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The word “inflammation” crops up a lot in health discussions, and that’s for good reason. Left unchecked, inflammation becomes a chronic health problem that spells serious trouble for your tissues and organs, immune function, and overall health. But inflammation stems from numerous possible causes, not all of which are under your control.
There’s a peptide, however, that might be able to police your body’s inflammatory response when you can’t. It’s called KPV.
In this guide, we explain how the KPV peptide works, break down the research into its effects, and discuss its availability to healthcare consumers.
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Our series on therapeutic peptides has taken us through articles on hundreds of clinical studies and other scientific sources on the subject, spread over more than 1,000 cumulative hours. KPV alone involved several dozen such sources and upwards of 30 hours. Along the way, we leaned on our relationships with people who know peptides on the ground level — both prescribers and patients. Although KPV isn’t an FDA-approved drug with widespread human use, these practical perspectives have allowed us to deduce its relative position in the larger peptide landscape.
Additionally, like all health-related content on this website, this guide was thoroughly vetted by one or more members of our Medical Review Board for accuracy and will continue to be monitored for updates by our editorial team.
KPV is a therapeutic tripeptide consisting of the amino acids lysine, proline, and valine (whose scientific abbreviations — K, P, and V — make up its name). Specifically, KPV is a fragment of alpha-melanocyte-stimulating hormone (α-MSH), a larger peptide with anti-inflammatory, antimicrobial, and fever-reducing properties.1 Even more specifically, the fragment in question is the C-terminal region of α-MSH, which is particularly good at neutralizing pathogens.2
While many therapeutic peptides are taken by needle, KPV stands apart in that it can also be administered as an oral capsule or chewable tablet. Its ability to be delivered through multiple routes may stem from a possible affinity for a peptide transporter, hPepT1, that occurs in the gastrointestinal tract.3 Researchers have also administered KPV topically or transdermally through technologies such as ionophoresis, which uses small electrical currents to drive the medication through the skin.4 There are even battery-integrated patches that use this technology.5 That being said, subcutaneous injection is likely the most rapid form of KPV drug delivery for systemic benefits.
KPV’s principal therapeutic value lies in its anti-inflammatory action. As your body’s natural response to harm from injury or illness, inflammation is essential for initiating the healing process. But when inflammation is severe or chronic, it becomes excessive and damages the body it’s meant to protect.6 Unless you get it back under control, it can contribute to serious health complications down the line — cardiovascular diseases, chronic obstructive pulmonary disease, cancer, and Alzheimer’s, to name a few.7 KPV’s role as a treatment is to prevent those complications from arising or worsening.
In addition, with its origins in α-MSH, KPV has demonstrated therapeutic value related to immune function, namely antimicrobial and wound-healing potential.
Of note, the research on KPV’s effects has been done primarily in animal models and human cell cultures, not in human subjects directly. Therefore, the support for its therapeutic uses is limited, albeit largely optimistic. Below, we discuss some of the most promising findings to date.
KPV’s anti-inflammatory mechanism of action isn’t fully understood, but it may have to do with a signaling pathway called NF-κB. In a 2012 study published in the International Journal of Physiology, Pathophysiology and Pharmacology, KPV was found to suppress NF-κB, which is known to induce the expression of inflammatory genes and regulate the survival, activation, and differentiation of inflammatory T cells.8 9 Having this suppressive property, KPV could be a potential treatment for serious inflammatory health conditions affecting the lungs or gastrointestinal tract, in which the NF-κB pathway plays a key role.8 10 Indeed, a 2017 study in a mouse model observed that KPV administration led to significant downregulation of TNF-α, a major cytokine encoded by the pro-inflammatory TNFA gene and which uses the NF-κB pathway.11 12
In 2000, the Journal of Leukocyte Biology published an in vitro study describing the effect that KPV (and α-MSH more broadly) could have on common pathogens. The pathogens in question were the bacterium Staphylococcus aureus and the fungus Candida albicans, which together account for nearly 150,000 infections and tens of thousands of deaths in the United States every year.13 14 The researchers found that even very small concentrations of the peptide not only killed significant amounts of these pathogens but also reduced their viability. Importantly, they noted that many anti-inflammatory drugs decrease the body’s immune function, but KPV doesn’t, concluding that its two-in-one action could be especially useful in the “treatment of disorders in which infection and inflammation coexist.”15
The melanocortin 1 receptor (MC1R) is a key protein for regulating skin and hair color, but it’s also expressed in cell types involved in cutaneous wound healing. Moreover, it has a high affinity for α-MSH, and researchers have theorized that this affinity, alongside MC1R’s other characteristics, is what allows KPV to promote faster wound healing.16 An earlier study, from 2006, demonstrated the extent to which the peptide could do so. In it, rabbits who’d had their corneas mechanically wounded were given topical applications of KPV four times per day and had their wounds measured. After four days’ treatment, the KPV-treated rabbits exhibited significantly smaller wounds compared to the control group, and cultures of their corneal epithelial cells were found to be stimulated after KPV exposure.17
The scientific literature says little about KPV’s safety profile, but there are concerns that it carries significant potential risks. From researchers, the most direct proclamation on the subject is found in the previously referenced 2017 mouse study, which described KPV as a “naturally derived tripeptide without any notable side effects,”11 but a weightier opinion given by the U.S. Food & Drug Administration (FDA) casts doubt on the study’s claim:
“FDA has not identified any human exposure data on drug products containing KPV administered via any route of administration. FDA lacks important information regarding any safety issues raised by KPV, including whether it would cause harm if administered to humans.”18
In other words, there have been no dedicated safety studies on KPV, so its status as a safe or unsafe therapy is up in the air. But notably, the FDA made this statement in a release about bulk drug substances (ingredients used to make medicines) that it considers to pose “potential significant safety risks,” so KPV’s lack of safety studies is a red flag in that regard.
Apart from its unclear safety profile, we can presume, based on our dealings with prescribers, that KPV administered subcutaneously can cause certain side effects that are common to most therapeutic peptide injectables: injection site reactions and mild, transient flu-like symptoms. We also know that certain populations — pregnant or breastfeeding women and people with a history of cancer — are contraindicated for peptide use.
Pharmaceutical-grade drugs meet high chemical purity standards and have been approved or indexed by the FDA as being fit for human consumption. Research-grade drugs do not meet such standards and so are intended for laboratory use only.
KPV is not an FDA-approved drug, so practically all commercially available KPV through an online vendor will undoubtedly be research-grade material that is not fit for human consumption. If consumed, its relatively high level of impurities will elevate the risk of immunogenicity (a state in which the body’s immune system interprets a substance as a danger and mounts a potentially life-threatening response against it).19
You might be able to get a prescription for pharmaceutical-grade KPV from a clinician, but you’ll first have to meet specific conditions. We discuss the matter further under “Where to find KPV” at the end of this guide.
No standard treatment protocol has yet been established for KPV, as it isn’t FDA-approved and few to no human trials have been conducted with it. The relatively scant number of reputable clinics that prescribe it may each have their own protocol that can’t be neatly homogenized here in summary. We can, however, deduce what the protocol is likely to be based on our findings in the existing literature, our familiarity with peptides in general, and the knowledge we’ve gained through relationships with prescribers and users of other therapeutic peptides:
As an injectable, KPV ought to come as a dry powder that must be reconstituted into a solution before use. The reconstitution process involves incorporating a measure of bacteriostatic water with the powder and gently mixing them together until the powder is dissolved.
In other forms (oral, topical), KPV should be good to go right out of the packaging — no preparation needed.
A standard KPV dose (injectable or oral) ought to start at around 0.2mg. That would be the human-equivalent dose of the amounts given to mice in the previously referenced study from 2017.12 Exact doses will depend on individual factors such as age, weight, and specific treatment circumstances.
For topical administration, a “dose” would be however much that minimally covers the target area.
KPV is likely to require daily administration, as in the previously referenced mouse and rabbit studies.12 17 As a preventive or a drug for managing chronic health conditions, treatment ought to be ongoing and may involve periodic breaks in dosing (cycling), which is common with many therapeutic peptides. But as a reactive treatment for acute inflammation, infection, or wounds, dosing should end once the condition has resolved.
Injectable KPV should be stored at a temperature of 4°C, or 39°F, per the U.K.’s National Institute for Biological Standards20 — in the refrigerator, that is. Oral or topical versions probably don’t need to be kept at such low temperatures but should at least be kept in a cool, dry environment.
We normally include information about a peptide’s timeline of benefits, but to do the same with KPV would require an unreasonable amount of unhelpful conjecture. We could say, for example, that KPV’s antimicrobial benefits take effect within two hours (as in the study from 2000),15 but in real-world use, the treatment itself would take place across a longer timeline whose exact length can vary from person to person, case to case.
Meanwhile, the user wouldn’t notice KPV’s benefits in the same way they would with a weight-loss or focus peptide, because its effects don’t manifest so visibly. At most, one might eventually acknowledge that they feel better compared to an earlier state, but that isn’t like seeing a lower weight on the bathroom scale or noticing increases in sustained cognitive effort. The only measurable data related to KPV’s benefits are inflammatory biomarkers, microbial counts, and wound sizes, but the average user probably doesn’t have the means or interest to record those.
In a world where KPV is a widely available prescription, the prime candidates for its use would be people with chronic inflammation, persistent bacterial or fungal infections, or stubborn wounds. Within these populations are people with risk factors that might make them better candidates than others, such as:
Other risk factors also contribute to the health conditions that KPV can help treat (e.g., poor nutrition, poor sleep, and smoking), but they’re more feasibly reversible with other interventions. That’s to say that a person would do better to fix their diet, take supplements to sleep better, and quit smoking than to take KPV to address the downstream effects of their lifestyle.
Additionally, like other therapeutic peptides, KPV is likely contraindicated for pregnant or breastfeeding women and people with a history of cancer.
More than a few online vendors offer KPV, but it’s highly unlikely that it’s a genuine pharmaceutical-grade peptide. What they’re really selling, probably, is research-grade material and just passing it off as pharma-grade. Remember, research-grade peptides are not suitable for human consumption, so taking stuff you bought online could lead to life-threatening circumstances.
Currently, as KPV remains on the FDA’s Category 2 list of restricted drugs, the only way to get the real deal is by qualifying for an exemption from the Federal Food, Drug, and Cosmetic Act.26 To do that, you have to meet at least two criteria:27
Your chances of fulfilling these criteria depend on your doctor’s willingness to have you try what’s effectively an experimental drug. To that end, there are reputable clinics in the United States that prescribe KPV and other restricted peptides, though they typically don’t deal in telemed or ship their treatments.
The FDA’s opinion on restricted peptides, not to mention the laws surrounding them, is subject to change. As more research is done, KPV may become more widely available. If that happens, we’ll update this guide accordingly and point you to the best pathways to prescription access.
Sources
Innerbody uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
Dall’Olmo, L., et al. (2023). Alpha-melanocyte stimulating hormone (α-MSH): Biology, clinical relevance and implication in melanoma. Journal of Translational Medicine, 21, 562.
Singh, M., & Mukhopadhyay, K. (2011). C-terminal amino acids of alpha-melanocyte-stimulating hormone are requisite for its antibacterial activity against Staphylococcus aureus. Antimicrobial Agents and Chemotherapy, 55(5), 1920-1929.
Viennois, E., et al. (2016). Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory pept1-mediated tripeptide KPV in a murine model. Cellular and Molecular Gastroenterology and Hepatology, 2(3), 340-357.
Pawar, K., et al. (2017). Transdermal iontophoretic delivery of lysine-proline-valine (KPV) peptide across microporated human skin. Journal of Pharmaceutical Sciences, 106(7), 1814-1820.
Zhou, Y., et al. (2023). An integrated Mg battery-powered iontophoresis patch for efficient and controllable transdermal drug delivery. Nature Communications, 14(1), 1-12.
Cleveland Clinic. (2024). Inflammation. Cleveland Clinic.
Pahwa, R., Goyal, A., & Jialal, I. (2023). Chronic inflammation. StatPearls [Internet].
Land, S. C. (2012). Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: Mechanism of KPV action and a role for MC3R agonists. International Journal of Physiology, Pathophysiology and Pharmacology, 4(2), 59-73.
Liu, T., Zhang, L., Joo, D., & Sun, S. (2017). NF-κB signaling in inflammation. Signal Transduction and Targeted Therapy, 2(1), 1-9.
Lu, D., & Zhao, H. (2020). Targeting NF-κB pathway for treating ulcerative colitis: Comprehensive regulatory characteristics of Chinese medicines. Chinese Medicine, 15, 15.
Xiao, B., et al. (2017). Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Molecular Therapy, 25(7), 1628-1640.
Hayden, M. S., & Ghosh, S. (2014). Regulation of NF-κB by TNF family cytokines. Seminars in Immunology, 26(3), 253-266.
U.S. Centers for Disease Control and Prevention. (2019). Vital signs: Epidemiology and recent trends in methicillin-resistant and in methicillin-susceptible Staphylococcus aureus bloodstream infections — United States. CDC.
U.S. Centers for Disease Control and Prevention. (2024). Data and Statistics on candidemia. CDC.
Cutuli, M., et al. (2000). Antimicrobial effects of alpha-MSH peptides. Journal of Leukocyte Biology, 67(2), 233-239.
Böhm, M., & Luger, T. (2019). Are melanocortin peptides future therapeutics for cutaneous wound healing? Experimental Dermatology, 28(3), 219-224.
Bonfiglio, V., et al. (2006). Effects of the COOH-terminal tripeptide α-MSH11–13 on corneal epithelial wound healing: Role of nitric oxide. Experimental Eye Research, 83(6), 1366-1372.
U.S. Food & Drug Administration. (2025). Certain bulk drug substances for use in compounding that may present significant safety risks. FDA.
De Groot, A. S., et al. (2023). Immunogenicity risk assessment of synthetic peptide drugs and their impurities. Drug Discovery Today, 28(10), 103714.
National Institute for Biological Standards and Control. (n.d.). Peptide handling, dissolution & storage. NIBSC.
Rosa, R. L., Johansen, H. K., & Molin, S. (2022). Persistent bacterial infections, antibiotic treatment failure, and microbial adaptive evolution. Antibiotics, 11(3), 419.
Guo, S., & DiPietro, L. (2010). Factors affecting wound healing. Journal of Dental Research, 89(3), 219-229.
Pugliese, G., et al. (2022). Obesity and infectious diseases: Pathophysiology and epidemiology of a double pandemic condition. International Journal of Obesity, 46(3), 449-465.
Khalid, K. A., et al. (2022). Aging and wound healing of the skin: A review of clinical and pathophysiological hallmarks. Life, 12(12), 2142.
Weyand, C. M., & Goronzy, J. J. (2016). Aging of the immune system. Mechanisms and therapeutic targets. Annals of the American Thoracic Society, 13(Suppl 5), S422-S428.
U.S. Food & Drug Administration. (2024). Bulk drug substances nominated for use in compounding under Section 503A of the Federal Food, Drug, and Cosmetic Act. FDA.
U.S. Food & Drug Administration. (2016). Prescription requirement under Section 503A of the Federal Food, Drug, and Cosmetic Act; Draft guidance for industry; Availability. FDA.