Kisspeptin-10 (Kp-10) is the C-terminal 10 amino acid active fragment of the KISS1 gene product — the endogenous ligand for the kisspeptin receptor (KISS1R, formerly GPR54). Kisspeptin neurons in the hypothalamic arcuate nucleus (KNDy neurons — co-expressing Kisspeptin, Neurokinin B, and Dynorphin) act as the GnRH pulse generator: kisspeptin release directly stimulates GnRH neuron firing, which drives pulsatile LH and FSH secretion from the anterior pituitary. Kisspeptin-10 is the most potent and widely studied active fragment — equivalent in KISS1R potency to the full-length kisspeptin-54 with much smaller size. It is the essential research tool for studying the upstream regulation of GnRH pulsatility, hypogonadotropic hypogonadism, pubertal timing, and sex steroid-mediated feedback on the HPG axis.
KISS1R
Primary receptor — hypothalamic KNDy neurons
~28 min
IV half-life
1302.4 g/mol
Molecular weight
GnRH → LH/FSH
Downstream hormonal cascade
≥99%
Purity — HPLC verified
Kisspeptin-10 — Specifications
Kisspeptin-10 — specifications
Property
Value
CAS Number
374683-27-9
Molecular Formula
C₆₃H₈₃N₁₅O₁₄
Molecular Weight
1302.4 g/mol
Half-life
~28 min (IV); longer SC
Class
Kisspeptin/KISS1R agonist — GnRH pulse generator
Purity
≥99% HPLC verified
COA
Janoshik independent third-party
⚙️
Mechanism of Action — Kisspeptin-10
Kisspeptin-10 activates KISS1R (Gq/11-coupled GPCR) on GnRH neurons and peripheral reproductive tissues:
KNDy neuron circuit: Arcuate KNDy neurons autosynchronise via NKB (neurokinin B) stimulation and dynorphin inhibition → kisspeptin released in synchronised pulse → GnRH pulse. This is the pulse generator mechanism.
Testosterone/oestrogen feedback: Sex steroids regulate kisspeptin neuron firing — oestrogen increases kisspeptin in AVPV (positive feedback for LH surge) and suppresses it in arcuate (negative feedback). Kisspeptin-10 allows HPG axis research downstream of this feedback.
Pituitary: KISS1R on gonadotrophs — kisspeptin-10 has direct LH-releasing effect at pituitary level independent of GnRH, providing a diagnostic tool for GnRH vs pituitary deficit distinction.
Kisspeptin-10 as a clinical diagnostic tool for hypogonadism
Kisspeptin-10 IV bolus is used clinically to distinguish hypothalamic from pituitary hypogonadism: if IV kisspeptin-10 stimulates LH release, the GnRH neuron and pituitary are intact — the deficit is upstream (kisspeptin neuron failure). If kisspeptin-10 fails to stimulate LH, the pituitary gonadotroph is the site of dysfunction. This diagnostic stratification is used in clinical research for congenital hypogonadotropic hypogonadism (CHH) and Kallmann syndrome — and is directly testable in rodent models with QSC kisspeptin-10.
Key Research Studies & Clinical Data
Key kisspeptin research
Study
Population/Model
Key finding
Dhillo et al. 2005 (J Clin Endo)
Healthy men, IV kisspeptin-10
Dose-dependent LH secretion — established kisspeptin-10 as a GnRH secretagogue in humans
Jayasena et al. 2014 (J Clin Endo)
Hypogonadal men, kisspeptin-54 SC
Kisspeptin restored LH pulsatility and testosterone in hypogonadotropic hypogonadism
Seminara et al. 2003 (NEJM)
KISS1R knockout patients
Loss-of-function mutations → hypogonadotropic hypogonadism — established KISS1R as essential for HPG axis
Research Protocols — Kisspeptin-10
Protocol 1: GnRH pulse generator characterisation
Kisspeptin-10 10 nmol/kg IV bolus in male rats. Serial LH blood draws (0, 5, 10, 15, 20, 30, 45, 60 min) — LH pulse amplitude and duration (ELISA). Compare vs GnRH bolus to distinguish hypothalamic vs direct pituitary action.
Protocol 2: Hypogonadotropic hypogonadism model
Hypothalamic lesion (bilateral arcuate nucleus) in rats → confirm LH/FSH suppression. Kisspeptin-10 10–100 nmol/kg IV — test LH rescue (intact pituitary with hypothalamic deficit). Compare vs GnRH analog.
Protocol 3: Testosterone feedback inhibition
Intact male rats + testosterone cypionate (HPG suppression) → kisspeptin-10 bolus. LH response vs vehicle-treated — quantifies testosterone-mediated kisspeptin suppression of GnRH axis.
Kisspeptin-10 is the C-terminal 10 amino acid active fragment of the KISS1 protein — the endogenous ligand for the KISS1R receptor. It is the master activator of GnRH neurons in the hypothalamus, controlling GnRH pulsatility and the downstream HPG axis (LH → FSH → gonadal steroidogenesis).
How does kisspeptin control GnRH pulsatility?
KNDy neurons (co-expressing Kisspeptin, Neurokinin B, Dynorphin) in the arcuate nucleus synchronise into pulses via NKB mutual stimulation and dynorphin-mediated negative feedback. Each synchronised kisspeptin burst triggers a GnRH pulse → LH/FSH pulse. Kisspeptin-10 is the direct activating signal at GnRH neurons.
What is Kallmann syndrome and how is kisspeptin-10 used in research?
Kallmann syndrome is hypogonadotropic hypogonadism with anosmia — caused by GnRH neuron migration failure. Kisspeptin-10 bolus in Kallmann patients fails to stimulate LH because the GnRH neurons are absent — confirming hypothalamic (not pituitary) deficit. Rodent models allow mechanistic study of this diagnostic application.
How does kisspeptin-10 differ from GnRH in research?
GnRH directly stimulates anterior pituitary gonadotrophs. Kisspeptin-10 acts one step upstream — on GnRH neurons. This distinction allows researchers to locate HPG axis deficits precisely. Kisspeptin-10 also has direct KISS1R on pituitary gonadotrophs, allowing parallel study of both hypothalamic and pituitary components.
What formats does QSC supply kisspeptin-10 in?
QSC supplies kisspeptin-10 as lyophilised research vials, ≥99% purity HPLC verified with Janoshik COA. Ships from domestic QSC warehouses in USA, EU, UK, Canada, and Australia.
Research Use Only: All QSC compounds are sold strictly for laboratory research purposes. Not for human use. Not approved by the FDA or equivalent regulatory bodies for human administration. All purchases confirm research intent and compliance with applicable local regulations.
