Kisspeptin-10 Nasal Spray 10mg

Kisspeptin-10 is a synthetic compound built from ten amino acids. The sequence corresponds to the final ten residues at the C-terminus of a larger protein encoded by the KiSS-1 gene. That parent protein, first characterised in 2001, was shown to be the natural ligand of a receptor that had until then sat unmatched in the genome (PMID 11385580, PMID 11457843). The shortest fragment that still binds and fully activates the receptor is this ten-residue piece, and that fragment is the compound supplied here as Kisspeptin-10.

The receptor it targets is KISS1R, a G-protein-coupled receptor originally catalogued under the name GPR54. Two structural points matter for activity. The peptide is amidated at its C-terminus, ending in an arginine-phenylalanine-amide motif; this RF-amide ending is conserved across the kisspeptin family and is required for the molecule to engage its receptor. The tryptophan and phenylalanine residues in the chain contribute the aromatic contacts that the binding pocket recognises. Truncate the C-terminus and activity falls away, which is why the ten-residue form, rather than a shorter piece, is the standard minimal agonist used in research.

The compound is supplied as a lyophilized — freeze-dried — white powder in a lyophilized in a 10 mL intranasal-spray bottle; reconstituted with the included 0.3% potassium sorbate solution. Each vial contains 10 mg of peptide. Reconstitution with bacteriostatic water is required before the peptide can be drawn into an insulin syringe. Reconstitution mechanics are covered in the Reconstitution accordion.

Kisspeptin-10 sits at the centre of a large reproductive-endocrinology literature that grew quickly after the receptor link was established. A pair of 2003 human-genetics studies tied loss-of-function mutations in the receptor to absent puberty and low gonadotropin output, which repositioned the whole kisspeptin system as a gatekeeper of the reproductive axis (PMID 12944565, PMID 14573733). A 2012 review in Physiological Reviews compiled the physiology in depth (PMID 22811428), and a 2014 review in Human Reproduction Update organised the human-focused findings across health and disease states (PMID 24615662).

Across this literature the compound appears under more than one name. Kisspeptin-10 and the abbreviation KP-10 are the most common. The fragment is also written as metastin 45-54, reflecting its position within the parent metastin sequence, and as KiSS-1 (112-121). These names refer to the same ten-amino-acid sequence. The CAS registry number 374675-21-5 and PubChem CID 25240297 are the canonical chemical identifiers.

No regulatory authority — Health Canada, the FDA, the EMA, the TGA, or any equivalent — has cleared Kisspeptin-10 for therapeutic use in humans or animals. Ronin Peptides ships the compound exclusively as a research-grade reagent for benchwork. Dosing protocols, treatment regimens, and administration instructions are out of scope and are not provided in any form.

The defining mechanistic finding is that Kisspeptin-10 binds KISS1R on gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus and drives those neurons to release GnRH (PMID 15665093). KISS1R is a Gq/11-coupled receptor; once kisspeptin engages it, the downstream cascade runs through phospholipase C activation, intracellular calcium mobilisation, and membrane depolarisation of the GnRH neuron. The net result documented across this work is increased GnRH secretion into the hypophyseal portal circulation.

That GnRH pulse is the first step in a three-tier signalling chain. Elevated GnRH reaching the anterior pituitary raises secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH); the raised gonadotropins in turn raise gonadal sex-steroid output. Research has positioned kisspeptin upstream of this entire hypothalamic-pituitary-gonadal axis rather than acting on the pituitary directly, with the GnRH neuron as the obligatory relay (PMID 22811428). This upstream position is why the 2003 receptor-mutation findings produced such a complete loss of reproductive-axis function (PMID 12944565, PMID 14573733).

One pharmacokinetic feature shapes how the ten-residue form is interpreted against its longer relatives. Kisspeptin-10 carries a short circulating half-life, reported in human work on the order of a few minutes, because it is cleared and degraded rapidly once in plasma. The 54-residue form, by contrast, produces a more sustained effect in vivo. A 2017 study examined the mechanistic basis for that difference, attributing the longer-form advantage to slower clearance and prolonged receptor exposure rather than to any difference in intrinsic receptor activation (PMID 28464043). For researchers, the short half-life of the decapeptide is a defining handling characteristic, not a defect.

Mechanism research on the system remains active. The receptor's expression has been mapped not only on GnRH neurons but across several peripheral tissues, and reviews have documented candidate roles beyond the classical reproductive-axis framing (PMID 24615662, PMID 39287750). The reproductive-axis pathway, however, remains the best-characterised and most-replicated mechanism in the literature.

The largest body of research on Kisspeptin-10 covers activation of the reproductive axis. Human administration studies have reported that kisspeptin raises circulating LH, FSH, and downstream sex steroids. A 2011 study examined this compound specifically and documented potent stimulation of LH together with an increase in LH pulse frequency in men (PMID 21632807). The pulse-frequency finding is significant because pulsatile GnRH signalling, rather than steady tonic signalling, is what the reproductive axis is built to read. This makes the compound useful as a probe of axis function in research settings.

Work on the longer 54-residue form sketched the same axis-activation picture earlier. A 2005 study reported that kisspeptin administration raised gonadotropins and testosterone in human males (PMID 16174713), and a 2007 study reported that the gonadotropin response in women varied with menstrual-cycle phase, peaking in the preovulatory window (PMID 17635940). A 2016 study examined subcutaneous infusion in women and documented that the response correlated with baseline oestradiol (PMID 26572695). Together these studies map a response that depends on dose, route, sex, and endocrine state.

The reproductive-genetics stream is the historical foundation of the field. Two independent 2003 studies linked loss-of-function mutations in the kisspeptin receptor to hypogonadotropic hypogonadism and failure to enter puberty (PMID 12944565, PMID 14573733). These human findings, paired with parallel mouse data, established that an intact kisspeptin-receptor system is required for normal reproductive maturation — a stronger claim than any pharmacology study alone could support.

Reviews have compiled the investigational reproductive-endocrinology applications that follow from this biology. A 2012 comprehensive review surveyed the physiological roles and regulatory mechanisms across species (PMID 22811428), and a 2014 review focused on the human kisspeptin-GnRH pathway in health and disease (PMID 24615662). A 2024 review examined the system in the context of functional hypothalamic amenorrhea and discussed its investigational therapeutic potential (PMID 39287750). Each of these is a review of research findings, not a statement of approved use.

Translation to approved clinical application has not occurred. The human studies above are mechanistic and investigational, conducted under research protocols, and the compound has not progressed through a drug-approval pathway. Researchers planning new work should review the most current literature before designing protocols, with attention to the short half-life of the ten-residue form and the dose- and route-dependence of the gonadotropin response.

Unopened lyophilized vials hold up well under dry ambient storage; usable activity persists for several weeks even without refrigeration. The recommended container is the unopened original vial — keep the seal intact until reconstitution. Refrigeration at 2–8 °C is appropriate once the working timeline extends past a month. A standard freezer at −20 °C handles archival storage; ultra-low storage at −80 °C is rarely needed for typical bench-research timescales.

Keep vials shielded from light, ideally in their original outer packaging. Repeated temperature cycling accelerates degradation noticeably more than steady storage at any single temperature inside the recommended bands — minimise transitions between cold and ambient.

After reconstitution, refrigerate the solution at 2–8 °C without delay. The typical working window for a reconstituted preparation is four to six weeks at fridge temperature. Past that window, peptide concentration drifts downward through chemical degradation pathways even though the bacteriostatic water's benzyl alcohol still suppresses microbial growth. The 0.9% benzyl alcohol holds back bacterial contamination — the dominant spoilage path — but does not arrest the slower hydrolysis, oxidation, and aggregation processes that accumulate in any aqueous peptide solution. The methionine-free sequence of this decapeptide reduces one oxidation route, but tryptophan remains oxidation-sensitive, so light protection still matters for a reconstituted solution.

When a research timeline extends past six weeks, common practice is splitting the reconstituted solution into single-use volumes and freezing them at −20 °C immediately. Ice-crystal formation during each freeze-thaw cycle inflicts mechanical damage on peptide chains, and pre-splitting eliminates the cumulative loss that comes from thawing one vial multiple times. Thaw individual aliquots overnight in a refrigerator — never at room temperature — and use them within a few days of thaw.

The reconstituted product should be visually clear and colourless. Discard any vial showing turbidity, suspended particulate, yellowing, or visible precipitate. The diluent of choice is USP-grade bacteriostatic water containing 0.9% benzyl alcohol — see the bacteriostatic water product page for reconstitution-grade water.

The closest relative to this compound is Kisspeptin-54, the longer fragment of the same parent protein. Both engage the same receptor through the same C-terminal motif; the practical difference researchers report is duration of action, since the ten-residue form clears faster than the 54-residue form (PMID 28464043). Selank and Semax are listed here as other short signalling peptides in the Ronin catalog, but they act through unrelated pathways and are not substitutes — they are included only to place the decapeptide among Ronin's research-peptide range. Each compound is typically investigated as a standalone reagent.

This nasal spray ships unreconstituted. The peptide is supplied lyophilized in a 10 mL intranasal-spray bottle together with the 0.3% potassium sorbate solution required to reconstitute it (included) — potassium sorbate acts as a preservative suited to an intranasal solution. Add the full 10 mL of the included solution to reconstitute; the resulting concentration is the bottle’s peptide load divided by 10 mL. A typical metered intranasal actuation delivers approximately 0.1 mL, so each spray delivers roughly one-hundredth of the total peptide load.

1. Bring the spray bottle and the included 0.3% potassium sorbate solution to room temperature.
2. Sanitise the stoppers with an alcohol swab.
3. Add the full 10 mL of the included 0.3% potassium sorbate solution to the lyophilized peptide, directing the liquid against the inner wall — never onto the lyophilized cake.
4. Invert slowly or swirl gently until dissolved. Do not vortex or shake.
5. Attach the spray pump to the bottle and prime it before first use.
6. Store the reconstituted solution refrigerated at 2–8 °C and avoid repeated freeze–thaw cycles.

1. Ohtaki T et al. Metastasis suppressor gene KiSS-1 encodes peptide ligand of a G-protein-coupled receptor. Nature. 2001;411(6837):613-617. PMID: 11385580 | doi:10.1038/35079135
2. Kotani M et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J Biol Chem. 2001;276(37):34631-34636. PMID: 11457843 | doi:10.1074/jbc.M104847200
3. de Roux N et al. Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54. Proc Natl Acad Sci U S A. 2003;100(19):10972-10976. PMID: 12944565 | doi:10.1073/pnas.1834399100
4. Seminara SB et al. The GPR54 gene as a regulator of puberty. N Engl J Med. 2003;349(17):1614-1627. PMID: 14573733 | doi:10.1056/NEJMoa035322
5. Messager S et al. Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54. Proc Natl Acad Sci U S A. 2005;102(5):1761-1766. PMID: 15665093 | doi:10.1073/pnas.0409330102
6. Messager S. Kisspeptin and its receptor: new gatekeepers of puberty. J Neuroendocrinol. 2005;17(10):687-688. PMID: 16159382 | doi:10.1111/j.1365-2826.2005.01357.x
7. Dhillo WS et al. Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. J Clin Endocrinol Metab. 2005;90(12):6609-6615. PMID: 16174713 | doi:10.1210/jc.2005-1468
8. Dhillo WS et al. Kisspeptin-54 stimulates gonadotropin release most potently during the preovulatory phase of the menstrual cycle in women. J Clin Endocrinol Metab. 2007;92(10):3958-3966. PMID: 17635940 | doi:10.1210/jc.2007-1116
9. George JT et al. Kisspeptin-10 is a potent stimulator of LH and increases pulse frequency in men. J Clin Endocrinol Metab. 2011;96(8):E1228-E1236. PMID: 21632807 | doi:10.1210/jc.2011-0089
10. Pinilla L et al. Kisspeptins and reproduction: physiological roles and regulatory mechanisms. Physiol Rev. 2012;92(3):1235-1316. PMID: 22811428 | doi:10.1152/physrev.00037.2010
11. Skorupskaite K et al. The kisspeptin-GnRH pathway in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. PMID: 24615662 | doi:10.1093/humupd/dmu009
12. d'Anglemont de Tassigny X et al. Mechanistic insights into the more potent effect of KP-54 compared to KP-10 in vivo. PLoS One. 2017;12(5):e0176821. PMID: 28464043 | doi:10.1371/journal.pone.0176821
13. Narayanaswamy S et al. Subcutaneous infusion of kisspeptin-54 stimulates gonadotrophin release in women and the response correlates with basal oestradiol levels. Clin Endocrinol (Oxf). 2016;84(6):939-945. PMID: 26572695 | doi:10.1111/cen.12977
14. Patel AH et al. Kisspeptin in functional hypothalamic amenorrhea: Pathophysiology and therapeutic potential. Ann N Y Acad Sci. 2024;1540(1):21-46. PMID: 39287750 | doi:10.1111/nyas.15220