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PEPTIDE · WHAT THE EVIDENCE SHOWS

KPV

Lysine-proline-valine, the C-terminal tripeptide of alpha-MSH. Below is what the published evidence establishes, what pathways it is reached for, and what we carry on those same pathways — with the grade on each.

Where it stands

The evidence position

FDA: “The molecular targets of KPV are unknown.” (slide 17)

FDA: “FDA did not identify data, such as clinical studies, on the use of KPV in humans.” (slide 19) The nomination did not include, and FDA did not identify, “any clinical studies or human exposure data for KPV via any route of administration.” (slide 22)

FDA did not identify nonclinical pharmacokinetic or toxicokinetic studies (slide 18), nor nonclinical toxicity studies to inform safety considerations (slide 20).

Not named on the WADA Prohibited List. Note that class S0 covers substances with no current approval for human therapeutic use, so absence from the list is not a clearance.

In July 2026 the US Food and Drug Administration reviewed KPV for the 503A Bulk Drug Substances list and proposed that it not be included. FDA briefing document, Pharmacy Compounding Advisory Committee, 23–24 July 2026.

The pathways it is reached for

1NF-κB — The Immune Alarm

The master inflammatory switch — indispensable to defend against threat, corrosive when it never stands down.

2ERK MAP Kinase Cascade — The Inflamed Accelerator

An inflammation-linked kinase that drives the exaggerated fat release seen in obesity.

3Intestinal Barrier — The Inner Gatekeeper

The intestinal barrier — the selective wall that admits nutrients, excludes toxins and anchors the gut–brain and immune dialogue.

4NLRP3 Inflammasome — The Sterile Alarm

The NLRP3 inflammasome — a sensor of cellular stress that ignites sterile, damage-driven inflammation.

5Systemic Inflammation — Inflammation Outside the Brain

Chronic low-grade inflammation in peripheral tissue — vessel wall, myocardium, follicle, joint.

6Adipose Tissue Inflammation — The Fat That Fights Back

Adipose tissue inflammation — immune cells accumulating in fat, forming crown-like structures around dying adipocytes and releasing cytokines locally.

7Neuroinflammation — The Brain Fog

Neuroinflammation — inflammatory activation within the brain that clouds cognition and depresses mood.

8Periodontal Inflammation

Gum breakdown starts as a bacterial signal.

9Skin Structure & Barrier — The Outer Surface

The body's largest organ and its most visible record. Collagen, elastin and barrier lipids degrade on a measurable schedule — and the evidence shows the degradation mechanisms specifically, because that is what the evidence actually witnesses.

What we carry on those pathways

1Rewire

Shares 5 of these pathways: NF-κB, Intestinal Barrier, NLRP3 Inflammasome, Neuroinflammation, Skin Structure & Barrier.

2Plush

Shares 4 of these pathways: NF-κB, Intestinal Barrier, Neuroinflammation, Skin Structure & Barrier.

3Ascendance

Shares 4 of these pathways: NF-κB, Intestinal Barrier, NLRP3 Inflammasome, Systemic Inflammation.

4Anti-Fatigue

Shares 4 of these pathways: NF-κB, NLRP3 Inflammasome, Systemic Inflammation, Neuroinflammation.

5Victorious

Shares 4 of these pathways: NF-κB, Intestinal Barrier, NLRP3 Inflammasome, Systemic Inflammation.

6Ceramide Blocker

Shares 3 of these pathways: NF-κB, Intestinal Barrier, Systemic Inflammation.

Intestinal Barrier → Ammonia. “This weakens the paracellular seal of the intestinal epithelium, enabling microbial products such as endotoxins, ammonia, and even whole microorganisms to translocate into the portal circulation.” — How the gut-liver axis shapes hepatic encephalopathy: mechanistic and therapeutic perspectives. Exploration of Digestive Diseases 2025;4:100597. doi:10.37349/edd.2025.100597 (no PMID exists — the journal is not MEDLINE-indexed; absence confirmed on file, not derived)

Intestinal Barrier → Oxygen-Carrying Capacity. “The two main causes are the villous atrophy of the mucosa at the site of iron absorption (the duodenum) and the resulting inflammation, which triggers the mechanism that leads to the anemia of chronic disease.” — Persistent Iron Deficiency Anemia in Patients with Celiac Disease Despite a Gluten-Free Diet. Nutrients, 2020, 12(8), 2176. doi:10.3390/nu12082176

Intestinal Barrier → Infection Resistance. “Unlike wildtype (WT) mice, infected Muc2−/− mice exhibited rapid weight loss and suffered up to 90% mortality.” — Muc2 Protects against Lethal Infectious Colitis by Disassociating Pathogenic and Commensal Bacteria from the Colonic Mucosa. PLoS Pathogens, 2010, vol 6, e1000902. doi:10.1371/journal.ppat.1000902

Intestinal Barrier → Micronutrient Status. “Micronutrient deficits, such as those in zinc and iron, can be caused by intestinal permeability and gut inflammation brought on by environmental enteric dysfunction.” — Environmental Enteropathy and Anaemia Status Among Under-Five Children, in Slum Areas of Jimma Town, Ethiopia. Pediatric Health, Medicine and Therapeutics, 2023, vol 14, 33-43. doi:10.2147/PHMT.S387747

NLRP3 Inflammasome → Caspase-1. “The NLRP3 inflammasome is a critical component of the innate immune system that mediates caspase-1 activation and the secretion of proinflammatory cytokines IL-1β/IL-18 in response to microbial infection and cellular damage.” — The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation. International Journal of Molecular Sciences, 2019, 20(13), 3328. doi:10.3390/ijms20133328

NLRP3 Inflammasome → Osteoarthritis. “Mechanistically, ERK5 interacted with the PYD domain of NLRP3 and mediated NLRP3 phosphorylation at serine 198, which facilitated mature inflammasome assembly, triggered pyroptosis and subsequently exacerbated OA progression.” — Inhibition of ERK5 activity ameliorates osteoarthritis by suppressing NLRP3 inflammasome-mediated chondrocyte pyroptosis. Bone Research; 2026; volume 14; article number 95. doi:10.1038/s41413-026-00573-x

What a grade means here

Every ingredient row on our formula pages carries one of these grades, fixed by a standard set before the evidence was gathered. The grades below are reproduced from those pages.

AHuman trial evidence

Randomized human trials, or a meta-analysis of them, measuring this pathway's own endpoint — either a clinical outcome or a validated biomarker.

B+Corroborated

Human data, or animal evidence replicated by an independent laboratory. It opens a pathway only alongside an independent corroborating driver.

BPreclinical

Mechanistic, cell or animal evidence. No single preclinical driver opens a pathway on its own.

What this page does not claim

Sharing a pathway is not the same as sharing an effect. Nothing here says a botanical formula does what KPV does, and nothing here recommends KPV. The pathways above are named because that is what the published work on KPV points at; the formulas below are listed because our own map records graded, published evidence on those same pathways. Read both columns and judge them yourself — every figure on our side carries its grade and its source.

Other peptides

BPC-157 · TB-500 · MOTS-c · Semax · Epitalon

Every pathway named, with the published study behind it.  ·  interstellarblends.com ·  Sign in