Kisspeptin
KISS1 Gene Product | Reproductive Neuropeptide
Kisspeptin is a family of neuropeptides encoded by the KISS1 gene that acts as a master regulator of the reproductive system. It potently stimulates gonadotropin-releasing hormone (GnRH) neurons, making it essential for puberty initiation, fertility, and reproductive function. Research explores its therapeutic potential for infertility, low libido, and reproductive disorders.
Daily dose
100-200mcg
Frequency
Once, or 2-3x/week
Cycle length
2-4 weeks
Storage
2-8°C
Key benefits
Potent reproductive hormone stimulation, fertility enhancement, sexual function support, and potential therapeutic applications for hypogonadotropic hypogonadism and HSDD.
How it works
Kisspeptin binds to KISS1R/GPR54 receptors on hypothalamic GnRH neurons, stimulating pulsatile GnRH release. This triggers pituitary LH and FSH secretion, which regulate gonadal steroid production and reproductive function. Kisspeptin serves as the master upstream regulator of the reproductive endocrine axis.
Dosage protocols
Goal
Gonadotropin stimulation
Dose
100-200mcg · 2-3x/week
Route
SubQ
Goal
Fertility support
Dose
0.4-1.0 nmol/kg · As directed
Route
SubQ (KP-54)
Goal
Sexual function (clinical)
Dose
1 nmol/kg/h · 75 min infusion
Route
IV
Goal
Research protocols
Dose
0.3-10 nmol/kg · Variable
Route
IV or SubQ
Research indications
reproductive
sexual
metabolic
Administration
Interactions
Safety notes
Use sterile injection technique
AVOID daily administration - causes desensitization
Use 2-3x per week maximum
Caution with cardiovascular disease (vasoconstrictor effects)
Not recommended during pregnancy or breastfeeding
Requires medical supervision for fertility applications
Research studies
Intranasal Kisspeptin Administration (2025)
Humans | 12.8 nmol/kg intranasal KP-54 | Healthy adults and HA patients
Intranasal kisspeptin-54 rapidly stimulated gonadotropin release in healthy men and women and patients with hypothalamic amenorrhea without side effects. Demonstrated non-invasive delivery method with stable formulation for 60 days at 4°C.
View study →Kisspeptin for Hypoactive Sexual Desire Disorder in Men (2023)
Humans | 32 men with HSDD | 1 nmol/kg/h IV infusion | 75 minutes | RCT
Kisspeptin significantly modulated brain activity in sexual processing networks, increased penile tumescence by up to 56% vs placebo, and enhanced behavioral measures of sexual desire. Brain imaging showed deactivation of self-monitoring regions and activation of sexual arousal centers.
View study →Kisspeptin for HSDD in Women (2022)
Humans | 32 women with HSDD | 1 nmol/kg/h IV infusion | 75 minutes | RCT
Kisspeptin administration modulated sexual and facial attraction brain processing. Exploratory analysis showed increased self-reported ratings of feeling sexy compared with placebo, suggesting potential therapeutic application.
View study →Kisspeptin as IVF Ovulation Trigger (2017)
Humans | Multiple doses tested | Subcutaneous KP-54 | Clinical trial
Kisspeptin-54 successfully triggered oocyte maturation in IVF patients at high risk of OHSS. Resulted in 45% live birth rate with zero cases of moderate-severe OHSS, establishing kisspeptin as safer alternative to hCG trigger.
View study →Kisspeptin Cardiovascular Effects Study (2017)
Human vessels and Apoe-/- mice | 4-week KP-10 infusion | Ex vivo studies
Kisspeptin-10 demonstrated vasoconstrictor properties comparable to angiotensin II and accelerated atherosclerotic lesion development in mice. Effects were completely reversed by GPR54 antagonist, raising cardiovascular safety considerations.
View study →Kisspeptin Effects on Metabolism and Obesity (2014)
Mice | Kiss1r knockout models | Long-term observation
Female Kiss1r knockout mice developed 30% increased body weight by 18 weeks despite reduced food intake, showing dramatically reduced energy expenditure, locomotor activity, and glucose tolerance.
View study →Discovery of Kisspeptin-GPR54 in Reproduction (2003)
Humans | Genetic studies | Inactivating GPR54 mutations identified
Landmark studies identified that mutations in GPR54 receptor cause hypogonadotropic hypogonadism and pubertal failure, establishing kisspeptin-GPR54 signaling as essential gatekeeper of human reproduction.
View study →