HormoneKP-10Metastin 45-54

Kisspeptin-10

Investigational reproductive-axis peptide · KISS1R (GPR54) agonist

Kisspeptin-10 (KP-10) is the short, ten–amino-acid business end of kisspeptin, the master "go" switch at the top of the reproductive hormone chain. It acts one step upstream of GnRH: it tells the GnRH neurons in the hypothalamus to fire, which makes the pituitary release LH and FSH, which in turn drive the testes or ovaries. Given to people in research settings, KP-10 produces a clean, dose-dependent rise in LH and — in men — testosterone, and it can increase the frequency of natural LH pulses; it also modulates how the brain processes sexual and emotional cues on fMRI. But it is investigational, not approved anywhere. Two honest caveats matter: most of the fertility and clinical-trial data actually uses kisspeptin-54 (the longer endogenous form), not KP-10, and KP-10 is so short-lived (a plasma half-life of minutes) that it works as a brief pulse rather than a sustained driver — continuous high-dose exposure tends to desensitize the system, not stimulate it further. The response is also cycle-dependent: KP-10 stimulates men and pre-ovulatory women but barely stimulates women in the early follicular phase. It is best understood today as a powerful physiology research tool, not a finished therapy or supplement.

The short version

Kisspeptin is the master "go" switch at the top of the HPG axis — the hypothalamic–pituitary–gonadal axis, the brain-to-gonad hormone chain that controls reproduction. Specialized neurons in the hypothalamus release kisspeptin, which acts on a receptor called KISS1R (also known as GPR54) on GnRH neurons. GnRH (gonadotropin-releasing hormone) then tells the pituitary to release LH and FSH (luteinizing and follicle-stimulating hormone), which drive the testes or ovaries to make testosterone or estrogen and to mature sperm or eggs. People born without working kisspeptin signaling don't go through puberty normally — so kisspeptin sits one crucial step upstream of GnRH.

Kisspeptin-10 (KP-10) is the short, ten–amino-acid piece of the natural hormone that still fully activates the receptor. Given to people in research, it produces a clean, dose-dependent rise in LH and, in men, testosterone, and can speed up the natural rhythm of LH pulses. Because it is so small, the body breaks it down within minutes, so its effect is brief and pulse-like. The response is also sexually dimorphic: KP-10 reliably stimulates men and women in the late, pre-ovulatory phase, but barely stimulates women in the early follicular phase — the gonad's hormonal state changes how the brain responds.

The buzz around kisspeptin — "natural testosterone booster," "libido peptide," "fertility hormone" — has a real kernel: research groups have shown it can stimulate the reproductive axis, enhance brain responses to sexual and bonding cues, and help trigger egg maturation in IVF with a lower risk of ovarian over-stimulation. But the catch is large: it is investigational, not approved; most of the clinical fertility and low-desire data uses the longer kisspeptin-54, not KP-10; and continuous high-dose infusion can desensitize the system rather than keep stimulating it.

Molecular identity

Specs

Molecular weight: 1302.4 g/mol
Molecular formula: C63H83N17O14
Monoisotopic mass: 1301.6305 Da
CAS / UNII: 374675-21-5 · FS1N52VS3S

Sequence: Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 (YNWNSFGLRF-NH2, 10 AA)PubChem CID 25240297
Structure / class: C-terminally amidated RFamide decapeptide; C-terminal fragment of kisspeptin-54PubChem CID 25240297
Molecular target: KISS1R / GPR54 agonist (on GnRH neurons)PMID 21632807
Half-life: ~4 min plasma (3.8 ± 0.3 min, IV in men)PMID 21976724Half-life curve →
Brand / approval: None — investigational; not approved anywhereResearch literature
Anti-doping status: Prohibited at all times by inference (WADA S2 peptide hormones / testosterone-stimulating peptides)WADA 2026

Plain English

Mechanism

Kisspeptin-10 is a high-potency agonist (a molecule that switches a receptor on) of KISS1R, also called GPR54 — a receptor sitting on the GnRH neurons of the hypothalamus. Switching it on makes those neurons fire and release GnRH, which then drives the pituitary to secrete LH and FSH, which drive the gonads. The key structural point is that KP-10 acts upstream of GnRH, not directly on the pituitary: its hormone effect depends on intact GnRH signaling. This cascade is established in both human and animal work.

The pulsatile-versus-continuous distinction is central. Healthy kisspeptin/GnRH signaling is naturally pulsatile, and acute KP-10 boluses or low-dose infusions raise LH and increase LH pulse frequency. But GnRH-axis signaling is prone to desensitization under sustained high agonist exposure — the same principle that makes continuous GnRH-agonist drugs end up suppressive rather than stimulating. A direct head-to-head infusion study found raw gonadotropin output ran GnRH greater than KP-54 greater than KP-10. The honest framing for anyone reading this is that kisspeptin works best as a brief, pulsatile stimulus, and continuous overdrive is not a route to sustained "more testosterone."

Two further features shape the response. It is cycle-dependent: KP-10 stimulates gonadotropin release in men and in pre-ovulatory women, but fails to stimulate women in the early follicular phase, because the ambient sex-steroid state gates the effect. And it has a behavioral arm: beyond the endocrine cascade, kisspeptin modulates limbic brain activity to sexual and emotional cues on fMRI, independent of simple hormone elevation, because KISS1R is also expressed in emotional-processing regions of the brain.

Sources:PMID 21632807 PMID 21976724 PMID 26089302 PMID 28112678

Why people reach for it

Potential benefits

Kisspeptin-10 is the reproductive-axis trigger people reach for to nudge their own LH and testosterone — a real physiology with genuinely large caveats. Here's the appeal, read against what the research actually supports.

Stimulate your own LH and testosterone — Its headline appeal. KP-10 switches on KISS1R at the top of the reproductive axis, telling the body to release GnRH → LH → and, in men, testosterone — a clean, dose-dependent rise shown in human research.
Works with your own axis, not around it — Because it acts upstream — driving the body's natural LH pulses rather than replacing the hormone — people reach for it when keeping the endogenous reproductive system engaged is the goal, not overriding it.
A brain-side effect on desire and arousal cues — Beyond the hormone cascade, kisspeptin modulated limbic brain responses to sexual and emotional cues on fMRI — a distinct, centrally-mediated arm that's part of why it draws interest for libido.
The top rung of an HPG-axis stack — It sits one step above GnRH, so it pairs logically with Gonadorelin (the pituitary rung) and hCG (the gonad rung) for people building a full-axis approach.
The honest counterweight — investigational, brief, and form-specific — KP-10 is approved nowhere, acts as a brief pulse (half-life of minutes, so more-is-better backfires via desensitization), and the strongest fertility data actually uses the longer kisspeptin-54, not KP-10 — and barely stimulates women in the early-follicular phase.

Sources:PMID 21632807 PMID 16174713 PMID 28112678 PMID 21976724

What people reach for Kisspeptin-10 for, drawn from what the research reports (investigational, monitored research settings only) and how it's used — not proven outcomes, a route to durable testosterone, or any medical claim.

Implied timing

Best time to dose

Implied best time

Morning (or per protocol)

For once-daily use most people dose KP-10 in the morning, when the body's own LH pulses run highest; research dosing varies by protocol.

LH pulses are naturally higher in the morning in men, so a morning dose lands the stimulus at the peak of the axis's own receptivity — the main reason morning is the common default.
KP-10's biology is pulsatile, not continuous: its plasma half-life is only ~4 minutes, so the value is in a brief, well-timed pulse — and for a twice-daily split, spacing the doses ~10–12 hours apart (e.g. 8 AM and 8 PM) to mimic natural LH-pulse intervals matters more than the exact clock time.
The response is also state-dependent rather than purely time-of-day — it stimulates men and pre-ovulatory women but barely stimulates early-follicular women, so "per protocol" carries real weight here.
In the human research, dosing was set by the study design (weight-based IV in monitored settings), not by time of day — so morning is a sensible community habit aligned with LH rhythm, not a studied clock schedule.

No study establishes an ideal time of day for Kisspeptin-10 — this is reasoned from natural LH-pulse rhythm and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; KP-10 leans earlier — morning, to ride the natural LH peak — with research dosing varying by protocol.

Sources:PMID 21976724 PMID 21632807

How to run it

Dosing & protocol

KP-10 is dosed here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. Human research uses intravenous administration at weight-based doses; community SubQ use extrapolates from that to a shorter-duration, bolus-style pulse. Read this as a map of how people actually run injectable KP-10 — not a validated prescription or approved protocol.

Community convention, not trial-proven: KP-10 has no approved dosing and no human subcutaneous trial; research doses were IV in monitored clinical settings. It is not an FDA-approved drug and is likely prohibited by WADA S2 inference. Every number here is a usage pattern, not evidence.

Tiered dose ranges

Community SubQ use aligns with KP-10's pulsatile biology — brief boluses, not continuous infusion.

Low / introductory:: 25–50 mcg per pulse once daily — used to assess individual response and tolerance; starting point for those new to the compound.
Standard:: 50–100 mcg per pulse, once or twice daily — the baseline range most reported in community use for HPG-axis stimulation goals.
Higher / twice-daily split:: 100 mcg twice daily (~8–12 h apart) — used for a more pronounced pulsatile stimulus; separate doses to mirror the body's natural LH pulse interval rather than compressing them.

Subcutaneous administration

KP-10 is injected into subcutaneous fat; site, timing, and pulse spacing are the actionable choices.

Injection site:: The abdomen (staying a couple of inches clear of the navel), the love-handle area, or the outer thigh. Rotate sites between doses so one spot is not used repeatedly — prevents local irritation and lipohypertrophy (fatty lumps).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard mix (5 mg vial + 2 mL bacteriostatic water = 2,500 mcg/mL): 25 mcg = 1 IU · 50 mcg = 2 IU · 100 mcg = 4 IU. The calculator handles any vial size.
Time of day:: Morning is the most common timing for once-daily dosing — LH pulses are naturally higher in the morning in men, so the stimulus lands at the peak of axis receptivity. For a twice-daily split, space doses ~10–12 hours apart (e.g., 8 AM and 8 PM) to mimic pulsatile physiology.
Food window:: SubQ KP-10 does not compete with food for absorption; it can be injected independently of meals.

Cycle & washout

Because KP-10 acts at the very top of the HPG axis, receptor desensitization is a real risk — the pulsatile-not-continuous principle applies to the whole cycle, not just each dose.

Standard cycle:: 2–4 weeks of daily use, then reassess. Shorter than most peptides, because the GnRH axis is particularly prone to tachyphylaxis (diminishing response) under sustained agonist exposure.
Washout:: 2–3 weeks off. Check LH and testosterone levels during the break to see whether the axis returns to its prior baseline. A washout that restores baseline is evidence the axis is not suppressed.
Pulsatile-not-continuous:: The biology actively works against daily extended use. Community preference is intermittent or semi-regular pulses (e.g., 5 days on / 2 days off within a 2–4-week block) rather than unbroken daily dosing, to preserve axis sensitivity.

Reconstitution at a glance

The on-page calculator does this live; the quick reference for a 5 mg vial:

Mixing:: 5 mg vial + 2 mL bacteriostatic water = 2,500 mcg per mL. On a 100-unit (1 mL) insulin syringe: 25 mcg = 1 IU · 50 mcg = 2 IU · 75 mcg = 3 IU · 100 mcg = 4 IU.
Why 2 mL:: Keeps the concentration high enough that small microgram doses still land on readable syringe units — 1–4 IU is a comfortable, measurable draw.

Sources:PMID 21632807 PMID 21976724 PMID 26089302

Substrate the signal needs

Nutritional cofactor precision

KP-10 presses the trigger at the top of the HPG axis — but the axis only delivers if it is fuelled and not stress-suppressed. Three questions organize the useful cofactors: What brake can a nutrient relieve? What steroid-building substrate does downstream hormone production need? What cost is there to offset? For KP-10, MITIGATE is minimal; the heavy lifting is AMPLIFY (energy + cortisol) and SUPPLY (steroid substrate).

Reasoned from HPG axis physiology and general steroidogenesis nutrition — not a KP-10 cofactor study. Supplement doses are community convention ranges, not KP-10-specific trial findings.

AMPLIFY — adequate energy availability

The HPG axis is energy-gated: this is real reproductive physiology, not a supplement claim.

Mechanism:: A meaningful caloric deficit or very low body fat suppresses GnRH/LH output — the same lever that disrupts menstrual cycles in under-fuelled athletes (functional hypothalamic amenorrhea) and causes low testosterone in men who are chronically under-eating. Pressing KP-10 while the body reads energy deficiency means working against a brake the hypothalamus is actively holding. The axis will not fully respond.
Protocol integration:: Maintain adequate energy intake and a healthy body-fat percentage (typically ≥10–12% for men, ≥17–22% for women) before and during KP-10 use. This is a precondition, not a supplement to add.

AMPLIFY — stress & cortisol management

Chronic cortisol suppresses the HPG axis at the same level KP-10 acts — they cancel each other.

Mechanism:: Chronic stress elevates cortisol, which inhibits GnRH pulsatility and blunts pituitary LH release — acting at exactly the hypothalamic level where KP-10 is trying to stimulate. High prolactin (another stress-driven elevation) adds further brake on GnRH. The stimulus and the suppression are working at the same switch.
Protocol integration:: Sleep 7–9 hours nightly (the single most powerful lever on hypothalamic GnRH rhythmicity); manage acute stress load (HRV training, parasympathetic-activation practices). Ashwagandha (KSM-66, 300–600 mg twice daily with meals) has cortisol-reducing + LH-supporting evidence in men and is a common on-cycle addition. Phosphatidylserine (400–800 mg/day with meals) is used to blunt exercise-induced cortisol spikes.

SUPPLY — steroid substrate & synthesis cofactors

Every hormone the axis ultimately produces is built from cholesterol; the enzymatic machinery that converts it needs specific micronutrients.

Mechanism:: Testosterone and estrogen are steroid hormones — cholesterol is their precursor. An extremely low-fat diet removes the raw material. Zinc is a cofactor in steroidogenesis (testosterone-synthesizing enzymes) and in LH receptor signaling; deficiency suppresses gonadal output even when LH signals are adequate. Vitamin D acts as a hormone-like regulator of testosterone synthesis. Magnesium supports free testosterone availability (competes with SHBG binding). Boron reduces SHBG, raising free testosterone — the active fraction.
Protocol integration:: Dietary cholesterol from eggs, meat, and full-fat dairy — do not aggressively restrict fat. Zinc 15–30 mg/day (picolinate or bisglycinate, with a meal) + 1–2 mg copper to prevent depletion on a long run. Vitamin D 2,000–5,000 IU/day with a fatty meal, dosed to a blood level of 50–80 ng/mL. Magnesium glycinate 300–400 mg nightly (doubles as sleep support). Boron 3–10 mg/day with a meal.

MITIGATE — minimal direct cost

KP-10 itself has no documented cofactor-requiring side effects at community doses; the axis desensitization risk is managed through cycling.

Mechanism:: The primary risk is receptor desensitization from overdosing or undercycling — not a nutrient-correctable effect, but a scheduling issue. Beyond that, KP-10 is well tolerated in research at acute doses with no consistent toxicity signal (though data is limited to monitored research settings).
Protocol integration:: Follow the 2–4-week on / 2–3-week off cycle structure in the dosing section. Monitor LH and testosterone at the start and end of washout to verify the axis is resetting, not staying suppressed.

Combinations + timing

Stacking notes + timing windows

KP-10 sits at the very top of the HPG axis — it triggers GnRH release. The natural stack family is the same axis at different rungs: each partner stimulates one step further down the chain, toward the gonad. These are not redundant duplicates of the same lever — they are complementary positions on one ladder. But stacking multiple axis-stimulators only matters if the axis is fuelled and the steroid substrate is present.

Axis-ladder reasoning from where each agent sits on the HPG cascade — not regimens studied head-to-head, and KP-10 is investigational. The pulsatile-not-continuous logic applies to the stack as much as to KP-10 alone; layering stimulators can blunt the response if the axis desensitizes. Doses are community convention.

KP-10 + Gonadorelin

Two rungs on the same axis: KP-10 triggers the GnRH pulse — Gonadorelin IS that GnRH, acting one step lower on the pituitary.

Why it works:: KP-10 tells the hypothalamus to release GnRH; gonadorelin delivers GnRH directly to the pituitary without waiting for the hypothalamic step. Together they can stimulate the pituitary from two angles — the upstream trigger and the direct signal. In research and fertility contexts this pairing appears where robust, multi-point HPG stimulation is the goal (e.g., post-cycle axis recovery alongside exogenous testosterone withdrawal).
The protocol:: KP-10 50–100 mcg SubQ + gonadorelin 100–200 mcg SubQ, each as separate pulses. A common timing: KP-10 in the morning (upstream trigger), gonadorelin ~6–8 h later (downstream signal), mimicking the natural cascade sequence. Pulsatile scheduling — not daily continuous — applies to both.
Outcome:: Reached for in HPG axis recovery and reproductive-function support contexts. Note: both act on the same axis ladder, so the desensitization risk applies doubly — shorter cycles and longer washouts are warranted.

KP-10 + hCG

The third rung: HCG mimics LH at the gonad, acting where the axis terminates — testis or ovary.

Why it works:: KP-10 fires at the hypothalamus (top of the axis); hCG acts at the bottom — it is an LH analog (luteinizing hormone mimic) that binds LH receptors on Leydig cells in the testes or theca cells in the ovaries, directly stimulating testosterone or estrogen synthesis. The two cover opposite ends of the same chain: signal origination at the brain and direct gonadal production. This is why hCG is the classic post-cycle option even when GnRH signaling is suppressed — it bypasses the upper axis entirely.
The protocol:: KP-10 50–100 mcg SubQ daily or EOD (hypothalamic stimulus) + hCG 250–500 IU SubQ every 3–4 days (gonadal stimulus), run in parallel. Because hCG acts downstream of KP-10, they are not redundant — KP-10 helps maintain the upper-axis signaling pattern while hCG supports direct gonadal output.
Outcome:: Reached for in testosterone maintenance, post-cycle support, and fertility-stimulation contexts. Honest caveat: no controlled human trial covers this combination; both are investigational in this context and KP-10 adds upstream HPG signaling that hCG alone does not provide.

KP-10 + Gonadorelin + hCG

The full axis ladder: hypothalamus (KP-10) → pituitary (gonadorelin) → gonad (hCG) — three rungs, one chain.

Why it works:: Each agent stimulates a distinct level of the HPG cascade. KP-10 fires the GnRH pulse upstream; gonadorelin delivers that GnRH signal to the pituitary directly; hCG acts on the gonad as an LH surrogate. All three are mechanistically distinct: removing any one still leaves two active. This is the most aggressive axis-support stack and reflects the logic of comprehensive HPG stimulation in the context of axis suppression recovery.
The protocol:: KP-10 50–100 mcg SubQ morning (hypothalamic pulse); gonadorelin 100 mcg SubQ ~6 h later (pituitary signal); hCG 250–500 IU SubQ every 3–4 days (gonadal direct). All three on a cycling schedule — 2–3 weeks on, minimum 2 weeks off — with LH and testosterone monitored at washout.
Outcome:: Reached for in structured post-cycle or TRT-pause protocols where maintaining endogenous axis function across all three levels is the goal. Doubly unproven: no controlled trial covers any two-peptide combination here, let alone three; desensitization risk is highest in this configuration and monitoring is not optional.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.04 mL
Doses per vial: 50
Concentration: 2.5 mg/mL

One vial lasts

Daily: 50 days
Every other day: 100 days
5×/week: 70 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

Across the published human trials — reproductive-axis stimulation, fMRI studies, the HSDD trial, and the IVF-trigger work — kisspeptin has generally been well tolerated, with no serious adverse events attributed to it. Reported effects are mild and transient, such as occasional flushing or minor infusion-related effects, with no consistent serious toxicity signal at research doses.

The honest limits are about what the data does not cover. These trials are small and short-term; there is no long-term or chronic-use safety data, and none at all in unsupervised, consumer settings. "Well tolerated in monitored research" is not the same as "safe for self-administration," and because the peptide acts on the reproductive hormone axis, sustained or repeated unsupervised use has unknown effects on that system.

Sources:PMID 16174713 PMID 28112678 PMID 25036713

As reported in literature

Research dosing ranges

These are doses tested in human research, shown separately so the trial evidence is never mistaken for a recommended regimen. The model column flags whether each study used kisspeptin-10 (KP-10) or the longer kisspeptin-54 (KP-54), because the strongest fertility and clinical data uses KP-54, not KP-10. All were given intravenously or subcutaneously in monitored research settings; none represents an approved or consumer regimen.

Dose	Route	Model	Outcome	Sources:
~0.3–4 µg/kg bolus; 1.5 µg/kg/h infusion	IV	Human men, KP-10 (n=6 bolus arm)	Dose-dependent LH rise (peak ~1 µg/kg); infusion increased LH pulse frequency	PMID 21632807
Single bolus / phase comparison	IV	Human men & women, KP-10	Stimulates LH/FSH in men and pre-ovulatory women; FAILS in early-follicular women (sexual dimorphism)	PMID 21976724
0.1 / 0.3 / 1.0 nmol/kg/h (3 h each)	IV continuous	Human men, KP-10 vs KP-54 vs GnRH	Gonadotropin output GnRH > KP-54 > KP-10 (direct head-to-head potency)	PMID 26089302
90-min infusion	IV	Human men, KP-54 (n=6)	↑ LH, FSH and testosterone vs saline (first-in-human HPG stimulation)	PMID 16174713
Infusion (fMRI paradigm)	IV	Human (men + HSDD women), kisspeptin	Enhanced limbic brain activity to sexual/bonding stimuli; well tolerated	PMID 28112678
Single bolus (trigger)	SC	Human women, IVF, KP-54 (n=53)	Triggered oocyte maturation with viable pregnancies; low ovarian-hyperstimulation risk	PMID 25036713

Quick answers

Frequently asked

Is kisspeptin-10 approved?

No. It is investigational worldwide — not approved by the FDA, EMA, or any other regulator for any use. All human use to date has been in research and clinical-trial settings.

What is the difference between KP-10 and KP-54?

KP-10 is the ten-residue C-terminal fragment — the smallest fully active piece — while KP-54 is the 54-residue major circulating form. They share the same receptor and core mechanism, but KP-54 lasts much longer in the blood and is the form used in most fertility and clinical trials, whereas KP-10 dominates acute mechanism studies. They are not interchangeable in the evidence.

Does it actually raise testosterone?

In men, intravenous KP-10 produces a clean, dose-dependent rise in LH, and kisspeptin-54 raised LH, FSH, and testosterone in the first-in-human study. But the effect is acute and pulsatile, not a route to durable testosterone elevation, and there is no approved regimen for that purpose.

Will it work the same in women?

No — the response is cycle-dependent. KP-10 stimulates women in the pre-ovulatory phase but barely stimulates women in the early follicular phase, because the ovary's hormonal state gates the brain's response.

Can you take it continuously for a bigger effect?

That is a mismatch with the biology. Kisspeptin/GnRH signaling is pulsatile, and sustained high exposure trends toward desensitization rather than greater stimulation. More is not better here — the biology actively works against continuous overdrive.

How is it given, and how long does it last?

In research it is given intravenously (KP-10) or subcutaneously (KP-54, IVF trigger); community SubQ use of KP-10 is convention, not trial-proven. KP-10's plasma half-life is only about minutes, though the hormonal response plays out over one to two hours. KP-54 lasts much longer.

Is kisspeptin banned in sport?

It is not named as a standalone entry on the 2026 WADA Prohibited List, but because it stimulates the body's own LH and testosterone production it falls under Category S2 (peptide hormones and related substances), which is banned at all times. This is an inference from the category language rather than an explicit listing, so athletes should treat it as prohibited and seek a definitive ruling from their anti-doping authority.

Primary sources

References

PubChem CID 25240297PubChem CID 25240297 (Kisspeptin-10)
PMID 21632807George et al., J Clin Endocrinol Metab 2011 (KP-10 ↑LH + pulse frequency in men)
PMID 21976724Jayasena et al., J Clin Endocrinol Metab 2011 (sexually dimorphic KP-10 response)
PMID 26089302Jayasena et al., Hum Reprod 2015 (KP-10 vs KP-54 vs GnRH head-to-head)
PMID 16174713Dhillo et al., J Clin Endocrinol Metab 2005 (KP-54 first-in-human, ↑testosterone)
PMID 28112678Comninos et al., J Clin Invest 2017 (kisspeptin modulates sexual brain processing)
PMID 36287566Thurston et al., JAMA Netw Open 2022 (kisspeptin in HSDD women)
PMID 25036713Jayasena et al., J Clin Invest 2014 (KP-54 IVF oocyte-maturation trigger)
WADA 2026WADA 2026 Prohibited List (S2 peptide hormones — kisspeptin prohibited by inference)

Research use only · Not medical advice · Updated 2026-06-01