Kisspeptin-10

clinical trials

Also known as: KP-10, Metastin fragment

Kisspeptin-10 (KP-10), a decapeptide fragment of the metastin/kisspeptin-1 protein, acts as a potent agonist at the KISS1 receptor (KISS1R, GPR54). Its primary mechanism involves direct activation of hypothalamic gonadotropin-releasing hormone (GnRH) neurons, thereby serving as an upstream regulator of the entire reproductive hormone axis. By stimulating pulsatile GnRH secretion, KP-10 indirectly promotes luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release from the anterior pituitary, making it a critical modulator of puberty onset, fertility, and gonadal function. Key research findings from clinical trials demonstrate that exogenous KP-10 administration robustly elevates LH and, to a lesser extent, FSH levels in healthy adults, with effects dependent on dose and route of administration. Studies have shown its utility in diagnosing and treating hypothalamic amenorrhea, hypogonadotropic hypogonadism, and certain forms of infertility, as it can restore endogenous GnRH pulsatility. Additionally, KP-10 has been investigated for its role in metabolic regulation, with evidence linking kisspeptin signaling to energy balance and glucose homeostasis, though these applications remain exploratory. Clinically, KP-10 is being evaluated as a diagnostic tool for assessing hypothalamic-pituitary-gonadal axis integrity and as a therapeutic agent for conditions characterized by impaired GnRH secretion, such as functional hypothalamic amenorrhea. Its rapid onset and short half-life offer advantages over traditional gonadotropin therapies, though further trials are needed to establish optimal dosing, safety, and long-term efficacy. For research purposes only — not medical advice.

Key data

Category
Sexual Health
Molecular weight
1302.4 g/mol
Molecular formula
C63H83N17O14
CAS number
374675-21-5
Administration
subcutaneous, intravenous
Research status
clinical trials
References
319
Tags
gnrh, reproductive, kiss1r

Research & studies

Enzymatic Stability and Comparative Effects of Kisspeptin-14, Kisspeptin-13 and Kisspeptin-10 on Beta-Cell Function, Glucose Homeostasis and Appetite Regulation
Metabolites · 2026 · PubMed
Structural basis for Kisspeptin-10 selectivity toward KISS1R: computational insights
In silico pharmacology · 2026 · PubMed
Chronic subcutaneous kisspeptin-10 stimulates gonadotropin secretion for 12 days in healthy men
European journal of endocrinology · 2026 · PubMed
Dynamic modulation of LH secretion by continuous kisspeptin infusion in healthy men
Hormones (Athens, Greece) · 2026 · PubMed
Kisspeptin-10 Ameliorates Obesity-Diabetes with Diverse Effects on Ileal Enteroendocrine Cells and Pancreatic Islet Morphology in High-Fat Fed Female Mice
Biomolecules · 2025 · PubMed

Kisspeptin-10 reduced body weight, blood glucose, and energy intake to normal diet levels in high-fat fed female mice.; In the ileum, kisspeptin-10 decreased crypt depth, restored villi length to ND levels, and increased the proportion of GIP-positive cells versus HFD mice and GLP-1-positive cells versus ND mice, while PYY immunoreactivity was unaltered.; Circulating GLP-1 and PYY were reduced to ND levels by kisspeptin-10, whereas plasma GIP was unchanged.; In the pancreas, kisspeptin-10 restored relative insulin area to ND levels, normalised glucagon radius and elevated glucagon-islet area, and increased beta-cell proliferation without altering beta-cell apoptosis.

Kisspeptin-10 Preserves the Blood-Brain Barrier's Integrity Post-Stroke by Augmenting Claudin-10 Expression
Clinical and experimental pharmacology & physiology · 2025 · PubMed

Kp-10 expression was reduced in cortical tissue after MCAO, and its administration alleviated neurological deficits and reduced BBB permeability (14C-sucrose leakage).; Kp-10 treatment upregulated Claudin-10 expression in the post-stroke cortex and in OGD/R-exposed HBMVECs, reducing endothelial permeability.; Kp-10 decreased mitochondrial ROS, increased SOD activity, and upregulated Nrf2 expression in vitro.; Nrf2 knockdown abolished Kp-10's protective effects on endothelial permeability and Claudin-10 expression, indicating the Nrf2 pathway is essential.

Oral Engineered Extracellular Vesicles Based on Ion Exchange Strategy for Multipronged Management of Wilson's Disease Complicated with Reproductive Dysfunction Therapy
Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025 · PubMed

CZGE penetrates intestinal and brain barriers after oral administration to target hypothalamic neurons.; Zn-Cur released from CZGE replaces excess Cu2+ via ion exchange, forming Cu-Cur and releasing Zn2+.; Cu-Cur reduces intracellular copper and neuroinflammation via the Nrf2/NLRP3 pathway, while Zn2+ inhibits extracellular copper influx by activating zinc transporter 1.; In WD mice, CZGE alleviates hypothalamic copper deposition, activates ERK1/2 phosphorylation, and repairs reproductive dysfunction by modulating the hypothalamic-pituitary-testicular axis.

Kisspeptin-10 protects against HIV-1 Tat-induced blood-brain barrier dysfunction and neuroinflammation via RhoA/ROCK pathway: Implications for HAND therapy
Neurotoxicology · 2025 · PubMed

Frequently asked questions

What is Kisspeptin-10?

Kisspeptin-10 (KP-10), a decapeptide fragment of the metastin/kisspeptin-1 protein, acts as a potent agonist at the KISS1 receptor (KISS1R, GPR54). Its primary mechanism involves direct activation of hypothalamic gonadotropin-releasing hormone (GnRH) neurons, thereby serving as an upstream regulator of the entire repro

How does Kisspeptin-10 work?

KISS1R agonist decapeptide that triggers hypothalamic GnRH release, upstream regulator of reproductive hormone axis.

What is the research status of Kisspeptin-10?

Kisspeptin-10 is currently classified as clinical trials, with 319 research references on record. This is for research purposes only and is not medical advice.

What is the molecular weight of Kisspeptin-10?

Kisspeptin-10 has a molecular weight of approximately 1302.4 g/mol (formula C63H83N17O14).

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