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Research peptide — not a dietary supplement
KPV is a research compound, not a regulated dietary supplement. It is typically administered by injection and sold “for research use only.” The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most KPV studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2008–2019.
Based on 6 studies
Confidence
LowBy outcome
The current evidence for KPV is insufficient to assign an evidence score, based on 6 indexed studies. A grey-market research peptide with NO completed human trials — every efficacy result below is from mice, rats, or cells. KPV is the C-terminal tripeptide (Lys-Pro-Val) of α-melanocyte-stimulating hormone (α-MSH), and it carries α-MSH's anti-inflammatory activity without the pigment-inducing effect. In mouse and rat models of ulcerative colitis it consistently reduces gut inflammation, and reviews flag related melanocortin tripeptides as candidates for skin-wound healing. But KPV has never been tested in a completed human efficacy trial, it is not an approved drug or a lawful dietary supplement, and it is sold online as an unregulated research chemical with no quality control. Its human dosing, route, and long-term safety are unknown. This entry exists to inform, not to recommend. Representative study: PMID 18061177.
The commonly studied dose of KPV is No legitimate or recommended dose — KPV is an unapproved grey-market research chemical with no completed human dosing data and no quality control. We do NOT provide a dosing protocol. Published dosing is in rodents only (e.g. KPV added to drinking water, or targeted nanoparticle/hydrogel delivery in colitis models), which does not translate to a human dose. Note that KPV is sold online in mutually inconsistent forms — oral capsules, topical creams, and injectables — none validated in humans.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
PT-141
Mostly mechanism / observationalA melanocortin-receptor (MC4R) agonist peptide for low sexual desire. Important honest framing: unlike most 'research peptides', bremelanotide is an FDA-APPROVED prescription drug — Vyleesi, approved 2019 — for acquired, generalized hypoactive sexual desire disorder (HSDD) in premenopausal women, self-injected subcutaneously on-demand. It has real phase-3 RCTs (the RECONNECT program). The catch: the approved-trial benefit was statistically significant but small (a fraction of a point on desire scales), nausea is very common, and it transiently raises blood pressure. Grey-market 'PT-141' vials sold online are NOT the approved drug and are unregulated.
Last reviewed June 2026 · evidence from 6 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
KPV (Lysine-Proline-Valine, α-MSH 11-13)
A grey-market research peptide with NO completed human trials — every efficacy result below is from mice, rats, or cells. KPV is the C-terminal tripeptide (Lys-Pro-Val) of α-melanocyte-stimulating hormone (α-MSH), and it carries α-MSH's anti-inflammatory activity without the pigment-inducing effect. In mouse and rat models of ulcerative colitis it consistently reduces gut inflammation, and reviews flag related melanocortin tripeptides as candidates for skin-wound healing. But KPV has never been tested in a completed human efficacy trial, it is not an approved drug or a lawful dietary supplement, and it is sold online as an unregulated research chemical with no quality control. Its human dosing, route, and long-term safety are unknown. This entry exists to inform, not to recommend.
Every efficacy result is preclinical — consistent anti-inflammatory effects in mouse colitis models and cells — but there are zero completed human trials, so the score reflects an unproven, emerging compound.
KPV (Lys-Pro-Val) is the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH) — corresponding to residues 11-13, hence the alias α-MSH(11-13).
The therapeutic interest comes from the fact that this minimal fragment retains the parent hormone's anti-inflammatory activity while shedding its melanocortin-receptor pigment-inducing action: it dampens pro-inflammatory signalling (NF-κB and MAP-kinase pathways) and lowers cytokines such as TNF-α and IL-6 in inflamed epithelial and immune cells.
Much of the mechanistic work centres on the gut: KPV is a substrate of the di/tripeptide transporter PepT1, which is normally expressed in the small intestine and becomes upregulated in the inflamed colon during inflammatory bowel disease, so PepT1-overexpressing colonocytes actively concentrate KPV at the site of inflammation.
In well-described mouse models of colitis (dextran-sodium-sulfate [DSS] colitis, TNBS colitis, and CD45RB-high transfer colitis), oral or targeted KPV reduced weight loss, histological inflammation, myeloperoxidase activity, and pro-inflammatory cytokine expression; one study even showed that KPV's anti-tumour effect in a colitis-associated-cancer model was lost in PepT1-knockout mice, tying the benefit mechanistically to the transporter.
A large body of nanoparticle/hydrogel drug-delivery work (hyaluronic-acid nanoparticles, thermosensitive and self-cross-linked hydrogels) uses KPV as the active anti-inflammatory payload, again in rodent colitis.
Separately, dermatology reviews propose truncated α-MSH peptides including KPV as future candidates for cutaneous wound healing and skin ulcers, on the strength of in-vitro, ex-vivo, and animal data. Here is the honest, load-bearing caveat: ALL of the efficacy evidence is preclinical.
There is no completed published human trial of KPV — not a phase-I safety study, not a pharmacokinetic study, not an IBD or skin efficacy trial.
It is not approved by any regulator, it is not a lawful dietary-supplement ingredient, and the material sold online (as an oral capsule, a topical/cream, or an injectable for 'research use only') is an unregulated grey-market research chemical with no guarantee of identity, purity, or sterility.
Human dose, route, and long-term safety are entirely uncharacterised. The evidence here is therefore UNSCORED: a genuinely interesting rodent-and-cell anti-inflammatory story with zero completed human data, sandboxed out of all goal- and stack-based recommendations.
KPV, the C-terminal tripeptide of α-MSH, inhibits activation of the NF-κB and MAP-kinase inflammatory signalling pathways and reduces secretion of pro-inflammatory cytokines (e.g. TNF-α, IL-6) in stimulated intestinal epithelial and immune cells. Demonstrated in cell and rodent systems — never measured in humans.
KPV is a substrate of the di/tripeptide transporter PepT1, which is upregulated in the inflamed colon during inflammatory bowel disease. PepT1-expressing colonocytes and immune cells actively transport KPV into the cytosol, concentrating it where inflammation is greatest. Established in mouse and cell models, with no human confirmation.
As the minimal active fragment of α-MSH, KPV retains the hormone's anti-inflammatory and cytoprotective activity but lacks its pigment-inducing melanocortin action; some of its colitis benefit appears even when MC1R signalling is non-functional. This is the proposed route to wound-healing and anti-inflammatory effects — shown in vitro and in animals only.
How KPV works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
No legitimate or recommended dose — KPV is an unapproved grey-market research chemical with no completed human dosing data and no quality control. We do NOT provide a dosing protocol. Published dosing is in rodents only (e.g. KPV added to drinking water, or targeted nanoparticle/hydrogel delivery in colitis models), which does not translate to a human dose. Note that KPV is sold online in mutually inconsistent forms — oral capsules, topical creams, and injectables — none validated in humans.
Can be taken without food
| Form | Type |
|---|---|
| 💊None — unapproved grey-market research chemical | Recommended |
There is no legitimate pharmaceutical form. KPV is a research peptide used in cell and rodent studies; it is not a medicine or a dietary supplement.
Minimum: 1 weeks
Optimal: 1 weeks
Cycling: Not required
Note: No approved or validated timing — the compound has never completed a human trial. This library does not endorse or schedule its use.
Dose-response data unavailable. The current published research for KPV does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
There is no completed published human trial of KPV — no safety study, no pharmacokinetics, no IBD or skin efficacy trial. Every effect listed here is from mice, rats, or cells and may not translate to people.
In DSS-, TNBS-, and transfer-colitis models, KPV reduced weight loss, histological inflammation, myeloperoxidase activity, and pro-inflammatory cytokine expression. A consistent preclinical signal — not demonstrated in humans.
Targeted KPV delivery promoted colonic mucosal healing and restored epithelial barrier/tight-junction proteins in rodent colitis. Mouse-only finding.
Dermatology reviews propose truncated α-MSH peptides including KPV as candidates for cutaneous wound healing and skin ulcers, based on in-vitro, ex-vivo, and animal data. Hypothesis-stage — no human efficacy trial.
Human dosing, the optimal route (oral vs topical vs injectable are all sold), and long-term safety are entirely uncharacterised because no human has been studied. Grey-market material has no purity or sterility guarantees.
Avoid — there are no completed human trials, no approved use, and no quality-controlled product. The rodent evidence does not justify human self-experimentation.
Avoid self-sourcing — interactions with immunosuppressants/biologics are unstudied. Discuss any IBD treatment only with a gastroenterologist.
Avoid entirely — completely unstudied.
KPV is anti-inflammatory and has been studied alongside agents like cyclosporine A in colitis models. Combining it with prescription immunosuppressants or IBD biologics has never been studied in humans; additive immunomodulation is theoretically plausible and unpredictable.
There are no completed human drug-interaction data of any kind. Effects on inflammatory signalling in people are uncharacterised, so interactions cannot be predicted.
Tip: No human has completed a study of KPV — the side-effect profile in people is genuinely unknown. This is itself the warning.
Tip: KPV is sold as a 'research-use-only' injectable with no sterility assurance; self-injection of non-sterile grey-market material risks infection and contamination.
Tip: Grey-market material has no identity/purity/sterility guarantees; contaminants are possible.
Timing is flexible for KPV — consistent daily use matters more than the time of day. There is no validated human dosing schedule because the compound has never completed a human trial.
KPV should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are unknown human side-effect profile, infection / contamination from injectable use, harm from an unregulated, impure product. Use caution if any of these apply to you: Not an approved medicine and not a regulated dietary supplement — unapproved grey-market research chemical; do not self-source; No completed human safety data exists — every safety conclusion would be an extrapolation from rodents; Pregnancy and breastfeeding (entirely unstudied).
Gonadorelin
Mostly mechanism / observationalA synthetic copy of gonadotropin-releasing hormone (GnRH), the hypothalamic decapeptide that drives the pituitary to release LH and FSH. Honest appraisal: it has genuine, trial-backed roles as a diagnostic agent (the GnRH/gonadorelin stimulation test) and — delivered in pulses by an infusion pump — for inducing ovulation in hypothalamic amenorrhea and spermatogenesis in men with congenital hypogonadotropic hypogonadism. Its now-trendy use in men's TRT clinics (compounded, to 'maintain testosterone/fertility' alongside testosterone, often replacing hCG) is largely off-label and has NOT been validated in controlled trials for that purpose.