Research and informational content only. Not medical advice. Many peptides discussed on this site are not approved for human use.
KPV
Research PeptideAlso known as: Lys-Pro-Val · α-MSH(11-13) · alpha-MSH C-terminal tripeptide · MSH 11-13
Animal Only
All therapeutic claims for KPV are derived from animal and in vitro studies: mouse colitis models (DSS-, TNBS-, and AOM/DSS-induced), rabbit corneal wound-healing models, and human-derived cell lines in vitro. The two research groups that produced most of the KPV-specific literature (the Catania lab at Milan for α-MSH fragment anti-inflammatory signaling, and the Merlin lab at Georgia State for PepT1-mediated colitis work) do most of the heavy lifting, and independent replication of the headline therapeutic findings has not been identified. A separate identity risk compounds the evidence problem: some vendors sell the N-acetylated, C-amidated form (Ac-KPV-NH2, ~383 Da) under the same "KPV" label as the free acid (H-KPV-OH, ~342 Da), these are structurally different compounds with different properties, and buyers cannot distinguish them without mass-spectrometry confirmation. KPV is for research use only and is not for human or animal consumption.
KPV is a fragment of α-MSH, but it is NOT Melanotan, and the mechanism is completely different
Online discussions routinely treat KPV as 'like Melanotan' or 'a type of MSH peptide', a framing that is mechanistically wrong and masks KPV's actual anti-inflammatory mechanism. KPV is the C-terminal tripeptide of α-MSH (residues 11–13), but it does NOT activate MC1-R, MC3-R, or MC4-R at pharmacological concentrations, demonstrated directly in MC1-R-deficient mice (where KPV's anti-inflammatory effect was preserved) and via MC3/4-R antagonist blockade (which also did not block the effect). KPV's documented anti-inflammatory mechanism is PepT1-mediated intracellular NF-κB suppression in intestinal epithelium, not melanocortin receptor agonism. That means no tanning, no MC4-R-mediated sexual arousal, no appetite dysregulation, no ghrelin-axis involvement. Melanotan I/II and KPV should not be discussed as functionally equivalent or as members of the same therapeutic class, the mechanism is genuinely different, and the safety profile differs as a direct consequence.
For laboratory research use only. Not for human or animal consumption.
Evidence Tier
Animal Only
Mol. Weight
342.41 Da
Last Reviewed
Apr 22, 2026
Claimed benefits by evidence tier
Column header colour matches the tier
Animal Only8
- Reduces intestinal inflammation in IBD (ulcerative colitis, Crohn's)
- Inhibits NF-κB inflammatory signaling at nanomolar concentrations
- Accelerates corneal epithelial wound healing
- Reduces skin inflammation (atopic dermatitis, eczema, psoriasis)
- May reduce colitis-associated colorectal cancer risk
- Systemic anti-inflammatory activity
- Does not activate melanocortin receptors (no tanning, no MC4-R effects)
- Immune system "balancing" / immunomodulation
Anecdotal1
- Repairs gut permeability / "leaky gut"
Unsupported1
- Anti-aging / longevity effects
About this peptide
Plain English
Your body produces a hormone called alpha-melanocyte-stimulating hormone (α-MSH) that, among other things, helps control inflammation. Scientists discovered that just the last three amino acids of this hormone, lysine, proline, and valine, abbreviated KPV, carry most of its anti-inflammatory activity without triggering the pigmentation effects associated with the full hormone. Research has focused on mouse models of gut inflammation (Crohn's, ulcerative colitis) and rabbit models of corneal wounds, where KPV accelerated healing. The evidence is limited to animal and in vitro studies. KPV is for research use only and is not for human or animal consumption.
Technical
KPV (L-Lys-L-Pro-L-Val; MW ~342 Da, free acid) is the C-terminal tripeptide of α-MSH, an endogenous tridecapeptide product of POMC cleavage. Unlike α-MSH, KPV does NOT activate canonical melanocortin receptors (MC1-R, MC3-R, MC4-R) at physiologically relevant concentrations, mechanistic differentiation established by Bhardwaj 2003 using MC3/4-R antagonist blockade and MC1-R-deficient mice. The primary documented mechanism in intestinal inflammation is transport-dependent: the proton-coupled di/tripeptide transporter PepT1 (SLC15A1), normally confined to small intestinal enterocytes but markedly upregulated in colonic epithelium and immune cells during active IBD, mediates KPV uptake; once intracellular, KPV inhibits NF-κB nuclear translocation and MAPK activation at nanomolar concentrations. A second proposed mechanism involves antagonism at IL-1β receptor binding sites, particularly characterized for the D-Pro diastereomer Lys-D-Pro-Val. In corneal epithelium, NO-mediated facilitation of re-epithelialization has been documented in rabbits. All mechanistic work is preclinical; pharmacokinetics, bioavailability, and pharmacodynamic characterization are limited to animal and in vitro studies. Critically, vendor labeling is inconsistent: the free acid (H-KPV-OH, ~342 Da) and the N-acetylated, C-amidated form (Ac-KPV-NH2, ~383 Da) are structurally distinct compounds sold under the same 'KPV' name, buyers cannot distinguish without mass spectrometry.
Mechanism of action
PepT1 (SLC15A1) oligopeptide transport → intracellular NF-κB / MAPK suppression
PepT1, a proton-coupled di/tripeptide transporter normally confined to small intestinal enterocytes, is markedly upregulated in colonic epithelium and immune cells during active IBD. KPV is recognized as a PepT1 substrate and transported intracellularly. Once inside, at nanomolar concentrations, KPV inhibits nuclear translocation of NF-κB (p65 subunit) and suppresses MAP kinase activation, reducing downstream transcription of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). The transporter-dependency is strict: KPV prevents tumorigenesis in PepT1-expressing mice but has no effect in PepT1-knockout mice (Laroui 2016). Human intestinal cell-line data (Caco2-BBE, HT29-Cl.19A, Jurkat) supports the intracellular mechanism in vitro.
Non-melanocortin-receptor anti-inflammatory signaling
The anti-inflammatory effect of KPV is NOT blocked by the MC3/4-R antagonist SHU9119 and is preserved in MC1-R-deficient mice (Bhardwaj 2003), distinguishing it definitively from α-MSH and melanocortin agonists like Melanotan II. The downstream anti-inflammatory signaling pathway in non-PepT1-expressing tissues is less well-characterized. The D-Pro diastereomer (Lys-D-Pro-Val), which can form as a synthesis impurity, has been shown to antagonize IL-1β at the receptor level in alveolar epithelium; whether this mechanism is relevant to L-KPV itself is unclear.
Nitric oxide–mediated corneal epithelial re-epithelialization
Topical KPV accelerated corneal re-epithelialization in rabbits (100% at 60 hours vs 0% in vehicle controls at 1–10 mg/mL, 4×/day). Pre-treatment with the NO-synthase inhibitor L-NAME substantially inhibited the wound-healing facilitation, implicating a NO-mediated component. Human keratinocyte cell-line work shows similar anti-inflammatory signaling but does not establish a wound-healing endpoint.
All mechanistic evidence is from rodent in vivo models, rabbit corneal models, and transformed or primary human cell lines. PepT1 expression in colonic tissue during IBD is documented in biopsy studies, which makes the mechanistic pathway biologically plausible, but plausibility is not efficacy. The estimated ~25–35 min serum half-life is derived from rodent data. Bioavailability, systemic distribution, and tissue penetration have only been characterized at the preclinical level. A critical nuance for the PepT1 pathway: PepT1 colonic upregulation is an IBD-specific phenomenon, so KPV may not be meaningfully absorbed or locally effective in intestinal tissue without active inflammatory disease.
Key studies
PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation (2008)
Dalmasso G, Nguyen HTT, Yan Y, Laroui H, Charania MA, Ayyadurai S, Sitaraman SV, Merlin D · Gastroenterology 134(1):166–178
- Participants
- No humans. DSS-colitis and TNBS-colitis mouse models; in vitro human intestinal epithelial cell lines (Caco2-BBE, HT29-Cl.19A) and Jurkat T-cells.
- Methodology
- Animal intervention (oral KPV in drinking water) plus in vitro mechanistic assays (NF-κB luciferase reporter, Western blot, ELISA, radiolabeled KPV uptake experiments).
- Result
- Nanomolar KPV inhibited NF-κB and MAPK activation in human intestinal cells. Oral administration reduced DSS- and TNBS-colitis severity (~50% reduction in myeloperoxidase activity; decreased pro-inflammatory cytokines). PepT1 identified as the mediating transporter.
Honest read
Foundational mechanistic paper, well-designed for preclinical work. All therapeutic claims rest on mouse colitis models. DSS and TNBS models capture acute mucosal inflammation but are imperfect surrogates for human chronic IBD. No human pharmacokinetics. No replication by an independent lab has been identified. The Merlin lab at Georgia State is responsible for essentially all KPV intestinal research to date, creating a single-group-dominance concern that is partially offset only by the Catania lab's parallel α-MSH-fragment signaling line.
Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides (2003)
Bhardwaj RS, Schwarz A, Becher E, Mahnke K, Schwarz T, Luger TA · J Pharmacol Exp Ther 307(1):197–204
- Participants
- No humans. Crystal-induced peritonitis mouse model; in vitro macrophage studies.
- Methodology
- In vivo peritonitis model with leukocyte migration readout; in vitro macrophage cytokine release; pharmacological receptor blocking (MC3/4-R antagonist SHU9119) plus MC1-R-deficient mouse experiments.
- Result
- KPV exhibited anti-inflammatory and anti-migratory effects that were NOT blocked by SHU9119 and were preserved in MC1-R-deficient mice. KPV mechanism is definitively not melanocortin-receptor mediated.
Honest read
Critical differentiation study. Relatively small animal experiment. Importantly establishes that KPV ≠ melanocortin agonist, which has real-world significance for safety, no tanning, no appetite effects, no MC4-R-mediated sexual-arousal effects. The flip side is that the non-MCR anti-inflammatory pathway is less well-characterized than α-MSH's canonical signaling. Luger group (Münster), different from the Merlin/Catania anchor labs, which modestly strengthens the multi-group picture for the non-MCR mechanism specifically.
Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis (2017)
Laroui H, Geem D, Xiao B, Viennois E, Gwon L, Dalmasso G, Merlin D, et al. · Molecular Therapy 25(1):69–80
- Participants
- No humans. DSS-induced ulcerative colitis mouse model.
- Methodology
- Nanoparticle engineering (HA-functionalized, KPV-loaded) plus in vivo mouse colitis intervention plus in vitro validation.
- Result
- HA-KPV nanoparticles achieved similar anti-colitis efficacy as free KPV at a 12,000× lower concentration, with dual action: mucosal healing acceleration and inflammation reduction.
Honest read
Elegantly designed proof-of-concept for targeted delivery, not clinical evidence. All data in mice. Nanoparticle formulations face significant translation hurdles, GI stability, manufacturing scalability, immunogenicity, reproducible loading. Merlin lab, consistent with the single-group pattern across the KPV intestinal-research line.
Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model (2016)
Laroui H, Viennois E, Xiao B, Canup BSB, Geem D, Bhatt M, Merlin D · Cell Mol Gastroenterol Hepatol 2(3):340–357
- Participants
- No humans. PepT1-transgenic, PepT1-knockout, and wild-type mice; AOM/DSS colitis-associated cancer model. Analysis of human colonic biopsy specimens (PepT1 expression only, not KPV treatment).
- Methodology
- Genetic mouse models plus pharmacological KPV intervention in the AOM/DSS CAC murine model; immunohistochemistry of human biopsy specimens.
- Result
- PepT1 overexpression promoted colitis-associated cancer; KPV prevented tumorigenesis in WT mice via PepT1 but had no effect in PepT1-KO mice, confirming transporter dependency. Human biopsy data showed elevated PepT1 in colorectal cancer specimens.
Honest read
The biopsy data is PepT1-expression analysis only, it does not measure any KPV effect. The cancer-prevention data is entirely from a chemically induced murine CAC model. The finding should not be extrapolated beyond the animal model. Merlin lab again.
Effects of the COOH-terminal tripeptide alpha-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide (2006)
Gabison EE, Huet E, Baudouin C, Menashi S, Nicoletti A, Behar-Cohen F, Brignole-Baudouin F · Experimental Eye Research 83(5):1062–1069
- Participants
- No humans. New Zealand white rabbits (n=8 per group in the main experiment).
- Methodology
- Bilateral mechanical corneal epithelial debridement; topical KPV (1, 5, 10 mg/mL, 4×/day); fluorescein photography every 12 hours; L-NAME pharmacological inhibition of NO synthase; in vitro rabbit corneal epithelial cell viability assay.
- Result
- 100% of KPV-treated corneas fully re-epithelialized by 60 hours vs 0% of vehicle controls (P<0.05). Effect substantially inhibited by L-NAME. In vitro cell viability stimulated at 1–10 µM concentrations.
Honest read
Clean, well-controlled small-animal study. n=8 is adequate for an ocular pharmacology animal study; the effect size is large and reproducible within the paper. However, rabbit cornea is a specific wound-healing model, it is not a surrogate for human skin or gut wounds. The NO mechanism is proposed but not fully characterized. Single paper; no replication identified. Different group from the Merlin/Catania anchors (Gabison et al., Paris / Créteil), one of the few KPV papers from a third research cluster.
alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells (2004)
Capsoni F, Ongari AM, Colombo G, Turcatti F, Catania A · J Investig Dermatol 123(3):562–567
- Participants
- No human subjects. Primary human keratinocyte cultures and keratinocyte cell lines.
- Methodology
- In vitro human keratinocyte cells stimulated with IL-1β or TNF-α; KPV NF-κB inhibition measured; receptor characterization.
- Result
- α-MSH and KPV attenuated inflammatory signaling in human keratinocytes; KPV did not signal through classical melanocortin receptors in these cells.
Honest read
Uses human-derived cells, more translatable than rodent models, but still not a clinical trial. Primary human keratinocyte cultures have known limitations for replicating in vivo skin physiology. Catania lab (Milan), which is the other major single-group contributor to KPV research alongside Merlin. No commercial affiliations identified in search results, though this should be independently verified before any definitive COI statement.
Research timeline
- 1993
Early 1990s, C-terminal tripeptide KPV identified from structure-activity dissection of α-MSH as the minimal sequence retaining anti-inflammatory activity. Initial work uses keratinocyte and macrophage cell lines from the Luger group (Münster) and the Catania group (Milan).
- 2001
Catania et al. show that the D-Pro diastereomer Lys-D-Pro-Val antagonizes IL-1β signaling at the receptor level in alveolar epithelium. Establishes that KPV-related tripeptides can act through IL-1R-level antagonism in addition to the α-MSH pathway, and that synthesis-impurity D-Pro material has distinct biology.
- 2003
Bhardwaj et al. demonstrate that KPV anti-inflammatory activity is NOT mediated by MC1-R, MC3-R, or MC4-R in a crystal-induced peritonitis mouse model, using MC3/4-R antagonist SHU9119 blockade plus MC1-R-deficient mice. Critical mechanistic differentiation from full α-MSH and from melanocortin-receptor agonists like Melanotan.
- 2004
Capsoni et al. (Catania lab) characterize α-MSH, KPV, and ACTH signaling in primary human keratinocyte cell cultures, one of the few KPV publications using human-derived cells directly, though still not a clinical trial.
- 2006
Gabison et al. demonstrate topical KPV accelerates corneal epithelial wound healing in rabbits via a NO-mediated pathway (100% re-epithelialization at 60 hours vs 0% vehicle).
- 2008
Dalmasso et al. (Merlin lab, Georgia State) identify PepT1 as the primary transporter mediating KPV anti-inflammatory effect in intestinal epithelium. Published in Gastroenterology; the foundational paper for the PepT1/NF-κB mechanistic line.
- 2008
Catania lab publishes major Endocrine Reviews synthesis of α-MSH and related tripeptide anti-inflammatory literature; Brzoska et al. publish a parallel review in British Journal of Pharmacology from the Luger group. Establishes the α-MSH-fragment anti-inflammatory class as a published review topic across multiple groups, not independent replication of the KPV-specific therapeutic data, but broader recognition of the class mechanism.
- 2016
Laroui et al. (Merlin lab) demonstrate KPV suppresses colitis-associated carcinogenesis in an AOM/DSS murine model, strictly PepT1-dependent (no effect in PepT1-knockout mice). Human biopsy data in the same paper is PepT1-expression analysis only.
- 2017
Laroui et al. (Merlin lab) publish hyaluronic-acid-functionalized nanoparticle delivery system for oral KPV in DSS colitis, achieves equivalent efficacy at 12,000× lower concentration vs free peptide. Preclinical proof-of-concept for targeted delivery.
- 2025
Ghazvini et al. systematic review in JGH Open includes KPV among preclinical-only anti-inflammatory peptide candidates for IBD. The evidence base as of 2025 is limited to animal and in vitro studies.
- 2026
Regulatory review activity ongoing for KPV. As of 2026, KPV remains a research-use-only compound with no approved therapeutic application. The preclinical evidence base has not advanced to any published human study.
What we don't know
- Efficacy for any indication beyond animal and in vitro studies. All therapeutic claims rest on preclinical data from mouse colitis models, rabbit wound models, and cell lines.
- Oral bioavailability in non-rodent systems. The fraction of orally administered KPV that reaches intestinal tissue, and how that fraction depends on PepT1 expression and disease state, has only been studied in mouse models.
- Systemic distribution and half-life beyond rodent data. The ~25–35 min serum half-life is estimated from rodent pharmacokinetics.
- Long-term safety at the preclinical level. No chronic administration safety data beyond acute animal studies. Theoretical concerns include sustained NF-κB suppression.
- Optimal dose, route, and schedule for any indication. Animal mg/kg dose ranges have not been formally characterized with validated pharmacokinetic support outside those animal models.
- Potential interactions with anti-inflammatory agents (corticosteroids, anti-cytokine biologics) and drugs that compete for PepT1 transport, as studied in relevant preclinical models.
- Whether PepT1 dependency limits oral bioavailability in non-inflamed tissue. PepT1 colonic upregulation is an IBD-specific phenomenon in animal models; KPV may not be meaningfully absorbed or locally effective in intestinal tissue without active inflammatory disease.
- Comparative efficacy of subcutaneous vs oral routes. Animal models have primarily used oral or intraperitoneal administration; subcutaneous pharmacokinetics and tissue distribution have not been published.
- Broader oncological context of NF-κB suppression. NF-κB has complex tumor-suppressor and tumor-promoter roles depending on cancer type and context. One mouse study showed anti-tumor activity in colitis-associated cancer; broader oncological implications in other preclinical models have not been studied.
- Whether the free acid (H-KPV-OH, ~342 Da), acetate salt, and amidated form (Ac-KPV-NH2, ~383 Da) are bioequivalent. These are distinct chemical entities with potentially different stability, absorption, and potency profiles. No comparative data exists.
- Independent replication of the PepT1/colitis line outside the Merlin lab, or of the α-MSH-fragment signaling line outside the Catania lab.
Stability & handling
- Lyophilized shelf life
- 2–3 years at −20°C is typical for small tripeptides under proper storage (standard peptide-handling guidance; no peer-reviewed KPV-specific stability study identified).
- Lyophilized storage
- Freeze at −20°C (long-term) or 2–8°C (short-term). Protect from moisture and light. Equilibrate sealed vials to room temperature before opening to avoid moisture condensation on the powder.
- Reconstitution diluents
- Bacteriostatic water for injection (0.9% benzyl alcohol in sterile water), standard for multi-dose research vials, Sterile water for injection (single-use only), Phosphate-buffered saline (PBS), for in vitro research applications
- Reconstituted (refrigerated)
- Research-market convention of ~28–30 days at 2–8°C with bacteriostatic water (benzyl alcohol provides antimicrobial protection). No peer-reviewed KPV-specific stability study.
- Reconstituted (room temp)
- Degradation accelerates above 8°C; use promptly if not refrigerated. No formal KPV-specific room-temperature stability data.
- OK to refreeze
- No
- Light sensitive
- Yes, protect from light
KPV's small size (3 amino acids) makes it generally more stable than larger peptides, but it has several compound-specific failure modes that matter for what is actually in the vial and should be reflected on the COA. (1) FREE ACID vs ACETATE SALT, KPV sold as 'KPV acetate' has higher MW than the free acid (+~60 Da per acetate counterion). A COA reporting '≥98% purity by HPLC' without specifying the form allows meaningful ambiguity; KPV free base and KPV acetate are distinct chemical entities for research purposes. Red flag: no salt-form declaration on the COA. (2) Ac-KPV-NH2 vs H-KPV-OH, the N-acetylated, C-amidated form (~383 Da) is a structurally different compound than the free acid (~342 Da). Some vendors sell it as 'KPV' without disclosure. Red flag: product labeled simply 'KPV' without N-terminal and C-terminal modifications explicitly stated; the label should match the research application. (3) PROLINE EPIMERIZATION (D-Pro impurity), Pro at position 2 is susceptible to epimerization during Fmoc synthesis under basic conditions, generating Lys-D-Pro-Val with distinct biology. Standard reversed-phase HPLC may not resolve L-Pro and D-Pro diastereomers. Red flag: no chiral analysis or explicit L-Pro configuration confirmation. (4) DELETION SEQUENCES (KP or PV dipeptide), in tripeptide synthesis, failure to add the first or last amino acid generates dipeptide deletion products that can partially co-elute with KPV on standard HPLC, artificially inflating apparent purity. Red flag: no mass-spectrometry confirmation (ESI-MS or MALDI) of the correct 342-Da mass. (5) TFA RESIDUAL, trifluoroacetic acid used in Fmoc deprotection and preparative HPLC can remain as a counterion. At 5 mg vial sizes, a 5% TFA contamination is 0.25 mg TFA, relevant for inflammatory cell-culture work and sensitive assays. Red flag: no residual-solvent panel, no statement of counterion type.
Frequently asked questions
Does KPV treat Crohn's disease or ulcerative colitis?
The evidence is limited to animal and in vitro studies. Mouse models of chemically induced colitis (DSS, TNBS) show significant anti-inflammatory effects, but those are animal models. IBD involves complex immune dysregulation that mouse DSS colitis only partially captures, and the research has not progressed beyond preclinical study.
Is KPV the same thing as Melanotan?
No, and this is the single most important distinction for KPV. α-MSH is the 13-amino-acid parent peptide; KPV is just its last three amino acids. α-MSH activates MC1-R (pigmentation), MC3-R, and MC4-R, producing broad hormonal effects. KPV does NOT activate any of these melanocortin receptors at pharmacological concentrations, its anti-inflammatory effect works via PepT1-mediated NF-κB inhibition, an entirely different pathway. Melanotan II is a synthetic non-selective MCR agonist causing intense tanning, sexual arousal via MC4-R in the CNS, and frequent nausea, KPV has none of those effects. Conflating KPV with Melanotan is a common online error and reflects unfamiliarity with melanocortin pharmacology.
Does KPV cause tanning or pigmentation?
No, based on mechanism. KPV does not activate MC1-R, the melanocortin receptor responsible for melanogenesis. This has been demonstrated directly in MC1-R-deficient mice (where the anti-inflammatory effect was preserved) and via MC3/4-R antagonist blockade (which also did not block the effect). Unlike Melanotan I/II, which are potent MC1-R agonists, KPV should not cause tanning. This is a real, meaningful differentiator, not a marketing talking point.
Is KPV on the WADA Prohibited List?
Not by name. The WADA 2026 S2 category includes a catch-all for substances with 'similar chemical structure or similar biological effects' to prohibited peptide hormones. KPV is a fragment of α-MSH, and some α-MSH analogs with potent MCR agonism have been associated with doping concerns, but KPV does not activate melanocortin receptors and has no documented performance-enhancing effect in any preclinical study. Practical doping risk appears low based on mechanism.
What should I look for on a KPV COA?
Five items, separately reported: (1) MASS SPECTROMETRY confirmation of the correct molecular mass (342 Da for H-KPV-OH free acid; 383 Da for Ac-KPV-NH2 amidated form), and an explicit statement of WHICH FORM the product is. Some vendors sell Ac-KPV-NH2 under the same 'KPV' label; the two are structurally different compounds. (2) SALT FORM DECLARATION, free acid vs acetate salt vs TFA counterion. 'KPV free base' and 'KPV acetate' are distinct chemical entities. (3) CHIRAL ANALYSIS or explicit L-Pro configuration confirmation, reverse-phase HPLC does not detect D-Pro epimerization impurity (Lys-D-Pro-Val), which has distinct biology. (4) HPLC PURITY plus a check for deletion-sequence dipeptides (KP or PV) that can partially co-elute with KPV and artificially inflate apparent purity, mass spec confirms correct molecular mass. (5) RESIDUAL TFA panel and statement of counterion type, particularly relevant at small vial sizes where percentage TFA contamination matters for inflammatory assays. A COA showing only '≥98% purity by HPLC' without these five items has not characterized what is actually in the vial.
Last researched: Apr 22, 2026
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