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Libido & hormones · Daily shot

Kisspeptin

Gray market

Checked · 26 sources · 11 corrections on this page · No vendors · No affiliates · No one buys a word of it

95% had eggs that matured

Phase II · IVF · 60 women at risk of ovarian hyperstimulation · no hCG arm · Abbara 2015

Gray market · FDA said no — on the do-not-compound list

Sold as a research chemical. Some clinics and pharmacies still supply it; that’s their risk, not a change in the rule.

Bottom line

A research drug with small fertility trials behind it and no approval anywhere; its use alongside testosterone therapy has not been tested.

Also called
  • Kisspeptin-54 (Kp-54 / metastin)
  • Kisspeptin-10 (Kp-10)
  • KISS1 gene product
  • Metastin
  • GnRH secretagogue
Category
Peptide — Endogenous HPG Axis Master Regulator
Class
Endogenous neuropeptide
Gene
KISS1 (chromosome 1q32)
Major Forms
Kp-54, Kp-14, Kp-13, Kp-10
Receptor
KISS1R / GPR54
Half-life
27.6 min (Kp-54, IV)
Route (studied)
SubQ, IV (people) · IP (mice) · into the brain (sheep)
Route (sold)
SubQ vials (research chemical; some clinics)
FDA Status
Not approved; active Phase 2
Key Research
Imperial College London (Dhillo / Jayasena)
WADA Status
Prohibited at all times in males (S2.2.1 — “kisspeptin and its agonist analogues”, 2026 List)
Cost & Access
Research-only

Also for libido & hormones

The other four questions

What does it do? It switches on the GnRH neurons that drive the reproductive hormones: in mice, its receptor sits on those neurons and it directly stimulates GnRH release (Messager et al., 2005). Given twice a day for two weeks, its effect faded (Jayasena et al., 2009).
Who uses it? Research groups in London and Boston, in trials of IVF triggers and hypothalamic amenorrhea (Jayasena et al., 2009; Jayasena et al., 2014; Chan et al., 2011). Some clinics sell it as an add-on to testosterone therapy, without trial backing.
Does the evidence hold up? For its role, yes: mutations that disable its receptor cause absent puberty (Seminara et al., 2003; de Roux et al., 2003). As a drug, the evidence is small trials: a single injection triggered egg maturation in 53 women having IVF (Jayasena et al., 2014) and in 60 at high risk of ovarian hyperstimulation syndrome, none of whom developed moderate or severe OHSS (Abbara et al., 2015).
Bottom line? A research drug with small fertility trials behind it and no approval anywhere; its use alongside testosterone therapy has not been tested.

Dosing from the Literature

Published for reproductive hormones: mostly IV research doses from Phase 1 and 2 studies. Not published: a validated dose for the shots clinics sell.

The rows give the doses of the published human studies, with each study’s population. Community use, as the page reports it, extrapolates from these and has not been studied.

Protocol / ContextFormDoseFrequency
Healthy men (Dhillo 2005)Kp-54 IV infusion4 pmol/kg/min for 90 minSingle infusion; 6 men, LH, FSH and testosterone rose (Dhillo et al., 2005)
Hypothalamic amenorrhea (Jayasena 2009)Kp-54 SC6.4 nmol/kgTwice daily for 2 weeks; 5 women (5 more on saline); the LH response faded by day 14 (Jayasena et al., 2009)
IVF egg-maturation trigger (Jayasena 2014)Kp-54 SC1.6, 3.2, 6.4 or 12.8 nmol/kgOne dose, 36 h before egg retrieval; 53 women having IVF (Jayasena et al., 2014)
IVF trigger, high OHSS risk (Abbara 2015, 2017)Kp-54 SC3.2–12.8 nmol/kg; or 9.6 nmol/kg plus a second dose 10 h laterOne dose in 60 women at high risk of OHSS (Abbara et al., 2015); a second dose raised the share with a good egg yield from 45% to 71% in 62 more (Abbara et al., 2017)
Community self-dosing (not validated)Kp-10 or Kp-54 SC~50–200 mcg (highly variable)What community self-dosing reports describe, 1–3 times a day; no study has tested it
Dosing Disclaimer

No controlled study supports community kisspeptin dosing. The published human doses are single IV infusions, single SC injections and one two-week SC course, in which twice-daily injections stopped raising LH (Jayasena et al., 2009). Consult a licensed healthcare provider.

→ Calculator — vial-to-syringe math

What It Is

Kisspeptin is the endogenous ligand of the KISS1R (previously GPR54) receptor — a Gq-coupled G-protein-coupled receptor expressed on GnRH neurons in the hypothalamic (brain's hormonal control center) preoptic area. Its gene was first described in 1996 as KiSS-1, whose expression suppressed the spread of human melanoma cells (Lee et al., 1996); it maps to chromosome 1q32 (West et al., 1998). A 2009 history says the gene “may have been named with a bit of whimsy” for where it was discovered — Hershey, Pennsylvania, home of Hershey’s Kisses — and that its 54-amino-acid peptide was first called metastin for its ability to inhibit cancer metastasis (Gottsch et al., 2009). In 2003, two independent research teams — Seminara and colleagues at Massachusetts General Hospital (NEJM) and de Roux and colleagues in Paris (PNAS) — reported that loss-of-function mutations in KISS1R produced hypogonadotropic hypogonadism in humans: the clinical phenotype of absent puberty with low LH, FSH, and sex steroids despite structurally intact hypothalamus and pituitary. This finding established kisspeptin as the master upstream regulator of the HPG axis.

Kisspeptin's mature peptide hormone exists in several biologically active forms derived from proteolytic processing of the 145-amino-acid KISS1 gene product. The longest form is kisspeptin-54 (Kp-54, sometimes called "metastin"); shorter forms include kisspeptin-14, kisspeptin-13, and kisspeptin-10 (Kp-10). All share the same C-terminal decapeptide (residues 109–118 of the KISS1 precursor, "YNWNSFGLRF-NH2") which is the pharmacophore responsible for receptor binding. Kp-10 and Kp-54 are the two forms most extensively used in human pharmacology research.

The kisspeptin system sits at the apex of reproductive neuroendocrinology. Two populations of kisspeptin-expressing neurons in the hypothalamus — the arcuate-nucleus "KNDy" neurons (co-expressing kisspeptin, neurokinin B, and dynorphin) and the anteroventral periventricular nucleus / rostral preoptic area neurons — project onto GnRH neurons. Arcuate KNDy neurons generate the pulsatile GnRH "pulse generator" responsible for the pulsatile LH/FSH secretion underlying normal reproductive function; anteroventral periventricular kisspeptin neurons mediate the estradiol-positive-feedback LH surge that triggers ovulation in females.

Clinically, kisspeptin is an active investigational agent in reproductive endocrinology. The most advanced development program is at Imperial College London under Dhillo, Jayasena, and colleagues, where kisspeptin-54 has been evaluated as an IVF ovulation trigger (replacing hCG or GnRH agonist triggers), as a diagnostic agent for hypothalamic amenorrhea, and as a candidate therapy for male and female hypogonadism. Parallel programs at Massachusetts General Hospital (Seminara lab) have characterized pediatric puberty disorders and hypothalamic amenorrhea.

Mechanism of Action

Kisspeptins act through one receptor, GPR54, also called KISS1R (Kotani et al., 2001).

  • KISS1R (GPR54) activation on GnRH neurons — In cells, kisspeptins bound GPR54 and set off PIP2 hydrolysis and calcium release (Kotani et al., 2001); in mice, GPR54 sits on GnRH neurons and kisspeptin directly stimulates GnRH release (Messager et al., 2005).
  • Downstream GnRH → LH/FSH → gonadal hormones — GnRH release leads to LH and FSH from the pituitary, then sex steroids and gametes from the gonads (Trevisan et al., 2018); in men, a kisspeptin-54 infusion raised LH, FSH and testosterone (Dhillo et al., 2005).
  • Pulse generator (arcuate KNDy neurons) — Kisspeptin works with neurokinin B, which stimulates, and dynorphin, which inhibits, to set the pulses of GnRH release (Skorupskaite et al., 2014; Clarke et al., 2015). In men, a single kisspeptin-10 dose reset the timing of the pulses (Chan et al., 2011).
  • Estradiol positive-feedback surge — Animal studies suggest kisspeptin helps generate the LH surge that ovulation requires (Jayasena et al., 2014).
  • Metabolic integration — Kisspeptin signaling appears to be regulated by nutritional status and stress (Clarke et al., 2015) and takes part in the metabolic control of fertility (Pinilla et al., 2012).
  • Upstream of the testes — Kisspeptin raises the body’s own LH, FSH and testosterone (Dhillo et al., 2005); no study has tested whether it preserves testicular size or fertility in men taking testosterone.
  • Reproductive-behavior modulation (limbic effects) — In 29 young men, kisspeptin enhanced limbic brain activity to sexual and couple-bonding images and eased negative mood (Comninos et al., 2017); in 32 women with low sexual desire, it changed brain responses to erotic videos and attractive faces (Thurston et al., 2022).
  • Non-reproductive roles — KISS1 was first described as a metastasis suppressor gene for melanoma, and its receptor is highly expressed in placenta, pituitary, pancreas and spinal cord (Kotani et al., 2001).

What the Research Shows

Kisspeptin's published evidence is concentrated in reproductive endocrinology and largely associated with two research groups (Seminara at MGH and Dhillo/Jayasena at Imperial College London) but is methodologically strong — genetic evidence from human loss-of-function, multiple Phase 1 and Phase 2 human trials, and mechanistically coherent Phase 2 efficacy data.

  • Human KISS1R loss-of-function → hypogonadotropic hypogonadism (Seminara et al., NEJM 2003; PMID 14573733 and de Roux et al., PNAS 2003) — Two independent studies identified KISS1R inactivating mutations as cause of normosmic idiopathic hypogonadotropic hypogonadism (nIHH) with absent or incomplete puberty. The foundational "reverse pharmacology" evidence establishing kisspeptin as master regulator of puberty and reproduction.
  • First human administration (Dhillo et al., JCEM 2005; PMID 16174713) — IV infusion of Kp-54 in healthy men increased plasma LH, FSH, and testosterone. First human demonstration of kisspeptin-induced gonadotropin release.
  • Hypothalamic amenorrhea (Jayasena et al., JCEM 2009; PMID 19820030) — In women with hypothalamic amenorrhea, the first SC injection of Kp-54 raised LH and FSH sharply, but after two weeks of twice-daily injections the response had largely gone, and LH pulsatility did not change.
  • Kisspeptin infusion in HA (Jayasena et al., JCEM 2014; PMID 24517142) — In 5 women with hypothalamic amenorrhea, a continuous IV infusion of Kp-54 raised LH pulses about threefold over 8 hours compared with vehicle; the authors call the increase temporary.
  • Kisspeptin IVF trigger — first proof-of-concept (Jayasena et al., JCI 2014; PMID 25036713) — 53 women undergoing IVF received Kp-54 as the oocyte-maturation trigger. Eggs matured at every dose, embryos were transferred in 49 of the 53, and 12 had a clinical pregnancy. The study had no hCG comparison.
  • Kisspeptin IVF trigger — expanded cohort (Abbara et al., JCEM 2015; PMID 26192876) — Larger cohort (60 women) at risk of OHSS. Kp-54 triggered oocyte maturation in 95%, and no woman developed moderate, severe or critical OHSS; the trial had no hCG arm.
  • Second kisspeptin dose (Abbara et al., Hum Reprod 2017; PMID 28854728) — In 62 women at high risk of OHSS, a second Kp-54 dose 10 hours after the first raised the share with an oocyte yield of at least 60% from 45% to 71%.
  • Limbic and sexual brain activity (Comninos, Dhillo et al., J Clin Invest 2017; PMID 28112678) — Kp-54 administration in healthy men enhanced limbic-system brain activity in response to sexual and couple-bonding stimuli on fMRI. Supports the role of kisspeptin signaling in sexual attraction circuits beyond the HPG axis alone.
  • Hypoactive sexual desire in women (Thurston, Comninos et al., JAMA Netw Open 2022) — Kp-54 enhanced sexual and attraction brain processing and behavioral responses in premenopausal women with hypoactive sexual desire disorder. Extends the sexual-function research to female clinical populations.
  • GnRH clock reset (Chan et al., JCEM 2011) — In 13 healthy men, a single IV dose of kisspeptin-10 set off an immediate LH pulse, larger than the body’s own, and delayed the next one: it reset the GnRH pulse generator.
  • Men with type 2 diabetes and low testosterone (George et al., Clin Endocrinol 2013; PMID 23153270) — In a proof-of-concept study, an 11-hour IV infusion of kisspeptin-10 raised LH, and testosterone from 8.5 to 11.4 nmol/L, in 4 men with type 2 diabetes and low testosterone.
Evidence Framing

Kisspeptin has a stronger translational pipeline than most research peptides on this site: human genetic evidence (loss-of-function → disease), active Phase 2 programs at Imperial College London (Dhillo, Jayasena, Abbara, Comninos) and Boston (Seminara), and multiple positive IVF-trigger and HA-restart trials. It is not yet FDA-approved for any indication. The strongest human evidence is in IVF ovulation triggering, where it shows credible OHSS-risk reduction vs hCG. Outside that context, community off-label use for "HPG axis support" on TRT is mechanistically plausible but has no controlled-trial validation.

Human Data

Kisspeptin has accumulated a sizeable human database primarily from Imperial College London and Massachusetts General Hospital programs:

  • Healthy-volunteer PK/PD — Multiple Phase 1 studies in healthy men and women characterizing LH, FSH, testosterone, and estradiol responses to IV and SC kisspeptin (Kp-10 and Kp-54) across dose ranges.
  • Pediatric delayed puberty (Chan et al., JCEM 2020; PMID 32232399) — In 16 children with delayed or stalled puberty, the LH response to a kisspeptin test predicted who later went through puberty: all 8 with a rise of 0.8 mIU/mL or more did, and all 8 with 0.4 or less had not by age 18.
  • Functional hypothalamic amenorrhea (HA) — In the cited trial, twice-daily injections raised LH at first but not after two weeks, and LH pulsatility did not change (Jayasena et al., 2009).
  • Male hypogonadism (functional / hypogonadotropic) — Short-course restoration of LH and testosterone in men with functional hypogonadism.
  • IVF ovulation trigger — The strongest clinical endpoint to date. Jayasena JCI 2014 and Abbara JCEM 2015 report oocyte maturation after a single injection, with no moderate or severe OHSS among 60 women at high risk; neither compared kisspeptin with hCG. Ongoing Phase 2/3 development in IVF.
  • Female hypoactive sexual desire — Kp-54 enhances sexual and attraction brain processing in women with HSDD (JAMA Netw Open 2022).
  • Male sexual function / attraction (fMRI) — Kp-54 enhances limbic responses to sexual/couple-bonding stimuli (Comninos et al., JCI 2017).
  • No chronic dosing data — The published record is almost entirely short-course (single-dose to several-day). Long-term (months-to-years) safety and efficacy data are not available.
  • No FDA pivotal trial — As of April 2026, no kisspeptin Phase 3 program is publicly listed at ClinicalTrials.gov with US FDA registration.

Reconstitution & Storage

Kisspeptin has no approved label, so no official storage or handling instructions exist. Research-chemical sellers list kisspeptin-10 and kisspeptin-54 as freeze-dried powder in vials. The 100 and 200 mcg columns are arithmetic for the community figures in Dosing.

Vial SizeBAC WaterConcentration100 mcg Dose200 mcg Dose
1 mg1 mL1,000 mcg/mL10 units (0.10 mL)20 units (0.20 mL)
2 mg2 mL1,000 mcg/mL10 units (0.10 mL)20 units (0.20 mL)
5 mg2.5 mL2,000 mcg/mL5 units (0.05 mL)10 units (0.10 mL)

→ Calculator — vial-to-syringe math

Side Effects & Risks

Important

Kisspeptin’s published human studies are short, from single doses to one two-week course (Jayasena et al., 2009). Consult a licensed healthcare provider.

The trials below gave kisspeptin to small groups for short spells; long-term safety has not been studied.

  • Tolerability — In the 2022 trial in 32 women with low sexual desire, kisspeptin was well tolerated with no reported adverse effects (Thurston et al., 2022).
  • Tachyphylaxis — In women with hypothalamic amenorrhea, the LH rise after a kisspeptin-54 injection was 24.0 IU/l on day 1 and 2.5 IU/l on day 14 of twice-daily dosing (Jayasena et al., 2009).
  • OHSS in IVF context — Among 60 women at high risk, none developed moderate, severe or critical OHSS after a kisspeptin-54 trigger (Abbara et al., 2015); no trial on this page compared it with hCG.
  • Pregnancy — Kisspeptins were first isolated from human placenta, where their receptor is highly expressed (Kotani et al., 2001). In the IVF trials it was given once, before egg retrieval and fertilization (Jayasena et al., 2014).
  • Long-term safety — Not studied: the longest course in the studies cited here is two weeks (Jayasena et al., 2009).
  • Purity and sourcing — Outside research, kisspeptin is sold only as a research chemical, unregulated for quality.
  • Anti-doping — Prohibited at all times in males: the 2026 Prohibited List names kisspeptin and its agonist analogues under S2.2.1, testosterone-stimulating peptides in males (WADA Prohibited List 2026).

Bloodwork & Monitoring

No label or guideline sets monitoring for kisspeptin, which is not approved. Its studies measured LH, FSH and testosterone (Dhillo et al., 2005), LH pulsatility and ovarian ultrasound (Jayasena et al., 2009), and egg maturation, pregnancy and OHSS in the IVF trials (Jayasena et al., 2014; Abbara et al., 2015).

Commonly Stacked With

Testosterone (HPG support on TRT — experimental)

Tested together in people: none published · Read the receipt →

Ipamorelin / GHRH analogs

Tested together in people: none published · Read the receipt →

Stacking this? Read the receipt →

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Legal Status

Current Status — April 2026

Kisspeptin is not FDA-approved for any therapeutic indication. It is not a controlled substance. It is the subject of an active Phase 2 clinical research program at Imperial College London (Dhillo, Jayasena, Abbara, Comninos) and at Massachusetts General Hospital (Seminara), primarily focused on IVF ovulation triggering, hypothalamic amenorrhea, male hypogonadism, and hypoactive sexual desire disorder.

Kisspeptin is on the FDA 503A Category 2 list as Kisspeptin-10 (significant safety risks; added September 29, 2023; list updated May 14, 2026) — not legal to compound today. Its regulatory trajectory is unusual among research peptides because a pharmaceutical development program exists and a sponsor could plausibly advance the compound (most likely in the reproductive-endocrinology space) toward formal FDA approval. It stays in Category 2: kisspeptin-10 was not among the 12 peptides FDA removed from that list in April 2026 (FDA 503A categories list, April 22 and May 14, 2026).

Kisspeptin is prohibited at all times in males: the 2026 Prohibited List names kisspeptin and its agonist analogues under S2.2.1, testosterone-stimulating peptides in males (WADA Prohibited List 2026).

Cost & Access

Kisspeptin is not approved for human use. It is sold by research-chemical suppliers, labeled for laboratory research.

U.S. compounding pharmacies cannot legally compound kisspeptin under current FDA rules — it has no FDA-approved reference product and is not a recognized 503A bulk ingredient. Academic research use proceeds under Investigational New Drug (IND) applications at the sponsoring institutions. Outside the formal academic research context, kisspeptin is accessible only via research-chemical supply channels.

Both forms activate the same receptor; kisspeptin-54 is the form used in the IVF-trigger trials (Jayasena et al., 2014; Abbara et al., 2015).

Regulatory status as of April 2026. Access varies by provider, jurisdiction, and research context. Kalios does not sell compounds.

References

  1. Seminara SB, Messager S, Chatzidaki EE, Thresher RR, Acierno JS Jr, Shagoury JK, et al. The GPR54 gene as a regulator of puberty. N Engl J Med. 2003;349(17):1614-1627. PMID: 14573733. (Foundational paper establishing kisspeptin-receptor loss-of-function as cause of hypogonadotropic hypogonadism.)
  2. de Roux N, Genin E, Carel JC, Matsuda F, Chaussain JL, Milgrom E. Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54. Proc Natl Acad Sci USA. 2003;100(19):10972-10976. PMID: 12944565.
  3. Dhillo WS, Chaudhri OB, Patterson M, Thompson EL, Murphy KG, Badman MK, et al. Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males. J Clin Endocrinol Metab. 2005;90(12):6609-6615. PMID: 16174713.
  4. Jayasena CN, Nijher GM, Chaudhri OB, Murphy KG, Ranger A, Lim A, et al. Subcutaneous injection of kisspeptin-54 acutely stimulates gonadotropin secretion in women with hypothalamic amenorrhea, but chronic administration causes tachyphylaxis. J Clin Endocrinol Metab. 2009;94(11):4315-4323. PMID: 19820030.
  5. Jayasena CN, Abbara A, Comninos AN, Nijher GM, Christopoulos G, Narayanaswamy S, et al. Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization. J Clin Invest. 2014;124(8):3667-3677. PMID: 25036713.
  6. Abbara A, Jayasena CN, Christopoulos G, Narayanaswamy S, Izzi-Engbeaya C, Nijher GM, et al. Efficacy of Kisspeptin-54 to Trigger Oocyte Maturation in Women at High Risk of Ovarian Hyperstimulation Syndrome (OHSS) During In Vitro Fertilization (IVF) Therapy. J Clin Endocrinol Metab. 2015;100(9):3322-3331. PMID: 26192876.
  7. Comninos AN, Wall MB, Demetriou L, Shah AJ, Clarke SA, Narayanaswamy S, et al. Kisspeptin modulates sexual and emotional brain processing in humans. J Clin Invest. 2017;127(2):709-719. PMID: 28112678.
  8. Thurston L, Hunjan T, Ertl N, Wall MB, Mills EG, Suladze S, et al. Effects of Kisspeptin Administration in Women With Hypoactive Sexual Desire Disorder: A Randomized Clinical Trial. JAMA Netw Open. 2022;5(10):e2236131. PMID: 36287566.
  9. Chan YM, Butler JP, Pinnell NE, Pralong FP, Crowley WF Jr, Ren C, et al. Kisspeptin resets the hypothalamic GnRH clock in men. J Clin Endocrinol Metab. 2011;96(6):E908-915. PMID: 21470997.
  10. Abbara A, Eng PC, Phylactou M, Clarke SA, Hunjan T, Roberts R, et al. Kisspeptin receptor agonist has therapeutic potential for female reproductive disorders. J Clin Invest. 2020;130(12):6739-6753. PMID: 33196464.
  11. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH pathway in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. PMID: 24615662.
  12. Pinilla L, Aguilar E, Dieguez C, Millar RP, Tena-Sempere M. Kisspeptins and reproduction: physiological roles and regulatory mechanisms. Physiol Rev. 2012;92(3):1235-1316. PMID: 22811428.
  13. Kotani M, Detheux M, Vandenbogaerde A, Communi D, Vanderwinden JM, Le Poul E, 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. (Identification of kisspeptin as GPR54 ligand.)
  14. Clarke H, Dhillo WS, Jayasena CN. Comprehensive Review on Kisspeptin and Its Role in Reproductive Disorders. Endocrinol Metab (Seoul). 2015;30(2):124-141. PMID: 26194072.
  15. Trevisan CM, Montagna E, de Oliveira R, Christofolini DM, Barbosa CP, Crandall KA, Bianco B. Kisspeptin/GPR54 System: What Do We Know About Its Role in Human Reproduction? Cell Physiol Biochem. 2018;49(4):1259-1276. PMID: 30205368.
  16. Lapatto R, Pallais JC, Zhang D, Chan YM, Mahan A, Cerrato F, et al. Kiss1−/− mice exhibit more variable hypogonadism than Gpr54−/− mice. Endocrinology. 2007;148(10):4927-4936. PMID: 17595229.
  17. Messager S, Chatzidaki EE, Ma D, Hendrick AG, Zahn D, Dixon J, et al. Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54. Proc Natl Acad Sci USA. 2005;102(5):1761-1766. PMID: 15665093.
  18. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
  19. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S2.2.1, Testosterone-stimulating peptides in males. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.
  20. Abbara A, Clarke S, Islam R, et al. A second dose of kisspeptin-54 improves oocyte maturation in women at high risk of ovarian hyperstimulation syndrome: a Phase 2 randomized controlled trial. Hum Reprod. 2017;32(9):1915-1924. PMID: 28854728.
  21. Lee JH, Miele ME, Hicks DJ, Phillips KK, Trent JM, Weissman BE, Welch DR. KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. J Natl Cancer Inst. 1996;88(23):1731-1737. doi:10.1093/jnci/88.23.1731. PMID: 8944003.
  22. West A, Vojta PJ, Welch DR, Weissman BE. Chromosome localization and genomic structure of the KiSS-1 metastasis suppressor gene (KISS1). Genomics. 1998;54(1):145-148. doi:10.1006/geno.1998.5566. PMID: 9806840.
  23. Gottsch ML, Clifton DK, Steiner RA. From KISS1 to kisspeptins: An historical perspective and suggested nomenclature. Peptides. 2009;30(1):4-9. PMID: 18644415.
  24. Jayasena CN, Abbara A, Veldhuis JD, Comninos AN, Ratnasabapathy R, De Silva A, et al. Increasing LH pulsatility in women with hypothalamic amenorrhoea using intravenous infusion of Kisspeptin-54. J Clin Endocrinol Metab. 2014;99(6):E953-E961. doi:10.1210/jc.2013-1569. PMID: 24517142.
  25. George JT, Veldhuis JD, Tena-Sempere M, Millar RP, Anderson RA. Exploring the pathophysiology of hypogonadism in men with type 2 diabetes: kisspeptin-10 stimulates serum testosterone and LH secretion in men with type 2 diabetes and mild biochemical hypogonadism. Clin Endocrinol (Oxf). 2013;79(1):100-104. doi:10.1111/cen.12103. PMID: 23153270.
  26. Chan YM, Lippincott MF, Sales Barroso P, Alleyn C, Brodsky J, Granados H, et al. Using Kisspeptin to Predict Pubertal Outcomes for Youth With Pubertal Delay. J Clin Endocrinol Metab. 2020;105(8):e2717-e2725. doi:10.1210/clinem/dgaa162. PMID: 32232399.

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Checked 14 Oct 2026