Pipeline compound

    Klotho (KP1)

    KP1 (Klotho-derived peptide 1) is a 30-amino-acid peptide taken from the human Klotho protein. In cell and mouse studies it binds TGF-beta receptor 2 and blocks the signal that drives fibrosis. It is often sold simply as Klotho, but it is a small fragment of a large protein, and the best-known Klotho findings come from the full protein, not from KP1. KP1 has never been tested in people. This profile summarises the research for laboratory readers.

    Also known as
    KP1, Klotho-derived peptide 1
    Source protein
    Human alpha-Klotho, residues 57 to 86 (30 amino acids)
    Reported target
    TGF-beta receptor 2 (TβR2)
    Evidence so far
    Cell and mouse studies; never tested in people

    Mechanism

    Klotho is a large protein made mainly in the kidney. The gene was described in 1997, when mice lacking it developed a syndrome resembling ageing, and in 2005 mice engineered to make extra Klotho lived longer. Alpha-Klotho sits in the cell membrane, where it works with FGF receptors as the co-receptor for FGF23, a hormone that controls phosphate. A soluble form is also released into the blood. Its size and complexity make the full protein hard to produce and study as a reagent.

    KP1 came from a search for a smaller piece that keeps one of Klotho's actions. Researchers screened a series of peptides taken from the human Klotho sequence and found that KP1, residues 57 to 86 near the start of the protein, bound TGF-beta receptor 2 and stopped TGF-beta from binding it. TGF-beta is the main signal that turns fibroblasts into scar-forming cells. In cultured kidney fibroblasts KP1 blocked TGF-beta-driven activation; in mouse models of kidney fibrosis it built up in injured kidneys after intravenous injection, reduced fibrosis, preserved kidney function and restored the kidneys' own Klotho production.

    Later studies from the same group extended this: fewer senescence markers in fibrotic mouse kidneys, linked to restored Klotho through a microRNA (miR-223-3p); protection in mouse models of acute kidney injury, through a mitochondrial protein called ATAD3A; and less fibrosis in mouse models of liver injury. A sister peptide, KP6, binds Wnt proteins instead and was studied in mouse diabetic kidney disease. All of this is cell and animal work.

    Clinical programme status

    • Research compound. KP1 is not a medicine anywhere, and no trial of KP1 is registered on ClinicalTrials.gov as of 30 October 2026.
    • Published KP1 evidence, all in cells and mice: kidney fibrosis (2022), senescence in fibrotic kidneys (2024), COVID-19-associated kidney injury (2024), liver fibrosis (2026) and acute kidney injury (2026). The five studies come from the group that discovered KP1 and have not yet been repeated independently.
    • The well-known Klotho results, longer life in mice and better memory in aged monkeys after a single low dose, used the full protein or other fragments, not KP1.
    • Human studies of Klotho itself are at the earliest stage: two small open-label pilot studies of Klotho gene therapy and a planned placebo-controlled phase 1b study of Klotho mRNA. None has published results. They are listed below.

    Registered trials

    From ClinicalTrials.gov, read 30 October 2026.

    • Klotho gene therapy pilotNCT07216781

      Klotho itself, not KP1: plasmid gene therapy in healthy adults, no placebo group, 14 people

      Phase 1 · Active, not recruiting · Started Oct 2025

    • Klotho and follistatin gene therapy pilotNCT07285629

      Klotho itself, not KP1: combined plasmid gene therapy in healthy adults, no placebo group, 14 people

      Early phase 1 · Completed, no results posted · Started Dec 2025

    • Klotho mRNA studyNCT07544420

      Klotho itself, not KP1: mRNA given into a vein, placebo-controlled, about 21 people

      Phase 1b · Not yet recruiting · Started Not started

    Published statements, quoted

    Reproduced verbatim from the sources named. Peptx makes no claim of its own on these points.

    “By screening a series of peptides derived from human Klotho protein, we identified KP1 that repressed fibroblast activation by binding to TGF-β receptor 2 (TβR2) and disrupting the TGF-β/TβR2 engagement.”
    Yuan Q, et al. Nature Communications, 2022 (PubMed 35064106), abstract.
    “KP1 acted as a competitive TGF-β receptor 2 (TβR2) antagonist, disrupted TGF-β1/TβR2 engagement, and suppressed both canonical and noncanonical TGF-β signaling in HSCs.”
    Tan H, et al. International Journal of Biological Sciences, 2026 (PubMed 41608630), abstract. HSCs are hepatic stellate cells, the liver's scar-forming cells.

    Not yet stocked

    Register interest

    Klotho (KP1) is not currently supplied by Peptx. Leave an email address and we will notify you once verified reference material is available. No purchase, no obligation, and the address is used for this notice only.

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    Frequently asked questions

    What is Klotho (KP1)?
    KP1, Klotho-derived peptide 1, is a 30-amino-acid peptide taken from the human Klotho protein (residues 57 to 86). In cell and mouse studies it binds TGF-beta receptor 2 and blocks TGF-beta signalling. It is a research compound and has never been tested in people.
    Is KP1 the same as the Klotho protein?
    No. Klotho is a large protein; KP1 is a small piece of it that was selected for one action, blocking TGF-beta receptor 2. Findings on lifespan in mice and memory in monkeys come from the full protein or other fragments, not from KP1.
    Has KP1 been tested in humans?
    No. As of October 2026 there is no registered human trial of KP1. The few human Klotho studies registered test gene therapy or mRNA designed to raise Klotho itself, and none has published results.
    What has KP1 been studied for?
    Fibrosis and injury in mouse kidneys and livers: kidney fibrosis, senescence in fibrotic kidneys, acute kidney injury and liver fibrosis. All of the published studies so far come from the group that discovered it.
    Does Peptx stock Klotho?
    No. Klotho (KP1) is not currently supplied by Peptx. You can register an email address on this page to be notified if verified reference material becomes available.

    Citations

    1. Yuan Q, et al. (2022). A Klotho-derived peptide protects against kidney fibrosis by targeting TGF-β signaling. Nature Communications. PubMed 35064106.
    2. Zhang X, et al. (2024). Klotho-derived peptide 1 inhibits cellular senescence in the fibrotic kidney by restoring Klotho expression via posttranscriptional regulation. Theranostics. PubMed 38164143.
    3. Zhang X, et al. (2026). Klotho-Derived Peptide 1 Protects against Acute Kidney Injury by Directly Targeting Mitochondrial ATAD3A. Advanced Science. PubMed 42640132.
    4. Tan H, et al. (2026). Klotho-derived peptide 1 ameliorates hepatic fibrosis induced by αKlotho deficiency and liver injury. International Journal of Biological Sciences. PubMed 41608630.
    5. Chen X, et al. (2022). Klotho-derived peptide 6 ameliorates diabetic kidney disease by targeting Wnt/β-catenin signaling. Kidney International. PubMed 35644285.
    6. Kuro-o M, et al. (1997). Mutation of the mouse klotho gene leads to a syndrome resembling ageing. Nature. PubMed 9363890.
    7. Kurosu H, et al. (2005). Suppression of aging in mice by the hormone Klotho. Science. PubMed 16123266.
    8. Urakawa I, et al. (2006). Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature. PubMed 17086194.
    9. Castner SA, et al. (2023). Longevity factor klotho enhances cognition in aged nonhuman primates. Nature Aging. PubMed 37400721.
    10. ClinicalTrials.gov registry search: studies with Klotho as an intervention.

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