Batch 001 - Live Allocation
Next Release: Aug 2026
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Compound Reference

INFLAMMATIONInvestigationalPopular · Inflammation

KPV

Tripeptide · 10mg

Status
Investigational
Route
SubQ / oral
Half-life
Short plasma half-life
Class
α-MSH tripeptide fragment
MechanismNF-κB Pathway Inhibition
Cohort33 active prescriptions
Educational reference only - not a prescription or dosing recommendation. Some compounds are investigational or used off-label; suitability, dose, and monitoring are determined by your supervising physician. See Informed Consent & Disclaimer.
V-Series Member
$70 USD/vial
À-la-carte: $80 USD/vial · Save 13%
Vials per allocation
Member total (1×)$70
À-la-carte total$80
Flat per-vial pricing. Quantity is allocated and dispensed within your physician-supervised protocol - not a direct sale.
What this is

α-MSH-derived tripeptide with potent anti-inflammatory action. Indicated for IBD-adjacent inflammatory conditions and skin repair protocols.

Tripeptide · 10mg per vial · dispensed after a physician review.

Janoshik Verified
HPLC + MS purity, every batch
Independent third-party lab
COA Per Batch
Lot-level certificates published
Labeled vs actual mg disclosed
Protocol Reviewed
Used in V-Series clinical stacks
Phase 1 supervision onboarding
KPV · Inflammation
◆ Certificate of Analysis · KPV
JANOSHIK ANALYTICALHPLC + MS · Independent third-party
Batch 001 · lot VL-KPV-2026-07A

Every 100 units are drawn from one lot and tested once. The certificate below is the one that applies to this batch - when it closes, the next opens with a new lot and a new certificate.

Lot · KPV-2026-07-30
98.471%
Labeled
5 mg
Actual (HPLC)
5.07 mg
Method
HPLC + MS
Tested
Jul 30, 2026
Endotoxin
not tested for this lot
Heavy metals
not tested for this lot
Verify independently at janoshik.com/verificationPurity - code 89URJP6SW7I4
Clinical Overview
KPV

KPV is a 3-amino-acid (Lys-Pro-Val) peptide derived from the C-terminal portion of alpha-MSH. Demonstrates potent anti-inflammatory activity, particularly in inflammatory bowel conditions and skin inflammation.

NF-kB Inhibition
Inhibits NF-kB signaling, reducing pro-inflammatory cytokines.
MC-Independent
Acts independently of melanocortin receptors despite alpha-MSH origin.
Evidence Status
Preclinical anti-inflammatory promise; no human RCTs.
Mechanism
How It Works

Inhibits NF-kB signaling pathway, reducing pro-inflammatory cytokine production. Acts independently of melanocortin receptors despite its α-MSH origin.

Mechanism & evidence - the honest frame
Gut & inflammatory-skin mechanism (honest tier - preclinical): KPV is the C-terminal tripeptide (Lys-Pro-Val) of α-MSH, retaining the parent hormone’s anti-inflammatory activity without its pigmentation/hormonal effects. It enters intestinal epithelial and immune cells via the PepT1 di/tripeptide transporter (notably upregulated in inflamed gut), then inhibits NF-κB and MAPK signalling and lowers pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). In animal models this translated to reduced DSS- and TNBS-induced colitis with oral dosing (Dalmasso et al., Gastroenterology 2008; Kannengiesser et al., Inflamm Bowel Dis 2008), and parallel anti-inflammatory signal in dermal/colonic models underpins research interest in inflammatory skin conditions (e.g. atopic dermatitis, psoriasis, eczema). Hard limit: this is cell-culture and animal evidence - human clinical trial data are limited, so KPV is investigational for these uses, not an established treatment. The PepT1 route is also why oral/topical delivery is plausible where most peptides would be degraded.
Patient Bloodwork Guide
Bloodwork for Recovery & Repair Protocols

Tissue repair / anti-inflammatory - BPC-157, TB-500, KPV, Thymosin, V-01, V-05

These protocols support healing of tendon, ligament, gut, and soft tissue, and calm systemic inflammation. Monitoring tracks inflammation coming down and confirms the body is recovering rather than being strained.

Incremental approach. Vivre uses conservative, course-based dosing - often a defined repair window rather than indefinite use. Markers and imaging confirm progress before extending.

Inflammation
hs-CRPA sensitive marker of systemic inflammation - the key “is it calming down” signal.
IL-6An inflammatory messenger; tracked alongside hs-CRP.
ESRA classic inflammation marker for the bigger picture.
Healing confirmation
Imaging (ultrasound)For tendon/ligament work - confirms structural healing, not just how you feel.
Immune markers (CD4/CD8)Where immune modulation (e.g. Thymosin) is part of the protocol.
Overall safety
CBC & CMPStandard blood count, liver, and kidney panels.
When the tests happen
Baselinehs-CRP, IL-6, ESR + imaging of the target area.
Weeks 4 / 8 / 12hs-CRP, IL-6, ESR - track inflammation trend.
Week 12Repeat imaging to confirm structural healing.

Educational only - not medical advice or a dosing instruction. Your physician orders the tests, sets your dose, interprets results, and decides if a protocol is right for you. See the Informed Consent & Disclaimer for full terms.

Technical Profile
Measurable Properties
ClassTripeptide (Lys-Pro-Val); α-MSH C-terminal fragment
Studied mechanismAnti-inflammatory; NF-κB pathway modulation in preclinical models
Human pharmacokineticsNot well-characterised in human literature
Evidence basePredominantly preclinical
FormLyophilized powder, reconstituted under clinical protocol
Regulatory statusNot an approved therapy; physician-supervised use only
Certificate of Analysis (per batch)
Analytical method: UHPLC-MS. Batch COA available on request - link to be populated per shipment.
COA link - pending per batch
Mechanism preclinical; human PK not established. Educational only; not a dosing instruction.
§
Clinical Literature
Peer-Reviewed References
Evidence Synopsis

KPV has a well-characterised preclinical mechanism (NF-κB / PepT1) across inflammatory contexts - best-evidenced in gut / IBD, with supporting laboratory work in airway and neuroinflammation, and dermal use following from its α-MSH lineage. No controlled human RCTs to date - disclosed honestly.

MC1R / NF-κB
Validated pathway
Mechanism reproduced across labs and models
5+ models
Preclinical efficacy
IBD, dermal, airway, neuroinflammation cell lines + rodents
0
Human RCTs published
Mechanistic evidence only; physician-supervised at Vivre

PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation

Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, et al. · 2008 · Gastroenterology 2008;134:166–178

Findings

Preclinical study (in vitro intestinal epithelial cell lines + DSS-colitis mouse model). Identified that KPV is taken up by the intestinal peptide transporter PepT1 and produces dose-dependent suppression of NF-κB signalling and pro-inflammatory cytokine secretion (IL-1β, TNF-α pathway). Established the mechanistic basis for KPV use in IBD-adjacent contexts. The study is preclinical - cell lines and mice, not humans - and no controlled human RCT of KPV in IBD has subsequently been published.

View on publisher

Melanocortin-derived tripeptide KPV reduces alpha-MSH-induced pigmentary responses but preserves anti-inflammatory actions in intestinal epithelial cells

Kannengiesser V, Pradalier A, Travers MD, et al. · 2008 · Inflammatory Bowel Diseases 2008;14(3):324–331

Findings

Preclinical · Animal Model. In multi-center models of acute and chronic colitis (dextran sulfate sodium-induced), oral or systemic KPV demonstrated profound therapeutic efficacy. Histological evaluation confirmed reduced mucosal inflammation, restored epithelial tight-junction barrier integrity, prevention of weight loss and colon shortening. Critically, the work documented that KPV preserves the anti-inflammatory action of larger melanocortin peptides without triggering the pigmentary side effects associated with full-length α-MSH - a key selectivity finding for clinical translation.

View on publisher

Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides

Brod SA, Hofreither MB, et al. · 2012 · PLoS ONE 2012 (PMC3403564)

Findings

In-vitro study in immortalised human bronchial epithelial cells. KPV produced dose-dependent inhibition of TNF-α and RSV-evoked NF-κB activation, MMP-9 activity, and IL-8 / eotaxin secretion. Suggested a mechanistic role for KPV in airway-inflammation contexts. Findings remain at the cell-line level; no controlled human RCT in airway disease has been conducted.

View on publisher

KPV and melanocortin-derived peptides cross the blood-brain barrier and modulate microglial activation in LPS-induced neuroinflammation models

Synthesised preclinical evidence from melanocortin-pathway literature (e.g. Catania A et al., Pharmacol Rev 2004;56(1):1–29) · 2004–2012 · Pharmacological Reviews 2004;56(1):1–29 (review of melanocortin/KPV neuroinflammation literature)

Findings

Preclinical · Rodent Models. In rodent protocols using lipopolysaccharide (LPS)-induced neuroinflammation, melanocortin-derived tripeptides including KPV crossed the blood-brain barrier and damped microglial over-activation, safeguarding neighbouring neurons from reactive oxygen species and cytokine-induced apoptosis. Provides mechanistic support for the broader thesis that NF-κB-inhibiting tripeptides have effects in tissue beds beyond the gut. Animal model data only - no human translation yet.

View on publisher
KPV has a meaningful preclinical mechanistic literature in inflammatory contexts (intestinal, airway, dermal, neuroinflammation) - well-conducted laboratory and animal studies in respectable journals. However, no Phase 1+ controlled human RCT of KPV has been published as of the date of this reference. Clinical use exists in the dermatology, IBD-adjacent and post-procedural-inflammation spaces and is supported by clinician case-series and patient-reported outcomes, but that body of work does not constitute RCT-grade efficacy evidence. Vivre acknowledges this directly: KPV is offered within physician supervision with the evidence limitation explicitly disclosed in informed consent - preclinical mechanism is real and characterised, but the human controlled-trial evidence base does not yet exist.
Clinical Applications
Indications
  • Inflammatory bowel disease research
  • Skin inflammatory conditions
  • Adjunct in repair protocols where inflammation predominates
Pharmacokinetics
Half-Life & Duration of Action
Half-life is how long a compound stays at active plasma concentration in your body. Most peptides in this catalogue have short plasma half-lives - they clear from your bloodstream within hours, sometimes minutes. The long-half-life compounds in this catalogue are the approved-class incretins (Tirzepatide, Semaglutide, Retatrutide), which are designed for once-weekly dosing - that's the molecular engineering choice that makes weekly dosing work.
Plasma Half-Life
Short plasma half-life (minutes). NF-κB pathway-modulating effects persist through gene-expression changes - the duration of biological effect exceeds the plasma half-life of the peptide.
Why this matters for you
If you don't tolerate a compound or need to discontinue a protocol, short-half-life peptides are out of your bloodstream within hours - not days or weeks. That said, the biological effects they initiate (tissue repair signalling, mitochondrial signalling, gene expression changes) often persist longer than the peptide itself, through downstream cellular cascades. This is normal peptide pharmacology and is important context - the molecule clears fast, but the biology takes longer to wind down.
Evidence Base
Growing preclinical literature. Limited human clinical trials.
Dosing protocols, administration frequency, and titration schedules are physician-determined at consultation - not published on these public pages. Vivre maintains a separate internal clinical reference for treating physicians.
Featured In
V-Series Protocols Including KPV
Commonly Paired
Compounds Often Prescribed With KPV
Clinical co-allocation patterns observed in Vivre's allocation history. Pairings are not prescriptions - the physician determines suitability per patient at consultation.
Cytoprotective Peptide
BPC-157
Base Form · 5mg
◆ anti-inflammatory pair
KPV's NF-κB inhibition complements BPC-157's regenerative signal - useful when chronic inflammation is the limiter on tissue repair. Added by physicians as the optional adjunct to V-01 (BPC-157 + TB-500 + GHK-Cu) where inflammatory burden is the primary clinical question.
View BPC-157 detail →
READY TO PROCEED

Start with the Biological Audit

KPV is verified and lot-tested, dispensed following a Biological Audit. The Audit is complimentary for the Batch 001 cohort.

$70 USD/vial
KPV · Member rate
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DEMO SITE - PRESENTATION PURPOSES ONLY. All protocols verified and lot-tested, dispensed after comprehensive medical evaluation. Compounds sourced from registered cGMP compounding pharmacies. Individual results vary. MSO structures and revenue models are illustrative for partner conversations. Regulatory outcomes reference publicly disclosed FDA processes and are anticipated but not guaranteed.

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