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 binding to KISS1R on hypothalamic gonadotropin-releasing hormone (GnRH) neurons, thereby stimulating GnRH secretion. This positions KP-10 as a critical upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis, modulating downstream luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release. Key research findings from clinical trials demonstrate that exogenous KP-10 administration reliably increases LH and FSH levels in healthy adults, with effects dependent on dose and baseline reproductive status. Studies have explored its utility in diagnosing and treating hypogonadotropic hypogonadism, including conditions such as functional hypothalamic amenorrhea and delayed puberty. Additionally, KP-10 has been investigated for its role in modulating reproductive function in assisted reproductive technologies, with evidence suggesting it can trigger an LH surge comparable to human chorionic gonadotropin (hCG) but with a shorter duration of action. Clinically, KP-10 is being evaluated as a diagnostic tool for assessing hypothalamic GnRH reserve and as a potential therapeutic agent for infertility disorders linked to impaired GnRH signaling. Its rapid onset and reversible action offer advantages over traditional hormonal therapies, though its short half-life necessitates careful dosing regimens. Ongoing trials aim to refine its application in reproductive medicine, particularly for conditions where precise control of gonadotropin release is required. For research purposes only — not medical advice.
Key data
C63H83N17O14Research & studies
Kisspeptin-10 is included in the 2024 WADA Prohibited List due to its testosterone-increasing effect.; Four metabolites (y9, y8, y7, y5) were identified and added to the initial testing procedure in full scan mode.; A degradation product likely resulted from oxidation of tryptophan to kynurenine.; A black-market vial showed more degradation than the reference standard but no unexpected impurities.
Gpr54 activation by Kp-10 recruits Dusp18 to dephosphorylate Src at Tyr 416.; Kiss1, Gpr54, and Dusp18 knockout mice exhibit osteoclast hyperactivation and bone loss.; Kp-10 treatment suppresses osteoclast activity and prevents bone loss in vivo.; Kp-10/Gpr54 is a promising therapeutic target for bone resorption via Dusp18-mediated Src dephosphorylation.
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 binding to KISS1R on hypothalamic gonadotropin-releasing hormone (GnRH) neurons, thereby stimulating GnRH secretion. This positions KP-10 as
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 308 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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