What the human kisspeptin studies reported: kisspeptin-10 versus kisspeptin-54, intravenous and subcutaneous doses, the IVF-trigger trials, tachyphylaxis, and reconstitution math for a 10 mg vial.
Kisspeptin is the KISS1-gene neuropeptide that sits at the top of the reproductive axis: it drives GnRH neurons in the hypothalamus, and through them pituitary LH and FSH. The research-grade material is kisspeptin-10, the ten-residue C-terminal fragment; most of the human literature, however, used the 54-residue kisspeptin-54. This page collects what those studies reported about how the peptide was given — route, amounts, cadence — the half-life context that explains those choices, and the reconstitution arithmetic for the vial sold here. It is a research reference beside the Kisspeptin profile, not a protocol and not medical advice.
Every kisspeptin fragment shares the same C-terminal ten residues and activates the same receptor, KISS1R, with essentially the same potency. Where they differ is stability. In human intravenous studies kisspeptin-54 had a half-life of roughly 28 minutes; kisspeptin-10 was cleared in about 4 minutes, a sevenfold gap. That difference shaped the study designs. The IVF trigger trials used kisspeptin-54 as a single subcutaneous injection because it persists long enough to drive an LH surge; most kisspeptin-10 work in men used intravenous boluses or infusion, because a bolus of the short fragment produces one LH pulse and is then gone. A figure reported for kisspeptin-54 in nmol/kg is therefore not a figure for kisspeptin-10, and the half-life calculator lists the two forms separately for that reason.
Both half-lives are far shorter than the downstream response: a single subcutaneous kisspeptin-54 injection produced an LH rise lasting many hours, because the pituitary and gonadal response outlasts the peptide.
Kisspeptin-54, intravenous infusion. Dhillo and colleagues (Journal of Clinical Endocrinology & Metabolism, 2005) infused kisspeptin-54 at 4 pmol/kg/min for 90 minutes in healthy men — the first human administration — and recorded rises in LH, FSH and testosterone, along with the ~28-minute half-life.
Kisspeptin-54, subcutaneous bolus. Later Imperial College work gave single subcutaneous boluses of 0.4 to 6.4 nmol/kg to women and showed that the LH response depended on menstrual-cycle phase, with the largest rise in the preovulatory phase.
Kisspeptin-10, intravenous. The 2011 JCEM study of kisspeptin-10 in men used intravenous boluses of 0.3 to 1 µg/kg and infusions of 4 µg/kg/h, reporting a faster onset than kisspeptin-54 and an increase in LH pulse frequency. This is the closest published data to the research-grade form, and it is intravenous — a route with no counterpart outside a research unit.
Converting between the unit systems needs the molar mass: kisspeptin-10 is about 1,302 g/mol, so 1 nmol is roughly 1.3 µg.
Jayasena and colleagues (Journal of Clinical Investigation, 2014) gave a single subcutaneous injection of kisspeptin-54 at 1.6 to 12.8 nmol/kg — roughly 0.1 to 0.9 mg for a typical adult — to women undergoing IVF in place of the standard hCG trigger. Oocyte maturation occurred in nearly all and live births followed. The 2015 follow-up (Abbara et al., JCEM) used 9.6 nmol/kg in women at high risk of ovarian hyperstimulation syndrome and reported no severe OHSS. These were Phase 2-scale studies of a single monitored dose timed against follicular stimulation; they established no regimen for anything else.
The finding that governs every later design came from Jayasena et al. (JCEM, 2009). Women with hypothalamic amenorrhoea received subcutaneous kisspeptin-54 at 6.4 nmol/kg twice daily. The first injections stimulated gonadotropins as expected, but with continued administration the response faded within two weeks — tachyphylaxis, the same desensitisation that GnRH agonists produce. Continuous exposure switches the axis off rather than driving it harder. Subsequent studies therefore moved to twice-weekly injections or short courses, and the cadences in this literature are single boluses, hours-long infusions, or widely spaced injections — never sustained daily dosing.
For a research design this is the single most important constraint: acute and chronic exposure produce opposite effects.
Reconstitution is a fixed calculation, independent of any dosing question: concentration = peptide mass ÷ diluent volume. For the KISSPEPTIN 10MG vial:
Because literature doses are per kilogram in nanomoles or micrograms, turning one into a volume is a two-step calculation — nanomoles to micrograms via the molar mass, then micrograms to syringe units at the chosen concentration. The dosing math guide works through an example, the dosage calculator automates it, and the vial planner shows how many measured volumes a given concentration yields. The full procedure is in Reconstitution 101. Because the peptide's tryptophan and tyrosine oxidise, reconstituted solution is refrigerated, kept dark and used within weeks.
Kisspeptin has more human exposure than most research peptides — several hundred volunteers and patients — but the data are physiology data. There is no validated dose for any clinical use, no approved product, and no dose-finding study with an outcome endpoint outside the IVF trigger trials. The kisspeptin-10 data are intravenous; the subcutaneous data are almost all kisspeptin-54. Every figure above is a data point from a specific study, to be checked against the primary source. The kisspeptin research overview covers the neuroendocrinology behind these designs.
In Canada, kisspeptin has no Health Canada market authorisation and no DIN; it is not a controlled substance and is sold here for research use only. Under the WADA Prohibited List, LH-releasing factors including kisspeptin are prohibited in male athletes.
What doses of kisspeptin appear in the published research? Kisspeptin-54 was infused intravenously at 4 pmol/kg/min for 90 minutes (Dhillo 2005), given subcutaneously at 0.4 to 6.4 nmol/kg in women, and used as an IVF trigger at 1.6 to 12.8 nmol/kg (Jayasena 2014). Kisspeptin-10 was given intravenously at 0.3 to 1 µg/kg as a bolus or 4 µg/kg/h as an infusion (2011). These are study parameters, not validated or recommended amounts.
Why do kisspeptin-10 and kisspeptin-54 have different half-lives? They activate the same receptor with the same potency, but the 54-residue peptide is cleared more slowly — about 28 minutes against about 4 minutes for kisspeptin-10 in human intravenous studies. That is why the IVF trials used kisspeptin-54 and why kisspeptin-10 studies relied on infusion.
What is tachyphylaxis and why does it matter here? Twice-daily subcutaneous kisspeptin-54 in women with hypothalamic amenorrhoea lost its gonadotropin-stimulating effect within two weeks (Jayasena 2009). Continuous exposure desensitises the axis, so later designs used spaced injections or short courses. Frequency, not amount, is the variable the literature handles most carefully.
How is a 10 mg kisspeptin vial reconstituted? With 2 mL of bacteriostatic water the concentration is 5 mg/mL, so each U-100 syringe unit holds 50 µg; with 5 mL it is 2 mg/mL and each unit holds 20 µg. Converting a per-kilogram literature figure uses the molar mass of about 1,302 g/mol (1 nmol is about 1.3 µg) before the syringe-unit step.
Is this medical advice? No. Kisspeptin-10 sold here is research-grade material for laboratory use only, not for human or veterinary use. Every number on this page describes what appeared in published studies under clinical monitoring; none of it is a protocol, a recommendation or medical advice.
