promoting hair growth and easing some effects of aging.
TB500 operates through two primary mechanisms:
- Actin Sequestration and Cell Motility Regulation:Within cells, TB500 binds to and sequesters actin, a key component of the cytoskeleton. This interaction is crucial for regulating cell movement, growth, and division. By enhancing cell motility, TB500 supports faster wound healing, improved immune cell trafficking, reduced inflammation, and increased angiogenesis (blood vessel formation).
- Gene Expression Modulation ("Moonlighting" Function): Beyond its structural role, TB500 also influences gene expression independent of actin binding. It modulates the expression of genes involved in nitric oxide (NO) production, angiogenesis, and cellular proliferation—paralleling several downstream effects observed with BPC-157. Through this regulatory function, TB500 affects cytokine secretion and modulates multiple signaling pathways associated with the inflammatory response. Notably, it downregulates pathways such as NF-κB and Toll-like receptor signaling, thereby suppressing pro-inflammatory cytokines like TNF-α and IL-1 receptor-associated kinases.
In addition to controlling inflammation, TB500 activates several tissue repair pathways, including PI3K/Akt/eNOS, Notch, and angiopoietin-1/Tie signaling. One of its most studied actions involves modulation of the TGF-β pathway, which plays a central role in reducing fibrosis (scarring)—making TB500 particularly valuable in the context of chronic injury and tissue regeneration.
As an aside, there is research to show that TB500 influences Wnt signaling. This has been shown to promote the formation of hair follicles and boost hair growth at the level of DNA expression patterns. The diagram below offers an overview of the complex and wide-ranging influences of TB500.
BPC-157 is a synthetic peptide made of 15 amino acids. It comes from a naturally occurring compound in the body known as Body Protective Compound (BPC). Originally isolated from human gastric juice, BPC has shown strong anti-inflammatory and wound-healing properties. In animal studies, BPC-157 has shown potential tissue regeneration benefits across various systems, including the gastrointestinal tract, liver, pancreas, ligaments, muscles, tendons, cornea, heart, brain, and nerves.
While the exact way BPC-157 works is not fully clear, several ideas have emerged. It is not yet known if the peptide acts by binding to cell surface receptors or by entering cells and directly influencing genetic activity. In truth, BPC-157 may work through both methods.
Research has consistently shown that BPC-157 greatly affects nitric oxide (NO) signaling—particularly through its regulation of endothelial nitric oxide synthase (eNOS). This is believed to explain many of its therapeutic effects because NO promotes the movement of vascular endothelial cells that are important in tissue repair and the growth of new blood vessels. There is recent evidence showing that BPC-157 promotes the phosphorylation of Src, Cav-1, and eNOS. It also reduces the binding interaction between Cav-1 and eNOS, an essential step in eNOS activation and NO production.
BPC-157 is known for its rapid absorption and spread throughout the body when taken by mouth or injected. Within 10 minutes of injection, the peptide is detectable throughout the body, including the kidneys, liver, stomach wall, thymus, reproductive organs, and spleen. Peak concentrations in tissues are typically reached about one hour after administration and gradually decline over the following 48 hours. The highest levels are usually found in the kidney, liver, thymus, and spleen, with moderate distribution in the lungs, muscles, brain, and skin.
Many of BPC-157's effects are thought to occur through changes in gene expression patterns. Again, the mechanism for this is not fully understood, but the peptide has been shown to clearly alter the expression patterns of:
• Egr,
• Nos (especially eNos),
• Srf,
• Vegr,
• Plcγ, and
• Kras.
These genes control the synthesis of a number of factors that affect cells of blood vessels and the immune system. BPC-157 has been shown to alter fundamental properties of cells like migration, adhesion, thrombosis, and inflammatory responses. These alterations result in changes to cell behavior that help regulate inflammation and improve tissue healing. Additional research shows that expression levels of each gene are increased or decreased based on the timeframe following administration of BPC-157. In other words, the length of time that BPC-157 is in the system is important in determining which genes are activated. This suggests that BPC-157 works through a complex regulatory mechanism that has fine control over a wide array of genes and their expression.
GHK-Cu is a naturally occurring copper complex made of a short peptide (GHK) bound to copper(II) ions. Initially isolated from human plasma, it has also been detected in saliva and urine. Animal studies have shown that GHK-Cu plays a significant role in wound healing and modulating inflammatory responses. It is particularly known for its ability to stimulate collagen production and promote the growth of skin fibroblasts, which has led to its widespread use in cosmetic formulations as an anti-aging compound.
GHK-Cu exerts its effects largely by regulating the activity of key enzymes involved in tissue remodeling. It stimulates the production of metalloproteinases, enzymes that break down damaged proteins to facilitate tissue repair. At the same time, it promotes the expression of anti-proteases, which help preserve healthy proteins from degradation. Much like BPC-157, GHK-Cu appears to orchestrate a delicate balance between protein synthesis and breakdown through gene regulation, supporting a highly coordinated wound healing process—especially within the skin and connective tissue.
KPV is a short, three-amino-acid peptide derived from the C-terminal end of alpha-melanocyte-stimulating hormone (α-MSH), making it the smallest peptide in this group. Despite its size, KPV exhibits a wide range of biological activities. It has been studied for its potential roles in modulating reduced blood flow, influencing sexual behavior and appetite, maintaining energy balance, and offering protection against UV radiation. Most notably, KPV is recognized for its potent anti-inflammatory properties, with effects observed in the gastrointestinal tract, lungs, and even the central nervous system. Additionally, it boasts excellent oral bioavailability, a rare feature among therapeutic peptides.
While KPV can bind to melanocortin receptors—particularly showing an affinity for MC1R—its mechanisms of action appear to be largely independent of these pathways. Unlike its parent molecule α-MSH, KPV does not rely on melanocortin receptor binding to exert its therapeutic effects. However, the precise molecular mechanisms behind its role in wound healing and inflammation resolution remain under investigation.
KPV's anti-inflammatory capabilities were first identified in 1984, when animal studies showed its effectiveness in reducing a wide range of inflammatory conditions, including fever, dermatitis, blood vessel inflammation, fibrosis, arthritis, eye inflammation, gastritis, and inflammation of the brain and lungs. Its broad anti-inflammatory action appears to involve modulation of several key biological pathways:
- Inhibition of nuclear factor-kappaB (NF-κB)
- Downregulation of adhesion molecules and chemokine receptors
- Suppression of pro-inflammatory cytokine production Regulation of T-cell activity and inflammatory cell migration
- Enhancement of antioxidant enzyme expression
- Modulation of cell death pathways
Although KPV is generally less potent than α-MSH in terms of anti-inflammatory activity, its superior oral bioavailability makes it a highly attractive therapeutic option. Additionally, KPV potency and half-life can be increased via glycoalkylation. Under experiments designed to mimic conditions within the body, unmodified KPV degraded to its three constituent amino acids within 24 hours but α-glycoalkylated KPV was completely stable. This indicates a successful modification of KPV to improve its chemical degradation without impacting its biological activity.
A particularly intriguing feature of KPV is its tissue-selectivity: it primarily acts in areas of excessive or pathological inflammation, while leaving healthy tissues and normal immune responses largely unaffected. Animal models suggest that KPV does not interfere with appropriate inflammatory responses, such as those involved in normal wound healing. This targeted action makes KPV both safe and easy to administer, with a very low risk of overdose or systemic side effects.
KLOW Anti-Inflammatory Effects
After briefly examining the limited but growing understanding of how BPC-157, TB500, GHK-Cu, and KPV function, it is essential to highlight their known therapeutic benefits—particularly the potential for synergistic effects when used in combination. The most significant commonality among all four peptides is their shared ability to modulate the inflammatory response, guiding it toward a state that promotes healing rather than harm.
Among the group, BPC-157 and KPV stand out for their pronounced anti-inflammatory properties. BPC-157, in particular, has consistently demonstrated the ability to suppress excessive inflammation across a wide range of preclinical studies. Chronic inflammation—a key driver of pain and tissue damage—is often the result of a dysregulated immune response, where the body fails to properly resolve inflammation. BPC-157 appears uniquely equipped to restore balance to this process. Remarkably, recent research has shown that BPC-157 was able to almost completely eliminate inflammation in a model of interstitial cystitis—a chronic bladder condition that has long been considered difficult, if not impossible, to cure.
BPC-157 regulates nitric oxide synthesis, one of its primary anti-inflammatory mechanisms of action. Nitric oxide, after all, is critical in the inflammatory processes, helping to regulate blood vessel dilation, immune response by cells like macrophages, cytokine release, tissue repair, and more. Nitric oxide (NO) is particularly important in regulating inflammation in the nervous system, with dysregulation of NO linked to multiple neurodegenerative diseases.
KPV regulates melanocortin signaling and controls cellular responses to inflammation at a very high level. Together, these properties allow the peptide to reduce pain, improve cell function, and reduce scarring. Tissue heals in a more organized way in the presence of KPV, which in turn leads to better long-term physiological outcomes. As a melanocortin modulator, KPV can also reduce the appearance of scars, helping to prevent the changes in skin tone and coloration often associated with scarring. This is true because KPV retains the healing properties of alpha-MSH without retaining the larger peptide’s pigmentation properties.
Unlike BPC-157 and KPV, TB500 appears to regulate inflammation by inhibiting the production of cytokines like TNF-α and interleukin-6. These cytokines are critical in mitigating and perpetuating the inflammatory response and are the targets of prescription monoclonal antibodies like Remicade and Humira. These cytokines are critical in starting and keeping the inflammatory response going and are the targets of prescription monoclonal antibodies like Remicade and Humira. Used together, these four peptides—BPC-157, TB500, GHK-Cu, and KPV—target inflammation through multiple complementary pathways, potentially leading to more effective suppression of excessive inflammatory responses, even at lower doses. This dose efficiency translates to enhanced therapeutic effects with a reduced risk of side effects.
Among these, GHK-Cu may play a particularly synergistic role due to its overlapping anti-inflammatory properties with both BPC-157 and TB500. Research has shown that GHK-Cu acts as a free radical scavenger and interacts with nitric oxide (NO) pathways to help limit the harmful effects of oxidative stress. While NO is critical for healing and immune function, excessive NO production can generate free radicals and cause tissue damage. By neutralizing these free radicals, GHK-Cu may help mitigate the risks associated with elevated NO levels, a potential side effect of peptides that promote NO signaling.
Additionally, GHK-Cu has been shown to suppress pro-inflammatory cytokines such as TNF-α and interleukin-6, further enhancing its anti-inflammatory profile. This not only supports TB500’s actions but may also relieve TB500 from having to "handle" inflammation, allowing it to more effectively engage in its other biological roles—particularly in promoting angiogenesis (blood vessel growth) and cell proliferation. The net result is a shift in TB500’s activity toward accelerating tissue regeneration rather than suppressing inflammation.
The healing process, like any construction process, produces a lot of waste. In the body, that waste comes in the form of free radicals, which are reactive molecules that can damage cells and extracellular matrix. By improving anti-oxidant responses, GHK-Cu can help to mitigate this damage and thus keep inflammation at a minimum while a wound is healing. Research shows that a reduction in free radicals can limit scar formation during wound healing, leading to improved long-term outcomes. In short, GHK-Cu helps to preserve the benefits of BPC-157 and TB500 while reducing collateral damage from the accelerated healing process.
It is in the setting of tissue repair that the addition of KPV really provides a boost to the other three peptides. The ability of KPV to reduce hypertrophic scarring and improve tissue organization works hand in hand with BPC-157 and GHK-Cu. Together, these peptides help to regulate the healing process so that it proceeds in a delimited, orderly manner. Recall that KPV is only active in the setting of excessive inflammation. This means that it tempers inflammatory processes that can lead to scarring but allows inflammatory processes necessary for tissue repair to proceed without interference. This helps to achieve a balance between the rapid healing and long-term outcomes that ensure strong, functional, healthy tissue repairs.
KLOW Anti-Bacterial Properties
While the antibacterial properties of these peptides are certainly relevant to wound healing, their effects in combating microbial growth are significant enough to warrant separate attention. Preventing bacterial and fungal overgrowth is essential for ensuring rapid, complication-free tissue repair—and these peptides contribute to that goal through distinct and complementary mechanisms.
TB500 offers multiple antimicrobial benefits. Not only does it exhibit direct antibacterial and antifungal properties, but it also enhances the penetration of both natural and synthetic antibiotics into tissues. This leads to higher local concentrations of antimicrobial agents at the site of infection or injury, improving their effectiveness where it matters most.
GHK-Cu, on the other hand, combats infection through a unique biochemical pathway. Studies have shown that GHK-Cu can reduce wound infection rates by up to 27%. It does so by interacting with fatty acids released from damaged tissue, forming a powerful antimicrobial complex that effectively targets both bacterial and fungal pathogens. This mechanism of action is different from that of TB500 and likely works synergistically with it to create an environment that is very hostile to microbial growth.
KPV actually has antimicrobial properties, though they have not been the focus of much research. KPV has known benefits against two of the most problematic pathogens to infect wounds: Staphylococcus aureus and Candida albicans. It is thought that KPV's ability to increase cellular cAMP levels improves the ability of cells in the immune system, particularly neutrophils, to respond to invading pathogens.
BPC-157 has no specific anti-microbial activity, but it does play a supporting role in preventing microbial growth. By increasing blood supply to a wounded area, BPC-157 helps to increase the penetration of immune system cells that fight off infection while simultaneously carrying away debris and damaged tissue that could foster microbial growth.
KLOW Anti-Aging Effects
Taken together, the combined benefits of BPC-157, TB500, GHK-Cu, and KPV in promoting tissue repair and reducing inflammation highlight their potent anti-aging properties. The human body relies on continuous repair and regeneration to maintain itself, but these processes gradually decline with age. This decline explains why recovery from injury slows down over time and why older individuals become more vulnerable to conditions such as infections, heart disease, and neurodegenerative disorders. Much of the aging process is driven by the breakdown of tissue repair mechanisms and the resulting chronic inflammation when these processes become dysregulated. This understanding suggests that by enhancing tissue repair and mitigating the adverse effects of impaired healing, we can potentially slow or even reverse aspects of aging. This principle underlies the widespread use of antioxidants and emphasizes the importance of exercise and diet in healthy aging. Ultimately, the aging process is influenced less by the initial damage itself and more by the body’s ability to recover from it.
TB500, in particular, is being investigated as a powerful tool in regenerative therapies, especially for addressing age-related tissue decline. Most adult organs, including the heart and brain, have very limited capacity to regenerate; for example, only about 0.5% to 2% of heart muscle cells renew, which is insufficient to recover from events like heart attacks or to combat gradual cell loss with aging. Enhanced regeneration is therefore critical to tackling these challenges. Research in mouse embryos has shown that TB500 plays a key role in cardiac cell migration and survival, while in adults, it promotes myocyte survival and improves cardiac function following coronary artery ligation. Additionally, TB500 activates epicardial progenitor cells, which serve as the source material necessary for heart repair. If this regenerative capacity can be harnessed, it holds the potential to significantly reduce cardiovascular disease, one of the leading causes of death worldwide. TB500 also exhibits strong anti-inflammatory effects. Monocytes produce TB500 sulfoxide in response to glucocorticoids, which inhibits neutrophil movement and suppresses inflammation. Furthermore, TB500 supports cell survival by reducing mitochondrial cytochrome c release, increasing levels of the anti-apoptotic protein BCL-2, and decreasing caspase activity. These protective effects are particularly important in conditions like sepsis, where excessive inflammation and F-actin accumulation in blood vessels contribute to tissue damage.
Beyond cardiovascular and inflammatory benefits, TB500 has shown promise in healing eye injuries and infections, such as corneal wounds and bacterial keratitis, as well as in supporting skeletal muscle regeneration. Phase 2 clinical trials have demonstrated its effectiveness in treating chronic skin wounds, including pressure ulcers and epidermolysis bullosa. Across these applications, TB500 has proven to be safe, well-tolerated, and a strong candidate for future regenerative medicine.
Similarly, BPC-157 offers cardiovascular benefits, improving blood flow to cardiac myocytes while reducing blood pressure and preventing blood clot formation—key factors that contribute to heart attacks. Research in mice indicates that BPC-157 lowers markers of necrosis and helps mitigate heart damage following injury, underscoring its potential role in preserving cardiac health and reducing cardiovascular risk. Thus, BPC-157 helps to prevent greater damage while TB500 promotes repair, resulting in vastly fewer long-term consequences following a cardiac insult. BPC-157 has been shown to have similar benefits in a number of tissues like the central nervous system, GI tract, kidneys, bladder, muscles, and bones. BPC-157 appears to be a universal healing peptide, helping to reduce inflammation and boost tissue regeneration throughout the body.
GHK-Cu is thought to suppress the activity of NFκB, provide a boost to DNA repair enzymes, and even enhance natural cell-cleaning processes carried out by proteasomes. Together, these effects enhance tissue repair—especially in vital organs like the heart—while simultaneously preventing excessive cell death and damage from occurring in the first place. GHK-Cu, in particular, has a broad influence on gene expression, modulating the activity of approximately 32% of human genes. It suppresses harmful genes linked to inflammation and tissue degradation, while promoting those involved in healing and regeneration.
GHK-Cu also reduces oxidative stress by neutralizing reactive oxygen species (ROS) and inhibiting pro-inflammatory cytokines such as TNF-α and interleukin-6. Additionally, it helps clear toxic byproducts of lipid breakdown, which are associated with conditions like diabetes and neurodegeneration. Animal studies have shown that GHK-Cu reduces brain inflammation and may modulate epigenetic pathways tied to cognitive decline.
Copper imbalances are implicated in neurodegenerative diseases including Alzheimer’s, Parkinson’s, and Wilson’s disease. GHK-Cu appears to regulate copper levels in the brain and prevent the aggregation of amyloid beta (Aβ), a key contributor to Alzheimer’s pathology. While it may not reverse existing plaques, GHK-Cu shows promise as a preventative agent.
An often overlooked but important aspect of KPV’s anti-aging effects lies in its action on the lungs. Though sometimes considered the “forgotten organ,” the lungs play a critical role in numerous regulatory processes and are essential for oxygenating the blood. Notably, the lungs are the primary site for converting angiotensin into angiotensin II, a powerful vasoconstrictor. Excess angiotensin II can lead to high blood pressure and stiffening of blood vessels—common features of aging. Several effective blood pressure medications work by blocking this conversion and have been linked to improved longevity and better recovery from cardiac injury. KPV’s ability to regulate inflammation in the lungs and prevent scarring indirectly supports heart and vascular health by promoting vascular flexibility and reducing arterial “hardening,” making it a potent anti-aging peptide in its own right.
Imagine the potential benefits of combining these peptides—each with vast anti-aging properties—to create a synergistic effect greater than any single peptide alone. Given their widespread impact on tissues throughout the body, this combination could not only extend lifespan but also significantly enhance overall health and well-being.
Summary
There is a tremendous amount to explore when it comes to BPC-157, TB500, GHK-Cu, and KPV—so much so that a single article can only scratch the surface of their full potential. Each of these peptides carries a wealth of unique properties and benefits, particularly in the realms of tissue repair, inflammation reduction, and protection against a broad spectrum of physiological insults. These range from acute events like heart attacks and strokes to chronic conditions including infections and neurodegenerative diseases. To truly appreciate their capabilities, it is highly recommended to delve into the individual profiles of each peptide, as doing so reveals just how powerful and multifaceted their effects can be.
While extensive research has been conducted on these peptides individually, their combined effects remain a frontier that has yet to be fully explored. Early evidence suggests that when used together, these peptides may interact synergistically, potentially amplifying their individual benefits in ways that could transform regenerative medicine and health optimization. Of particular significance is their emerging role in addressing the underlying mechanisms of aging. Aging is a complex, multifactorial process marked by declining cellular repair, increasing inflammation, and diminished resilience to stress and injury. BPC-157, TB500, GHK-Cu, and KPV each target different aspects of these processes, offering a multi-pronged approach to not only slow down but possibly reverse some aging-related changes at the cellular and systemic levels.
These peptides represent a groundbreaking glimpse into how modern science can go beyond simply extending lifespan, instead focusing on enhancing healthspan—the length of time that an individual remains healthy. They hold promise not just for healing injuries and combating disease but also for promoting overall vitality, resilience, and longevity.
For researchers and clinicians, the potential of these peptides opens exciting new avenues for investigation. Understanding how they work in concert—how their combined gene regulation, anti-inflammatory, regenerative, and protective effects interact—could unlock revolutionary treatments for tissue repair, chronic disease prevention, and anti-aging therapies. The future of medicine may well lie in harnessing such synergistic combinations to optimize human health at the molecular level, thereby offering people a better quality of life well into their later years.
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