KissPeptin-10

A short form of kisspeptin, the hormone that sits at the top of your reproductive hormone system. It directly tells the brain to release the signals that kick off the whole chain — FSH, LH, and ultimately testosterone or estrogen. Researchers are studying it as a possible alternative to other fertility hormones, with potentially fewer issues of the body 'getting used to' it.

Dosage

Research only — 0.1-1 nmol/kg IV or subcutaneous

Dosages shown are for research reference only. Always consult a qualified healthcare provider.

Half-Life

28 minutes (shorter than full-length kisspeptin-54)

Half-Life Calculator →

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Effects

HPG Axis Stimulation

Master upstream regulator — triggers the entire reproductive hormone cascade.

Fertility

May help trigger ovulation and restore reproductive hormone function.

Hormone Regulation

Master upstream signal that controls the entire reproductive hormone chain.

Mechanism of Action

KissPeptin-10 is the shortest bioactive fragment of the kisspeptin family, derived from the 145-amino-acid precursor protein encoded by the KISS1 gene. The kisspeptin system was identified as the master upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis when loss-of-function mutations in its receptor (KISS1R/GPR54) were found to cause hypogonadotropic hypogonadism — complete failure of puberty and reproductive function.

Kisspeptin-10 binds to KISS1R (formerly GPR54), a Gq/11-coupled GPCR expressed predominantly on GnRH neurons in the hypothalamus, specifically in two key nuclei: the arcuate nucleus (ARC) and the anteroventral periventricular nucleus (AVPV). KISS1R activation stimulates phospholipase C, generating IP3 and DAG, which raise intracellular calcium and activate protein kinase C in GnRH neurons. This depolarizes the neurons and triggers GnRH release into the hypophyseal portal system, which then stimulates FSH and LH secretion from anterior pituitary gonadotrophs.

What makes kisspeptin extraordinary is its position at the very apex of the reproductive hormone cascade. It sits upstream of GnRH itself, integrating metabolic, circadian, and hormonal signals to determine when and how strongly GnRH pulses fire. Kisspeptin neurons in the ARC co-express neurokinin B and dynorphin (forming the 'KNDy' neuron population) and function as the GnRH pulse generator — the fundamental oscillator that drives pulsatile reproductive hormone secretion. Estradiol and testosterone feed back to kisspeptin neurons (not directly to GnRH neurons) to regulate the HPG axis, making kisspeptin the integration point for sex steroid feedback. This upstream position makes kisspeptin-10 a uniquely powerful tool for stimulating the entire reproductive axis from the top, with clinical potential for triggering ovulation in IVF protocols and restoring fertility in functional hypogonadism.

Regulatory Status

Not FDA approved. Active clinical research for fertility disorders and hypogonadism. Imperial College London conducting key trials. Promising but still investigational.

Risks & Safety

Common

facial flushing, headache, feeling warm.

Serious

repeated dosing can cause unpredictable swings in reproductive hormones; continuous use can suppress hormone production instead of boosting it; very limited human safety data.

Rare

allergic reactions.

Compare KissPeptin-10 With

Research Papers

30
Integrated transcriptomics and miRNA-mRNA network analysis reveals Kisspeptin-10 mediated regulation of EMT and apoptosis in glioblastoma.

Published: April 9, 2026

AI Summary

Kisspeptin-10 influenced genes and pathways linked to cell migration and death in glioblastoma, with hub genes like CDK1 and JUN and miRNAs like miR-200. Lab experiments supported its effects on these markers, suggesting it could be useful for diagnosis and treatment of this aggressive brain cancer.

Dual role of Kisspeptin-10 in modulating neuroinflammation: Downregulation of NLRP3 inflammasome activation and Caspase-1-mediated pyroptosis, and activation of BAG3-dependent aggrephagy in microglial cells.

Published: February 5, 2026

AI Summary

Kisspeptin-10 reduced NLRP3 inflammasome activation and pyroptosis in microglia while promoting BAG3-dependent aggrephagy. The dual effect suggests kisspeptin-10 could help control neuroinflammation in neurodegenerative diseases.

High-Fat Diet Promotes Glycolysis in Hepatocellular Carcinoma by Suppressing Hepatic Kisspeptin Signaling in Mice.

Published: February 1, 2026

AI Summary

A high-fat diet suppressed liver kisspeptin signaling and promoted liver cancer in mice, while kisspeptin-10 slowed tumor growth and reduced glycolytic enzyme levels. The results point to kisspeptin as a possible target for liver cancer in people with metabolic syndrome.

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

Published: November 12, 2025

AI Summary

Kisspeptin-10 normalized weight, blood sugar, and gut and pancreatic cell changes in obese female mice. It increased GIP and GLP-1 cells in the gut and improved insulin area and beta-cell growth in the pancreas, revealing a metabolic role for kisspeptin beyond reproduction.

Intravenous kisspeptin 112-121 bolus does not acutely impact circulating vasopressin in humans.

Published: January 21, 2026

AI Summary

An intravenous kisspeptin bolus did not change vasopressin levels in healthy adults, so it does not appear useful as a provocative test for vasopressin deficiency. The lack of effect may be due to dose, route, or species differences.

Decidual cell invasion and decidualization at the trophoblast-decidual interaction in the progression of cesarean scar pregnancy.

Published: December 24, 2025

AI Summary

Lower KISS1 in decidual cells was linked to cesarean scar pregnancy, and restoring KISS1 increased cell invasion and migration via the PI3K/AKT pathway. The work suggests KISS1 helps balance trophoblast–decidua interactions and may be relevant to scar pregnancy.

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

Published: October 7, 2025

AI Summary

Kisspeptin-10 reduced triple-negative breast cancer cell growth and migration, reactivated KISS1, reversed EMT, and promoted apoptosis. The findings support exploring kisspeptin-10 as a treatment for this aggressive breast cancer subtype.

Kisspeptin-10 Improves Gestational Diabetes Mellitus Symptoms in Rats by Suppressing Insulin Resistance in Placental Trophoblast Cells by Activating the Cyclic AMP/Protein Kinase A Pathway.

Published: September 7, 2025

AI Summary

Kisspeptin-10 improved blood sugar, insulin sensitivity, and fetal outcomes in gestational diabetes rats by restoring the cAMP/PKA pathway and glucose uptake in placental cells. The results suggest it could help treat insulin resistance in GDM.

Kisspeptin as a marker for male infertility: a comparative study of serum and seminal plasma kisspeptin between fertile and infertile men.

Published: November 10, 2025

AI Summary

Serum and seminal kisspeptin were compared between fertile and infertile men with abnormal semen. The work aims to determine whether kisspeptin can serve as a biomarker for male infertility.

Associations between kisspeptin hormone level and its genetic polymorphisms with polycystic ovary syndrome.

Published: January 23, 2026

AI Summary

Kisspeptin levels and gene variants were examined in women with PCOS, given its role in reproductive hormone regulation. Prior studies have been inconsistent, and this work aims to clarify the relationship.

The association between 1st trimester serum kisspeptin level and antenatal complications.

Published: July 14, 2025

AI Summary

First-trimester serum kisspeptin was evaluated as a predictor of pregnancy complications. The work aims to determine whether this biomarker can identify women at higher risk early in pregnancy.

Kisspeptin Suppresses the Growth of Primary Pterygial Cells via Inhibiting Chemokine (C-X-C Motif) Ligands in Microenvironment.

Published: September 23, 2025

AI Summary

Kisspeptin slowed growth of pterygium cells by blocking chemokine ligands in the microenvironment. The findings may support new biomarkers and treatments for this common eye condition.

Hypothalamic kisspeptin alleviates myasthenia gravis by regulating Th1/Th17/Treg balance through Inhibition of NF-κB signaling pathway.

Published: June 15, 2025

AI Summary

Kisspeptin improved myasthenia gravis in a mouse model by rebalancing Th1, Th17, and Treg cells and inhibiting NF-kappaB. The results suggest kisspeptin may influence autoimmune disease through neuroendocrine–immune crosstalk.

Effects of Kisspeptin on rabbit ovulation: a comprehensive study of ovulatory, endocrine and histological response.

Published: September 30, 2025

AI Summary

Kisspeptin-10 induced ovulation in 87.5% of rabbits, matching GnRH, though progesterone was lower. The peptide promoted follicle development and blood vessel growth, suggesting it could be an alternative to GnRH for ovulation induction in rabbits.

Kisspeptin system-physiology and clinical perspectives.

Published: July 27, 2025

AI Summary

Kisspeptin affects cancer cell migration and controls the reproductive axis. The review summarizes current knowledge on its physiology and potential clinical uses.

Kisspeptin Receptor Agonists and Antagonists: Strategies for Discovery and Implications for Human Health and Disease.

Published: May 19, 2025

AI Summary

The kisspeptin receptor system is involved in reproduction, cancer, diabetes, and heart disease. The article reviews methods for finding agonists and antagonists and discusses challenges and future directions for drug development.

Kisspeptin-10 Protects Against TNF-α-Induced Chondrocyte Senescence via the SIRT1/p53/p21 Signaling.

Published: June 11, 2025

AI Summary

Kisspeptin-10 reduced TNF-induced chondrocyte senescence in osteoarthritis by restoring SIRT1 and suppressing the p53/p21 pathway. The findings suggest kisspeptin-10 could help protect cartilage and slow OA progression.

Kisspeptin-10 Prevents the Development of Cerebral Aneurysms by Reducing the Expression of Egr-1.

Published: May 2, 2025

AI Summary

Kisspeptin-10 reduced Egr-1 expression and limited cerebral aneurysm development in a mouse model. The work explores whether the kisspeptin/GPR54 system could be a target for preventing or treating brain aneurysms.

Adult Neurogenesis Is Regulated by the Endocannabinoid and Kisspeptin Systems.

Published: April 22, 2025

AI Summary

Kisspeptin-10 and the endocannabinoid anandamide both reduced hippocampal neurogenesis in adolescent rats via ERK signaling, with TRPV1 as a shared mediator. The results suggest crosstalk between these systems in regulating brain plasticity.

The effect of COVID-19 on placental functioning in South African pregnancies: investigation of kisspeptin expression and vascular and inflammatory alterations.

Published: May 4, 2025

AI Summary

Placentas from COVID-19 pregnancies in South Africa had higher kisspeptin expression and more inflammation and vascular problems. The findings support ongoing monitoring of mothers and babies after COVID-19 during pregnancy.

Kisspeptin 10 Inhibited the Proliferation, Migration, and Stemness of Esophageal Cancer Cells via Regulating the SIX1/Wnt/β-Catetin Signaling.

Published: April 10, 2025

AI Summary

Kisspeptin-10 slowed esophageal cancer cell growth, migration, and stemness by blocking the SIX1/Wnt/beta-catenin pathway. The results suggest kisspeptin-10 could be a therapeutic target for this aggressive cancer.

Can kisspeptin be a new treatment for sexual dysfunction?

Published: November 4, 2025

AI Summary

Kisspeptin activates reproductive hormones and brain regions involved in sexual and emotional processing, making it a candidate for treating low sexual desire. Better delivery methods and understanding of sex-specific effects are needed before clinical use.

New Insights in Bovine Follicular Cysts.

Published: March 19, 2025

AI Summary

Cows with follicular cysts had higher kisspeptin-10, GnIH, LH, and estrogen, and lower GPR54 in cystic follicles. The findings suggest hormonal imbalance in the hypothalamic–pituitary–ovarian axis contributes to cyst formation.

Kisspeptin Administration Stimulates Reproductive Hormones but Does Not Affect Anxiety in Humans.

Published: October 15, 2025

AI Summary

Kisspeptin increased reproductive hormones in humans but did not change anxiety levels. The results clarify that kisspeptin’s clinical potential lies in reproductive and psychosexual disorders rather than anxiety.

Association between PFAS exposure and metabolic-related biomarkers in Spanish adolescents.

Published: May 14, 2025

AI Summary

PFAS exposure was linked to metabolic biomarkers in Spanish adolescents, with kisspeptin possibly involved. The work explores how these chemicals may disrupt the endocrine–metabolic axis.

Sex-dependent increases in oxytocin levels in response to intravenous kisspeptin in humans.

Published: March 2, 2025

AI Summary

Intravenous kisspeptin increased oxytocin levels in healthy adults, with a stronger effect in women. The results support kisspeptin as a possible provocative test for oxytocin deficiency.

Dysregulated serum levels of kisspeptin, NKB, GABA in women with polycystic ovary syndrome and their association with hormonal profiles.

Published: December 10, 2025

AI Summary

Serum kisspeptin, NKB, and GABA were altered in Chinese women with PCOS and linked to hormone profiles. The work explores whether these markers could help characterize or diagnose PCOS.

Association of Kisspeptin and KISS1 Gene Polymorphism (rs35431622) with Circulating Sex Hormones and Male Infertility.

Published: March 4, 2025

AI Summary

Infertile men with low sperm count had lower kisspeptin and free testosterone and higher LH and FSH. A KISS1 gene variant was more common in infertile men, suggesting kisspeptin may be a marker for male reproductive health.

The Neuroendocrine Regulation of Reproductive Behavior and Emotional Control by Kisspeptin.

Published: May 18, 2025

AI Summary

Kisspeptin regulates reproductive behavior and emotional state through brain regions beyond the hypothalamus. The evidence supports exploring kisspeptin-based therapies for reproductive and psychosexual disorders.

Distribution of the kisspeptin system and its relation with gonadotropin-releasing hormone in the hypothalamus.

Published: June 24, 2025

AI Summary

Kisspeptin, originally identified as a metastasis suppressor, is now known as a key regulator of puberty and GnRH release. The chapter discusses its distribution and role in reproduction across rodents, fish, and birds.

Frequently Asked Questions

What is KissPeptin-10?

A short form of kisspeptin, the hormone that sits at the top of your reproductive hormone system. It directly tells the brain to release the signals that kick off the whole chain — FSH, LH, and ultimately testosterone or estrogen. Researchers are studying it as a possible alternative to other fertility hormones, with potentially fewer issues of the body 'getting used to' it.

What is KissPeptin-10 used for?

A short form of kisspeptin, the hormone that sits at the top of your reproductive hormone system. It directly tells the brain to release the signals that kick off the whole chain — FSH, LH, and ultimately testosterone or estrogen. Researchers are studying it as a possible alternative to other fertility hormones, with potentially fewer issues of the body 'getting used to' it.

What is the dosage for KissPeptin-10?

Clinical trials: 0.1-1 nmol/kg intravenous bolus or subcutaneous. No established therapeutic dosing protocol. Research protocols vary significantly between studies.

What are the side effects of KissPeptin-10?

Common: facial flushing, headache, feeling warm. Serious: repeated dosing can cause unpredictable swings in reproductive hormones; continuous use can suppress hormone production instead of boosting it; very limited human safety data. Rare: allergic reactions.

How does KissPeptin-10 work?

KissPeptin-10 is the shortest bioactive fragment of the kisspeptin family, derived from the 145-amino-acid precursor protein encoded by the KISS1 gene. The kisspeptin system was identified as the master upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis when loss-of-function mutations in its receptor (KISS1R/GPR54) were found to cause hypogonadotropic hypogonadism — complete failure of puberty and reproductive function. Kisspeptin-10 binds to KISS1R (formerly GPR54), a Gq/11-coupled GPCR expressed predominantly on GnRH neurons in the hypothalamus, specifically in two key nuclei: the arcuate nucleus (ARC) and the anteroventral periventricular nucleus (AVPV). KISS1R activation stimulates phospholipase C, generating IP3 and DAG, which raise intracellular calcium and activate protein kinase C in GnRH neurons. This depolarizes the neurons and triggers GnRH release into the hypophyseal portal system, which then stimulates FSH and LH secretion from anterior pituitary gonadotrophs. What makes kisspeptin extraordinary is its position at the very apex of the reproductive hormone cascade. It sits upstream of GnRH itself, integrating metabolic, circadian, and hormonal signals to determine when and how strongly GnRH pulses fire. Kisspeptin neurons in the ARC co-express neurokinin B and dynorphin (forming the 'KNDy' neuron population) and function as the GnRH pulse generator — the fundamental oscillator that drives pulsatile reproductive hormone secretion. Estradiol and testosterone feed back to kisspeptin neurons (not directly to GnRH neurons) to regulate the HPG axis, making kisspeptin the integration point for sex steroid feedback. This upstream position makes kisspeptin-10 a uniquely powerful tool for stimulating the entire reproductive axis from the top, with clinical potential for triggering ovulation in IVF protocols and restoring fertility in functional hypogonadism.

How is KissPeptin-10 administered?

KissPeptin-10 is administered via subcutaneous or intravenous injection.

What is the half-life of KissPeptin-10?

The half-life of KissPeptin-10 is 28 minutes (shorter than full-length kisspeptin-54).

Is KissPeptin-10 legal?

Not FDA approved. Active clinical research for fertility disorders and hypogonadism. Imperial College London conducting key trials. Promising but still investigational.

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