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Research Overview

Kisspeptin: Neuroendocrine & Reproductive Axis Research Overview

Research Use Only — Not for human or veterinary use, consumption, or administration.

Research At a Glance

Research Category
Reproductive & Endocrine Signaling Research
Peptide Length
10 amino acids (kisspeptin-10 fragment)
Purity
≥ 98% (HPLC)
Published Studies
3,800+ indexed
Storage
Lyophilized: −20 °C long term, 2–8 °C short term. Reconstituted: 2–8 °C, use within 30 days.
Research Use Only

Published-study figures are approximate PubMed result counts and indicate the volume of available literature only. Purity reflects third-party analytical testing on the corresponding lot; see the Quality Assurance Center for lot-matched certificates.

Overview

Kisspeptin refers to a family of neuropeptides encoded by the KISS1 gene, acting through the G-protein-coupled receptor GPR54 (also known as KISS1R). The kisspeptin/GPR54 system is one of the most important upstream regulators of gonadotropin-releasing hormone (GnRH) neurons, making it a central focus of neuroendocrine reproductive research. Kisspeptin neurons in the hypothalamus integrate signals from gonadal steroids, metabolic factors such as leptin, and photoperiod/seasonal cues, positioning the kisspeptin system as a key gatekeeper linking metabolic and reproductive status.

Citation: Oakley A.E., et al., PubMed, 2007

History

KISS1 was originally characterized as a metastasis-suppressor gene in breast cancer and melanoma research before its peptide products were identified as the natural ligand for GPR54. The reproductive significance of the kisspeptin/GPR54 system was established when loss-of-function mutations in GPR54 were found to cause hypogonadotropic hypogonadism in both humans and mice, and gain-of-function mutations were linked to gonadotropin-dependent precocious puberty. This dual discovery — from cancer biology to reproductive neuroendocrinology — established kisspeptin as a critical node for studying the onset of puberty and the broader hypothalamic-pituitary-gonadal (HPG) axis.

Citation: de Roux N., et al., PNAS, 2003; Seminara S.B., et al., NEJM, 2003

Structure

Full-length Kisspeptin (KP-54)Molecular Formula: varies by fragment length (KP-10, KP-13, KP-14, KP-54 are all biologically active cleavage products)
KP-54 Molecular Weightapproximately 6234 g/mol
CAS # (KP-10, most commonly used research fragment)274901-16-5
GeneKISS1
ReceptorGPR54 / KISS1R
FormatLyophilized powder
Purity≥ 98% (HPLC)
Storage−20 °C long term; 2–8 °C short term. Reconstituted: 2–8 °C, use within 30 days.

Research Findings

Kisspeptin has been studied extensively in neuroendocrine, reproductive, and metabolic research models.

Key Areas of Research:

  • Neuroendocrine: GnRH neuron activation, direct stimulation of gonadotropin (LH, FSH) secretion in human and animal studies
  • Reproductive: Puberty onset regulation, sexually dimorphic KISS1 expression patterns, ovulation induction research
  • Metabolic gating: Modulation of KISS1 expression by leptin and nutritional status, linking energy balance to reproductive function
  • Oncology: Original characterization as a metastasis-suppressor gene product in breast cancer and melanoma models; elevated plasma kisspeptin as a marker in gestational trophoblastic neoplasia

Summary: Together, these findings position kisspeptin as a central signaling system bridging metabolic status, puberty, and reproductive hormone regulation. Acute intravenous kisspeptin administration in healthy human male volunteers has been shown to increase LH, FSH, and testosterone, representing some of the more direct human research data among compounds in this catalog, alongside a substantial preclinical literature in rodent models.

Citation: Dhillo W.S., et al. (human kisspeptin administration research)

Source

Review literature available via PubMed — kisspeptin neuroendocrine research .

References

Oakley A.E., Clifton D.K., Steiner R.A. (2007). Kisspeptin signaling in the brain. Endocrine Reviews.

de Roux N., Genin E., Carel J.C., Matsuda F., Chaussain J.L., Milgrom E. (2003). Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54. Proceedings of the National Academy of Sciences.

Seminara S.B., et al. (2003). The GPR54 gene as a regulator of puberty. New England Journal of Medicine.

Dhillo W.S., et al. Kisspeptin-54 stimulates gonadotropin release in healthy men. Journal of Clinical Endocrinology & Metabolism.

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Research Use Only. This content is for laboratory and educational research purposes only. Not a drug, food, cosmetic, or dietary supplement. Not intended for human or veterinary use, consumption, administration, or diagnostic purposes.