| Pack Size | Single Vial, 10-Pack |
|---|
KPV is a synthetic tripeptide consisting of three amino acids — Lys-Pro-Val — corresponding to the C-terminal residues of α-melanocyte-stimulating hormone (α-MSH). The compound retains anti-inflammatory activity attributed to the parent hormone through cytokine-modulation pathways but does not engage the melanocortin receptors that mediate parent-hormone signalling. Research has investigated the compound across intestinal-inflammation, ulcerative-colitis, and inflammatory-bowel-disease model systems, with a literature spanning more than two decades. Every Ronin batch is independently verified by Janoshik Analytical using HPLC for purity and mass spectrometry for identity, with the minimum acceptance threshold set at 99 percent purity by HPLC. Supplied as a lyophilized powder in a sealed glass vial, 10 mg per vial. For laboratory research use only — not for human or veterinary use.
Description
KPV is a synthetic three-residue tripeptide whose sequence — Lys-Pro-Val, written one-letter as KPV — corresponds to the C-terminal three amino acids of the larger α-melanocyte-stimulating hormone (α-MSH) parent hormone. The α-MSH parent is a 13-residue post-translationally modified peptide derived from pro-opiomelanocortin (POMC), a precursor protein cleaved into multiple bioactive peptides including ACTH, β-endorphin, and the three melanocyte-stimulating hormones α-MSH, β-MSH, and γ-MSH.
The KPV tripeptide retains a portion of the parent hormone's anti-inflammatory activity but operates through a distinct mechanism. Whereas α-MSH binds the melanocortin receptors (MC1R through MC5R) to mediate its pigmentary, energy-balance, and anti-inflammatory effects, KPV does not engage these receptors. Research has characterised PepT1-mediated cellular uptake as the principal route by which KPV enters target cells, with downstream cytokine-modulation activity contributing to the compound's anti-inflammatory profile in intestinal and dermal research models.
The compound is supplied as a lyophilized white-to-off-white powder in a sealed amber-glass vial under inert gas. Each vial contains 10 mg of peptide. Reconstitution with bacteriostatic water is required before the peptide can be drawn into an insulin syringe. Researchers planning bench preparations should review the Reconstitution accordion below for mechanics.
KPV has been the subject of an expanding preclinical literature centred on intestinal inflammation, ulcerative colitis, and inflammatory bowel disease. A 2008 paper in Gastroenterology documented PepT1-mediated cellular uptake of KPV and reduction of intestinal inflammation in murine model systems (PMID 18061177). A 2008 paper in Inflammatory Bowel Diseases characterised the melanocortin-derived tripeptide in murine IBD model systems (PMID 18092346). A 2016 paper in Cellular and Molecular Gastroenterology and Hepatology examined the role of PepT1-mediated KPV delivery in colitis-associated cancer model systems (PMID 27458604). A 2017 paper in Molecular Therapy characterised hyaluronic-acid-functionalised nanoparticles for orally targeted KPV delivery in ulcerative colitis model systems (PMID 28143741). A 2021 paper in ACS Biomaterials Science and Engineering examined a self-cross-linked hydrogel format for KPV in TNBS colitis model systems (PMID 34547895).
Across the literature the compound appears under several alternate identifiers. KPV, the one-letter sequence representation, is the most common research-context name. α-MSH(11-13), referring to residues 11 through 13 of the α-MSH parent, is also used. The descriptive name Lys-Pro-Val tripeptide and CAS registry number 67727-97-3 anchor the canonical chemical identifiers.
No regulatory authority — Health Canada, the FDA, the EMA, the TGA, or any equivalent — has cleared KPV for therapeutic use in humans or animals. The compound has not progressed through a drug-approval pathway in any major jurisdiction, although the parent α-MSH has been investigated through Phase 2/3 clinical trials for select indications. Ronin Peptides ships the compound exclusively as a research-grade reagent for benchwork. Dosing protocols, treatment regimens, and administration instructions are out of scope and not provided in any form.
Mechanism in research literature
The mechanistic anchor for KPV is its anti-inflammatory activity through cytokine-modulation pathways. Unlike the α-MSH parent hormone — which binds melanocortin receptors (MC1R-MC5R) on target cells — KPV does not engage these receptors. The 2008 Kannengiesser paper in Inflammatory Bowel Diseases characterised the tripeptide as melanocortin-derived but receptor-independent in its anti-inflammatory profile (PMID 18092346).
PepT1-mediated cellular uptake is the principal route by which KPV enters target cells. PepT1 is an oligopeptide transporter expressed on the apical membrane of intestinal epithelial cells and, under inflammatory conditions, on additional cell types in the gut and other tissues. The 2008 Dalmasso paper in Gastroenterology documented PepT1-mediated uptake of KPV with downstream reduction of intestinal inflammation in murine colitis model systems (PMID 18061177). The 2016 Viennois paper extended the PepT1-mediated framework into colitis-associated cancer research (PMID 27458604).
Cytokine modulation following cellular uptake forms the downstream mechanism. Research has documented suppression of pro-inflammatory cytokines including TNF-α, IL-6, IL-1β, and IFN-γ in cell-culture and animal-model systems exposed to KPV, alongside upregulation of anti-inflammatory cytokines including IL-10 in some contexts. The cytokine-modulation profile is broadly consistent with the parent α-MSH's anti-inflammatory activity but does not require receptor binding.
Recent biomaterial-integrated research has produced novel delivery formats. A 2017 paper in Molecular Therapy characterised hyaluronic-acid-functionalised nanoparticles for orally targeted KPV delivery in ulcerative colitis model systems, observing improved colonic accumulation and reduced systemic exposure (PMID 28143741). A 2021 paper in ACS Biomaterials Science and Engineering examined a cysteamine-grafted γ-polyglutamic acid hydrogel format for KPV stabilisation in TNBS colitis model systems (PMID 34547895). The biomaterial-delivery work represents one active translation track for the compound.
Structure-activity relationship research has examined modifications to the KPV scaffold. A 2018 paper in PLoS One characterised reductive glycoalkylation of the lysine residue and its effect on the compound's pharmacological profile (PMID 29953505). The 2000 Cutuli paper characterised antimicrobial activity of α-MSH(11-13) — the same KPV sequence — alongside the parent hormone's antimicrobial profile (PMID 21222263). A 2020 paper compiled the broader α-MSH-derivative anti-inflammatory research literature (PMID 32945357).
Studied properties
Intestinal-inflammation and IBD research forms the largest application bracket for KPV. The 2008 Dalmasso PepT1-mediated mechanism paper anchored this stream (PMID 18061177). The 2008 Kannengiesser paper extended findings into broader IBD model systems (PMID 18092346). The 2016 Viennois paper documented benefits of PepT1-mediated KPV in colitis-associated cancer model systems (PMID 27458604). The pattern of consistent findings across multiple research groups has shaped KPV's research-context positioning as a candidate compound for combined-mechanism anti-inflammatory protocols.
Ulcerative colitis research forms a closely related second stream. The 2017 Xiao paper in Molecular Therapy characterised hyaluronic-acid-functionalised nanoparticles for orally targeted KPV delivery in ulcerative colitis model systems (PMID 28143741). The 2021 Sun paper extended biomaterial-integrated research into TNBS colitis model systems (PMID 34547895). These biomaterial-delivery findings address one of the practical challenges in KPV research — the tripeptide's susceptibility to proteolytic degradation in the gastrointestinal tract.
Dermal-inflammation research represents a third stream, building on the parent α-MSH's documented activity in dermal-inflammation model systems. KPV-specific dermal findings are narrower than the IBD literature but include cytokine-modulation observations in keratinocyte and dermal fibroblast cell-culture systems.
Antimicrobial research provides a fourth stream. The 2000 Cutuli paper documented antimicrobial activity of the α-MSH(11-13) sequence alongside the parent hormone's antimicrobial profile (PMID 21222263). The antimicrobial findings overlap mechanistically with the cytokine-modulation work in some interpretive frameworks but represent a distinct experimental endpoint.
Translation to human clinical application has been narrower than the breadth of the preclinical literature. The PepT1-mediated mechanism, the biomaterial-delivery research, and the consistent IBD findings collectively position KPV in an active expansion-era research stream. Recent broader peptide-therapy reviews (PMID 41966639, PMID 41490200) compile contemporary framings around the wider compound class.
Compound specifications
| Specification | Value |
|---|---|
| Common name | KPV |
| Alternate names | Lys-Pro-Val tripeptide; α-MSH(11-13); melanocortin-derived tripeptide |
| Molecular formula | C16H30N4O4 |
| Molecular weight | ~342.4 g/mol |
| CAS number | 67727-97-3 |
| Sequence (one-letter) | KPV |
| Sequence (three-letter) | Lys-Pro-Val |
| Length | 3 amino acids (tripeptide) |
| Parent hormone | α-melanocyte-stimulating hormone (α-MSH) |
| Mechanism niche | α-MSH C-terminal tripeptide; cytokine modulation; PepT1-mediated uptake |
| Form | Lyophilized white-to-off-white powder |
| Vial contents | 10 mg peptide, sealed amber-glass vial under inert gas |
| Purity | ≥99% by HPLC (verified per batch by Janoshik Analytical) |
Storage and handling
Unopened lyophilized vials hold up well under dry ambient storage; usable activity persists for several weeks even without refrigeration. Refrigeration at 2–8 °C is appropriate once the working timeline extends past a month. A standard freezer at −20 °C handles archival storage; ultra-low storage at −80 °C is rarely needed for typical bench-research timescales.
Keep vials shielded from light, ideally in their original outer packaging. Repeated temperature cycling accelerates degradation noticeably more than steady storage at any single temperature inside the recommended bands.
After reconstitution, refrigerate the solution at 2–8 °C without delay. The typical working window for a reconstituted preparation is four to six weeks at fridge temperature. The 0.9% benzyl alcohol in bacteriostatic water suppresses microbial growth but does not arrest hydrolysis, oxidation, or aggregation processes accumulating in any aqueous peptide solution. KPV's relatively short three-residue length makes it more susceptible to proteolytic degradation than longer peptides; researchers should attend to fresh-preparation practices and avoid extended room-temperature exposure.
When a research timeline extends past six weeks, common practice is splitting the reconstituted solution into single-use volumes and freezing them at −20 °C immediately. Ice-crystal formation during each freeze-thaw cycle inflicts mechanical damage on peptide chains. Thaw individual aliquots overnight in a refrigerator — never at room temperature.
The reconstituted product should be visually clear and colourless. Discard any vial showing turbidity, suspended particulate, yellowing, or visible precipitate. The diluent of choice is USP-grade bacteriostatic water containing 0.9% benzyl alcohol — see the bacteriostatic water product page for reconstitution-grade water.
Compare with similar compounds
| Compound | Primary research area | Documented mechanism (preclinical) | Format at Ronin |
|---|---|---|---|
| KPV | Anti-inflammatory; intestinal/dermal research | α-MSH C-terminal tripeptide; cytokine modulation; PepT1 uptake | 10 mg vial |
| BPC-157 | Tissue repair; gastric protection | VEGFR2-Akt-eNOS pathway; gastric cytoprotection | 10 mg vial |
| GHK-Cu | Skin remodelling; antioxidant | Cu(II) carrier; ECM remodelling; gene-expression modulation | 50 mg vial |
| KLOW Blend | Combined four-niche research | KPV + GHK-Cu + BPC-157 + TB-500 in one vial | 80 mg blend vial |
KPV occupies an anti-inflammatory mechanism niche distinct from Ronin's tissue-repair compounds (BPC-157, TB-500), the dermal-research GHK-Cu, and the GH-axis compounds. Researchers studying combined anti-inflammatory + tissue-repair protocols often examine KPV alongside one or more of the recovery-category compounds — see the KLOW Blend for a four-component format that pairs KPV with GHK-Cu, BPC-157, and TB-500.
Reconstitution and laboratory handling
A 10 mg vial of KPV reconstituted with 2 mL of bacteriostatic water yields a final concentration of 5 mg/mL, or 5,000 mcg/mL. Other diluent volumes scale linearly: 1 mL gives 10 mg/mL, 5 mL gives 2 mg/mL.
Reconstitution procedure:
- Bring both vials — peptide and bacteriostatic water — to room temperature before opening.
- Sanitise both rubber stoppers with an alcohol swab.
- Pull the chosen diluent volume into a sterile transfer syringe.
- Direct the water against the inner wall of the peptide vial as it is injected — never onto the lyophilized cake, since direct impact foams the solution and denatures peptide at the air-water interface.
- Invert slowly or swirl gently until everything dissolves. Do not vortex; do not shake.
- Refrigerate at 2–8 °C the moment reconstitution completes.
A finished preparation should be visually transparent with no suspended particulate. If the solution is hazy or contains visible material, treat it as degraded or contaminated and discard.
For dose-volume calculations on insulin syringes, use the Ronin peptide reconstitution calculator. The calculator pre-loads KPV with default reconstitution volumes and converts target doses to U-100 syringe units automatically.
In published preclinical research, KPV has been administered across rodent IBD model systems with oral, intraperitoneal, and intracolonic routes characterised across the literature (PMID 18061177, PMID 18092346, PMID 27458604). Biomaterial-integrated delivery formats have been characterised for nanoparticle and hydrogel-encapsulated KPV (PMID 28143741, PMID 34547895). These figures are research-reference only — Ronin Peptides does not provide dosing recommendations or administration instructions for any non-laboratory purpose.
Frequently asked questions
What is KPV?
KPV is a synthetic three-residue tripeptide (Lys-Pro-Val) corresponding to the C-terminal three amino acids of α-melanocyte-stimulating hormone (α-MSH). Research has investigated KPV across intestinal-inflammation, ulcerative-colitis, and inflammatory-bowel-disease research model systems. The compound's anti-inflammatory activity operates through cytokine-modulation pathways with PepT1-mediated cellular uptake, distinct from the parent α-MSH's melanocortin-receptor-mediated signalling. Ronin supplies KPV as a lyophilized vial reconstituted with bacteriostatic water at the bench. Sale is limited to laboratory research applications; human and veterinary use are excluded.
What does KPV stand for?
KPV is the one-letter sequence representation of the tripeptide — K for Lysine, P for Proline, V for Valine — written in three-letter code as Lys-Pro-Val. The compound is also referred to as α-MSH(11-13), reflecting its derivation from residues 11 through 13 of the α-melanocyte-stimulating hormone parent. The CAS registry number 67727-97-3 anchors the canonical chemical identifier.
How does KPV differ from α-MSH?
α-MSH is a 13-residue post-translationally modified peptide hormone that binds the melanocortin receptors MC1R through MC5R to mediate its pigmentary, energy-balance, and anti-inflammatory effects. KPV is just the C-terminal three residues of α-MSH (residues 11-13) and does not engage the melanocortin receptors. Instead, KPV's anti-inflammatory activity operates through PepT1-mediated cellular uptake and downstream cytokine-modulation pathways. The KPV tripeptide retains a portion of the parent hormone's anti-inflammatory profile but operates through a distinct mechanism.
What is the regulatory status of KPV?
No regulatory body — Health Canada, the FDA, the EMA, the TGA, or any equivalent — has approved KPV as a drug for human or veterinary use. The compound has not progressed through a drug-approval pathway in any major jurisdiction.
KPV is not listed as a scheduled controlled substance under the international drug-control conventions or under the major national scheduling systems. It sits within the regulatory layer covering laboratory reagents and research chemicals.
Ronin Peptides supplies the compound as a research-grade reagent for laboratory and bench-research applications. Buyers operate under their own jurisdictional laws and any applicable institutional review protocols when handling the compound — Ronin Peptides assumes no oversight of downstream lab practice.
How is KPV verified?
Each batch passes through Janoshik Analytical — an independent peptide-analytics lab — for HPLC purity quantification and MS identity confirmation, with the minimum acceptance threshold set at 99 percent purity by HPLC. Every Janoshik COA includes a verification key that resolves at janoshik.com. To pull the COA covering the batch on your order, email support@roninpeptides.ca from the address used at checkout, with your order number; the typical reply turnaround is well under 24 hours.
How is KPV reconstituted?
The standard preparation is 2 mL of bacteriostatic water added to a 10 mg vial, producing a 5 mg/mL solution. Inject the water against the inside wall of the vial — never directly onto the lyophilized powder. Swirl gently or invert slowly until fully dissolved (typically 30–60 seconds). Refrigerate at 2–8 °C immediately. Use the Ronin reconstitution calculator for non-standard volumes.
How do I receive the COA for my batch?
Email support@roninpeptides.ca from the email address used at checkout, with your order number (e.g., RP-CA-1234) and the compound name. We reply within 24 hours — typically the same business day — with the COA PDF attached. The COA includes the Janoshik verification key, which you can check independently at janoshik.com to confirm the test results match what the laboratory ran on your specific batch. COAs are not published publicly to protect supply-chain privacy and prevent competitor scraping.
References
- Cutuli M et al. Antimicrobial activity of the tripeptide α-MSH(11-13). J Leukoc Biol. 2000;67(2):233-239. PMID: 21222263 | doi:10.1189/jlb.67.2.233
- Dalmasso G et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166-178. PMID: 18061177 | doi:10.1053/j.gastro.2007.10.026
- Kannengiesser K et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008;14(3):324-331. PMID: 18092346 | doi:10.1002/ibd.20334
- Viennois E et al. Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV. Cell Mol Gastroenterol Hepatol. 2016;2(3):340-357. PMID: 27458604 | doi:10.1016/j.jcmgh.2016.01.006
- Xiao B et al. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles. Mol Ther. 2017;25(7):1628-1640. PMID: 28143741 | doi:10.1016/j.ymthe.2016.11.020
- Songok AC et al. Structural modification of the tripeptide KPV by reductive glycoalkylation. PLoS One. 2018;13(6):e0199686. PMID: 29953505 | doi:10.1371/journal.pone.0199686
- Lv S. α-MSH peptide and its derivatives in inflammatory pathology. Int J Mol Med. 2020. PMID: 32945357 | doi:10.3892/ijmm.2020.4701
- Sun J et al. Self-Cross-Linked Hydrogel of Cysteamine-Grafted γ-Polyglutamic Acid Stabilized Tripeptide KPV. ACS Biomater Sci Eng. 2021. PMID: 34547895 | doi:10.1021/acsbiomaterials.1c00792
- Mendias CL et al. Safety and Efficacy of Approved and Unapproved Peptide Therapies for Musculoskeletal Injuries. Sports Med. 2026. PMID: 41966639 | doi:10.1007/s40279-026-02437-0
- Rahman OF et al. Therapeutic Peptides in Orthopaedics. J Am Acad Orthop Surg Glob Res Rev. 2026. PMID: 41490200 | doi:10.5435/JAAOSGlobal-D-25-00236
