Kisspeptin-10 is an investigational research peptide with no approved human dose. The figures below document what published studies administered, under intravenous control with continuous hormone sampling. They are not transferable to self-administration and are not a protocol.
Why the pharmacology resists a "dose"
Kisspeptin-10 is the minimal kisspeptin sequence retaining full intrinsic bioactivity. It acts on the KISS1 receptor at GnRH neurons — one step above the hormones it ultimately releases — and it is cleared quickly. In the phase 1 work on a related analog, maximum plasma concentration occurred within 0.25 to 0.5 hours and median terminal half-life ran 1.4 to 5.3 hours (PMID 24762108).
Because the peptide acts on a pulsatile system and clears fast, the meaningful variable in every published study is the delivery pattern, not a milligram figure. A bolus and an infusion of comparable total exposure produce qualitatively different — and at the extreme, opposite — hormonal outcomes.
The doses used in human research
Published human protocols, all intravenous (PMID 21632807):
- Bolus dose-ranging in men: 0.01 to 3.0 µg/kg, against vehicle. LH rose rapidly and dose-dependently, with maximal stimulation at 1 µg/kg (4.1 → 12.4 IU/L at 30 minutes, n=6).
- Low-rate infusion: 1.5 µg/kg·h raised mean LH from 5.2 to 14.1 IU/L, increased LH pulse frequency from 0.7 to 1.0 pulses/hour, and increased secretory burst mass from 3.9 to 12.8 IU/L.
- High-rate infusion: 4 µg/kg·h for up to 22.5 hours raised LH from 5.4 to 20.8 IU/L and testosterone from 16.6 to 24.0 nmol/L — but LH pulses were obscured entirely at that secretion rate.
A separate study used molar dosing and found the threshold differed by sex and cycle phase: men showed elevated LH from 0.3 nmol/kg and FSH from 1.0 nmol/kg, women in the follicular phase showed no gonadotropin change at the doses tested, and women in the preovulatory phase responded (PMID 21976724). Note that these two literatures use different units — µg/kg and nmol/kg — which is one reason quoted figures circulate incoherently.
The pattern matters more than the amount
Two published findings make the amount a secondary consideration.
First, the acute dose-response has a peak rather than a plateau: 3 µg/kg elicited a reduced LH response compared with 1 µg/kg. Escalating past the optimum lost effect within a single session.
Second, duration reverses the direction of the hormonal effect. In the phase 1 program for the kisspeptin analog TAK-448, a single bolus or 2-hour infusion raised testosterone roughly 1.3- to 2-fold by 48 hours — but a 14-day infusion at doses above 0.1 mg/day dropped testosterone below baseline by 60 hours and to a sustained below-castration level by day 8 (PMID 24762108). The compound was being developed as an androgen-deprivation therapy; the suppression was the goal.
This is the standard behaviour of GnRH-axis pharmacology — pulsatile stimulates, continuous desensitizes — and it means "how much" is the wrong first question. "How often, and for how long" determines whether the axis goes up or down.
Why these numbers do not transfer
Every figure above comes with conditions that do not exist outside a research unit:
- Route. The dose-response data are intravenous. Subcutaneous bioavailability and time course for kisspeptin-10 are not established by these studies, so a µg/kg number does not carry across routes.
- Sampling. The endpoints are deconvolution analyses of frequent LH measurements. Without them there is no way to know which side of the peak a given dose landed on.
- Population. Participants were healthy volunteers screened into a protocol, and the response varied by sex and menstrual cycle phase.
- Sample size. Several of the infusion arms had n=4 to n=6.
Research doses answer research questions. They were never designed to generalise into a regimen.
Why oversight matters
The clinical development of kisspeptin is proceeding through supervised protocols — for example, investigating whether it could trigger oocyte maturation during IVF with a lower OHSS risk than hCG, precisely because it evokes the body's own LH surge rather than substituting a long-acting analogue (PMID 36147569). That work depends on controlled timing, monitored hormone responses, and a defined clinical question. Outside those conditions there is no dose, no route-appropriate data, no biomarker feedback, and a documented mechanism by which sustained exposure suppresses the very hormones the peptide acutely raises.