Kisspeptin-10
clinical trialsAlso 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
C63H83N17O14Research & studies
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.
Kp-10 ameliorated TNF-α-induced senescence in chondrocytes, reducing SA-β-gal staining and increasing telomerase activity.; Kp-10 modulated expression of hTERT and TERF2, and suppressed the p53/p21 pathway.; Kp-10 restored SIRT1 expression, which was downregulated by TNF-α.; Silencing SIRT1 abolished Kp-10's protective effects, indicating SIRT1 is essential for its anti-senescence action.
KP-10 levels were reduced in both cerebral aneurysm patients and mouse models.; KP-10 reduced cerebral aneurysm size in wild-type mice but not in Gpr54 knockout mice.; KP-10 inhibited Ang II-induced proliferation, tube formation, and VEGF-A expression in HBMVECs by reducing Egr-1.; The effects of KP-10 were dependent on Gpr54, as they were abolished in Gpr54 knockdown conditions.
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 313 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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