What is the standard Kisspeptin-10 dosage?

The most common community Kisspeptin-10 dosage is 100–500 mcg administered subcutaneously 1–2 times daily. Starting doses are typically 100–200 mcg once daily to assess individual response, with titration upward based on symptom improvement and tolerance. Kisspeptin-10 is the minimal active fragment (10 amino acids) of the full-length Kisspeptin-54 and is the form most commonly available for research use.

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

Kisspeptin-54 (also called metastin) is the full-length peptide encoded by the KISS1 gene — 54 amino acids long. Kisspeptin-10 is the minimal C-terminal fragment (the last 10 amino acids) that retains full receptor binding activity at the KISS1R (GPR54) receptor. Both activate the same receptor and stimulate GnRH release. Kisspeptin-54 has been used in clinical trials (primarily IV at 1.6–12.8 nmol/kg), while Kisspeptin-10 is more commonly available in community settings and is typically dosed in micrograms subcutaneously. Kisspeptin-54 may have a longer duration of action due to its larger size and slower degradation.

How does Kisspeptin differ from Gonadorelin (GnRH)?

This is the most important distinction to understand. Gonadorelin IS synthetic GnRH — it directly stimulates the pituitary GnRH receptors to release LH and FSH. Kisspeptin acts one level upstream: it stimulates the hypothalamic GnRH neurons to release their own endogenous GnRH in a natural pulsatile pattern. This means Kisspeptin preserves the physiological hypothalamic signaling rhythm rather than bypassing it. The practical consequence is that Kisspeptin is less likely to cause the pituitary desensitization seen with continuous GnRH agonist exposure, because the GnRH release it triggers follows the body’s own pulsatile pattern.

Can Kisspeptin restore testosterone levels?

Kisspeptin stimulates the full HPG (hypothalamic-pituitary-gonadal) axis cascade: Kisspeptin → GnRH release → LH and FSH release → testicular testosterone production. Clinical studies have demonstrated that Kisspeptin-54 administration acutely increases LH and testosterone levels in healthy men. Community protocols using Kisspeptin-10 (100–500 mcg SubQ daily) report improvements in testosterone-related symptoms over 4–8 weeks. However, the testosterone-raising effect requires intact pituitary and gonadal function — Kisspeptin will not raise testosterone if the pituitary cannot produce LH or the testes cannot respond to it.

Does Kisspeptin cause pituitary desensitization like GnRH agonists?

This is one of Kisspeptin’s key advantages. Continuous GnRH agonist exposure (like long-acting leuprolide) causes pituitary GnRH receptor downregulation, leading to suppressed LH/FSH and ultimately lower testosterone — the basis of chemical castration therapy. Kisspeptin does NOT directly activate pituitary GnRH receptors. Instead, it stimulates hypothalamic neurons to release endogenous GnRH in a natural pulsatile fashion. This preserved pulsatility is believed to protect against the desensitization seen with continuous direct GnRH stimulation. Clinical studies with repeated Kisspeptin dosing have shown sustained LH responses without evidence of pituitary desensitization.

Is Kisspeptin used in IVF or fertility treatment?

Yes. Kisspeptin-54 has been investigated in clinical trials as an alternative to hCG for triggering final oocyte maturation in IVF cycles. The rationale is that Kisspeptin triggers a more physiological LH surge (through endogenous GnRH) compared to exogenous hCG, potentially reducing the risk of ovarian hyperstimulation syndrome (OHSS) — a serious complication of IVF. Clinical doses used as IVF triggers are typically Kisspeptin-54 at 1.6–12.8 nmol/kg administered intravenously. This is a clinical application under physician supervision, not a community protocol.

Does Kisspeptin affect libido and sexual function?

Yes, through two pathways. First, by restoring testosterone levels via HPG axis stimulation, Kisspeptin indirectly supports libido and sexual function. Second, neuroimaging studies have shown that Kisspeptin-54 administration modulates brain regions associated with sexual arousal and attraction (limbic structures) independently of its hormonal effects. Clinical trials have demonstrated that Kisspeptin enhances brain responses to sexual stimuli in both men and women. Community users frequently report improved libido as one of the earliest noticed effects, often within 1–2 weeks of starting a protocol.

Can women use Kisspeptin?

Yes. Kisspeptin plays a fundamental role in female reproductive physiology — it is essential for GnRH pulsatility, the LH surge that triggers ovulation, and the onset of puberty. Clinical research has explored Kisspeptin for hypothalamic amenorrhea (where impaired GnRH pulsatility causes absent menstrual periods) and as an IVF trigger. Women should only use Kisspeptin under medical guidance, as stimulating the HPG axis affects the menstrual cycle, ovulation timing, and reproductive hormones. Dosing may differ from male protocols. Kisspeptin is not recommended during pregnancy.

How long does it take for Kisspeptin to work?

Kisspeptin produces acute hormonal effects quickly — LH levels rise within 30–60 minutes of a single subcutaneous dose, and testosterone levels increase within hours in clinical settings. However, sustained clinical benefits (improved energy, libido, body composition) require consistent dosing over weeks. Most community users report noticeable improvements in libido and energy within 1–2 weeks, with fuller testosterone restoration effects developing over 4–8 weeks of consistent daily use.

Kisspeptin (Kisspeptin-10 / Kisspeptin-54) Dosage Guide

Q: Is Kisspeptin safe for long-term use?

Available clinical data suggests Kisspeptin has a favorable safety profile with no evidence of pituitary desensitization during study periods. Because it works through the body’s own GnRH pulsatile mechanism rather than bypassing it, the theoretical risk of hormonal axis disruption is lower than with direct GnRH analogs. However, long-term human safety data beyond clinical trial durations is limited. Cycling (4–8 weeks on, 2–4 weeks off) is recommended by community practitioners to periodically reassess HPG axis function and avoid prolonged reliance on exogenous stimulation.

Evidence-based protocols for the master upstream regulator of the HPG axis — Kisspeptin-10 and Kisspeptin-54 dosing for endogenous GnRH stimulation, testosterone restoration, fertility support, IVF triggers, libido enhancement, and stacking strategies.

Compiled by PeptideWiki Editorial Team

What Is Kisspeptin?

Kisspeptin is a family of peptides encoded by the KISS1 gene that function as the master upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis. The full-length form, Kisspeptin-54 (also called metastin), is a 54-amino-acid peptide. The minimal active fragment, Kisspeptin-10, is the C-terminal 10 amino acids that retain full binding activity at the KISS1R (GPR54) receptor. Both forms are used in research and clinical settings.

Kisspeptin's mechanism is fundamentally different from direct GnRH analogs like Gonadorelin. Rather than bypassing the hypothalamus and directly stimulating pituitary GnRH receptors, Kisspeptin acts on KISS1R receptors on GnRH neurons in the hypothalamus. This triggers the release of endogenous GnRH in its natural pulsatile pattern, which then stimulates pituitary LH and FSH secretion, ultimately driving gonadal hormone production (testosterone in men, estrogen and progesterone in women). The critical distinction is that Kisspeptin preserves the body's own hypothalamic signaling rhythm.

This “upstream” mechanism gives Kisspeptin a key advantage: it is significantly less likely to cause the pituitary GnRH receptor desensitization that occurs with continuous direct GnRH agonist exposure. Clinical studies have demonstrated sustained LH responses with repeated Kisspeptin dosing, supporting its potential as a more physiological approach to HPG axis stimulation.

Use our Peptide Dosage Calculator to calculate your exact subcutaneous dose based on vial size and concentration.

Important: Kisspeptin is not FDA-approved for general human use. It is classified as a research peptide. Kisspeptin-54 has been used in clinical trials (primarily for IVF triggers and reproductive endocrinology research), but it is not an approved pharmaceutical outside of clinical trial settings. All dosing information in this guide is derived from clinical research data and community protocols — not from approved pharmaceutical labeling. Consult a healthcare provider before using any research peptide.

Key Characteristics:

Master upstream regulator of the HPG axis — Kisspeptin → GnRH release → LH/FSH release → testosterone/estrogen production; the top of the reproductive hormone cascade
Preserves endogenous GnRH pulsatility — stimulates hypothalamic GnRH neurons to release GnRH in natural pulses, rather than bypassing the hypothalamus like direct GnRH analogs
Resists pituitary desensitization — does NOT directly activate pituitary GnRH receptors, so it avoids the receptor downregulation seen with continuous GnRH agonist exposure
Two main forms — Kisspeptin-54 (full-length, 54 amino acids, used in clinical trials) and Kisspeptin-10 (minimal active fragment, 10 amino acids, most common in community use)
Clinical research areas — IVF oocyte maturation trigger, hypothalamic amenorrhea, testosterone restoration, sexual function, puberty disorders
Neurological effects on sexual function — activates limbic brain regions associated with sexual arousal and attraction independently of hormonal effects; enhances brain response to sexual stimuli

For cross-reference on the downstream target, see the Gonadorelin dosage guide. New to peptides? Start with the Beginner's Guide to Peptides.

How Kisspeptin Dosage Is Determined

Kisspeptin dosing is informed by a combination of clinical trial data (primarily for Kisspeptin-54), translational pharmacology, and community experience (primarily for Kisspeptin-10). The evidence base is stronger than many research peptides due to published clinical trials in reproductive endocrinology.

Clinical Trials — Kisspeptin-54

Dhillo et al. (2005) demonstrated that intravenous Kisspeptin-54 at doses of 0.4–12.8 nmol/kg potently stimulated LH, FSH, and testosterone release in healthy men. Jayasena et al. explored Kisspeptin-54 as an IVF trigger at 1.6–12.8 nmol/kg IV, showing it could induce oocyte maturation while potentially reducing OHSS risk compared to hCG triggers. These landmark studies established Kisspeptin's dose-response relationship for acute HPG axis stimulation.

Subcutaneous Pharmacokinetics

Clinical research has also evaluated subcutaneous Kisspeptin-54 administration, demonstrating effective LH stimulation via this more practical route. Subcutaneous delivery produces a slower absorption curve with more sustained plasma levels compared to IV bolus, which may better support physiological GnRH pulsatility. This subcutaneous data underpins the community's adoption of SubQ as the standard route.

Kisspeptin-10 Community Protocols

Kisspeptin-10, the minimal active fragment, is the form most commonly available for research use. Community dosing protocols (100–500 mcg SubQ, 1–2x daily) are extrapolated from clinical Kisspeptin-54 data, adjusted for the shorter peptide fragment's potentially different pharmacokinetics (Kisspeptin-10 has a shorter half-life than Kisspeptin-54). These ranges represent the most commonly reported effective doses across peptide research communities.

Reproductive Endocrinology Research

Extensive research into Kisspeptin's role in hypothalamic amenorrhea (Jayasena et al.) has demonstrated that exogenous Kisspeptin can restore GnRH pulsatility in women with impaired hypothalamic signaling. Studies in men with functional hypogonadotropic hypogonadism have shown Kisspeptin can stimulate the HPG axis when the hypothalamus is the weak link. This body of research supports Kisspeptin's potential for restoring natural hormone production in conditions of hypothalamic origin.

Strength of evidence: Strong clinical for Kisspeptin-54, moderate community for Kisspeptin-10. Kisspeptin-54 has robust published clinical trial data in reproductive endocrinology, including randomized controlled trials for IVF triggers. Kisspeptin-10 community protocols are extrapolated from this data and refined by user experience. The underlying receptor pharmacology (KISS1R activation) is the same for both forms, supporting the translation. This is stronger evidence than most research peptides have.

Standard Kisspeptin Dosage Ranges

Dosing depends on which form of Kisspeptin you are using. Kisspeptin-10 (community standard) and Kisspeptin-54 (clinical form) have different molecular weights and pharmacokinetics, so their dosing protocols are not interchangeable.

Kisspeptin-10 — Subcutaneous (Community Standard)

Level	Dose per Injection	Frequency	Daily Total	Notes
Starting	100 mcg	1x daily	100 mcg	Assess individual HPG axis response; check LH/testosterone at 2–4 weeks
Standard	200–300 mcg	1–2x daily	200–600 mcg	Most common community protocol for testosterone support and libido
Higher Range	500 mcg	1–2x daily	500–1,000 mcg	Upper end of community dosing; for individuals with suboptimal response at standard doses

Kisspeptin-54 — Clinical Dosing (Reference)

Application	Dose	Route	Context
Acute LH stimulation	0.4–12.8 nmol/kg	IV bolus	Clinical research; dose-response studies in healthy men
IVF trigger	1.6–12.8 nmol/kg	IV or SubQ	Clinical trials; alternative to hCG for oocyte maturation
Hypothalamic amenorrhea	6.4 nmol/kg twice weekly or pulsatile infusion	SubQ or IV infusion	Clinical trials; restoring GnRH pulsatility in women

Do NOT mix up dosing units. Kisspeptin-54 clinical data uses nmol/kg (nanomoles per kilogram of body weight). Kisspeptin-10 community protocols use mcg (micrograms) as flat doses. These are different peptide forms with different molecular weights (Kisspeptin-54: ~5.9 kDa; Kisspeptin-10: ~1.3 kDa). Do not attempt to convert between them without accounting for these differences. If you have Kisspeptin-10 (the most common community form), use the mcg-based Kisspeptin-10 table above.

Administration Routes Compared

Kisspeptin has been studied via multiple routes. The choice depends on the clinical context, form of Kisspeptin, and whether acute or sustained HPG axis stimulation is desired.

Parameter	Subcutaneous	Intravenous	Intranasal
Typical Use	Community & clinical	Clinical trials only	Experimental / early research
Form Used	Kisspeptin-10 or Kisspeptin-54	Kisspeptin-54 (clinical)	Kisspeptin-10 (experimental)
Onset	30–60 minutes (LH rise)	5–15 minutes (fastest)	Variable / uncertain
Duration	More sustained (slower absorption)	Acute peak, shorter duration	Unknown / limited data
Bioavailability	Good (well-characterized)	100% (direct bloodstream)	Low to moderate (mucosal)
Practicality	Most practical (self-administered)	Requires clinical setting	Easy but unproven efficacy
Community Popularity	Standard route	Clinical only	Very limited
Key Advantage	Sustained absorption; supports pulsatility	Precise dosing; fastest onset	Non-invasive; brain-targeted potential

Subcutaneous is the standard community route. SubQ injection of Kisspeptin-10 provides well-characterized absorption kinetics, supports the sustained plasma levels needed for physiological GnRH pulsatility, and is practical for self-administration. IV dosing is confined to clinical trial settings. Intranasal Kisspeptin is experimental with very limited efficacy data — it is not recommended as a primary route at this time.

Calculate Your Kisspeptin-10 Dose

Kisspeptin-10 is supplied as a lyophilized (freeze-dried) powder, typically in 2 mg or 5 mg vials. You reconstitute it with bacteriostatic water, then draw your dose using an insulin syringe. The concentration depends on how much water you add to the vial.

Worked Example:

Vial size: 5 mg (5,000 mcg) of Kisspeptin-10
Bacteriostatic water added: 2 mL
Concentration: 5,000 mcg ÷ 2 mL = 2,500 mcg per mL
Target dose: 250 mcg
Volume to draw: 250 ÷ 2,500 = 0.1 mL = 10 units on an insulin syringe

Quick Reference — 5 mg Vial

Bac Water Added	Concentration	200 mcg Dose	500 mcg Dose
1 mL	5,000 mcg/mL	4 units (0.04 mL)	10 units (0.1 mL)
2 mL	2,500 mcg/mL	8 units (0.08 mL)	20 units (0.2 mL)
2.5 mL	2,000 mcg/mL	10 units (0.1 mL)	25 units (0.25 mL)
5 mL	1,000 mcg/mL	20 units (0.2 mL)	50 units (0.5 mL)

Quick Reference — 2 mg Vial

Bac Water Added	Concentration	100 mcg Dose	200 mcg Dose
1 mL	2,000 mcg/mL	5 units (0.05 mL)	10 units (0.1 mL)
2 mL	1,000 mcg/mL	10 units (0.1 mL)	20 units (0.2 mL)

Skip the Math — Use Our Calculator

Enter your vial size, water volume, and desired dose — get instant calculations with zero manual math.

Kisspeptin Dosage by Goal

Kisspeptin's HPG axis stimulation supports several related but distinct goals. The optimal protocol varies depending on whether testosterone restoration, fertility support, libido enhancement, or post-cycle recovery is the primary objective.

Testosterone Restoration & Optimization

For men with suboptimal testosterone due to hypothalamic dysfunction (secondary hypogonadism), age-related decline, or general HPG axis sluggishness. Kisspeptin stimulates the full cascade: GnRH → LH → testicular testosterone production. Requires intact pituitary and gonadal function.

Form: Kisspeptin-10
Route: Subcutaneous injection
Dose: 200–500 mcg per injection
Frequency: 1–2x daily (morning preferred for first dose)
Duration: 4–8 weeks; verify with bloodwork (LH, total/free testosterone) at 4 weeks
Stack: + Gonadorelin 100 mcg SubQ for dual-level HPG axis support (Kisspeptin at hypothalamus + Gonadorelin at pituitary)

Libido & Sexual Function Enhancement

Kisspeptin enhances sexual function through two pathways: indirect testosterone elevation and direct neurological effects on brain regions controlling sexual arousal. Clinical neuroimaging studies have demonstrated that Kisspeptin modulates limbic brain activity in response to sexual stimuli in both men and women. Users frequently report libido improvements as one of the earliest effects.

Form: Kisspeptin-10
Route: Subcutaneous injection
Dose: 200–300 mcg per injection
Frequency: 1x daily
Duration: 4–8 weeks; effects often noticed within 1–2 weeks
Note: Some users report acute effects within hours of dosing (likely the neurological pathway), with sustained improvements developing over weeks (testosterone pathway)

Fertility Support (Male)

For men seeking to improve fertility markers (sperm count, motility) through HPG axis stimulation. Kisspeptin drives both LH (testosterone production) and FSH (spermatogenesis support). This is particularly relevant for men with secondary hypogonadism or those transitioning off TRT who need to restore spermatogenesis.

Form: Kisspeptin-10
Route: Subcutaneous injection
Dose: 200–500 mcg per injection
Frequency: 1–2x daily
Duration: 8–12 weeks (spermatogenesis takes ~74 days; allow sufficient time)
Monitoring: Semen analysis at baseline and 8–12 weeks; LH, FSH, testosterone bloodwork at 4–6 weeks
Stack: + Gonadorelin 100 mcg for additional FSH support

Post-Cycle Therapy (PCT)

For individuals recovering HPG axis function after anabolic steroid or prohormone cycles. Kisspeptin provides top-down stimulation starting at the hypothalamus, encouraging the entire axis to restart natural function. Can be combined with SERMs and/or Gonadorelin for a multi-level PCT approach.

Form: Kisspeptin-10
Route: Subcutaneous injection
Dose: 300–500 mcg per injection
Frequency: 1–2x daily
Duration: 4–8 weeks post-cycle
Stack: + Enclomiphene 12.5–25 mg oral daily (SERM to block estrogen negative feedback at pituitary) ± Gonadorelin 100 mcg SubQ (pituitary-level GnRH support)
Important: Begin PCT only after the exogenous compounds have cleared (timing depends on the compounds used). Do not begin Kisspeptin while still on cycle.

Fertility Support (Female) — Under Medical Supervision Only

Kisspeptin-54 has been studied for hypothalamic amenorrhea (restoring GnRH pulsatility and menstrual cycles) and as an IVF oocyte maturation trigger (alternative to hCG with potentially lower OHSS risk). These are clinical applications that require specialist reproductive endocrinology supervision and are NOT standard community protocols.

Form: Kisspeptin-54 (clinical)
Route: IV or SubQ (clinical setting)
Dose: 1.6–12.8 nmol/kg (IVF trigger); variable for amenorrhea
Context: Requires fertility specialist supervision; not a self-directed protocol

Verify with bloodwork. Kisspeptin's value lies in stimulating endogenous hormone production. The only way to confirm it is working is to measure LH, FSH, and total/free testosterone (or estradiol/progesterone in women) at baseline and 4–6 weeks into the protocol. Subjective improvements in libido, energy, and well-being are encouraging but should always be verified with objective lab values.

Cycling & Duration

One of Kisspeptin's key advantages is that it stimulates endogenous GnRH pulsatility rather than directly activating pituitary GnRH receptors. This means it carries a lower theoretical risk of pituitary desensitization compared to continuous GnRH agonist exposure. However, cycling is still recommended to periodically assess natural HPG axis function without exogenous stimulation and to follow best practices for research peptide use.

Protocol	On-Period	Off-Period	Notes
Standard (Testosterone)	4–8 weeks	2–4 weeks off	Most common; bloodwork at week 4 to assess response; reassess during off-period
Fertility	8–12 weeks	4 weeks off	Longer on-period to support spermatogenesis (~74-day cycle); semen analysis at 8–12 weeks
PCT	4–8 weeks	Reassess HPG recovery	Duration depends on suppression severity; bloodwork guides when to stop
Libido / Short Course	4 weeks	2–4 weeks off	Shorter cycles for targeted libido enhancement; neurological effects may persist into off-period
Maintenance (Advanced)	Ongoing at lower dose	Periodic bloodwork	Some users maintain at 100–200 mcg/day; limited long-term data; requires regular monitoring

Lower desensitization risk than direct GnRH agonists: Because Kisspeptin triggers endogenous GnRH release in natural pulses (rather than continuously flooding pituitary GnRH receptors), the risk of pituitary desensitization is theoretically much lower. Clinical data supports this — repeated Kisspeptin dosing has shown sustained LH responses. However, long-term continuous use data is limited, so periodic off-periods remain prudent to confirm the HPG axis can function independently.

When to Extend or Shorten a Cycle

Extend beyond 8 weeks for fertility protocols (spermatogenesis requires ~74 days) or if testosterone is improving but has not yet reached target levels by week 8.
Shorten to 4 weeks if bloodwork at 4 weeks shows robust LH and testosterone response, or if the primary goal (libido improvement) has been achieved.
During the off-period: Check bloodwork (LH, FSH, total/free testosterone) to assess whether the HPG axis maintains improved function without exogenous Kisspeptin stimulation. If levels remain adequate, a longer off-period is fine. If they drop significantly, consider another cycle.
PCT cycling: Guided entirely by bloodwork recovery. Continue until LH and testosterone levels are satisfactorily restored. There is no fixed duration — suppression severity varies by compounds and cycle length.

Kisspeptin Stacking Protocols

Kisspeptin's position at the top of the HPG axis cascade makes it a natural stacking partner with compounds that act at lower levels of the axis. The principle is multi-level HPG axis support: stimulate the hypothalamus (Kisspeptin), the pituitary (GnRH / SERMs), and optionally the gonads (hCG) for comprehensive axis recovery or optimization.

Kisspeptin + Gonadorelin — Dual-Level HPG Axis Stimulation (Most Popular)

The most logical and popular Kisspeptin stack. Kisspeptin stimulates GnRH neurons at the hypothalamic level, while Gonadorelin provides direct GnRH receptor stimulation at the pituitary. This dual-level approach targets both the upstream trigger and the downstream effector for maximal LH/FSH output.

Compound	Dose	Route	Purpose
Kisspeptin-10	200–300 mcg, 1x daily	SubQ	Hypothalamic GnRH neuron stimulation; endogenous GnRH pulsatility
Gonadorelin	100 mcg, 1–2x daily	SubQ	Direct pituitary GnRH receptor stimulation; LH/FSH release

Protocol note: Space the doses if using both daily. Some users take Kisspeptin in the morning and Gonadorelin in the evening to provide two distinct stimulatory signals at different levels of the axis throughout the day. Others administer them together. Both approaches are reported in community protocols.

Kisspeptin + Enclomiphene (SERM) — HPG + Anti-Estrogen Feedback

Combines Kisspeptin's hypothalamic stimulation with Enclomiphene's blockade of estrogen negative feedback at the pituitary. Enclomiphene (the active trans-isomer of clomiphene) blocks estrogen receptors on pituitary gonadotrophs, removing the brake that estrogen puts on LH/FSH secretion. Together, you get upstream stimulation (Kisspeptin) plus removal of downstream inhibition (Enclomiphene).

Compound	Dose	Route	Purpose
Kisspeptin-10	200–300 mcg, 1x daily	SubQ	Hypothalamic GnRH stimulation; drives LH/FSH from the top
Enclomiphene	12.5–25 mg, 1x daily	Oral	Blocks estrogen negative feedback at pituitary; removes LH/FSH brake

Kisspeptin + Gonadorelin + Enclomiphene — Comprehensive PCT Stack

The full multi-level PCT approach for recovery from significant HPG axis suppression. Kisspeptin restarts the hypothalamus, Gonadorelin stimulates the pituitary directly, and Enclomiphene removes estrogen-mediated negative feedback. This three-pronged strategy targets every level of the axis simultaneously.

Compound	Dose	Route	Purpose
Kisspeptin-10	300–500 mcg, 1x daily	SubQ	Hypothalamic restart; endogenous GnRH pulsatility
Gonadorelin	100 mcg, 1–2x daily	SubQ	Direct pituitary GnRH stimulation; LH/FSH support
Enclomiphene	12.5–25 mg, 1x daily	Oral	Estrogen feedback blockade; potentiates LH output

Kisspeptin as an HCG Alternative (On-TRT Fertility Preservation)

Some practitioners explore Kisspeptin as an alternative to HCG for maintaining testicular function during TRT. However, this is theoretically problematic because exogenous testosterone suppresses the HPG axis via negative feedback, which may blunt Kisspeptin's upstream signaling. HCG, which directly mimics LH at the testicular level, bypasses this suppression entirely. Kisspeptin is generally better suited as a TRT alternative (instead of testosterone) rather than a TRT adjunct (alongside testosterone).

Kisspeptin on TRT is theoretically limited. Exogenous testosterone suppresses hypothalamic and pituitary function through negative feedback. Since Kisspeptin works at the hypothalamic level, its efficacy is likely reduced when the feedback loop is suppressed by exogenous hormones. For on-TRT testicular preservation, HCG (which works directly at the gonadal level, bypassing the suppressed hypothalamus/pituitary) remains the more established approach. Kisspeptin is best used as a standalone HPG axis stimulator or in PCT contexts.

Explore more combinations with our Peptide Stack Builder or browse the Top 10 Peptide Stacks guide.

Safety, Side Effects & Contraindications

Safety Profile: Kisspeptin has demonstrated a favorable safety profile in published clinical trials, with no serious adverse events reported at clinical doses. Because it works through the body's own GnRH pulsatile mechanism rather than bypassing it, the theoretical risk of pituitary desensitization or hormonal axis disruption is lower than with direct GnRH agonists. However, Kisspeptin does stimulate the HPG axis and will affect reproductive hormone levels — it is not a benign supplement. Use under medical guidance is recommended.

Reported Side Effects

Generally mild and infrequent (based on clinical trial data and community reports):

Injection site reactions — minor redness, soreness, or swelling at the injection site; standard for any subcutaneous peptide
Headache — reported in a minority of clinical trial participants; typically mild and self-resolving
Facial flushing — transient warmth or flushing shortly after injection; related to acute hormonal changes
Mild nausea — reported rarely; usually transient and dose-related
Abdominal discomfort — reported occasionally in female clinical trial participants, particularly at higher doses

Important hormonal considerations:

Kisspeptin will raise LH, FSH, and sex hormones (testosterone/estrogen) — this is the intended effect, but it means hormonal monitoring is necessary
In men, elevated testosterone may also increase estradiol (via aromatization) — monitor estradiol alongside testosterone if symptoms of high estrogen develop
In women, Kisspeptin stimulates ovulation-related hormones — unintended ovulation induction is a risk if used without medical supervision
No evidence of pituitary desensitization in clinical study periods (a key advantage over continuous GnRH agonists)

Compared to GnRH agonists: Continuous GnRH agonist exposure (like long-acting leuprolide) causes paradoxical suppression through pituitary GnRH receptor downregulation — ultimately lowering testosterone (the basis of chemical castration). Kisspeptin does NOT cause this effect because it does not directly activate pituitary GnRH receptors. It stimulates endogenous GnRH in natural pulses, preserving the pulsatile signaling that maintains receptor sensitivity. This is Kisspeptin's fundamental safety advantage in the HPG axis peptide category.

Contraindications

Pregnancy — Kisspeptin stimulates gonadotropins and could affect pregnancy hormones. Avoid entirely during pregnancy. In IVF contexts, Kisspeptin use is strictly controlled by fertility specialists.
Hormone-sensitive cancers — any cancer that is stimulated by sex hormones (breast, prostate, ovarian) is a contraindication for HPG axis stimulation. Raising testosterone or estrogen levels could accelerate hormone-dependent tumor growth.
Concurrent use with exogenous testosterone or anabolic steroids — exogenous hormones suppress the HPG axis via negative feedback, counteracting Kisspeptin's mechanism. Use Kisspeptin as an alternative to exogenous hormones, not alongside them.
Primary hypogonadism (testicular failure) — if the testes cannot respond to LH, upstream HPG axis stimulation will not raise testosterone. Kisspeptin requires intact gonadal function to produce its intended hormonal effects.
Pituitary tumors or disorders — stimulating GnRH release in the presence of pituitary pathology could produce unpredictable hormonal responses. Consult an endocrinologist.
Known hypersensitivity — discontinue if allergic reactions occur (rash, hives, difficulty breathing).

When to Stop or Reduce Dose

Signs of estrogen excess (in men): gynecomastia tenderness, excessive water retention, mood changes — may indicate testosterone is aromatizing excessively
Any signs of allergic reaction (rash, hives, swelling, difficulty breathing)
Persistent headache or flushing that does not resolve with dose reduction
Bloodwork showing excessively elevated LH or testosterone beyond target ranges
In women: any unintended menstrual cycle changes, ovarian discomfort, or signs of ovarian hyperstimulation — seek medical attention immediately
Any symptom that feels unusual or concerning — err on the side of caution

Regulatory Status: Kisspeptin is not FDA-approved for general human use. Kisspeptin-54 has been used in clinical trials (primarily in the UK for IVF and reproductive endocrinology research) under investigational protocols. Kisspeptin-10 is available as a research peptide. Regulations vary by jurisdiction — verify your local laws before purchasing.

Common Kisspeptin Dosing Mistakes

Avoid these common errors to get the most out of your Kisspeptin protocol:

Confusing Kisspeptin with GnRH (Gonadorelin)

Kisspeptin and GnRH are NOT the same peptide and work at different levels of the HPG axis. Kisspeptin acts upstream on hypothalamic GnRH neurons to stimulate endogenous GnRH release. Gonadorelin IS synthetic GnRH that directly stimulates the pituitary. They should not be used interchangeably, and their dosing protocols are completely different.

Using continuous high-frequency dosing expecting faster results

More is not better with Kisspeptin. The HPG axis responds to pulsatile stimulation — continuous high-dose exposure could theoretically blunt the GnRH response over time, undermining the very advantage Kisspeptin has over continuous GnRH agonists. Stick to 1–2 daily doses and allow the natural pulsatile rhythm to work.

Expecting results with primary hypogonadism (testicular failure)

Kisspeptin stimulates the HPG axis from the top down: Kisspeptin → GnRH → LH/FSH → testosterone. If the testes cannot respond to LH (primary hypogonadism due to testicular damage, Klinefelter’s, etc.), no amount of upstream stimulation will raise testosterone. Kisspeptin only works when the pituitary and gonads are functionally intact.

Mixing up Kisspeptin-10 and Kisspeptin-54 dosing units

Kisspeptin-54 clinical trials use nmol/kg (nanomoles per kilogram) dosing, while Kisspeptin-10 community protocols use mcg (micrograms). These are completely different units and peptide forms. Do not apply Kisspeptin-54 clinical doses to Kisspeptin-10 or vice versa without proper molecular weight conversion. Most community-available product is Kisspeptin-10.

Not monitoring bloodwork to verify HPG axis response

Kisspeptin’s value is its ability to stimulate endogenous hormone production. Without bloodwork (LH, FSH, total and free testosterone at baseline and 4–6 weeks), you cannot confirm whether the protocol is actually working. Subjective improvements in libido or energy are helpful but insufficient — verify with lab values.

Using Kisspeptin while on exogenous testosterone or anabolic steroids

Exogenous testosterone suppresses the HPG axis via negative feedback — it shuts down GnRH, LH, and FSH production. Kisspeptin cannot override this suppression because the feedback loop operates independently of Kisspeptin signaling. Using Kisspeptin while on TRT or a steroid cycle is counterproductive. Kisspeptin is appropriate for post-cycle therapy or as an alternative to TRT, not alongside it.

Storing reconstituted Kisspeptin improperly

Like all reconstituted peptides, Kisspeptin solution should be stored refrigerated (2–8°C) and used within 3–4 weeks. Kisspeptin peptides are susceptible to degradation at room temperature. Use bacteriostatic water for reconstitution to prevent bacterial growth, and avoid repeated freeze-thaw cycles.

Expecting Kisspeptin to work like an HCG replacement at the same dose

While both Kisspeptin and HCG stimulate testosterone production, they work through entirely different mechanisms. HCG mimics LH and directly stimulates the testes. Kisspeptin works upstream on the hypothalamus. Their dose ranges, timing, and response profiles are different. Kisspeptin is not a drop-in replacement for HCG — it is a fundamentally different approach to HPG axis support.

Frequently Asked Questions

Key Takeaways

Kisspeptin is the master upstream regulator of the HPG axis — it stimulates hypothalamic GnRH neurons to release endogenous GnRH in natural pulsatile patterns, driving LH, FSH, and sex hormone production
Preserves physiological GnRH pulsatility — unlike direct GnRH agonists, Kisspeptin does not cause the pituitary desensitization associated with continuous GnRH receptor stimulation
Two forms: Kisspeptin-54 (clinical trials, nmol/kg dosing) and Kisspeptin-10 (community standard, 100–500 mcg SubQ daily) — do not mix up dosing units between forms
Standard Kisspeptin-10 protocol: 200–300 mcg SubQ 1–2x daily for testosterone support, libido, and general HPG axis stimulation
Dual effect on sexual function: indirect (testosterone elevation) and direct (neurological modulation of brain sexual arousal centers)
Best stacking partner: Gonadorelin for dual-level HPG axis support (hypothalamus + pituitary); add Enclomiphene for comprehensive PCT
NOT effective alongside exogenous testosterone: TRT suppresses the HPG axis via negative feedback, counteracting Kisspeptin's upstream mechanism. Use Kisspeptin as an alternative to TRT, not alongside it.
Requires intact pituitary and gonads: Kisspeptin stimulates from the top down. It will not work in primary hypogonadism (testicular failure) or pituitary failure.
Cycling: 4–8 weeks on, 2–4 weeks off — lower desensitization risk than GnRH agonists, but periodic off-periods allow HPG assessment
Favorable safety profile — no serious adverse events in clinical trials; headache, injection site reactions, and flushing are uncommon and mild. Monitor bloodwork.
Verify with bloodwork — LH, FSH, total/free testosterone at baseline and 4–6 weeks is essential to confirm the protocol is working

This article is for educational and informational purposes only. Kisspeptin (Kisspeptin-10 and Kisspeptin-54) is not approved by the FDA for general human use and is classified as a research peptide. Kisspeptin-54 has been used in clinical trials under investigational protocols. This information is not intended to diagnose, treat, cure, or prevent any disease. Consult a qualified healthcare provider before using any research peptide, especially if you have pre-existing medical conditions, are taking medications, or are pregnant or nursing. See our Medical Disclaimer.

References

Dhillo WS, et al. “Kisspeptin-54 stimulates the hypothalamic-pituitary gonadal axis in human males.” J Clin Endocrinol Metab. 2005;90(12):6609-6615.
Jayasena CN, et al. “Kisspeptin-54 triggers egg maturation in women undergoing in vitro fertilization.” J Clin Invest. 2014;124(8):3667-3677.
Jayasena CN, 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.
Seminara SB, et al. “The GPR54 gene as a regulator of puberty.” N Engl J Med. 2003;349(17):1614-1627.
de Roux N, et al. “Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54.” Proc Natl Acad Sci USA. 2003;100(19):10972-10976.
Comninos AN, et al. “Kisspeptin modulates sexual and emotional brain processing in humans.” J Clin Invest. 2017;127(2):709-719.
George JT, et al. “Kisspeptin-10 is a potent stimulator of LH and increases pulse frequency in men.” J Clin Endocrinol Metab. 2011;96(8):E1228-E1236.
Abbara A, 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.
Chan YM, et al. “Kisspeptin resets the hypothalamic GnRH clock in men.” J Clin Endocrinol Metab. 2011;96(6):E908-E915.
Topaloglu AK, et al. “Inactivating KISS1 mutation and hypogonadotropic hypogonadism.” N Engl J Med. 2012;366(7):629-635.

Next Steps

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