Peptides & growth hormone

Kisspeptin-10

Updated · 24 sources · Editorial policy

Kisspeptin-10 is a 10-amino-acid peptide, the shortest naturally occurring form of kisspeptin. Kisspeptin is the hypothalamic signal that switches on gonadotropin-releasing hormone (GnRH) neurons, which in turn drive the pituitary to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In men, more LH means the testes make more testosterone.

Kisspeptin-10 is not an approved drug anywhere. It has been given to people only in small physiology studies, mostly single injections or infusions lasting hours to days, run by academic groups in London, Edinburgh and Boston. It acts for only minutes in the blood, with a measured plasma half-life of about 4 minutes. In 2023 the FDA placed it on its list of bulk substances that may present significant safety risks in compounding.

This page summarizes what the human studies and regulators report. It is for education only and is not medical advice.

Property Detail
Class Endogenous neuropeptide; kisspeptin receptor (KISS1R, formerly GPR54) agonist
Also called KP-10, metastin 45–54, kisspeptin-10 (human)
Structure Linear decapeptide with an amidated C-terminus; formula C₆₃H₈₃N₁₇O₁₄, MW 1302.4 g/mol
Studied routes Intravenous bolus or infusion; subcutaneous infusion
Studied doses IV bolus 0.01–3.0 µg/kg; IV infusions 1.5–12.5 µg/kg/h; SC infusions 150–180 nmol/h
Plasma half-life About 4 min after IV infusion in men and women
Main effect Releases the body’s own GnRH, raising LH, FSH and (in men) testosterone
Approval Not approved by the FDA; research use only
FDA compounding Category 2 bulk substance (503A) since September 29, 2023
WADA Prohibited at all times in males (S2.2.1, “kisspeptin and its agonist analogues”)

What it is

The KiSS-1 gene was first described in 1996 as a gene that suppressed metastasis in human melanoma cells (Lee et al., JNCI 1996). In 2001, two groups showed that the gene encodes peptides that activate an orphan receptor, GPR54. Takeda’s group isolated a 54-amino-acid peptide from human placenta and named it metastin (Ohtaki et al., Nature 2001). A second group isolated 54-, 14- and 13-amino-acid forms with the same C-terminal end and named them kisspeptins (Kotani et al., J Biol Chem 2001).

Kisspeptin-10 is the last 10 amino acids shared by all of these forms, corresponding to amino acids 112–121 of the precursor protein (Chan et al., JCEM 2011). It ends in the “RF-amide” motif (arginine followed by an amidated phenylalanine) that the receptor recognizes. It is described as the minimal kisspeptin sequence with full intrinsic activity at the receptor (George et al., JCEM 2011). PubChem lists it as metastin 45–54, formula C₆₃H₈₃N₁₇O₁₄ and molecular weight 1302.4 g/mol (PubChem CID 25240297).

Its importance for reproduction came from genetics. In 2003, two groups found that people with inactivating mutations in GPR54 never went through puberty, a condition called hypogonadotropic hypogonadism (low sex hormones because the brain and pituitary do not signal the gonads) (Seminara et al., NEJM 2003; de Roux et al., PNAS 2003). Mice lacking the receptor had the same picture but still responded to injected GnRH, placing kisspeptin above GnRH in the hormonal chain.

Step Signal What acts on it
1. Hypothalamus Kisspeptin activates KISS1R on GnRH neurons Kisspeptin-10, kisspeptin-54
2. Hypothalamus to pituitary GnRH released in pulses Gonadorelin (synthetic GnRH) acts here
3. Pituitary to gonads LH and FSH released hCG mimics LH here
4. Testes Testosterone and sperm production —

Because it works at the top of this chain, kisspeptin-10 only raises testosterone if the GnRH neurons, pituitary and testes are working. This differs from hCG, which bypasses the brain and pituitary, and from enclomiphene, which raises LH by blocking estrogen feedback.

Pharmacokinetics

Kisspeptin-10 is cleared from the blood very quickly:

Measure Value Source
Plasma half-life in people (after IV infusion) About 4 min, no significant difference between men and women Jayasena et al., JCEM 2011
Compared with kisspeptin-54 About 7-fold shorter Jayasena et al., JCEM 2011
Breakdown in rat plasma at 37 °C (in vitro) Decomposition half-life 1.7 min; main product lacks the first tyrosine Liu et al., J Chromatogr B 2013
Rats, 1.0 mg/kg IV bolus Undetectable in plasma by 30 min Liu et al., J Chromatogr B 2013

The short half-life shapes how it has been studied. Most human protocols use IV boluses to trigger a single LH pulse, or continuous infusions to keep levels up. The Imperial College group noted that the longer kisspeptin-54 can be given as a subcutaneous injection because of its longer half-life, while kisspeptin-10 is cheaper to make because it is shorter (Jayasena et al., Hum Reprod 2015). The most recent chronic studies gave kisspeptin-10 under the skin by infusion pump rather than by single injection (Yeung et al., Eur J Endocrinol 2026).

Regulatory status

  • Not an approved medicine. No kisspeptin product is approved by the FDA. In several of the studies below, kisspeptin-10 was custom-synthesized to GMP standards specifically for the research.
  • FDA compounding list. On September 29, 2023, FDA added kisspeptin-10 to category 2 of its interim policy for 503A compounding. FDA said compounded kisspeptin-10 “may pose risk for immunogenicity” for certain routes, may have problems with peptide-related impurities and characterization, and that it has little or no safety information for the proposed routes (FDA category 2 list).
  • Not a controlled substance. Kisspeptin-10 is not among the anabolic steroids named in Schedule III (21 CFR 1308.13).
  • Banned in sport. The WADA list names “kisspeptin and its agonist analogues” under S2.2.1, testosterone-stimulating peptides in males, prohibited at all times (WADA 2026 Prohibited List).

What the research shows

All of the data below come from small physiology studies, typically 4–15 people per experiment. None was designed to test a treatment for low testosterone, libido or fertility over weeks or months.

Single doses in healthy men

The first dose-finding study gave healthy men IV boluses of 0.01–3.0 µg/kg (George et al., JCEM 2011):

  • LH rose quickly and in a dose-dependent way.
  • The maximum response was at 1 µg/kg: LH rose from 4.1 to 12.4 IU/L at 30 minutes (n = 6).
  • A higher dose, 3 µg/kg, gave a smaller response than 1 µg/kg.

In the Imperial College study, IV boluses raised LH at doses as low as 0.3 nmol/kg and FSH at 1.0 nmol/kg in men (Jayasena et al., JCEM 2011).

A Boston study in 13 men showed that a single 0.24 nmol/kg IV bolus produced an immediate LH pulse, larger than natural pulses (amplitude 5.0 vs 2.1 mIU/mL). It also reset the timing of the next natural pulse, which the authors interpreted as kisspeptin resetting the hypothalamic GnRH “clock” (Chan et al., JCEM 2011).

In men of different ages given a 1 µg/kg IV bolus, LH rose in every age group, but testosterone rose significantly only in the youngest adult group (Ullah et al., Andrologia 2019).

Infusions over hours to days

Study Men Protocol LH Testosterone
George 2011 4 healthy IV 4 µg/kg/h for 22.5 h 5.4 → 20.8 IU/L 16.6 → 24.0 nmol/L (≈ 479 → 692 ng/dL)
George 2011 4 healthy IV 1.5 µg/kg/h 5.2 → 14.1 IU/L; pulse frequency 0.7 → 1.0 per h Not reported
George 2013 4 with type 2 diabetes and low testosterone IV 4 µg/kg/h for 11 h 3.9 → 20.7 IU/L 8.5 → 11.4 nmol/L (≈ 245 → 329 ng/dL)
Naveed 2026 3 healthy IV 12.5 µg/kg/h for 24 h 5–8-fold peak at 12–20 h, then fell 13–47% by the end Rose modestly
Yeung 2026 4 healthy SC 180 nmol/h continuously for 5 days Back to vehicle levels by day 5 Still elevated
Yeung 2026 7 healthy SC 150 nmol/h, 8 h a day for 12 days Mean rise +1.68 IU/L on day 1 and +1.14 IU/L on day 12 vs −0.16 with vehicle Sustained increase reported

Two points stand out:

  • The rise in testosterone is modest. In healthy men, a near-day-long IV infusion raised testosterone from 16.6 to 24.0 nmol/L. In men with type 2 diabetes, obesity (mean BMI 40.6) and low testosterone, an 11-hour infusion raised it from 8.5 to 11.4 nmol/L.
  • Continuous exposure blunts the response. In the 2026 Imperial study, gonadotropins fell back to placebo levels after 5 days of round-the-clock infusion, while an 8-hours-on, 16-hours-off pattern kept LH raised for 12 days. In the Boston 24-hour infusion, LH peaked and then partly declined. The authors of both papers framed these as early steps toward designing longer-term protocols, not as treatments.

Kisspeptin-10 is less potent than GnRH itself. When the same molar doses were infused for 3 hours in healthy men (5 per group), LH exposure was about 3-fold higher with GnRH than with kisspeptin-10, and kisspeptin-10 and kisspeptin-54 gave similar responses (Jayasena et al., Hum Reprod 2015).

Women

The response in women depends on the menstrual cycle phase. In the follicular (early) phase, kisspeptin-10 did not change LH or FSH even at the highest doses tested: 10 nmol/kg IV bolus, 32 nmol/kg subcutaneous bolus, or a 720 pmol/kg/min infusion. In the preovulatory phase, a 10 nmol/kg IV bolus did raise LH and FSH (Jayasena et al., JCEM 2011).

Diagnostic and research uses

  • Genetic GnRH disorders. In patients with mutations in the neurokinin B pathway who had not gone through puberty, a 1.5 µg/kg/h IV infusion of kisspeptin-10 for 12 hours restored pulsatile LH secretion (Young et al., Neuroendocrinology 2013).
  • Delayed puberty. In 15 children with delayed or stalled puberty, responses to a kisspeptin-10 bolus ranged from robust to none. All 6 children with spontaneous overnight LH pulses responded (Chan et al., JCI Insight 2018). Whether this predicts later puberty was still being followed.

Libido and sexual function

Kisspeptin is listed for libido because of brain-imaging studies, but these used kisspeptin-54, not kisspeptin-10:

  • In 29 healthy young men, a kisspeptin-54 infusion increased limbic brain activity in response to sexual and couple-bonding images (Comninos et al., J Clin Invest 2017).
  • In a randomized crossover trial in 37 men (32 completed) with hypoactive sexual desire disorder, a 75-minute kisspeptin-54 infusion changed brain activity to sexual videos and increased penile tumescence by up to 56% more than placebo (mean difference 0.28 units, 95% CI 0.04–0.52) (Mills et al., JAMA Netw Open 2023).

These were single 75-minute IV infusions measured in the lab. No study has tested kisspeptin-10 for libido, and no study has tested any kisspeptin for sexual function at home or over weeks.

Kisspeptin-54 in IVF

The longer isoform has also been used as a single subcutaneous injection to trigger egg maturation in 53 women undergoing IVF, with a clinical pregnancy rate of 23% (Jayasena et al., J Clin Invest 2014). This is a different peptide and route, so the result does not carry over to kisspeptin-10.

Side effects and risks

What the human studies report

The published kisspeptin-10 studies report no adverse events, but they are small and short:

  • George 2011: blood pressure, heart rate, oxygen levels, liver and kidney tests and blood counts stayed stable, and no adverse events were reported (George et al., JCEM 2011).
  • Chan 2011: no adverse events related to kisspeptin immediately or at 2-week follow-up (Chan et al., JCEM 2011).
  • Young 2013 and Chan 2018: no adverse events, or no major adverse events, during infusions and follow-up (Young et al., 2013; Chan et al., 2018).

For kisspeptin in general (tested with kisspeptin-54 in 95 men and women), a randomized crossover study found no effect on anxiety, cortisol, blood pressure or heart rate (Mills et al., JCEM 2025).

Taken together, the kisspeptin-10 studies are small (most under 20 participants per experiment), mostly used IV dosing, and lasted at most 12 days. There are no data on use over months, on repeated self-injection, or on use alongside anabolic steroids.

Desensitization

Continuous kisspeptin-10 stops working over days: in the 5-day infusion study, LH and FSH returned to placebo levels (Yeung et al., Eur J Endocrinol 2026). The receptor still responded to a fresh bolus after the 12-day intermittent protocol, but long-term effects on the body’s own hormone rhythm have not been studied.

Product quality

FDA’s category 2 listing points to the main practical risks of non-pharmaceutical kisspeptin-10: possible immune reactions to the peptide or its impurities, and uncertain identity and purity of the material. FDA said it lacks the information to know whether compounded kisspeptin-10 would cause harm (FDA category 2 list). Products sold as “research peptides” are not reviewed for dose, sterility or identity.

Cancer biology

The KiSS-1 gene was discovered as a suppressor of metastasis, and metastin reduced lung metastasis of engineered melanoma cells in an animal model (Ohtaki et al., Nature 2001). This is animal and cell-culture work. It does not show any anticancer benefit, or any cancer risk, from taking kisspeptin-10.

Key takeaways

  • A brain-level switch for the reproductive axis. Kisspeptin-10 releases the body’s own GnRH, which raises LH, FSH and testosterone only if the hypothalamus, pituitary and testes work.
  • Very short-acting. Its plasma half-life is about 4 minutes, so human studies used IV boluses or continuous infusions.
  • Modest testosterone rises in short studies. IV infusions lasting 11–22.5 hours raised testosterone in groups of 4 men, from 16.6 to 24.0 nmol/L in healthy men.
  • The effect fades with constant exposure. Gonadotropins returned to baseline after 5 days of continuous infusion; an intermittent schedule kept them raised for 12 days.
  • Libido data are for kisspeptin-54. No study has tested kisspeptin-10 for sexual function.
  • Research only. It is not FDA-approved, FDA lists it as a compounding safety concern, and WADA bans it in male athletes.

Sources

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