Description
PrymaLab · Research Use Only
Preloaded Autoinjector | KPV | 3ml Pen | 5mg/ml
Lys-Pro-Val tripeptide in solution · 3ml at 5mg/ml
The KPV autoinjector is a preloaded 3ml research device containing the Lys-Pro-Val tripeptide in solution at 5mg/ml, giving 15mg of total peptide and approximately 14.6 millimolar. Among the solution-state devices in this catalogue, a three-residue peptide carrying no oxidation-prone residues is the least demanding to hold stable.
Specification Table
| Property | Value |
|---|---|
| Device format | Preloaded autoinjector pen, glass cartridge |
| Fill volume | 3 ml |
| Concentration | 5 mg/ml |
| Total compound in device | 15 mg |
| Molar concentration | Approximately 14.6 mM |
| Compound | KPV, Lys-Pro-Val |
| CAS number | 67727-97-3 |
| Molecular formula | C16H30N4O4 |
| Molecular weight | 342.43 g/mol |
| Parent molecule | α-MSH residues 11 to 13 |
| Transport route | PepT1 (SLC15A1) |
| Reported downstream target | NF-κB signalling |
| Oxidation-prone residues | None. No cysteine, methionine, tryptophan, tyrosine or histidine |
| Disulfide bonds | None |
| Reconstitution required | None. Supplied as solution |
| Excipient system | Not published on the product record |
| Solution pH | Not published on the product record |
| Solution stability | Not established over device shelf life, though composition is favourable |
| Storage | 2-8°C, protected from light |
| Purity | Per lot-specific certificate of analysis |
| Regulatory status | No approved human or veterinary formulation in any jurisdiction |
Why Is a Tripeptide Comparatively Safe in Solution?
Solution-state supply worries most peptides. The KPV autoinjector is a genuine exception. The reasons read straight off the sequence.
Lys-Pro-Val contains no cysteine whatsoever, so no disulfide bonds exist to scramble or reduce. It contains none of methionine, tryptophan, tyrosine or histidine, which are the residues most vulnerable to oxidative attack. There is essentially no secondary structure to lose. Three residues cannot form a stable fold.
Aggregation, the failure mode that dominates for larger peptides in solution, requires extended hydrophobic surface to drive association. A tripeptide with a charged lysine and a polar backbone has very little of that.
What remains is hydrolysis of the two amide bonds, which proceeds slowly at neutral pH and refrigerated temperature, and the proline in the central position confers some resistance to enzymatic cleavage though not to chemical hydrolysis.
None of this means shelf-life data is unnecessary. It means the prior expectation for this compound in solution is more favourable than for anything else supplied this way in the catalogue.
What Does the Device Concentration Support?
Five milligrams per millilitre is approximately 14.6 millimolar, which sits in a convenient range for cell-based work.
Published KPV work uses concentrations spanning roughly the micromolar range in cell systems. Reaching 10 micromolar from a 14.6 millimolar stock is a 1,460-fold dilution, comfortably achievable in two serial steps with good accuracy.
That compares favourably with the picomolar arithmetic GHK-Cu demands, where reaching the published active range from a concentrated stock requires several steps and accumulates error at each one.
For work needing lower concentrations the device still serves, it simply requires one additional dilution step. For work needing higher concentrations than the device provides, a lyophilized vial reconstituted to a stronger stock is the better route, since concentrating a solution is not practical.
How Should the KPV Autoinjector Be Verified?
Visual inspection is less informative for the KPV autoinjector than for the copper-containing devices, because a colourless solution gives no colour cue to degradation. That places more weight on the other checks.
Before each draw, inspect for particulate and haze against light and dark backgrounds in turn. Clarity is the available visual signal and it should be complete.
Gravimetric verification of delivered volume is the substantive check. Actuate onto a tared weighing vessel, record delivered mass, convert using solution density, and repeat across several actuations to capture accuracy against nominal volume and precision between draws. Perform it at the temperature of intended use.
Discard the first actuation after any rest period rather than measuring it, since air ingress and seal relaxation both cause under-delivery on first use.
Where the work is quantitative, periodic concentration confirmation by chromatography is worth considering for a device used over many weeks, since it substitutes measurement for the absent shelf-life data.
Does PepT1 Competition Affect Device Use?
It affects the experiment rather than the device, but it belongs in any discussion of how this compound reaches its target.
PepT1 carries a broad range of di- and tripeptides without strong sequence selectivity. Anything else small and peptidic in the same system competes for transport, and serum-containing media contain peptide fragments that qualify.
For a single-component device this is simpler than for a blend, since the only competing peptides are whatever the assay medium contributes rather than three other deliberately added compounds. A device delivering only KPV avoids the transporter competition that a four-component blend introduces.
That is a genuine advantage of the single-compound format for mechanism work. Where the research question concerns PepT1-mediated uptake specifically, a preparation containing one transportable peptide is the cleaner tool.
Serum-free or defined-medium conditions reduce the background further, and where serum is required its batch becomes a variable worth recording.
What Concentration Range Does the Literature Use?
Matching the device concentration to the published work is worth doing deliberately rather than by default, and the numbers make the exercise straightforward.
Published cell work with KPV generally operates in the micromolar range. The device holds approximately 14.6 millimolar, so reaching 10 micromolar requires roughly a 1,460-fold dilution and reaching 1 micromolar roughly 14,600-fold.
Two serial steps of about 40-fold each, or one of 100-fold followed by one of about 15-fold, cover the first case comfortably. The second needs three steps or two larger ones, and each additional step adds pipetting error.
Working from a written dilution scheme rather than improvising at the bench is worth the two minutes it takes. Serial dilutions performed from memory are where concentration errors originate, and a factor-of-ten mistake in a three-step scheme is easy to make and hard to detect afterward.
Where the design needs concentrations far below the micromolar range, preparing an intermediate stock and storing it briefly is preferable to a long chain of transfers on the day.
What Does the Device Not Solve?
A preloaded format removes preparation variability and leaves everything else exactly as it was. Worth stating, so the format is not credited with more than it delivers.
It does nothing about transporter dependence. A device delivering a precise volume into a system lacking PepT1 delivers precision into a null.
Adsorptive loss occurring downstream remains entirely untouched by any of this. Once drawn, the solution meets whatever plasticware the assay uses. Losses there are unaffected by storage.
Nor does it address the absence of shelf-life data, which applies here as much as to any solution-state format.
What it does address is real. No reconstitution, no dissolution uncertainty, no shear, and no variable interval between preparation and use. That is a meaningful reduction in variance and it is not the whole problem.
Handling the Device in Laboratory Practice
Store at 2-8°C protected from light. The light requirement is precautionary here rather than mechanism-specific, since the compound carries no chromophore and no photosensitive metal.
Allow the device to reach ambient temperature before actuating. Cold solution is more viscous and viscosity affects delivered volume in a spring-driven mechanism, which is the most common avoidable error with pen devices.
Log the device lot, the date it was first actuated, storage conditions and the volume taken at each session. Shelf-life stability is unpublished, so the interval between first use and each later draw remains a variable even here.
Where downstream work involves measuring PepT1 expression or activity, record that alongside, since transport capacity is part of what determines whether the delivered compound reaches its target at all.
A Note on Vehicle Controls
The excipient system in this device is unpublished, which makes a matched vehicle control more important than it would be with a known formulation.
Whatever buffer, tonicity agent or preservative the solution contains enters the assay alongside the peptide. Benzyl alcohol, common in multi-use peptide preparations, is not inert in cell culture at all concentrations.
A vehicle arm requires the same formulation without the active compound, which a supplier may or may not be able to provide. Where they cannot, the fallback is to test the highest planned dilution of the device solution against a known-inactive comparator.
Neither is perfect. Both are better than assuming the excipients sit there doing nothing at all. Both are better than assuming the excipients are silent.
Where Does KPV Come From, and What Does the Literature Report?
This tripeptide has a clearer origin story than most research peptides, and the origin explains the anti-inflammatory interest in it.
Alpha-MSH, alpha-melanocyte-stimulating hormone, is a 13-residue hormone with well-characterised anti-inflammatory activity alongside its pigmentation role.
Its final three amino acids are lysine, proline and valine. Lysine-proline-valine, abbreviated KPV, is that C-terminal tripeptide isolated from the parent hormone.
The finding that made it interesting is that the anti-inflammatory activity of alpha-MSH survives the truncation while the pigmentation activity does not.
So KPV peptide retains an anti-inflammatory property without the melanocortin receptor engagement that drives the rest of the parent hormone’s effects.
Reported mechanisms centre on interference with inflammatory signalling inside the cell, reducing pro-inflammatory cytokines rather than blocking a receptor at the surface.
The proposed mechanism of action is worth stating in more detail, because it is the part that distinguishes this compound from its parent.
Alpha-MSH acts through melanocortin receptors, principally MC1R, the melanocortin-1 receptor, and MC3R. Losing ten residues removes most of that receptor engagement.
What the truncated peptide is reported to do instead is act intracellularly, interfering with NF-κB activation and with MAPK signalling once inside the cell.
NF-kB is the transcription factor that drives most inflammatory gene expression, so blocking its nuclear translocation reduces production of inflammatory mediators broadly rather than selectively.
Reported downstream effects include lower TNF-α and IL-1β output from immune cells, which is the cytokine signature that shows up across the preclinical work.
Reduced oxidative stress is reported alongside that in some models, which follows from lower inflammatory activity rather than from a separate antioxidant mechanism.
Antimicrobial activity is a separate reported property inherited from the parent hormone. Alpha-MSH has documented antimicrobial properties, and this fragment retains some activity against organisms including Candida albicans in culture.
That antimicrobial finding is genuinely interesting and it is also in-vitro work, which is a different claim from anything about an infection in an animal.
The best-known work is in colitis models. Dalmasso and colleagues reported in 2008 that oral KPV reduced inflammation in mouse models of colitis at very low concentrations.
That paper is also the source of the transport story, since uptake was shown to occur through PepT1, a peptide transporter expressed in intestinal epithelium and upregulated during colitis.
Those experiments used DSS-induced colitis, the standard chemical model, where intestinal inflammation is produced deliberately and then scored.
Reported effects in inflamed intestinal tissue include reduced inflammatory signalling in intestinal epithelial cells and improved tight junction integrity.
Tight junctions are what leaky gut refers to when the phrase is used precisely, so that finding is the mechanistic root of the leaky gut claims attached to this compound.
Subsequent work in inflammatory bowel disease models followed the same pattern, which is why this compound appears throughout gut health and gut healing marketing.
Uptake occurs through the PepT1 transporter, also written hPepT1 in the human literature, and PepT1-mediated tripeptide KPV uptake is the specific phrase that work established.
Wound healing and tissue repair are the other reported areas, mostly from topical application in dermal models rather than from systemic administration. Reported tissue repair there follows the reduction in inflammatory signalling rather than a separate growth effect.
What Does the Skin Literature Report?
Dermatology is the second research area for this compound and it is separate enough from the gut work to deserve its own treatment.
Skin inflammation models are where most of it sits, with reported reductions in inflammatory signalling in keratinocyte cultures and in mast cells.
Psoriasis, eczema and dermatitis are the inflammatory skin conditions named most often in discussions of that work, since all three involve the cytokine pathways this peptide is reported to interrupt.
No controlled human trial of this tripeptide in psoriasis, eczema or any other dermatological condition has been published.
Corticosteroids remain the mainstay for those conditions and have decades of trial evidence, and NSAIDs occupy a comparable position for general inflammation.
An anti-inflammatory peptide with mouse and cell-culture data is not a replacement for either, and nothing here is offered as one.
Topical formulations of this anti-inflammatory tripeptide are widely sold on the strength of that preclinical record, and the cosmetic market moves faster than the evidence does.
What Is the Compounding and Regulatory Position?
The compounding status of this compound changed recently enough that many listings still describe the old position.
Compounding pharmacies in the United States supplied it for a period, usually as an oral capsule or a topical preparation, prescribed for gut or skin complaints.
The FDA’s Pharmacy Compounding Advisory Committee reviewed a number of peptides for the 503A bulks list, and this compound did not secure a place on it.
So compounded preparations are no longer lawfully available in the United States, whatever a given clinic page still says.
Side effects of KPV are not characterised in humans, because no human trial has been run to characterise them.
Injection site reactions are the effect reported anecdotally for any subcutaneous route, and they reflect the formulation as much as the compound.
KPV peptide therapy as marketed usually means a compounded prescription or an unapproved research product used off-label, and this device is the second thing rather than the first.
Peptide therapy clinics group this compound with growth hormone secretagogues such as sermorelin and ipamorelin. Those act on an entirely different axis and share nothing with an anti-inflammatory tripeptide.
Claims about autoimmune conditions, immune balance, IBS, food sensitivities and inflammatory bowel conditions generally follow the same shape as the rest: animal plausibility, no human outcomes.
Is KPV a Treatment for Colitis or IBD?
No. The distance between the mouse work and that claim is the thing this section exists to describe.
Every colitis result cited for this compound comes from rodent models. No controlled human trial of KPV in inflammatory bowel disease, ulcerative colitis or Crohn’s disease has been published.
It is not FDA-approved for anything, in any formulation, in any jurisdiction.
Anyone managing IBD is managing a serious condition with real approved treatments behind it, including immunosuppressants and biologics with decades of trial evidence.
Substituting an unapproved research compound for those, or adding it without telling a treating clinician, is a decision with consequences that this page cannot make safer.
Claims about chronic inflammation, systemic inflammation and immune response generally follow the same pattern: mechanistic plausibility from animal work, no human outcome data.
This device is supplied for laboratory research only and is not for administration to humans or animals.
What Do the Different Routes Actually Support?
This compound is sold in several formats and the published work does not support them equally, which is unusual and worth setting out.
The strongest published route is oral. Oral KPV is what the colitis work used, and PepT1-mediated uptake in intestinal epithelium is the mechanism that makes an oral route coherent for this molecule specifically.
Topical application has the second-best support, from dermal wound models where the compound is applied directly to the site.
A topical route is also where the cosmetic interest sits, and topical formulations of this tripeptide are widely sold on that basis.
Subcutaneous injection is what this device format supports, and it is the route with the least published work behind it for this compound.
That is an awkward thing for a product page to say and it is accurate. The evidence and the format point in different directions here.
Where a systemic question is being asked, an injected route is the reasonable choice regardless. Where a gut question is being asked, the oral literature is the one to replicate.
BPC-157 is the compound most often paired with this one in peptide therapy marketing, usually for gut applications, and no study has tested the two in combination.
Published Literature
Traced to publisher records or primary indexes. All concern the compound and its transport biology rather than this delivery format, which has no published data.
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. Gastroenterology. 2008;134(1):166-178.
- Kannengiesser K, Maaser C, Heidemann J, et al. Inflammatory Bowel Diseases. 2008;14(3):324-331. DOI: 10.1002/ibd.20334
- Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. Endocrine Reviews. 2008;29(5):581-602.
- Getting SJ, Perretti M. Trends in Pharmacological Sciences. 2000;21(9):327-329.
- Daniel H. Annual Review of Physiology. 2004;66:361-384.
Frequently Asked Questions
What is the KPV autoinjector?
A preloaded 3ml research device holding the Lys-Pro-Val tripeptide in solution at 5mg/ml, giving 15mg in total and roughly 14.6 millimolar in the cartridge. No reconstitution needed. Laboratory research use only. No approved human or veterinary formulation exists anywhere in the world.
Why is a tripeptide safer in solution than larger peptides?
The sequence carries none of the vulnerabilities that normally cause trouble in solution. No cysteine, so nothing to scramble. No methionine, tryptophan, tyrosine or histidine, so oxidation is largely closed off. Three residues cannot fold, so there is no structure to lose.
What about aggregation?
Unlikely for the KPV autoinjector, and the reason is structural. Aggregation requires extended hydrophobic surface to drive association between molecules, and a tripeptide carrying a charged lysine on a polar backbone offers very little of it. The dominant failure mode for larger peptides is a minor one here.
What degradation route does remain?
Hydrolysis of the two amide bonds, proceeding slowly at neutral pH and refrigerated temperature. The proline in the central position confers some resistance to enzymatic cleavage. It offers nothing against chemical hydrolysis, which is an entirely separate process operating on a different timescale.
What concentrations does the device support?
Roughly 14.6 millimolar in the cartridge. Published KPV work operates at micromolar concentrations in cell systems, so reaching 10 micromolar means a 1,460-fold dilution, comfortably done in two serial steps with good accuracy.
How does that compare with other compounds here?
Favourably, and the contrast with GHK-Cu is instructive. That compound is active at picomolar concentrations, so reaching its published range from a concentrated stock takes several dilution steps with error accumulating at each. The KPV autoinjector needs two steps from cartridge to working concentration.
How should the device be verified?
Gravimetrically, since a colourless solution gives no visual cue to degradation the way a copper-containing one does. Actuate onto a tared vessel, record delivered mass, convert by density, and repeat at the temperature of intended use.
Does a single-compound device avoid transporter competition?
It reduces it. PepT1 carries a broad range of di- and tripeptides without strong sequence selectivity, so any small peptide present competes. A device delivering only KPV avoids the deliberate competition a four-component blend introduces, leaving only whatever the medium contributes.
Is that an advantage for mechanism work?
Yes, materially so. Where the question concerns PepT1-mediated uptake, one transportable peptide beats four. Serum-free conditions reduce background further. Where serum is required, its batch becomes a variable worth recording explicitly.
What should be recorded per session?
Lot number, first-actuation date, storage conditions, and volume taken. Where the downstream work involves PepT1 expression or activity, record that too, since transport capacity determines whether the delivered compound reaches its target at all.
What dilution does the device require?
Published cell work generally operates in the micromolar range. The device holds approximately 14.6 millimolar, so reaching 10 micromolar requires roughly a 1,460-fold dilution and reaching 1 micromolar roughly 14,600-fold, which needs three steps or two larger ones.
Why write the dilution scheme down?
Because serial dilutions performed from memory are where concentration errors originate. A factor-of-ten mistake in a three-step scheme is easy to make and very hard to detect afterward, and the two minutes spent writing it out stops that class of error.
What if very low concentrations are needed?
Prepare an intermediate stock and store it briefly rather than running a long chain of transfers on the day. Each additional transfer adds pipetting error, and the error compounds multiplicatively rather than averaging out across steps.
Why does the unpublished excipient system matter?
Because whatever buffer, tonicity agent or preservative the solution contains travels into the assay alongside the peptide and nothing on the record says what that is. Benzyl alcohol is common in multi-use preparations. It is not inert in cell culture at all concentrations.
What vehicle control is possible?
Ideally the same formulation without the active compound, which a supplier may or may not provide. Where they cannot, test the highest planned dilution of the device solution against a known-inactive comparator. Neither is perfect and both beat assuming the excipients are silent.
What is KPV?
The C-terminal fragment of alpha-MSH: lysine-proline-valine. KPV retains the anti-inflammatory properties of the parent hormone while losing its pigmentation activity, which is what made this anti-inflammatory tripeptide interesting in the first place.
How does KPV work?
Intracellularly rather than through melanocortin receptors. Reported work has KPV interfering with NF-κB activation and MAPK signalling inside immune cells, lowering TNF-α and IL-1β output. NF-kB drives most inflammatory gene expression, so blocking it reduces inflammatory mediators broadly.
Is KPV peptide a treatment for colitis or IBD?
No. Every colitis result comes from rodent DSS models of intestinal inflammation. No controlled human trial in inflammatory bowel disease exists, and KPV is not FDA-approved for anything. IBD has real approved treatments including immunosuppressants and biologics.
Which route does the evidence actually support?
Oral, for gut questions. The colitis work used oral KPV taken up through the PepT1 transporter in intestinal epithelium. Topical has the next-best support from dermal models. Subcutaneous injection, which this device format supports, has the least published work behind it.
Does KPV help psoriasis or eczema?
No human trial exists in either. The skin inflammation work is in keratinocyte cultures and mast cells. Corticosteroids remain the mainstay for those conditions with decades of trial evidence, and this compound is not a replacement for them.
Can a compounding pharmacy still supply KPV?
Not lawfully in the United States. The FDA’s Pharmacy Compounding Advisory Committee reviewed peptides for the 503A bulks list and this one did not secure a place, so compounded preparations are no longer available whatever a clinic page still says about KPV peptide therapy.
Is it usually stacked with BPC-157?
In marketing, yes, generally for gut applications. No study has tested KPV and BPC-157 in combination in anything. Clinics also group both with sermorelin and ipamorelin, which act on a different axis entirely and share nothing with an anti-inflammatory tripeptide.
What are the side effects of KPV?
Not characterised, because no human trial has been run to characterise them. Injection site reactions are what gets reported anecdotally for any subcutaneous route, and those reflect the formulation as much as the compound. Claims about immune modulation and gut inflammation rest on animal work.
Compliance Statement
The KPV autoinjector is sold exclusively for laboratory research use. It is not a drug, food, or cosmetic product, and it is not a dietary product of any kind. It is not approved by the FDA or any comparable authority for human or veterinary use. This product is not intended to diagnose, treat, cure, or prevent any disease. It must not be given to humans or animals. Purchase is restricted to qualified researchers and institutions operating within applicable laws. All handling is the responsibility of the purchasing laboratory.
Other formats of KPV
KPV is also stocked as KPV (5mg), KPV (10mg) and KPV 10mg Nasal Spray. Each listing states its own quantity and concentration, and the pen and vial comparison explains what changes between formats.
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