KPV Peptide 10 mg (Lys-Pro-Val; α-MSH C-Terminal Tripeptide)

$49.99

Buy KPV Peptide 10 mg Online from SourceTides. CAS 67727-97-3 | Lys-Pro-Val (H-Lys-Pro-Val-OH) | α-MSH C-terminal fragment (positions 11–13) | MW 342.43 g/mol | C₁₆H₃₀N₄O₄ | ≥99% HPLC purity | Endotoxin <1 EU/mg (LAL) | Full CoA | Lyophilised | Dry-ice cold chain. NF-κB + MAPK inhibition. PepT1-mediated intracellular delivery. Active at nanomolar concentrations. Oral efficacy in IBD colitis models (Dalmasso 2008; Gastroenterology). No melanocortin receptor activity. WADA not prohibited. For in-vitro laboratory research use only. Not for human consumption.

SKU: ST-KPV-10MG Categories: Immune Support & Inflammation Peptides, Peptides by Goal, Regenerative & Repair Peptides, Research Peptides

Description
Additional information

Buy KPV Peptide 10 mg Online | Lys-Pro-Val | α-MSH C-Terminal Fragment | ≥99% Purity | CoA | SourceTides

Buy KPV Peptide 10 mg Online from SourceTides.
KPV (Lys-Pro-Val; CAS 67727-97-3) is a synthetic tripeptide corresponding to positions 11–13 of alpha-melanocyte-stimulating hormone (α-MSH) — the C-terminal three amino acids of the parent tridecapeptide.
Despite containing just three amino acids and having a molecular weight of only 342.43 g/mol, KPV retains the powerful anti-inflammatory activity of full-length α-MSH while entirely lacking the receptor-binding sequence responsible for melanocortin effects on pigmentation, appetite, and arousal.
KPV operates through a mechanistically distinct pathway: it is transported into inflamed intestinal epithelial cells and immune cells by the PepT1 (SLC15A1) di/tripeptide transporter — a transporter that is dramatically upregulated during intestinal inflammation — and once inside, inhibits NF-κB and MAP kinase inflammatory signalling at nanomolar concentrations.
It is one of the very few research peptides for which oral bioavailability in the target tissue (inflamed colon) is actually enhanced by the disease state being studied.
Every SourceTides vial is lyophilised, tested at ≥99% HPLC purity, and ships with a full lot-specific Certificate of Analysis.
For in-vitro laboratory research use only. Not for human consumption.

KPV Peptide 10 mg — Technical Specifications

Parameter	Specification
Common Name	KPV (Lys-Pro-Val tripeptide)
Full Name	Lysine-Proline-Valine; α-MSH(11-13); C-terminal α-MSH tripeptide
CAS Number	67727-97-3
Molecular Formula	C₁₆H₃₀N₄O₄
Molecular Weight	342.43 g/mol
PubChem CID	73455
Peptide Length	3 amino acids (tripeptide); H-Lys-Pro-Val-OH; linear; all L-configured; free N- and C-terminus
Origin	C-terminal fragment (positions 11–13) of α-melanocyte-stimulating hormone (α-MSH; SYSMEHFRWGKPV); first identified as autonomous anti-inflammatory unit by Hiltz & Lipton (1989)
Key Structural Feature	Central proline residue imposes conformational rigidity; absent the His-Phe-Arg-Trp core sequence responsible for MC1R-MC4R binding — no melanocortin receptor activity at physiological concentrations
Primary Mechanism	NF-κB pathway inhibition; MAP kinase (MAPK/ERK/p38) suppression; PepT1-mediated intracellular delivery in inflamed epithelial and immune cells; pro-inflammatory cytokine reduction (TNF-α, IL-1β, IL-6)
Active Concentration (in vitro)	Active at nanomolar concentrations (10 nM shown to inhibit NF-κB in Caco2-BBE intestinal cells; Dalmasso et al. 2008)
PepT1 Transport	Transported into cells by PepT1 (SLC15A1); PepT1 is upregulated in inflamed colon in IBD — disease-enhanced tissue uptake; active in both intestinal epithelial cells and immune cells
Oral Viability	Orally active in IBD research models; tripeptide size allows PepT1-mediated intestinal uptake; oral delivery effective in DSS and TNBS colitis mouse models; gastric acid stable
Physical Form	White lyophilised powder; hygroscopic
Purity	≥99% (RP-HPLC); identity confirmed by ESI-MS
Endotoxin	<1 EU/mg (LAL chromogenic assay)
Solubility	Freely soluble in sterile water and PBS pH 7.4; 1–5 mg/mL stock recommended; hygroscopic — keep desiccated and sealed
Storage — Lyophilised	−20°C long-term (stable 24 months); 2–8°C short-term (up to 4 weeks); protect from moisture; equilibrate sealed vial to room temperature before opening
Storage — Reconstituted	2–8°C for up to 7 days; −20°C for longer; avoid freeze-thaw cycles; aliquot for single use
Certificate of Analysis	Lot-specific CoA with every order; HPLC chromatogram + MS data + endotoxin result
Regulatory Status	Not FDA, EMA, TGA, or Health Canada approved; research compound only; not a controlled substance in any jurisdiction
WADA Status	Not listed on the 2024–2025 WADA Prohibited List; not prohibited

What Is KPV?

KPV stands for Lysine-Proline-Valine — the three C-terminal amino acids of alpha-melanocyte-stimulating hormone (α-MSH). To understand what makes KPV scientifically important, you need to understand its parent molecule and why the trimming away of ten amino acids made something more useful, not less.

α-MSH is a 13-amino acid peptide produced by the pituitary gland and locally in skin keratinocytes. It is best known for driving skin pigmentation — but it also has powerful anti-inflammatory and immunomodulatory properties. The problem with α-MSH in research and potential therapeutic contexts is that its melanocortin receptor-binding sequence (the His-Phe-Arg-Trp core at positions 6–9) is responsible not only for its anti-inflammatory effects but also for all its other biological activities: melanin synthesis, appetite regulation, sexual behaviour, and cardiovascular effects through MC1R, MC3R, MC4R, and MC5R. This broad receptor activity makes α-MSH a poor tool for studying inflammation in isolation — every experiment is confounded by multiple parallel receptor-mediated effects.

KPV resolves this problem. When researchers in the late 1980s identified that the C-terminal fragment (positions 11–13: Lys-Pro-Val) of α-MSH retained potent anti-inflammatory activity, they also observed that this minimal sequence lacked the His-Phe-Arg-Trp melanocortin receptor binding core. Hiltz and Lipton (1989) confirmed that KPV produces anti-inflammatory effects comparable to — and in some assays stronger than — full-length α-MSH, while showing no melanocortin receptor activation. The 11-13 fragment was not merely a weaker version of the parent. It was a pharmacologically cleaner version: all the anti-inflammatory signal, none of the receptor-mediated hormonal noise.

The second discovery that elevated KPV’s research significance was made decades later: KPV is a substrate for PepT1 (SLC15A1), the intestinal di/tripeptide transporter. PepT1 is expressed throughout the small intestine under normal conditions. During intestinal inflammation — Crohn’s disease, ulcerative colitis — PepT1 expression is dramatically upregulated in the colon. This means KPV is more efficiently taken up by inflamed colonic epithelial cells and immune cells than by normal tissue. The disease state enhances the therapeutic delivery. This pharmacological behaviour is mechanistically unique and explains why oral KPV is effective in IBD research models despite being a tripeptide that would normally face significant degradation in the gut. When you buy KPV Peptide 10 mg from SourceTides, you receive ≥99% HPLC-pure Lys-Pro-Val with full lot-specific CoA for in-vitro research.

KPV vs α-MSH: Why the Smaller Fragment Is the Better Research Tool

Property	α-MSH (full-length)	KPV (C-terminal tripeptide)
Length	13 amino acids	3 amino acids
MW	1,665 g/mol	342.43 g/mol
Melanocortin receptor binding	Yes — MC1R, MC3R, MC4R, MC5R via His-Phe-Arg-Trp core	No — lacks the His-Phe-Arg-Trp binding pharmacophore; no MCR activity at physiological concentrations
Pigmentation effect (MC1R)	Yes — activates melanogenesis	None
Appetite / CNS effect (MC4R)	Yes — appetite suppression, arousal	None
Anti-inflammatory potency	Potent; active at nanomolar concentrations	Equally or more potent at NF-κB inhibition; active at nanomolar concentrations; independent of MCR
PepT1 transport	No — too large for di/tripeptide transporter	Yes — tripeptide size is the PepT1 substrate class; disease-enhanced uptake in inflamed colon
Oral efficacy in IBD models	Limited — larger peptide; systemic effects complicate GI research	Confirmed — oral KPV reduces DSS- and TNBS-induced colitis in mice (Dalmasso et al. 2008; Gastroenterology)
Research tool value	Multiple confounding MCR-mediated effects; difficult to attribute specific findings to anti-inflammatory mechanism	Clean anti-inflammatory probe; MCR-independent; ideal for dissecting NF-κB and MAPK pathways in isolation
Comparison with Melanotan-1	Full-length α-MSH is the parent of both; Melanotan-1 targets MC1R pigmentation + NER DNA repair; KPV targets inflammation independent of MC1R	Complementary research tools from the same parent molecule with completely different applications

How KPV Works — Mechanism of Action

Step 1 — PepT1-Mediated Cellular Entry: The Disease-Enhanced Uptake Mechanism

KPV’s entry into cells is the key to understanding its unique pharmacology. Most anti-inflammatory peptides act on cell-surface receptors — they bind from outside the cell and trigger intracellular signalling through receptor-coupled pathways. KPV works differently: it is actively transported into the cell by PepT1 (Peptide Transporter 1; SLC15A1) and then directly inhibits intracellular inflammatory signalling.

PepT1 is a proton-coupled oligopeptide transporter expressed on the apical membrane of small intestinal enterocytes. Its normal physiological function is to absorb dietary di- and tripeptides from the gut lumen — it recognises and transports any peptide of two or three amino acids, making KPV an ideal substrate. Crucially, PepT1 expression in the colon is minimal under normal conditions — but during intestinal inflammation (Crohn’s disease, ulcerative colitis), colonic PepT1 is strongly upregulated. This means KPV is preferentially taken up by inflamed tissue. The diseased colon is more permeable to KPV than healthy colon — a pharmacological property almost exactly opposite to most drugs, which face reduced bioavailability in inflamed tissue.

PepT1 is also expressed in macrophages, dendritic cells, and T-lymphocytes — and its expression in these immune cells is upregulated during inflammation. This means KPV is not only taken up by inflamed epithelial cells lining the gut, but also by the infiltrating immune cells driving the inflammatory response. This dual epithelial + immune cell uptake explains the breadth of KPV’s anti-inflammatory effects in IBD models: it reaches both the tissue barrier cells and the immune effectors causing the damage.

Step 2 — NF-κB Pathway Inhibition

Once inside the cell, KPV inhibits NF-κB (Nuclear Factor kappa-light-chain-enhancer of activated B cells) — the master transcriptional regulator of inflammatory gene expression. NF-κB controls the transcription of over 150 genes involved in inflammation, including TNF-α, IL-1β, IL-6, IL-8, COX-2, iNOS, and ICAM-1. In the resting state, NF-κB is held inactive in the cytoplasm by IκB (Inhibitor of kappa B) proteins. Pro-inflammatory stimuli (TNF-α, IL-1β, LPS) activate IKK (IκB kinase), which phosphorylates IκB and triggers its degradation, freeing NF-κB to translocate to the nucleus and drive inflammatory gene transcription.

KPV inhibits this pathway. In intestinal epithelial cells (Caco2-BBE and HT29-Cl.19A) and T-lymphocytes (Jurkat cells) stimulated with IL-1β, nanomolar concentrations of KPV reduced NF-κB activation as measured by a luciferase reporter assay — confirming intracellular NF-κB transcriptional inhibition, not just upstream receptor blockade. The landmark study (Dalmasso et al. 2008; Gastroenterology; PMC2431115) showed that 10 nM KPV significantly suppressed NF-κB activation and subsequent cytokine production (IL-8, TNF-α) in multiple human cell lines at concentrations achievable via PepT1-mediated uptake.

Step 3 — MAP Kinase (MAPK/ERK/p38) Pathway Suppression

Parallel to its NF-κB inhibition, KPV also suppresses the MAP kinase inflammatory cascade — specifically the ERK1/2 (extracellular signal-regulated kinase) and p38 MAPK pathways. Both of these kinase cascades are activated by inflammatory stimuli and feed into the same pro-inflammatory cytokine production that NF-κB drives, but through different transcription factor targets (AP-1, ATF2). By inhibiting both NF-κB and MAPK simultaneously, KPV produces a broader and more complete suppression of inflammatory gene expression than compounds that target only one pathway.

A 2025 study published in Toxicology confirmed that KPV inhibits the ERK/p38 MAPK pathway and caspase-1 activation in human keratinocytes (HaCaT cells) exposed to particulate matter (PM10) — extending the MAPK inhibition mechanism beyond intestinal research into skin and respiratory inflammation biology. This study showed KPV restored cell viability, reduced IL-1β secretion, and blocked ROS-driven MAPK activation at 50 µg/mL, demonstrating that the dual NF-κB and MAPK inhibition mechanism operates across multiple cell types and inflammatory stimuli.

Step 4 — Pro-Inflammatory Cytokine Suppression

The downstream consequence of NF-κB and MAPK inhibition is reduced production of all three primary inflammatory cytokines: TNF-α (the master cytokine of acute inflammation and IBD pathogenesis), IL-1β (the pyroptosis-initiating cytokine with roles in gut and skin inflammation), and IL-6 (the chronic inflammation mediator linking gut inflammation to systemic metabolic effects). KPV reduces the mRNA transcription and secreted protein levels of all three in multiple published cell models. In the DSS and TNBS colitis mouse studies (Dalmasso 2008; Kannengiesser 2008), oral KPV produced measurable reductions in colonic TNF-α, IL-1β, IL-6, and IL-12 at the tissue level — confirming that the in-vitro cytokine suppression translates to in-vivo anti-inflammatory tissue effects.

Step 5 — Colitis-Associated Cancer Protection (Colonic Tumorigenesis Prevention)

The most striking research finding for KPV beyond simple anti-inflammatory activity is its effect on colitis-associated cancer (CAC). IBD patients with long-standing colitis have a significantly elevated risk of colorectal cancer. The PepT1-KPV axis appears to play a role in preventing the inflammatory microenvironment that promotes colonic tumour development. Dalmasso et al. (2016; Cell Mol Gastroenterol Hepatol; PMC4957955) demonstrated that KPV dramatically reduced colonic tumorigenesis in an AOM/DSS mouse model of colitis-associated cancer — reducing tumour numbers, sizes, and overall burden. Critically, the anti-tumorigenic effect was completely abolished in PepT1-knockout mice, confirming that PepT1-mediated KPV uptake is essential for the cancer-protective effect. This finding places KPV at the intersection of GI inflammation research and colitis-associated cancer biology.

KPV Research Evidence

Research Area	Evidence Level	Key Finding	Source
Intestinal Inflammation — PepT1 Mechanism	In vitro (Caco2-BBE, HT29, Jurkat cells) + in vivo (DSS and TNBS colitis mice; oral KPV)	10 nM KPV inhibits NF-κB and MAPK in intestinal epithelial and immune cells; PepT1-mediated uptake confirmed; oral KPV reduces colitis severity (body weight loss, MPO, histology, cytokine mRNA) in two independent mouse colitis models	Dalmasso et al. 2008 — Gastroenterology — PMC2431115
IBD Models — Melanocortin-Derived Anti-inflammatory	In vivo (TNBS and DSS colitis mice; i.p. and intracolonic KPV)	KPV reduces colonic inflammation in two standard IBD mouse models; reduced colonic damage scores, MPO activity, and IL-1β, IL-6, TNF-α levels; confirms anti-inflammatory effect via multiple routes	Kannengiesser et al. 2008 — Inflamm Bowel Dis — PubMed PMID: 18215434
Colitis-Associated Cancer Prevention	In vivo (AOM/DSS murine colitis-associated cancer model; PepT1-KO vs WT mice)	KPV dramatically reduced colonic tumour number, size, and burden; effect abolished in PepT1-KO mice — confirms PepT1 dependence; identifies KPV as protective against IBD-associated carcinogenesis; PepT1 as therapeutic target for CAC	Dalmasso et al. 2016 — Cell Mol Gastroenterol Hepatol — PMC4957955
Nanoparticle-Enhanced Delivery (Proof-of-Concept)	In vitro + in vivo (nanoparticle-encapsulated KPV in colitis models)	KPV in nanoparticles (1 pmol/L) more effective than free KPV (100 µmol/L in drinking water) — ~100-million-fold dose reduction; hyaluronic acid-functionalized nanoparticles (272 nm) targeted inflamed colonic cells via CD44; demonstrates targeted delivery feasibility	Laroui et al. 2010 — Gastroenterology — PubMed PMID: 20600962
Skin / Keratinocyte Anti-inflammatory (2025)	In vitro (HaCaT human keratinocytes; PM10 exposure model)	KPV (50 µg/mL) restored cell viability, reduced IL-1β secretion, and inhibited ROS-driven ERK/p38 MAPK activation and caspase-1-driven pyroptosis in keratinocytes exposed to particulate matter; MAPK inhibition mechanism confirmed in skin cells	Zhang et al. 2025 — Toxicology — PubMed
KPV + FK506 Nanoparticle Combination (2024)	In vivo (acute and chronic colitis models; combined KPV + tacrolimus nanoparticle)	Combined KPV + FK506 in PepT1-targeted nanoparticles improved body weight, colon length, and disease activity index while reducing TNF-α, IL-1β, and IL-6 in both acute and chronic colitis models; demonstrates KPV as a combinable anti-inflammatory agent	Zhang et al. 2024 — Front Pharmacol — PubMed
Bronchial Epithelial Anti-inflammatory	In vitro (human bronchial epithelial cells; CALU-3 and 16HBE)	KPV inhibits cellular and systemic inflammation cues in bronchial epithelial cells; mechanism involves MC3R agonism in addition to NF-κB inhibition in this specific cell type; extends KPV anti-inflammatory research beyond GI into respiratory biology	Land SC 2012 — Int J Physiol Pathophysiol Pharmacol — PMC2095288
α-MSH Fragment Anti-inflammatory Discovery	Foundational in vitro and in vivo (Hiltz & Lipton 1989 + Catania et al. review)	Original identification of KPV as autonomous anti-inflammatory unit; KPV exerts similar or stronger anti-inflammatory activity than full α-MSH without MCR activation; first demonstration of MCR-independent melanocortin anti-inflammatory mechanism	Catania et al. 2007 — PMC2095288

The PepT1 System: Why KPV Is Unique in IBD Research

Most anti-inflammatory drugs face a pharmacological paradox in IBD: the inflamed gut is harder to reach. Mucosal barrier disruption, altered blood flow, increased luminal degradation, and immune infiltration all reduce drug bioavailability in the target tissue. KPV navigates this paradox in reverse — PepT1 upregulation in inflamed colon means more KPV is taken up by diseased tissue than healthy tissue. The disease itself enhances delivery to the target.

How PepT1 Expression Changes in IBD

Under normal conditions, PepT1 is expressed predominantly in the small intestine — its natural role is absorbing dietary peptides. The colon has minimal PepT1 expression. In IBD patients (both Crohn’s disease and ulcerative colitis), colonic PepT1 expression is strongly upregulated in both epithelial cells and infiltrating immune cells (macrophages, T-cells). This is not a subtle change — colonic PepT1 mRNA and protein are dramatically elevated in inflamed versus non-inflamed segments of the same IBD patient. Non-inflamed colon in IBD patients has near-normal PepT1 levels; the inflamed segments show the elevated expression.

This tissue-specific upregulation creates a natural targeting mechanism for KPV: the peptide selectively accumulates in the tissue compartments with the highest inflammatory burden. When Dalmasso et al. performed PepT1-knockout mouse experiments, oral KPV completely lost its anti-colitis efficacy — confirming that PepT1 transport is not merely one route of entry but the essential mechanism. Without PepT1, KPV cannot enter the cells where NF-κB inhibition needs to occur.

Implications for Research Design

The PepT1 dependence of KPV’s activity has important implications for experimental design. For maximum anti-inflammatory signal in intestinal research models: DSS or TNBS colitis induction (which upregulates colonic PepT1) will produce stronger KPV responses than non-inflamed intestinal cell culture. Oral delivery in colitis models will produce more relevant results than systemic injection for gut-targeted research — because oral KPV reaches the inflamed colon directly via luminal PepT1 uptake. For epithelial cell culture studies: Caco2-BBE cells (which express functional PepT1) are the validated cell line for KPV mechanistic studies; non-PepT1-expressing cell lines will require higher concentrations. For confirming PepT1 dependence: PepT1-knockout cells or PepT1 siRNA knockdown provides the definitive control — as demonstrated in the CAC study where the anti-tumorigenic effect was PepT1-dependent.

What Is KPV Used for in Research?

Research Field	Application	Why KPV
Inflammatory Bowel Disease (IBD)	DSS/TNBS colitis models; Crohn’s and UC cell models; mucosal healing; colon barrier function; cytokine profiling	Most extensively published anti-inflammatory peptide for intestinal research; two validated mouse colitis models; PepT1-mediated targeted delivery to inflamed colon; nanomolar active concentration; oral efficacy confirmed in vivo
NF-κB Biology	NF-κB pathway inhibition; IκB phosphorylation; cytokine gene transcription; NF-κB luciferase reporter assays	Active at 10 nM (extremely potent NF-κB inhibitor); MCR-independent mechanism allows clean pathway attribution; validated in multiple cell types; ideal probe for dissecting NF-κB from parallel inflammatory pathways
Colitis-Associated Cancer	AOM/DSS murine CAC models; colorectal carcinogenesis; tumour prevention; PepT1 oncology biology	Published RCT-level preclinical data showing KPV reduces CAC tumorigenesis (Dalmasso 2016); PepT1-dependent mechanism; connects IBD inflammation research to cancer biology; unique research compound at this mechanistic intersection
PepT1 Transporter Pharmacology	PepT1 substrate studies; transporter kinetics; IBD-induced PepT1 upregulation; targeted drug delivery research	KPV is the most published PepT1 substrate with documented anti-inflammatory activity; ideal probe for studying PepT1 transport biology and the therapeutic implications of intestinal inflammation-induced transporter upregulation
Skin Inflammation / Dermatology	Contact dermatitis models; keratinocyte inflammation; wound healing; pollution-induced skin inflammation; MAPK/NF-κB in skin cells	2025 keratinocyte data confirms ERK/p38 MAPK and caspase-1 inhibition; no pigmentation effects (unlike Melanotan-1); clean anti-inflammatory tool for skin research without MC1R confounders; complements BPC-157 for wound healing research panels
Nanoparticle Drug Delivery	PepT1-targeted nanoparticle design; colon-targeted delivery; dose reduction studies; encapsulation efficacy	100-million-fold dose reduction via nanoparticle encapsulation documented (Laroui 2010); hyaluronic acid-KPV nanoparticles validated; KPV is the canonical payload for PepT1-targeted colonic nanoparticle research
Respiratory Inflammation	Bronchial epithelial inflammation; airway hyperresponsiveness; pulmonary cytokine biology	Published data in human bronchial epithelial cells (Land SC 2012); extends beyond GI to respiratory biology; MC3R agonism in this tissue type adds receptor dimension not seen in gut cells
Gut-Brain Axis Research	Gut inflammation and neuroinflammation connections; vagal afferent signalling; intestinal cytokine-brain axis	KPV’s origin in α-MSH connects gut and neuroendocrine biology; studied alongside DSIP and Selank Amidate in gut-brain axis neuroinflammation panels

KPV Pharmacokinetics and Experimental Considerations

Parameter	Value / Notes	Research Implication
Active In-Vitro Concentration	10 nM for NF-κB inhibition in PepT1-expressing intestinal cells; 50 µg/mL (~146 µM) for MAPK inhibition in keratinocytes; variable by cell type and endpoint	Run full dose-response (1 nM – 10 µM) in your specific cell system; PepT1-expressing cells (Caco2-BBE, HT29-Cl.19A) require lower concentrations than non-expressing cells; confirm PepT1 expression status of your cell line before comparing to published data
Plasma Half-Life	Short — tripeptides are rapidly degraded by plasma peptidases; in-vivo effects outlast circulating peptide due to intracellular accumulation via PepT1; exact half-life not formally characterised	Measure intracellular endpoints (NF-κB reporter, cytokine mRNA, phosphorylation states) 30–120 minutes after addition; for in-vivo colitis models, endpoint measurement (histology, MPO, cytokines) at 24–72 hours reflects sustained intracellular effects
Routes of Administration (research)	Oral (validated in colitis models — most relevant for IBD research); SC/IP injection (for systemic anti-inflammatory endpoint studies); topical (for skin research; active in wound healing and dermatitis models); intracolonic (for direct mucosal delivery studies)	Choose oral for IBD/gut-targeted research — PepT1 transport is the primary delivery mechanism and is active via oral route; choose SC/IP for systemic inflammatory endpoint studies; choose topical for skin inflammation research
Oral Dose in Colitis Models	1–1000 µg/mouse/day in drinking water or by gavage (published range); Laroui 2010 nanoparticle study achieved 1 pmol/L equivalent; free KPV requires higher concentrations due to luminal degradation	Free KPV: start at 10 µg/mouse/day via gavage; establish dose-response from 1–1000 µg/day; nanoparticle formulation dramatically reduces required dose if targeted delivery is the research question
Gastric Acid Stability	Reasonably stable at gastric pH 1–2; tripeptide size and Pro residue provide some conformational protection; some degradation by intestinal peptidases expected — mitigated by PepT1 uptake at intestinal epithelium	Oral route is viable for intestinal research; for maximum mucosal bioavailability, consider enteric-coated delivery or nanoparticle encapsulation in experimental designs requiring very low doses
Cell Line Selection	PepT1-expressing: Caco2-BBE (best validated), HT29-Cl.19A, primary human colonocytes; Immune cells: Jurkat (T cells), THP-1 (macrophages); Non-PepT1: use as controls for PepT1-dependence confirmation	Always confirm PepT1 expression in your cell line before assuming published nanomolar concentrations apply; non-PepT1-expressing cells require micromolar concentrations for equivalent effect — which is useful as an internal negative control for mechanism confirmation

KPV Side Effects and Safety Profile

Important: KPV is not approved by the FDA, EMA, TGA, or Health Canada. No human clinical trials have been completed. All safety data comes from in-vitro cell studies and rodent models. SourceTides supplies KPV for in-vitro laboratory research use only. Not for human consumption.

Concern	Evidence	Protocol Note
No adverse effects reported in published studies	No adverse events documented in any published KPV animal study; excellent tolerability in all colitis mouse models; no toxicity signals at any dose tested in published literature	KPV is an endogenous tripeptide fragment of a naturally occurring hormone — the body already produces and processes it; metabolites (Lys, Pro, Val) are standard amino acids with no toxicity
No melanocortin receptor activity	Confirmed lack of MCR binding at physiological concentrations (lacks the His-Phe-Arg-Trp pharmacophore); no pigmentation, appetite, or sexual side effects — distinct from parent α-MSH and Melanotan-1	Clean safety advantage over full-length α-MSH analogs; pigmentation and CNS confounders absent from KPV research designs
Hygroscopicity handling risk	Highly hygroscopic lyophilised powder; moisture absorption causes dosing inaccuracy	Equilibrate sealed vial to room temperature before opening; weigh quickly; reseal immediately; use desiccant; same protocol as other hygroscopic tripeptides (Pinealon, Thymalin)
Critical data gap: no human safety data	No human clinical trials completed; all evidence from in-vitro and rodent studies; formal toxicology battery not published	Treat as a preclinical research compound with a favourable animal safety profile but insufficient human characterisation; appropriate for in-vitro research and well-designed preclinical models
WADA not prohibited	Not on 2024–2025 WADA Prohibited List; no performance-enhancing mechanism identified	Verify WADA list annually; list updated each year

KPV Quality Control at SourceTides

Every batch of KPV Peptide 10 mg from SourceTides passes these tests before release. The endotoxin specification is critical for KPV specifically — LPS contamination activates NF-κB, the exact pathway KPV is studied for inhibiting, making endotoxin the most important confounder for this compound’s primary research application.

Test	Method	Specification	Why It Matters
Purity	RP-HPLC (C18; UV 220 nm)	≥99% peak area purity	KPV synthesis produces Lys-Pro (KP dipeptide) and Pro-Val (PV dipeptide) as common by-products; these lack the full anti-inflammatory sequence and reduce specific activity if present above 1%; ≥99% confirms correct tripeptide dominates
Identity	ESI-MS ([M+H]⁺ = 343.44 Da)	Confirmed MW 342.43 g/mol; H-Lys-Pro-Val-OH sequence	Confirms correct tripeptide identity vs dipeptide by-products (KP at 243 Da; PV at 215 Da); also distinguishes from the related K(D)PT peptide (D-Pro substitution)
Endotoxin	LAL chromogenic assay	<1 EU/mg	The most critical QC parameter for KPV: LPS activates NF-κB and the MAPK cascade — both of which KPV is studied for inhibiting. Endotoxin contamination would confound every NF-κB reporter, cytokine ELISA, and inflammatory signalling assay by activating the pathway you are measuring KPV’s ability to suppress
Appearance	Visual inspection	White powder; no clumping, discolouration	Clumping indicates moisture absorption; discolouration indicates oxidation or contamination; both affect dosing accuracy and potency
Moisture	Karl Fischer titration	<5% w/w	Low moisture ensures dosing accuracy and prevents hydrolytic degradation of the Lys-Pro peptide bond (the most hydrolysis-prone bond in the sequence)
Cold-Chain Dispatch	Dry-ice packaging; temperature-logged	≤−20°C throughout	Maintains lyophilised peptide integrity; prevents hygroscopic moisture absorption during transit
Certificate of Analysis	Lot-specific PDF	HPLC + MS + endotoxin + moisture + dates	Required for GLP research environments; endotoxin specification particularly noted for NF-κB research use

KPV Regulatory Status

Jurisdiction	Status	Notes
USA (FDA)	Not approved; not a DEA controlled substance; research compound only	KPV has no approved indication in the USA. Not scheduled under the Controlled Substances Act. Sold as a research chemical for laboratory use only.
Australia (TGA)	Not listed on ARTG; research compound	Not registered as a therapeutic good. Laboratory research access only.
United Kingdom (MHRA)	Unlicensed; not a controlled drug; research compound	No MHRA marketing authorisation. Not listed under the Misuse of Drugs Act 1971.
Canada (Health Canada)	Unapproved new drug; research access only	Not a CDSA controlled substance. Not authorised for therapeutic sale.
European Union (EMA)	No EMA marketing authorisation; research use	No authorised medicinal product in any EU member state.
WADA	Not listed on the 2024–2025 WADA Prohibited List; not prohibited	No performance-enhancing classification. Not a melanocortin receptor agonist. Verify WADA list annually at wada-ama.org.

KPV vs Related Anti-inflammatory Research Peptides

Compound	Mechanism	Primary Research Focus	Key Difference vs KPV	SourceTides
KPV (this product)	NF-κB + MAPK inhibition; PepT1 transport; MCR-independent	IBD; intestinal inflammation; NF-κB biology; PepT1 pharmacology; colitis-associated cancer; skin inflammation	—	Buy KPV 10 mg
BPC-157	VEGFR2/NO/FAK; angiogenesis; tissue repair	GI cytoprotection; tendon/ligament; wound healing; mucosal barrier	Both have GI protective properties but via completely different mechanisms — BPC-157 via angiogenesis/NO, KPV via NF-κB/MAPK/PepT1; often studied together in gut inflammation and healing panels; BPC-157 is WADA-prohibited, KPV is not	Buy BPC-157 Capsules
Melanotan-1 (afamelanotide)	MC1R agonist; cAMP-CREB-MITF; NER DNA repair; melanogenesis	Photoprotection; EPP; melanogenesis; DNA repair; skin biology	Same parent molecule (α-MSH) but completely different fragment — Melanotan-1 carries the MC1R-binding His-Phe-Arg-Trp core; KPV lacks it entirely; complementary tools for dissecting melanocortin vs non-melanocortin anti-inflammatory mechanisms	Buy Melanotan-1 10 mg
Selank Amidate	GABAergic gene modulation; IL-6 suppression; BDNF; tuftsin-derived immunomodulation	Anxiety; neuroimmunology; neuroinflammation; IL-6 biology	Both modulate inflammatory cytokines (IL-6) but via different systems — Selank via CNS-immune axis, KPV via GI epithelial NF-κB/PepT1; studied together in neuroinflammation-gut axis research	Buy Selank Amidate 10 mg
Thymalin	Thymic polypeptide; T-cell differentiation; immunosenescence	Immune ageing; T-cell biology; immunosenescence	Both address immune function but at different levels — Thymalin restores T-cell production capacity, KPV directly suppresses active inflammatory signalling; complementary in IBD (where both dysregulated T-cell responses and NF-κB overactivation are pathogenic)	Buy Thymalin 10 mg

Peer-Reviewed References

#	Citation	Link
1	Dalmasso G et al. (2008). PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation. Gastroenterology. 134(1):166–178. PMID: 18061177.	PMC2431115 — Gastroenterology 2008
2	Dalmasso G et al. (2016). Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of KPV in a murine model. Cell Mol Gastroenterol Hepatol. 2(3):340–357. PMC4957955.	PMC4957955 — CAC / PepT1 2016
3	Kannengiesser K et al. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 14(3):324–331. PMID: 18215434.	PubMed PMID: 18215434
4	Laroui H et al. (2010). Nanoparticle-encapsulated KPV reduces colitis at 100 million-fold lower dose than free KPV in drinking water. Gastroenterology. 138(5):1672–1683. PMID: 20600962.	PubMed PMID: 20600962
5	Land SC. (2012). Inhibition of cellular and systemic inflammation in bronchial epithelial cells by melanocortin-related peptides; mechanism of KPV action and a role for MC3R agonists. Int J Physiol Pathophysiol Pharmacol. 4(2):59–73.	PMC3399072
6	Catania A et al. (2007). α-MSH related peptides: a new class of anti-inflammatory and immunomodulating drugs. Review covering KPV discovery, mechanisms, and C-terminal fragment autonomy. PMC2095288.	PMC2095288 — α-MSH Fragment Review
7	Xiao B et al. (2017). KPV loaded into hyaluronic acid-functionalized nanoparticles (~272 nm) targets inflamed colonic epithelial cells and macrophages. Molecular Therapy. 2017.	PubMed PMID: 27804996
8	Wikipedia: KPV tripeptide. Structure, function, anti-inflammatory mechanism, skincare research applications.	Wikipedia: KPV tripeptide
9	PubChem. KPV (Lys-Pro-Val). CID 73455. CAS 67727-97-3. National Library of Medicine.	PubChem CID 73455

Frequently Researched Alongside KPV

These compounds are commonly studied alongside KPV in gut inflammation, immune biology, and anti-inflammatory research:

BPC-157 Capsules — The most common research partner for KPV in gut biology; BPC-157 addresses tissue repair and angiogenesis (VEGFR2/NO pathway) while KPV addresses active inflammatory signalling (NF-κB/MAPK/PepT1 pathway); complementary mechanisms in IBD, mucosal healing, and gut barrier research
BPC-157 Injectable Vials — Injectable format for systemic gut and tissue repair research; paired with KPV in protocols studying combined anti-inflammatory and regenerative biology
Melanotan-1 10 mg — The MC1R-active complement to KPV from the same parent α-MSH molecule; studying KPV (MCR-independent anti-inflammation) and Melanotan-1 (MC1R-dependent photoprotection) together allows complete dissection of the α-MSH biological repertoire
Selank Amidate 10 mg — GABAergic anxiolytic with IL-6 suppression; studied alongside KPV in neuroinflammation-gut axis research where central (Selank/IL-6) and peripheral (KPV/NF-κB) anti-inflammatory mechanisms are studied together
Thymalin 10 mg — Thymic T-cell bioregulator; studied alongside KPV in IBD models where both T-cell dysregulation (Thymalin target) and epithelial NF-κB overactivation (KPV target) contribute to pathogenesis
Thymosin Alpha-1 — Thymic peptide with immune modulation and antiviral properties; studied alongside KPV in combined immune regulation and gut inflammation research panels
Pinealon 10 mg — Neuroprotective antioxidant via SOD2/GPX1; studied with KPV in gut-brain axis research combining intestinal (KPV) and CNS (Pinealon) anti-inflammatory endpoints
DSIP Peptide 5 mg — Sleep and antioxidant neuropeptide; studied with KPV in gut-brain axis protocols where gut inflammation (KPV target) and sleep/stress (DSIP target) intersect
Semaglutide — GLP-1R agonist; has independent gut anti-inflammatory effects via GLP-1 receptor on intestinal immune cells; studied alongside KPV in metabolic-inflammatory overlap research (NASH, obesity-associated gut inflammation)
LIPO-C Injectable — Multi-nutrient lipotropic; hepatic fat metabolism and gut health; studied with KPV in gut-liver axis research where intestinal inflammation (KPV) and hepatic lipid accumulation (LIPO-C) are co-studied as features of MASLD
NAD⁺ Injectable — Sirtuin substrate; SIRT1 has anti-inflammatory effects through NF-κB deacetylation and p65 activity suppression — mechanistically complementary to KPV’s direct NF-κB inhibition; studied together in inflammation-ageing intersection research

Frequently Asked Questions

You can buy KPV Peptide 10 mg (Lys-Pro-Val; CAS 67727-97-3) directly from SourceTides. Every order includes a lot-specific Certificate of Analysis with the RP-HPLC chromatogram (≥99% purity; confirms correct tripeptide vs dipeptide by-products), ESI-MS identity confirmation (MW 342.43 Da; H-Lys-Pro-Val-OH sequence), and the LAL endotoxin result (<1 EU/mg). All vials are lyophilised and dispatched on dry-ice cold chain. See the SourceTides shipping policy for dispatch details.

KPV and Melanotan-1 both derive from α-MSH (alpha-melanocyte-stimulating hormone), but they represent opposite ends of the parent molecule and have completely different biological activities.

Melanotan-1 (afamelanotide) retains the His-Phe-Arg-Trp melanocortin receptor binding core at positions 6–9 of α-MSH — the sequence responsible for MC1R activation, melanogenesis, eumelanin production, and NER-enhanced DNA repair. It is FDA-approved (as Scenesse) for EPP. It is WADA-prohibited.

KPV is positions 11–13 (the C-terminal end) — it lacks the His-Phe-Arg-Trp core entirely. It produces no melanocortin receptor activation at physiological concentrations. Instead, it works through a completely different mechanism: PepT1-mediated intracellular delivery and direct NF-κB / MAPK pathway inhibition. It is the clean anti-inflammatory tool from α-MSH biology, stripped of all pigmentation and hormonal activity. It is not WADA-prohibited.

For researchers: use Melanotan-1 when your question is about MC1R pharmacology, melanogenesis, or UV-DNA repair. Use KPV when your question is about NF-κB inflammatory signalling, gut inflammation, or PepT1-mediated delivery. Studying them together allows complete dissection of the α-MSH biological repertoire.

KPV has three properties that make it exceptionally well-suited for IBD research specifically — and each is mechanistically distinct.

First, PepT1-mediated delivery. PepT1 is the intestinal di/tripeptide transporter that is dramatically upregulated in inflamed colon in both Crohn’s disease and ulcerative colitis. KPV is a natural substrate for PepT1 — and because PepT1 is most active where inflammation is worst, KPV accumulates preferentially in the most inflamed tissue. This is drug-to-target self-targeting at the tissue level.

Second, intracellular NF-κB inhibition. Most anti-inflammatory biologics work at cell-surface receptors. KPV enters the cell via PepT1 and directly inhibits the NF-κB transcription factor that drives production of TNF-α, IL-1β, IL-6, and COX-2 — the core inflammatory genes in IBD pathogenesis. At nanomolar concentrations. That potency is extraordinary for a tripeptide.

Third, oral efficacy. The landmark Dalmasso et al. 2008 study (Gastroenterology; PMC2431115) showed that oral KPV reduced both DSS-induced and TNBS-induced colitis in mice — confirming that the PepT1 route delivers sufficient KPV to inflamed colonic tissue to produce measurable anti-inflammatory effects. This makes KPV orally viable for IBD gut research in a way that most anti-inflammatory peptides are not. SourceTides supplies KPV 10 mg for this specific research application.

For NF-κB luciferase reporter assays, cytokine ELISA (TNF-α, IL-1β, IL-6, IL-8), MAPK phosphorylation assays (ERK, p38), and cell viability studies, ≥99% HPLC purity is the minimum. Two quality issues are specific to KPV. First, dipeptide by-products (KP and PV) appear at 243 Da and 215 Da respectively — both easily detected by MS but requiring ≥99% HPLC to control below 1% of total peak area. These dipeptides may have some biological activity of their own, confounding KPV-specific interpretations if present above trace levels. Second, and most critically: endotoxin (<1 EU/mg by LAL). LPS activates NF-κB and the MAPK cascade — the exact pathways KPV inhibits. If your KPV preparation contains endotoxin, the LPS will activate NF-κB before KPV has a chance to inhibit it, and you will likely see no KPV inhibitory effect in your reporter assay — a false negative caused by endotoxin competition. Every SourceTides KPV 10 mg batch is tested to <1 EU/mg before release.

KPV can be purchased as a research compound in all major Western jurisdictions. It is not a controlled substance in any jurisdiction — it is a tripeptide fragment of a naturally occurring hormone. In the USA, it is not DEA-scheduled. In the UK, it is not controlled under the Misuse of Drugs Act 1971. In Australia, it is available as a laboratory research compound. In Canada, it is accessible for research use. KPV is not WADA-prohibited. SourceTides supplies for in-vitro laboratory research use only. See the SourceTides shipping policy for jurisdiction-specific dispatch information.

KPV has a focused but high-quality preclinical evidence base. The key published findings:

IBD — NF-κB and MAPK inhibition (Dalmasso 2008): 10 nM KPV inhibits NF-κB and MAP kinase inflammatory pathways in human intestinal epithelial cells and T-lymphocytes; PepT1 identified as transport mechanism; oral KPV reduces DSS- and TNBS-induced colitis in mice.

IBD — Colitis-associated cancer (Dalmasso 2016): KPV dramatically reduces colonic tumorigenesis in AOM/DSS cancer model; effect abolished in PepT1-knockout mice; identifies KPV as a CAC-protective agent with PepT1 as the target.

Nanoparticle delivery (Laroui 2010): KPV in nanoparticles is ~100-million-fold more effective than free KPV in drinking water — demonstrates dramatic dose reduction possible with targeted delivery.

Skin inflammation (2025): KPV inhibits ERK/p38 MAPK and caspase-1-driven pyroptosis in human keratinocytes exposed to particulate matter pollution.

Key limitation: No human clinical trials completed. All data is in-vitro and rodent models. All references on the SourceTides KPV product page.

Equilibrate the sealed vial to room temperature before opening to prevent condensation (KPV is hygroscopic). Dissolve lyophilised KPV in sterile water or PBS (pH 7.4) to a stock of 1 mg/mL (approximately 2.92 mM given MW 342.43). KPV dissolves readily in aqueous buffers — no organic cosolvent required. Filter through a 0.22 µm syringe filter before use in cell culture (the solution is already sterile from manufacturing, but filtration is standard practice). For NF-κB reporter assays and cytokine ELISAs in PepT1-expressing intestinal cells (Caco2-BBE): start with 1–100 nM working concentration; the published active concentration is 10 nM in these cells. For keratinocyte MAPK assays: 10–100 µg/mL working range (as in 2025 HaCaT study). For in-vivo colitis models (oral gavage): dissolve 1–100 µg in 200 µL sterile saline per mouse per day — this gives the range validated in published DSS/TNBS colitis protocols. Full reconstitution notes are in the CoA with every SourceTides KPV order.

KPV and BPC-157 are both studied for gut biology but through entirely different mechanisms — which is why they are frequently studied together rather than as alternatives. KPV is an anti-inflammatory agent: it suppresses NF-κB and MAPK inflammatory signalling in inflamed epithelial and immune cells via PepT1-mediated intracellular delivery. It directly reduces cytokine production and inflammatory gene transcription in the diseased gut. BPC-157 is a tissue repair agent: it promotes angiogenesis (VEGFR2/NO/FAK pathway), restores mucosal barrier integrity, accelerates wound healing, and has gastrointestinal cytoprotective effects from its gastric origin. KPV addresses the inflammatory signalling causing gut damage; BPC-157 addresses the physical repair of the damaged gut tissue. In IBD models, the ideal research combination studies both: KPV to suppress the inflammatory driving force, BPC-157 to promote mucosal healing of the damaged tissue. BPC-157 is WADA-prohibited (S0); KPV is not. SourceTides supplies both KPV 10 mg and BPC-157 capsules.

Yes — and this is one of KPV’s most distinctive research properties. Unlike most research peptides that require injection for systemic bioavailability, KPV can be administered orally and achieves therapeutic anti-inflammatory effects in the inflamed gut via PepT1-mediated uptake. The published evidence is direct: Dalmasso et al. 2008 demonstrated that orally administered KPV (in drinking water or by gavage) reduced both DSS-induced and TNBS-induced colitis in mice at the tissue level, measured by histological inflammation scores, myeloperoxidase activity, and colonic cytokine mRNA. The PepT1 transporter expressed in inflamed colonocytes takes up KPV directly from the gut lumen — bypassing the need for systemic absorption. For gut-targeted IBD research, oral administration is therefore not just convenient but pharmacologically justified as the most relevant delivery route. Note: for systemic anti-inflammatory endpoint studies (outside the GI tract), SC/IP injection provides more reliable and quantifiable systemic exposure. All SourceTides KPV 10 mg is supplied as lyophilised powder suitable for reconstitution for any of these routes.

SourceTides accepts Visa, Mastercard, American Express, cryptocurrency, and bank transfers for institutional orders. All payments go through secure, encrypted gateways. For institutional purchase orders, bulk research procurement, or custom quantities, contact the team via the SourceTides contact page. Orders are reviewed for research compliance before dispatch.

Research Use Only

All SourceTides products, including KPV Peptide 10 mg (CAS 67727-97-3; Lys-Pro-Val), are for in-vitro laboratory research use only. They are not approved by the FDA, EMA, TGA, or Health Canada. They are not for human consumption. By purchasing, the buyer confirms authorised researcher status and accepts responsibility for compliance with all applicable laws and regulations.

Weight	0.01 lbs
Dimensions	5 × 5 × 5 in
Purity	≥99% (HPLC-verified)
Size	10 mg
Form	Lyophilised Powder
CAS Number	67727-97-3

KPV Peptide 10 mg (Lys-Pro-Val; α-MSH C-Terminal Tripeptide)