Public educational draft · 04 November 2026Clinical review pending →
Kisspeptin-10 reference card with source-verified molecular imagery and original research-informed diagrams. Evidence levels and limitations are marked; full citations accompany the card on the website.

Visual summary only. The research findings, limitations and references accompany the card on this page.

The chemical drawing shows source-verified two-dimensional connectivity and stereochemistry, not an experimental three-dimensional conformation. The biological setting is an illustration. Original study diagrams summarize cited research without reproducing publication artwork or inventing quantitative results.

Verified chemical reference record

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Melanocortin / reproductive

Kisspeptin-10

KISS1R → GnRH axis

Human kisspeptin C-terminal decapeptide; free N-terminus, C-terminal phenylalaninamide
Molecular formula
C63H83N17O14
Molecular weight
1302.4 g/mol
Class
Amidated decapeptide
Identity
H-Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2

Research snapshot

Kisspeptin-10 is the bioactive C-terminal fragment shared by longer kisspeptins. Small human studies show gonadotropin responses and altered LH pulse timing, but these are physiological endpoints, not established fertility or wellness outcomes.

Small human physiology studies

Identity & representation

Reference parent, not an AXON formulation or salt.

Educational reference only. Not a dosing guide, treatment recommendation or product endorsement.

Human kisspeptin C-terminal decapeptide · free N-terminus · Phe amide[1]

View the chemical structure →

Sources checked: 2026-11-06. Identity and evidence limits are stated above. Independent specialist review is pending.

ClassAmidated decapeptide

Research contextKISS1R → GnRH axis

EvidenceSmall human physiology studies

StatusExperimental reproductive-endocrine research

What researchers study

Kisspeptin-10 is the bioactive C-terminal fragment shared by longer kisspeptins. Small human studies show gonadotropin responses and altered LH pulse timing, but these are physiological endpoints, not established fertility or wellness outcomes.

  • GnRH pulse-generator physiology

  • LH secretion in human experiments

  • Reproductive-axis responses in selected endocrine conditions

Mechanism in context

  1. Kisspeptin-10 activates KISS1R signaling
  2. GnRH secretion is stimulated
  3. Pituitary LH / FSH responses follow

Human GnRH effects are often inferred from peripheral LH measurements. Results from kisspeptin-54 or modified agonists must not be transferred without labeling the different compound.

Simplified publication-grounded schematic, not a solved protein structure or proof of clinical benefit.

Selected evidence

Small human physiology studies

Kisspeptin resets the hypothalamic GnRH clock in men.[2]

Acute human physiology experiment · 13 healthy adult men · Single experimental exposure with serial sampling

Observed: Kisspeptin10 elicited an LH pulse and shifted subsequent pulse timing.

Kisspeptin10 elicited an LH pulse and shifted subsequent pulse timing. GnRH timing inferred from LH; no fertility or long-term therapeutic outcome.

Limit: GnRH timing inferred from LH; no fertility or long-term therapeutic outcome.

Exploring the pathophysiology of hypogonadism in men with type 2 diabetes: kisspeptin-10 stimulates serum testosterone and LH secretion in men with type 2 diabetes and mild biochemical hypogonadism.[4]

Small human proof-of-concept physiology study · 5 men with T2DM and 7 healthy comparators; infusion subgroup 4 · Acute experimental sessions

Observed: LH responses and testosterone increases were observed in selected men.

LH responses and testosterone increases were observed in selected men. Very small surrogate-endpoint study, not an established hypogonadism treatment trial.

Limit: Very small surrogate-endpoint study, not an established hypogonadism treatment trial.

Reference identity in detail

Sequences and form distinctions describe the cited reference substance, not a verified supplier preparation.

Read the sequence and form notes
Sequence
H-Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2
Residue count
10
Molecular formula
C63H83N17O14
Molecular weight (g/mol)
1302.4

Research scope

Targeted source verification, not a systematic review. Citation quality and molecule-specific applicability are stated separately.

Safety & evidence limits

  • Human studies are small and mainly measure short-term hormonal surrogates.

  • Longer kisspeptins and experimental analogs differ in pharmacokinetics and cannot substitute for kisspeptin-10 evidence.

  • Effects vary by physiological context; long-term reproductive efficacy and safety remain unestablished here.

Practical identity notes

  • Human kisspeptin C-terminal decapeptide; free N-terminus, C-terminal phenylalaninamide
  • No original PubChem 3D conformer was available for this exact reference in the checked endpoint; use exact 2D structure.
  • Reference identity is not confirmation of product contents, purity, sterility or therapeutic equivalence.

The 10-second takeaway

A reproductive-signaling fragment with human hormonal-response evidence, not established general fertility or testosterone therapy.

What the visual panels show

Original diagrams summarize the cited research or documented evidence search. They are not copied publication figures or claims of treatment benefit.

  • MECHANISM / STUDY CONTEXT[3]

    Publication-grounded mechanism schematic · Original publication-grounded diagram

    KISS1R signaling activated · GnRH secretion stimulated · Pituitary LH / FSH responses measured

    Interpretation: Human GnRH effects are often inferred from peripheral LH measurements. Results from kisspeptin-54 or modified agonists must not be transferred without labeling the different compound.

  • Reproductive-axis signals[3]

    HUMAN PHYSIOLOGY · Original publication-grounded diagram

    Hormonal responses follow kisspeptin signaling

    Human GnRH timing is often inferred from peripheral LH.

    Interpretation: Human GnRH timing is often inferred from peripheral LH. Original conceptual illustration only; no fabricated data, docking geometry or clinical extrapolation.

  • LH pulse timing[2]

    HUMAN EXPERIMENT · Original publication-grounded diagram

    LH pulse elicited; later pulse timing shifted

    13 healthy men; acute experiment, not a fertility trial.

    Interpretation: 13 healthy men; acute experiment, not a fertility trial. Original conceptual illustration only; no fabricated data, docking geometry or clinical extrapolation.

  • Hormones are surrogate endpoints[4]

    SMALL PHYSIOLOGY STUDY · Original publication-grounded diagram

    LH and testosterone responses observed

    5 men with T2DM; 7 controls; long-term clinical benefit unestablished.

    Interpretation: 5 men with T2DM; 7 controls; long-term clinical benefit unestablished. Original conceptual illustration only; no fabricated data, docking geometry or clinical extrapolation.

Follow the evidence

Sources & what they support

  1. PubChem CID 25240297: source reference graph

    Supports: Exact reference graph, stereochemistry, formula and mass

    Original structure record · Download source SDF

    Original PubChem 2D source structure record.

  2. Kisspeptin resets the hypothalamic GnRH clock in men.

    PMID: 21470997 · DOI: 10.1210/jc.2010-3046

    Supports: 13-man acute LH-pulse experiment

  3. Kisspeptin-10 is a potent stimulator of LH and increases pulse frequency in men.

    PMID: 21632807 · DOI: 10.1210/jc.2011-0089

    Supports: Kisspeptin10 human bolus/infusion physiology

  4. Exploring the pathophysiology of hypogonadism in men with type 2 diabetes: kisspeptin-10 stimulates serum testosterone and LH secretion in men with type 2 diabetes and mild biochemical hypogonadism.

    PMID: 23153270 · DOI: 10.1111/cen.12103

    Supports: Small T2DM endocrine proof-of-concept

Source-linked educational drafts. Scientific and clinical review is pending. These cards describe molecules and study context, not product quality, approval or treatment recommendations.

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