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database / hormone

Kisspeptin-10

in clinical study hormone reproductiveendocrine modified — mass check n/a
OOOOOOOOOOOOOONNNNNNNNNNNNNNNNNHHHHHHHHHHHHHHHHHHHHHHHH
94 heavy atoms · 181 bonds · drag to pan, scroll to zoom C63N17O14

Skeletal structure drawn from the computed atomic coordinates in PubChem CID 25240297. Carbons are implicit vertices; hydrogens on carbon are suppressed, as in any structural formula. Nothing here is estimated — every atom sits where PubChem placed it.

Research reference only. The observations below are recorded in the cited literature. Nothing here is advice or a recommendation, and no dosing information is published on this site.

Sequence

YNWNSFGLRF

Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe

1. Tyr — Tyrosine · aromatic · hydropathy -1.3 · charge 0Y12. Asn — Asparagine · polar · hydropathy -3.5 · charge 0N3. Trp — Tryptophan · aromatic · hydropathy -0.9 · charge 0W4. Asn — Asparagine · polar · hydropathy -3.5 · charge 0N5. Ser — Serine · polar · hydropathy -0.8 · charge 0S6. Phe — Phenylalanine · aromatic · hydropathy 2.8 · charge 0F67. Gly — Glycine · glycine · hydropathy -0.4 · charge 0G8. Leu — Leucine · hydrophobic · hydropathy 3.8 · charge 0L9. Arg — Arginine · positive · hydropathy -4.5 · charge +1R10. Phe — Phenylalanine · aromatic · hydropathy 2.8 · charge 0F10

Modified molecule. C-terminal amide; the RF-amide motif is required for receptor activation.

Backbone carries modifications, so computed backbone mass is not comparable to the reported mass of the complete molecule.

Molecular data

Chemical fields come from the PubChem compound record; computed values are derived from the sequence shown above.
molecular formulaC63H83N17O14
molecular weight1302.4 Da (PubChem)
computed backbone mass1303.44 Da
length10 residues
net charge (pH 7.4)+1
mean hydropathy-0.55
half-lifenot characterised
delivery routeintravenous, subcutaneous
PubChem CID25240297
PDBnot characterised
UniProt parentQ15726

Mechanism

KISS1R agonist upstream of GnRH release.

Reported targets: KISS1R

Experimental structure

No experimental structure of this peptide is deposited in the PDB. Nothing is rendered here — a predicted fold would not be a structure, and this site does not draw one.

Position in the parent protein

exact match at residues 112–121 of Metastasis-suppressor KiSS-1 (138 aa)

…APHSRQIPAPQGAVLVQREKDLPNYNWNSFGLRFGKREAAPGNHGRSAGRG

Parent sequence from UniProt Q15726. Kisspeptin-10 is the shortest active C-terminal fragment of KISS1.

Reported effects

Each row is an outcome described in the literature indexed for this peptide. Reported in the cited work — not a claim, not a recommendation.

Reported observations and the corpus they are drawn from.
reported outcomewhere it appears
LH release in trialsChronic subcutaneous kisspeptin-10 stimulates gonadotropin secretion for 12 … European journal of endocrinology 2026
reproductive-axis activationKisspeptin-10 attenuates pulmonary arterial hypertension via restoration of … Neuropeptides 2026

Registered trials

Records from ClinicalTrials.gov. Listed for reference — this project sponsors no trial and is not involved in any of them.
NCTtitlestatusphase
NCT02514629Testosterone, Metformin, or Both, for Hypogonadism in Obese MalesCOMPLETEDPHASE3
NCT01952782Neuropeptides in Human ReproductionCOMPLETEDPHASE1
NCT05971836The Molecular Basis of Inherited Reproductive DisordersCOMPLETED
NCT02369796A Phase 2a Pharmacodynamic Study of TAK-448 in Participants With Hypogonadotropic HypogonadiTERMINATEDPHASE2
NCT07224438Kisspeptin Administration Subcutaneously to Patients With Hypothalamic AmenorrheaRECRUITINGPHASE2

Literature (8)

Chronic subcutaneous kisspeptin-10 stimulates gonadotropin secretion for 12 days in healthy men — European journal of endocrinology 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 42549827 · DOI 10.1093/ejendo/lvag134

Kisspeptin-10 attenuates pulmonary arterial hypertension via restoration of mitochondrial function in pulmonary artery smooth muscle cells — Neuropeptides 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 41955717 · DOI 10.1016/j.npep.2026.102611

Kisspeptin Restores Placental mTOR Signaling and Improves Glucose Homeostasis Mediators Disrupted by Maternal Hypothyroidism in Rats — Acta physiologica (Oxford, England) 2026

AimReduced placental mTOR signaling is associated with intrauterine growth restriction and impaired maternal and placental metabolism. Since maternal hypothyroidism induces intrauterine growth restriction, and maternal treatment with kisspeptin-10 (Kp10) has been shown to improve feto-placental development in hypothyroid rats, this study aimed to evaluate the effects of maternal hypothyroidism, with and without kisspeptin-10 treatment, on maternal energy homeostasis and placental expression of mTOR and glucose metabolism mediators.MethodsMaternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8.ResultsMaternal hypothyroidism caused glucose intolerance, decreased insulin and HDL levels, reduced fetal and placental weights, and thinned the placental interhaemal barrier. It also increased INSRβ and AKT, while downregula…

open access ↗ · PMID 41782211 · DOI 10.1111/apha.70188

Kisspeptin-10 Ameliorates Obesity-Diabetes with Diverse Effects on Ileal Enteroendocrine Cells and Pancreatic Islet Morphology in High-Fat Fed Female Mice — Biomolecules 2025

Kisspeptin is a neuropeptide recognised for a pivotal role within the reproductive system, but potentially important endocrine metabolic effects are less well understood. We examined effects of twice-daily intraperitoneal administration of saline vehicle or kisspeptin-10 ([dose redacted]), for 21 days, on glucose homeostasis, energy balance, circulating hormones as well as the morphology-function of enteroendocrine and islet cells in high-fat diet (HFD) fed female mice, with normal diet (ND) mice as an additional control group. Kisspeptin-10 decreased body weight, blood glucose and energy intake to ND levels. HFD increased circulating follicle-stimulating hormone (FSH) levels, which were further enhanced by kisspeptin-10 along with luteinising hormone (LH) concentrations. Neither HFD nor kisspeptin-10 affected progesterone or corticosterone. In the ileum, kisspeptin-10 decreased crypt depth a…

open access ↗ · PMID 41301510 · DOI 10.3390/biom15111591

Integrated transcriptomics and miRNA-mRNA network analysis reveals Kisspeptin-10 mediated regulation of EMT and apoptosis in glioblastoma — Computational biology and chemistry 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 41389577 · DOI 10.1016/j.compbiolchem.2025.108826

Exogenous Kisspeptin-10 inhibits ovarian cancer progression through targeting the SP1-hTERT-ZEB1 regulatory axis — Cytotechnology 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 42292313 · DOI 10.1007/s10616-026-01005-8

Kisspeptin-10 regulates glycosaminoglycan and decorin content in human cardiac fibroblast cultures — Pharmacological reports : PR 2026

abstract not reproduced — this record is not open-access, so it is linked rather than copied.

publisher record ↗ · PMID 42159865 · DOI 10.1007/s43440-026-00870-6

Exogenous kisspeptin-10 treatment shows pleiotropy via induction of KISS1 expression, metastasis suppression, and promotes apoptosis in triple-negative breast cancer — Scientific reports 2025

Triple-negative breast cancer (TNBC) is an aggressive subtype lacking ER, PR, and HER2 receptors making it highly clinically challenging subtype pf breast cancer. In this study, we investigated the effect of exogenous Kisspeptin-10 (Kp-10), on MDA-MB-231 and MDA-MB-468 cells. TNBC cells using both in vitro and in silico approaches. Kp-10 treatment significantly reduced cell viability and migration and induced a dose-dependent upregulation of KISS1 mRNA, suggesting a positive feedback loop. Alongside this, Kp-10 modulated key transcription factors-upregulating GATA2, CDX2, and FLI1 while downregulating ZEB1-indicating a shift towards a less aggressive transcriptional state. EMT reversal was evident from increased E-cadherin and β-catenin, and reduced N-cadherin, CD44, and Vimentin. Pro-apoptotic genes CASP3, CASP8, CASP9, and BAX were upregulated, while BCL2 was suppressed, suggesting act…

open access ↗ · PMID 41062590 · DOI 10.1038/s41598-025-19140-1

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