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Kisspeptin-10 (Metastin 45-54) — a 10-amino acid C-terminal fragment of the KISS1 gene product. This neuropeptide is a potent endogenous ligand for the GPR54 (KISS1R) receptor and plays a central role in the regulation of the hypothalamic-pituitary-gonadal (HPG) axis. Supplied as a 10mg lyophilized powder in a 3ml vial for research applications studying reproductive endocrinology, GnRH secretion, and neuroendocrine signaling.
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In-depth findings from peer-reviewed preclinical and clinical studies
Kisspeptin-10 (Metastin 45-54) is a 10-amino acid C-terminal fragment of the KISS1 gene product and a potent endogenous ligand for the GPR54 (KISS1R) receptor. It serves as a master upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis, directly stimulating gonadotropin-releasing hormone (GnRH) neurons. Kisspeptin signaling is essential for puberty onset, reproductive function, and neuroendocrine regulation, and has been extensively studied in both preclinical and clinical settings.
Kisspeptin is the most potent known endogenous stimulator of GnRH neurons. Acting via the KISS1R (GPR54) receptor, kisspeptin-10 triggers robust GnRH release from the hypothalamus, leading to dose-dependent increases in circulating LH and FSH in multiple species including humans.
Nature (2001)Loss-of-function mutations in KISS1R (GPR54) cause hypogonadotropic hypogonadism and failure of puberty in humans, establishing kisspeptin signaling as essential for normal sexual maturation. Hypothalamic kisspeptin expression increases dramatically at puberty onset.
New England Journal of Medicine (2003)Intravenous administration of kisspeptin-10 to healthy human volunteers produced a rapid, dose-dependent rise in plasma LH levels, confirming its role as a potent gonadotropin secretagogue in humans and its potential as a diagnostic and therapeutic tool in reproductive medicine.
Journal of Clinical Endocrinology & Metabolism (2005)Kisspeptin neurons in the arcuate nucleus and anteroventral periventricular nucleus serve as critical relay stations for sex steroid feedback. They express estrogen receptor alpha and integrate circulating estradiol and progesterone signals to modulate pulsatile GnRH release.
Endocrinology (2005)Kisspeptin neurons integrate metabolic signals including leptin, insulin, and glucose availability with reproductive output. Caloric restriction suppresses hypothalamic kisspeptin expression, linking energy status to fertility, while kisspeptin administration can rescue metabolic suppression of the HPG axis.
Journal of Neuroscience (2009)Kisspeptin challenge tests have been investigated as a diagnostic tool for distinguishing between hypothalamic and pituitary causes of hypogonadotropic hypogonadism, and for assessing GnRH neuron function in conditions such as hypothalamic amenorrhea and polycystic ovary syndrome.
Peptides (2009)All findings above are sourced from peer-reviewed journals for educational reference. This product is for research purposes only — not for human consumption. Preclinical results may not translate to human outcomes.
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