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Explore  /  Kisspeptin-10 (KP-10)
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Kisspeptin-10 (KP-10)

B
lead outcome
Stimulating the reproductive axis (LH/FSH…
grades vary by outcome ↓
Peptide
also called — Kisspeptin-10 · KP-10 · metastin (the parent's original name)
reproductive-axis stimulation (GnRH→LH/FSH)fertility / IVF triggeringsexual desire / arousal (HSDD)(research tool for reproductive endocrinology)

The reproductive "master switch" — with real modern clinical science and three great backstories. This is one of the register's stronger entries: a genuine upstream controller of human reproduction, backed by actual randomized trials (Imperial College London), yet still research-only. Three threads of intrigue: (1) it's named after Hershey's Kisses chocolate; (2) it was discovered in cancer research (as a metastasis suppressor) before anyone knew it ran reproduction; (3) recent placebo-controlled trials show it modulates the "attraction" and desire circuits of the brain — a real, published sexual-desire signal, not gray-market folklore.

In brief

Kisspeptin-10 is the minimal active fragment of kisspeptin — the hypothalamic peptide that sits at the top of the reproductive hormone axis and acts as its master switch. It works upstream: activating KISS1R on GnRH neurons, which drives pulsatile GnRH → LH/FSH → testosterone/estradiol. Its story is unusually rich: the gene was named after Hershey's Kisses chocolate, was discovered in cancer research (as the metastasis suppressor "metastin") before its reproductive role was known, and proved essential when people lacking it were found not to undergo puberty. Crucially — and unlike most compounds here — kisspeptin has real, current clinical science behind it: Imperial College London teams have run trials in hypogonadism, IVF triggering, hypothalamic amenorrhea, and hypoactive sexual desire disorder, where randomized placebo-controlled studies showed it modulates the brain's arousal/"attraction" circuits and reduces sexual aversion. The honest caveats: it's still research-only (not approved), its strongest data are in specific clinical settings (not the bodybuilding "testosterone restart" use it's often sold for), and it has a very short half-life. Bottom line: a genuinely important hormone with real translational momentum — promising and well-studied, but not yet an approved therapy.

Legal standing, by region
European Union
Not FDA-approved (gray-market)

research use only; not approved by FDA or EMA for any therapeutic use. But — unlike most gray-market peptides — it has an active, legitimate clinical-trial pipeline (Phase 1/2), so its "unproven" status is "not yet approved, actively being developed," not "fringe."

Evidence, by outcome
How we grade →

An honest grade per outcome — drawn from the evidence, not any catalogue. Hype and undemonstrated marketing claims grade low.

OutcomeEvidence base · effectGrade
Stimulating the reproductive axis (LH/FSH release)
Well-established physiology in controlled settings; short-acting; response shows sexual dimorphism (differs by sex and menstrual-cycle phase)
Robust, repeatedly demonstrated in humans (IV kisspeptin → rapid LH/FSH rise); genetics confirm necessity
B
IVF / egg-maturation triggering
Promising, actively developed; not yet a standard/approved trigger
Clinical trials: kisspeptin can trigger oocyte maturation with lower OHSS risk than standard hCG
B
Hypoactive sexual desire disorder (HSDD) — arousal/attraction
Real RCT signal on brain processing + self-report — but early, small, mechanistic endpoints; not an approved HSDD drug
2 randomized placebo-controlled trials (JAMA Netw Open 2022/2023, 32 women + 32 men): modulated sexual-processing brain networks, ↑"sexy" ratings, ↓aversion
C
Idiopathic hypogonadotropic hypogonadism / hypothalamic amenorrhea
Coherent, promising; still investigational
Mechanistic + clinical studies restoring axis activity
C
"PCT / natural-testosterone restart" (the bodybuilding use)
Not clinically established for this purpose; short half-life and pulsatility make casual self-use dubious
Extrapolated from LH/FSH stimulation
F
Safety
Reported well-tolerated with no significant adverse events in trials; but off-protocol self-dosing of an upstream reproductive hormone is unstudied; product quality unverified
Controlled-setting trials
Disclosure

Vallydia sells its own cosmetic serums, and some ingredients graded here belong to the same categories as those products. Grades are drawn from the published evidence by the method we publish, and applied to our own ingredients on the same terms — our copper-peptide serum is graded no more kindly than the peptides it competes with. We disclose the interest so you can weigh it.

Trade names shown here (for example Matrixyl, Argireline, Syn-Ake) are the property of their respective owners and are used only to identify the ingredient under discussion. Their appearance implies no affiliation with, or endorsement by, the proprietor.

Evidence changes

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Identity an endogenous decapeptide — the minimal fully-active fragment of kisspeptin, the hypothalamic peptide that sits at the very top of the reproductive hormone axis. The KISS1 gene (chromosome 1q32) makes a 145-aa precursor, cleaved to kisspeptin-54 (metastin) and shorter fragments including KP-10, which retains full activity at the KISS1R (GPR54) receptor. Unlike hormones that act on the gonads directly, kisspeptin acts upstream — it "controls the controllers." ## Mechanism (as proposed) kisspeptin neurons (in the hypothalamic arcuate and AVPV nuclei) release kisspeptin, which binds KISS1R (GPR54) — a Gq/11-coupled GPCR — on GnRH neurons, activating phospholipase C → IP3/DAG → calcium and ERK1/2/p38 signalling. This makes GnRH neurons fire and release GnRH in pulses into the pituitary portal circulation; the pituitary then secretes LH and FSH, which drive the gonads to make testosterone/estradiol. Kisspeptin is thus the dominant "gate" for GnRH pulse generation — the reason it's called the reproductive master regulator. It's also sensitive to sex-steroid feedback and metabolic cues (linking body energy status to fertility). The separate arousal/attraction effects appear to involve limbic brain activity and are reported to be partly independent of the downstream hormone rise — i.e. kisspeptin may act on desire circuits directly, not only via testosterone/estradiol.

Chemical identifiers

Cross-reference identifiers for the authoritative external databases — not a recipe, and nothing about how to use it.

PubChem CID25240297
InChIKeyRITKWYDZSSQNJI-INXYWQKQSA-N
SMILESCC(C)C[C@@H](C(=O)N[C@@H](CCCN=C(N)N)C(=O)N[C@@H](CC1=CC=CC=C1)C(=O)N)NC(=O)CNC(=O)[C@H](CC2=CC=CC=C2)NC(=O)[C@H](CO)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CC3=CNC4=CC=CC=C43)NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CC5=CC=C(C=C5)O)N

via PubChem exact-name match (Kisspeptin-10) · high confidence

Sources — 5 cited
01Lee JH, Welch DR, et al. KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. (1996) — discovery/naming; Ohtaki et al. 2001 (metastin/KISS1R).
02Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH pathway in human reproductive health and disease. Hum Reprod Update. 2014; Koysombat et al. (Dhillo/Abbara), Physiol Rev. 2025 (current synthesis).
03Thurston L, et al. Effects of kisspeptin administration in women with HSDD: a randomized clinical trial. JAMA Netw Open. 2022; Mills EG, et al. …in men with HSDD. JAMA Netw Open. 2023 (the RCT arousal/attraction data).
04Comninos AN, et al. — kisspeptin and attraction/olfaction brain processing (JCI Insight, 2020).
05Human genetics: KISS1/KISS1R loss-of-function → idiopathic hypogonadotropic hypogonadism. (Research-use-only; not FDA/EMA-approved as of 2026.)
Updated 2026-07-13 (active clinical pipeline — watch for Phase 2/3 progress in IVF triggering and HSDD; approval would move several grades)

Grades reflect the published evidence, not our interest. No dosing, reconstitution, or administration is published for research compounds — that restraint is deliberate.

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