KPV Peptide: Complete Research Guide — Alpha-MSH C-Terminal Fragment, NF-κB Inhibition & IBD Model Data (2026)
- KPV (CAS: 65001-60-7; Lys-Pro-Val; MW: 356.44 Da) is a synthetic tripeptide representing amino acids 11–13 of α-melanocyte-stimulating hormone (α-MSH), the C-terminal tripeptide of the 13-amino acid neuropeptide. KPV retains α-MSH’s anti-inflammatory potency while completely lacking the melanocortin receptor binding sequence (His-Phe-Arg-Trp, positions 6–9) — making it the smallest known α-MSH-derived peptide with documented anti-inflammatory activity.
- KPV operates through a melanocortin-receptor-independent mechanism: it inhibits NF-κB activation at nanomolar concentrations in intestinal epithelial cells, T cells, macrophages, keratinocytes, and endothelial cells — without binding MC1R–MC5R, without elevating cAMP, and without producing melanogenesis pathway activity.
- Dalmasso et al. (2008) published the landmark mechanistic study in Gastroenterology demonstrating that KPV is transported into colonic epithelial cells via the PepT1 (SLC15A1) peptide transporter — which is upregulated specifically in inflamed colonic tissue in IBD research subjects — providing a disease-site-targeted oral delivery mechanism (PMID: 18061177). Oral KPV reduced DSS- and TNBS-induced colitis severity in mice.
- Viennois et al. (2016) published in Cellular and Molecular Gastroenterology and Hepatology (PMID: 27458604) that KPV dramatically reduced colonic tumorigenesis in a mouse model of colitis-associated cancer via PepT1, with no effect in PepT1-knockout mice, confirming PepT1 dependence.
- Research-grade KPV is available in a 10mg configuration (Research Use Only) with batch-specific COAs through the YPB catalog.
- ~8,000 monthly US searches; the smallest bioactive α-MSH fragment in the catalog; unique NF-κB and IBD research tool entirely distinct from BPC-157’s GI mechanism. Updated April 2026.
What Is KPV and What Makes It Unique Among Anti-Inflammatory Research Peptides?
Melanocortin-Receptor-Independent NF-κB Inhibition
PepT1-Mediated IBD Delivery Mechanism
KPV (Lys-Pro-Val; CAS: 65001-60-7; MW: 356.44 Da) is the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH), corresponding to amino acids 11–13 of the 13-residue neuropeptide. Updated April 2026. The discovery that this three-amino acid fragment retains potent anti-inflammatory activity independent of melanocortin receptor binding was a paradigm-shifting finding in α-MSH pharmacology — published by Hiltz & Lipton (1989) in FASEB Journal — establishing that the anti-inflammatory and the pigmentation/receptor-binding functions of α-MSH are carried by entirely different regions of the molecule. The melanocortin receptor pharmacophore sits at positions 6–9 (His-Phe-Arg-Trp); KPV at positions 11–13 has no binding affinity for MC1R through MC5R and produces no melanogenesis pathway activity.
This receptor independence is KPV’s defining research property. Where Melanotan II and PT-141 activate melanocortin receptors to produce their effects, KPV operates through a fundamentally different intracellular mechanism — direct NF-κB inhibition — that is not shared by any other compound in the YPB anti-inflammatory category. This makes KPV a distinct research tool from both the melanocortin receptor agonists and from GI-focused compounds like BPC-157 (VEGFR2/NO mechanism), addressing a specific molecular target — NF-κB — through a pathway that neither class can replicate.
Key Characteristics
| Parameter | Value |
|---|---|
| Chemical Name | L-Lysyl-L-prolyl-L-valine (Lys-Pro-Val) |
| Common Names | KPV; α-MSH(11–13); Lys-Pro-Val tripeptide; C-terminal α-MSH fragment |
| CAS Number | 65001-60-7 |
| Molecular Formula | C16H30N4O4 |
| Molecular Weight | 356.44 Da |
| Amino Acids | 3 (tripeptide; C-terminal sequence of α-MSH) |
| Half-Life | Short (unprotected tripeptide; susceptible to peptidase cleavage in plasma); in vivo activity supported by PepT1-mediated cellular uptake reaching intracellular NF-κB |
| Melanocortin Receptor Activity | None — does not bind MC1R–MC5R; does not elevate cAMP; no melanogenesis pathway activity |
| Primary Mechanism | NF-κB inhibition (p65/p50 nuclear translocation inhibited at nanomolar concentrations); MAP kinase pathway modulation; PepT1-mediated intestinal epithelial uptake |
| Transport Mechanism | PepT1 (SLC15A1) di/tripeptide transporter — normally expressed in small intestine; upregulated in inflamed colon in IBD; provides disease-site-targeted delivery |
| FDA Status | Not research-grade. Research Use Only (RUO). |
| WADA Status | Not listed on WADA Prohibited List 2025 (anti-inflammatory tripeptide; no GH-axis or melanocortin receptor activity) |
| Storage | Lyophilized: −20°C. Reconstituted: 2–8°C, use within 14 days |
| Research Context | IBD inflammation research; NF-κB pathway biology; dermatitis and skin inflammation; colitis-associated cancer models |
How Does KPV Work? The NF-κB Inhibition Mechanism
KPV’s anti-inflammatory mechanism operates at the transcription factor level — inhibiting NF-κB, the master regulator of inflammatory gene expression, without engaging any known membrane receptor. This intracellular mechanism explains why KPV remains active despite having no measurable melanocortin receptor affinity.
Direct NF-κB Inhibition at Nanomolar Concentrations
NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) is a transcription factor complex that controls the expression of hundreds of inflammatory genes including those encoding TNF-α, IL-1β, IL-6, IL-8, ICAM-1, and iNOS. Under basal conditions, NF-κB (primarily as the p65/p50 heterodimer) is sequestered in the cytoplasm by inhibitory IκB proteins. Pro-inflammatory stimuli (LPS, TNF-α, IL-1β) activate IκB kinase (IKK), which phosphorylates IκB proteins, targeting them for degradation and releasing NF-κB to translocate to the nucleus and activate inflammatory gene transcription.
Published data using NF-κB luciferase reporter constructs in human intestinal epithelial cells (Caco2-BBE, HT29-Cl.19A) and human T cells (Jurkat) documents that KPV inhibits NF-κB nuclear translocation at nanomolar concentrations under stimulation with TNF-α, IL-1β, and LPS. This inhibition reduces downstream TNF-α, IL-1β, IL-6, IL-8, and nitric oxide production in published cell culture studies. KPV also modulates the MAP kinase (MAPK) inflammatory signaling pathway, providing a second anti-inflammatory signaling mechanism (Dalmasso et al., Gastroenterology, 2008 — PMID: 18061177).
PepT1-Mediated Intestinal Targeting: The IBD-Specific Delivery Mechanism
KPV’s research significance in IBD biology was transformed by the Dalmasso et al. (2008) discovery that KPV is a substrate for PepT1 (SLC15A1, the intestinal di/tripeptide transporter). PepT1 is normally expressed at high levels in the small intestinal brush border and at low levels in healthy colon. During intestinal inflammation — specifically in IBD research subjects and in DSS/TNBS colitis mouse models — PepT1 expression is dramatically upregulated in the colonic epithelium. This means that orally used KPV is preferentially transported into colonic epithelial cells precisely at inflamed sites where PepT1 is overexpressed — creating a disease-site-targeted delivery mechanism that does not require nanoparticle formulation or chemical modification to achieve local colonic compound exposure (Dalmasso et al., Gastroenterology, 2008 — PMID: 18061177).
Subsequent work using PepT1 gene silencing confirmed that PepT1-mediated uptake is not merely facilitatory but necessary for KPV’s intestinal anti-inflammatory activity — when PepT1 expression was knocked down, KPV’s anti-inflammatory effects in colitis models were abolished.
What Systems Has KPV Been Investigated For?
KPV’s published research applications center on intestinal inflammation, skin inflammation, and general NF-κB biology — reflecting its anti-inflammatory mechanism across multiple tissue types where NF-κB is active.
Intestinal Inflammation and IBD Research Models
The most extensive published KPV research is in IBD models. Dalmasso et al. (2008) documented that oral KPV in drinking water (205 μg/day) reduced disease severity in both DSS-induced (dextran sulfate sodium) and TNBS-induced (trinitrobenzenesulfonic acid) colitis in C57BL/6 mice, with histological evidence of reduced mucosal inflammation and decreased pro-inflammatory cytokine expression at the colonic level. This data, published in one of the highest-impact gastroenterology journals, represents the primary preclinical evidence base for KPV in IBD research and has been extensively cited in subsequent IBD peptide compound delivery literature.
Colitis-Associated Cancer Research
Viennois et al. (2016) published a significant extension of the KPV/IBD literature in Cellular and Molecular Gastroenterology and Hepatology, demonstrating that KPV dramatically reduced colonic tumorigenesis in a mouse model of colitis-associated cancer (AOM/DSS model). Tumor numbers, sizes, and overall burden were decreased in KPV-treated wild-type mice. Critically, this anti-tumor effect was entirely absent in PepT1-knockout mice, confirming that PepT1-mediated delivery is the essential mechanism — and simultaneously validating PepT1 as a potential therapeutic target for colitis-associated cancer research (Viennois et al., Cell Mol Gastroenterol Hepatol, 2016 — PMID: 27458604).
Skin Inflammation and Dermatitis Research
KPV’s anti-inflammatory activity extends to skin tissue, where NF-κB is a central driver of inflammatory dermatoses. Published data documents NF-κB inhibition in human keratinocytes and dermal endothelial cells, reduction of contact hypersensitivity responses, and anti-inflammatory effects in dermatitis models. KPV’s lack of melanocortin receptor activity is a specific advantage in dermal research contexts where MC1R activation would confound experiments by simultaneously activating melanogenesis. Researchers studying skin inflammation without the pigmentation-pathway confound of full α-MSH or Melanotan II can use KPV to isolate the NF-κB anti-inflammatory mechanism.
Peritonitis and Leukocyte Migration Research
Larange et al. (2003, PMID: 12750433) published a mechanistic dissection of α-MSH anti-inflammatory fragments in a crystal-induced peritonitis model, confirming that KPV reduced accumulation of polymorphonuclear leukocytes in the peritoneal cavity. Importantly, this antimigratory effect was not blocked by the MC3/4 receptor antagonist SHU9119, further establishing that KPV’s anti-inflammatory activity is mechanistically independent of melanocortin receptor signaling.
What Does the Human Research Data Show So Far?
KPV does not have published human clinical trial data for synthetic KPV as a standalone compound. The evidence base is primarily preclinical (mouse colitis models) and in vitro (human cell lines). The parent compound α-MSH has been studied in human contexts, and KPV’s mechanism is derived from the α-MSH literature, but researchers should not attribute α-MSH human data to synthetic KPV specifically.
Human Relevance Summary
| Evidence Type | Study | Model | Key Finding | Adverse Events | Year |
|---|---|---|---|---|---|
| In vitro human cell cultures | Dalmasso et al. — NF-κB reporter assay | Human intestinal epithelial cells (Caco2-BBE, HT29-Cl.19A), T cells (Jurkat) | NF-κB luciferase activity inhibited at nanomolar KPV concentrations under TNF-α, IL-1β stimulation; PepT1-dependent uptake confirmed | In vitro; adverse event framework not applicable | 2008 |
| In vitro human cell cultures | Luger et al. / Brzoska et al. — NF-κB EMSA | Human dermal microvascular endothelial cells (HDMEC); human keratinocytes | KPV partially reduced NF-κB nuclear translocation in skin cells; K(D)PT showed stronger effect; effect independent of cAMP / melanocortin receptor | In vitro; adverse event framework not applicable | Published pre-2007 |
| Human IBD relevance | PepT1 expression in human IBD biopsies — Dalmasso et al. | Human colonic biopsies (IBD research subjects) | PepT1 expression significantly upregulated in inflamed colonic mucosa of IBD research subjects vs. healthy controls — establishing the in-human rationale for PepT1-mediated KPV delivery at disease sites | N/A (observational biopsy data; no KPV administration) | 2008 |
| Synthetic KPV human RCT | No published RCT as of April 2026 | N/A | No human interventional trial data for synthetic KPV in published literature as of April 2026 | N/A | N/A |
How Does KPV Compare to Other Anti-Inflammatory Research Peptides?
KPV occupies a unique position in the YPB catalog: the only compound with a primary NF-κB inhibition mechanism and PepT1-mediated intestinal targeting. It complements rather than competes with BPC-157 and other GI-focused compounds by addressing inflammation at the transcription factor level rather than through vascular or receptor signaling mechanisms.
| Parameter | KPV | BPC-157 | GHK-Cu | α-MSH |
|---|---|---|---|---|
| Origin | α-MSH C-terminal tripeptide (positions 11–13); no receptor binding sequence | Gastric juice BPC fragment; synthetic pentadecapeptide | Endogenous plasma tripeptide-copper; Pickart 1973 | POMC-derived neuropeptide; full 13-AA sequence |
| Melanocortin Receptor Activity | None — lacks His-Phe-Arg-Trp pharmacophore | None (VEGFR2 mechanism, not melanocortin) | None | Full MC1R–MC5R activity (all subtypes) |
| Primary Anti-Inflammatory Mechanism | NF-κB inhibition (p65/p50 nuclear translocation blocked at nanomolar); MAP kinase modulation | VEGFR2/NO pathway; local tissue repair; GI mucosa protection | Gene expression reprogramming (4,000+ genes including anti-inflammatory) | MC1R activation → cAMP → downstream NF-κB suppression (indirect) |
| GI/IBD Mechanism | PepT1-mediated uptake in inflamed colon; direct mucosal NF-κB inhibition; disease-site-targeted oral delivery | VEGFR2/NO-mediated GI mucosal repair; Phase 2 IBD trial ongoing | Not primarily GI-targeted | Systemic anti-inflammatory; no specific GI delivery mechanism |
| Melanogenesis Activity | None — no MC1R; no tanning effect | None | None | Full melanogenesis activity via MC1R |
| Published Human Data | In vitro human cell data (Caco-2, HT29, Jurkat, HDMEC); PepT1 upregulation in human IBD biopsies; no published human RCT | Phase 2 GI trial ongoing; no published human RCT results | Cosmeceutical topical data; dermal studies | Human pharmacology published; Vyleesi-class context (PT-141) |
| PubMed Publications | 100+ (KPV / α-MSH C-terminal fragment) | 800+ | 300+ | 2,000+ (full α-MSH) |
| Research-Grade Available? | Yes — RUO | Yes — RUO | Yes — RUO | Yes (research reagent) |
Researchers studying IBD and intestinal inflammation can use KPV for NF-κB inhibition research and PepT1-targeted delivery models, while using BPC-157 for GI mucosal vascular repair research — the two mechanisms are non-overlapping and can be combined for comprehensive intestinal inflammation research protocols. The GHK-Cu Research Guide covers the gene expression approach to anti-inflammatory research that complements KPV’s NF-κB targeted inhibition. Researchers cross-referencing melanocortin receptor pharmacology should see the Melanotan II Research Guide for the non-selective receptor agonist context from which KPV is deliberately differentiated.
What Should Researchers Know About KPV Stability and Handling?
KPV at 356.44 Da is the smallest peptide in the YPB catalog by molecular weight. As an unprotected linear tripeptide of all L-amino acids, it is susceptible to peptidase cleavage — a consideration that the PepT1-mediated cellular uptake mechanism partly addresses in the intestinal setting by getting the tripeptide inside cells before it can be fully degraded in the luminal environment.
Storage and Reconstitution
Lyophilized KPV is stable at −20°C for up to 24 months when protected from moisture and light. Its small size makes it highly water soluble and easy to reconstitute; bacteriostatic water is recommended. Once reconstituted, solutions should be held at 2–8°C and used within 14 days. KPV’s susceptibility to plasma peptidases means that in in vivo research protocols, route of administration significantly affects bioavailability and delivery to target tissues; the PepT1-mediated uptake mechanism is specifically relevant for oral/intestinal administration models.
COA Verification
At 356.44 Da, KPV is straightforward to verify by HPLC (≥98% purity) and MS confirmation at the correct molecular weight. L-amino acid configuration at all three residues should be confirmed. The small size means peptide synthesis yield is typically high and impurity profiles are simpler than for larger peptides. All YPB KPV batches include lot-traceable COA documentation accessible through the COA Library.
Key Research Findings: KPV in 2026
Key Research Findings
- NF-κB inhibition at nanomolar concentrations: Documented in human intestinal epithelial cells, T cells, macrophages, keratinocytes, and endothelial cells — the broadest cell-type coverage of any NF-κB inhibiting compound in the YPB catalog.
- Melanocortin-receptor-independent mechanism: KPV lacks the MC1R–MC5R binding pharmacophore (His-Phe-Arg-Trp); confirmed not to bind melanocortin receptors, not to elevate cAMP, and not to produce melanogenesis pathway activity.
- PepT1-mediated IBD targeting confirmed (Dalmasso 2008, PMID: 18061177): KPV is a PepT1 substrate; PepT1 is upregulated in inflamed human colon in IBD; oral KPV reduced DSS- and TNBS-colitis severity in mice via this mechanism.
- PepT1 dependence confirmed by knockout model: KPV’s anti-inflammatory effects in intestinal models were abolished in PepT1-KO mice, confirming PepT1-mediated transport as necessary (not merely facilitatory) for intestinal activity.
- Colitis-associated cancer reduction via PepT1 (Viennois 2016, PMID: 27458604): KPV reduced colonic tumorigenesis in AOM/DSS model in wild-type mice; effect absent in PepT1-KO mice.
- No published human RCT as of April 2026: All evidence is preclinical (mouse colitis models) or in vitro (human cell lines); human PepT1 upregulation in IBD tissue is observational, not interventional.
- Hiltz & Lipton (1989, FASEB J): Original characterization of KPV anti-inflammatory activity from α-MSH C-terminal fragment — foundational paper establishing melanocortin-receptor-independent inflammation biology for this class.
- Skin inflammation research: NF-κB inhibition documented in human keratinocytes and dermal microvascular endothelial cells without melanogenesis activity — distinct advantage for skin inflammation research where MC1R activation would confound experiments.
Browse the Full Research Catalog
Market Demand and Research Interest
KPV generates approximately 8,000 monthly US searches — a consistent audience of researchers studying IBD biology, NF-κB pharmacology, and the α-MSH peptide family.
Market Demand Indicators
| Demand Indicator | KPV Data Point |
|---|---|
| Monthly US searches | ~8,000/mo |
| PubMed publications (total) | 100+ (KPV / α-MSH C-terminal fragment) |
| Key publications (2008+) | Dalmasso 2008 (Gastroenterology, PMID: 18061177); Viennois 2016 (PMID: 27458604); nanoparticle delivery studies 2010–2022 |
| Human relevance signal | PepT1 upregulation confirmed in human IBD biopsy tissue — direct mechanistic rationale for IBD research translation |
| NF-κB niche | Only compound in YPB catalog with primary NF-κB inhibition mechanism — no direct competitor in this research space |
| Keyword difficulty range | Low competition (KD <10) |
| Research pairing | BPC-157 (VEGFR2/GI repair) + KPV (NF-κB/IBD) covers complementary intestinal research mechanisms |
How Can Researchers Offer KPV Under Their Own Brand?
KPV Wholesale Pricing & Margin Analysis
| SKU | Compound | Premier ($497/mo) | Core ($297/mo) | Suggested MSRP | Premier Margin |
|---|---|---|---|---|---|
| YPB.265 (RUO) | KPV (Lys-Pro-Val) 10mg | $43.27 | $51.92 | $120.00 | $76.73 (64%) |
Use the YPB Profit Calculator to model projected monthly revenue. KPV at Premier tier generates $76.73 gross margin per unit at $120 MSRP (64%). White-label brands offering both KPV and BPC-157 capture intestinal inflammation research buyers at both the NF-κB (KPV) and VEGFR2/GI repair (BPC-157) mechanism levels — the two most-researched molecular mechanisms in the GI anti-inflammatory peptide research space. Download the full catalog for all anti-inflammatory SKU pricing.
Methodology & Data Sources
Methodology & Data Sources
Scientific literature: PubMed searched for “KPV,” “Lys-Pro-Val,” “alpha-MSH C-terminal,” “MSH(11-13),” and CAS 65001-60-7. Search conducted through April 2026.
Key sources: Hiltz & Lipton (1989) FASEB J (foundational C-terminal anti-inflammatory characterization); Larange et al. (2003, PMID: 12750433) (peritonitis model, receptor independence); Dalmasso et al. (2008) Gastroenterology (PMID: 18061177, PepT1 mechanism, IBD models); Viennois et al. (2016) Cell Mol Gastroenterol Hepatol (PMID: 27458604, colitis-associated cancer); Luger et al./Brzoska et al. (NF-κB in skin cells).
Search volume data: Google Ads keyword data via DataForSEO, April 2026.
Pricing data: YPB Full Pricing Catalog, current as of April 2026. Margin calculated as MSRP minus Premier wholesale.
Limitations: No published RCT for synthetic KPV in human subjects. All efficacy data is preclinical (mouse colitis models) or in vitro (human cell lines). The PepT1 human biopsy data is observational, not interventional. This article is for educational purposes and does not constitute medical or research protocol advice.
References
- Hiltz, M. E., & Lipton, J. M. (1989). Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB J, 3(11), 2282–2284. (Foundational characterization of KPV anti-inflammatory activity.)
- Larange, A., Antonios, D., Pallardy, M., Kerdine-Römer, S., & Orsini, S. (2003). Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides. J Leukoc Biol, 74(2), 244–251. PMID: 12750433
- Dalmasso, G., Charrier-Hisamuddin, L., Nguyen, H. T., Yan, Y., Sitaraman, S., & Merlin, D. (2008). PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology, 134(1), 166–178. PMID: 18061177
- Viennois, E., Xiao, B., Ayyadurai, S., Wang, L., Wang, P. G., Zhang, Q., Chen, Y., & Merlin, D. (2016). Critical role of PepT1 in promoting colitis-associated cancer and potential wellness benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model. Cell Mol Gastroenterol Hepatol, 2(4), 340–357. PMID: 27458604
- Catania, A., Gatti, S., Colombo, G., & Lipton, J. M. (2004). Targeting melanocortin receptors as a novel strategy to control inflammation. Pharmacol Rev, 56(1), 1–29.
- Luger, T. A., Scholzen, T. E., Brzoska, T., & Böhm, M. (2003). New insights into the functions of alpha-MSH and related peptides in the immune system. Ann N Y Acad Sci, 994, 133–140.
- Brzoska, T., Luger, T. A., Maaser, C., Abels, C., & Böhm, M. (2008). Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory, and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases. Endocr Rev, 29(5), 581–602.
- Kannengiesser, K., et al. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of IBD. Inflamm Bowel Dis, 14(3), 324–331.
- Laroui, H., Dalmasso, G., Nguyen, H. T., Yan, Y., Sitaraman, S. V., & Merlin, D. (2010). compound-loaded nanoparticles targeted to the colon with polysaccharide hydrogel reduce colitis in a mouse model. Gastroenterology, 138(3), 843–853.
Frequently Asked Questions
KPV (Lys-Pro-Val; CAS: 65001-60-7; MW: 356.44 Da) is a synthetic tripeptide representing amino acids 11–13 of α-melanocyte-stimulating hormone (α-MSH). It is the smallest known α-MSH-derived fragment with documented anti-inflammatory activity. In research models, published data demonstrates KPV inhibits NF-κB nuclear translocation at nanomolar concentrations in human intestinal epithelial cells, T cells, macrophages, keratinocytes, and endothelial cells without binding melanocortin receptors or elevating cAMP. KPV is transported into inflamed colonic epithelial cells via PepT1 (SLC15A1), which is specifically upregulated in IBD; oral KPV reduced DSS- and TNBS-colitis severity in mice (Dalmasso et al., Gastroenterology, 2008, PMID: 18061177). No published human RCT as of April 2026. Research Use Only (RUO). Updated April 2026.
Full α-MSH (all 13 amino acids) activates MC1R through MC5R via its pharmacophore sequence His-Phe-Arg-Trp at positions 6–9, producing melanogenesis, appetite regulation, and immune modulation via receptor-cAMP signaling. Melanotan II is a cyclic analog retaining and amplifying this full melanocortin receptor activity. KPV (positions 11–13, Lys-Pro-Val) lacks the pharmacophore entirely: it has no measurable MC1R–MC5R binding affinity, does not elevate cAMP, and produces no melanogenesis pathway activity. Its anti-inflammatory activity operates through a different mechanism entirely — direct NF-κB inhibition in the cytoplasm after PepT1-mediated cellular uptake. The two activities of α-MSH (melanocortin receptor signaling and NF-κB inhibition) are carried by different regions of the molecule; KPV isolates the NF-κB mechanism as a pure research variable (Larange et al. 2003, PMID: 12750433).
PepT1 (SLC15A1) is a proton-coupled di/tripeptide transporter expressed in the small intestinal brush border at high levels, and at low levels in healthy colon. During intestinal inflammation (IBD, colitis), PepT1 expression is specifically upregulated in the inflamed colonic mucosa — a finding confirmed in both mouse colitis models and human IBD research subjects biopsies. Dalmasso et al. (2008) demonstrated that KPV is a PepT1 substrate and that oral KPV is preferentially transported into colonic epithelial cells specifically at inflamed sites where PepT1 is overexpressed. Subsequent PepT1 gene silencing experiments confirmed this transport is essential: without functional PepT1, KPV’s intestinal anti-inflammatory effects are abolished. This makes PepT1 upregulation in IBD a disease-site-targeted delivery mechanism — the inflamed tissue itself creates the preferential uptake condition (PMID: 18061177).
At 356.44 Da, KPV is the smallest peptide in the YPB catalog. As an unprotected linear tripeptide of all L-amino acids, it is susceptible to peptidase cleavage under physiological conditions — this explains the emphasis on PepT1-mediated cellular uptake as the delivery mechanism in published research, since intracellular delivery avoids the extracellular peptidase environment. Lyophilized KPV is stable at −20°C for 24 months. Reconstituted solutions should be held at 2–8°C and used within 14 days. Its small size confers high water solubility and simple reconstitution. COA verification requires HPLC purity (≥98%) and MS at 356.44 Da with L-amino acid configuration confirmation.
No published randomized controlled trial for synthetic KPV in human subjects exists as of April 2026. Human-level evidence is limited to: in vitro studies in human cell lines (Caco-2, HT29, Jurkat intestinal epithelial cells and T cells; HDMEC and keratinocytes for skin inflammation); and observational data from human IBD tissue biopsies confirming PepT1 upregulation in inflamed colon. The parent compound α-MSH has been studied in humans in other contexts, but this data cannot be attributed to synthetic KPV specifically. Researchers should treat KPV’s efficacy data as preclinical (primarily mouse colitis models) and its human relevance data as mechanistic (PepT1 upregulation confirmed in human IBD tissue). All YPB KPV is Research Use Only.
Yes. YourPeptideBrand.com provides white-label dropship for KPV in a 10mg configuration at $43.27 Premier wholesale, with a suggested MSRP of $120 generating $76.73 gross margin per unit (64% margin). White-label storefronts include pre-built RUO-compliant product pages with molecular data tables, NF-κB mechanism descriptions, PepT1 delivery context, and COA library links. Storefronts launch within 30 days with no inventory requirements. Use the profit calculator to model projected revenue.
Every KPV batch includes a lot-specific COA from an independent third-party laboratory: qualitative ID (HPLC + MS confirmation at 356.44 Da), HPLC purity (≥98%), L-amino acid configuration at all three residues (Lys, Pro, Val), endotoxin (<1 EU/mg), TAMC, and TYMC. KPV’s small size and all-L-configuration make it one of the simpler tripeptides to verify analytically. Documentation is accessible through the batch-specific COA library per order.
Premier tier members ($497/mo) access KPV 10mg at $43.27 wholesale, generating $76.73 gross margin per unit at the $120 MSRP (64% margin). Core tier ($297/mo) pricing is $51.92. White-label brands pairing KPV ($76.73) with BPC-157 10mg ($64.77 Premier margin) create a dual-mechanism GI anti-inflammatory research catalog covering NF-κB inhibition and VEGFR2/NO vascular repair — two non-overlapping intestinal inflammation mechanisms from a single GI research buyer audience. The combined two-SKU GI anti-inflammatory basket generates $141.50 margin per dual-order transaction at Premier pricing.
Key Takeaways
Research Takeaways
- Smallest bioactive α-MSH fragment: KPV (positions 11–13) is the minimal anti-inflammatory sequence of α-MSH, established by Hiltz & Lipton (1989) — the smallest peptide in the YPB catalog at 356.44 Da.
- Melanocortin-receptor-independent NF-κB inhibition: No MC1R–MC5R binding; no cAMP; no melanogenesis. NF-κB p65/p50 nuclear translocation blocked at nanomolar concentrations via a separate intracellular mechanism.
- PepT1-mediated disease-site-targeted delivery (Dalmasso 2008, PMID: 18061177): PepT1 is specifically upregulated in inflamed human colon in IBD; oral KPV is transported preferentially into inflamed colonic epithelium. PepT1-KO abolished KPV’s intestinal effects.
- IBD and colitis-associated cancer preclinical data: DSS- and TNBS-colitis severity reduced with oral KPV; colonic tumorigenesis reduced in AOM/DSS model (Viennois 2016, PMID: 27458604).
- No published human RCT as of April 2026 — all efficacy data is preclinical; human PepT1 upregulation in IBD tissue is observational.
- Complements BPC-157 in GI research: KPV (NF-κB inhibition, PepT1 delivery) and BPC-157 (VEGFR2/NO, mucosal repair) address non-overlapping intestinal mechanisms that can be combined in comprehensive GI protocols.
Business Takeaways
- $76.73 gross margin per unit at Premier tier (64%) — strong margin with unique NF-κB narrative and PepT1 IBD story.
- ~8,000 monthly searches at low KD — IBD research, NF-κB biology, and α-MSH fragment audiences combined.
- Only NF-κB inhibitor in YPB catalog — no competitor within the platform for this specific mechanism.
- KPV + BPC-157 GI pair = $141.50 combined margin per order; covers both primary intestinal inflammation research pathways from a single GI research buyer.
Ready to add KPV to your research catalog? Book a consultation with the YPB team.
[ypb_studies peptide=”kpv”]