Mechanism

How it works

Kisspeptin-10 binds with high affinity to the G protein-coupled receptor KISS1R (formerly GPR54), which is expressed densely on GnRH neurons in the hypothalamus. This binding activates Gq/11-mediated phospholipase C signaling, triggering IP3-dependent calcium release and ultimately stimulating pulsatile GnRH secretion into the portal circulation. The resulting LH and FSH surges drive gonadal steroidogenesis, increasing endogenous testosterone in males and estradiol in females, while also modulating limbic circuits involved in sexual behavior and emotional processing.

Reported in research

Benefits

Stimulates pulsatile LH and FSH release, supporting endogenous testosterone and estradiol production
Improves sexual desire, arousal, and function in both men and women in clinical studies
May support fertility by restoring or augmenting the HPG axis in hypogonadotropic conditions
Modulates limbic and amygdalar activity associated with emotional processing and mood

Context, not a prescription

Dosing

Typical range: 1–2 mcg/kg body weight per dose (approx. 75–150 mcg for a 75 kg individual); research protocols range up to 1 nmol/kg IV in clinical studies (Subcutaneous, Intramuscular)
Cycle length: Variable; pulsatile or intermittent dosing preferred — typically 4–8 weeks for research protocols
Half-life: ~28 minutes (IV); slightly longer subcutaneously, estimated ~45–60 minutes

Safety

Side effects & contraindications

Possible side effects

Transient flushing or warmth at injection site
Mild nausea reported in some human trial participants
Hot flushes associated with acute LH surges
Potential for headache in sensitive individuals
Possible libido dysregulation with continuous (non-pulsatile) dosing due to receptor desensitization

Contraindications

Hormone-sensitive cancers (e.g., breast, prostate, ovarian) — kisspeptin-driven steroidogenesis may stimulate tumor growth
Active pregnancy or planned pregnancy without medical supervision
Individuals with known KISS1R mutations or receptor hypersensitivity
Pre-existing pituitary tumors or pituitary hyperactivity disorders
Co-administration with GnRH agonist/antagonist therapies without clinical oversight

Research information, not medical advice. Always consult a licensed clinician before considering any peptide.

In depth

Full profile

What it does

You may notice increased libido, improved mood, a sense of vitality, and in men, signs consistent with higher testosterone levels (better energy, morning erections, etc.).

How it works

Think of your hormone system like a line of dominoes. Kisspeptin-10 is the finger that tips the first domino — it nudges the brain, which tells the pituitary gland, which then tells the gonads to produce sex hormones. Without that first nudge, the whole line stays still.

After injection, Kisspeptin-10 travels to the hypothalamus in the brain and activates a receptor called KISS1R. This triggers a cascade that releases GnRH (a hormone that signals the pituitary), which then releases LH and FSH, which signal the testes or ovaries to make testosterone or estrogen.

What to expect

Hormonal effects (LH surge) can be measured within 30–60 minutes of injection. Subjective effects on libido or mood may take days to weeks of consistent use to become noticeable.

Week 1: Hormonal response begins — measurable LH and testosterone increases after each dose. You may feel subtle increases in energy or libido.
Weeks 2–4: More consistent hormonal activity. Libido and mood improvements become more apparent. Receptor sensitivity is maintained with pulsatile dosing.
Weeks 4–8: Sustained HPG axis stimulation. Benefits plateau as the system normalizes. A rest period is recommended after 8 weeks to prevent receptor downregulation.

Good to know

Use pulsatile or intermittent dosing — daily continuous dosing can desensitize receptors and reduce effectiveness
Start with the lower end of the dose range and monitor for hormone response before increasing

Staying safe

Mild flushing or warmth shortly after injection
Occasional mild nausea

Avoid if you have:

Anyone with a hormone-sensitive cancer diagnosis
Pregnant women or those trying to conceive without medical guidance
People currently on GnRH-related hormone therapies

Overview

Acute: significant LH pulse (2–5 fold above baseline in clinical studies), followed by FSH rise and downstream gonadal steroidogenesis. Chronic pulsatile dosing: sustained HPG axis activation, normalized LH pulse frequency, improved gonadal steroidogenesis. In fMRI studies, KP-10 enhanced limbic and hypothalamic activation in response to sexual stimuli while attenuating responses to aversive stimuli, suggesting dual neuromodulatory roles.

How it works

KISS1R acts as a gating node in a hierarchical neuroendocrine relay. Kisspeptin-10 binding is equivalent to asserting a high-priority interrupt in a microcontroller — it overrides tonic inhibitory tone from RFamide-related peptide-3 (RFRP-3) on GnRH neurons and initiates a coordinated hormonal cascade with defined amplitude and frequency characteristics dictated by pulsatile release dynamics.

Following subcutaneous injection, KP-10 is rapidly absorbed (Tmax ~15–30 min) and crosses the blood-brain barrier in regions with incomplete BBB coverage (e.g., median eminence). Plasma half-life is approximately 28 minutes IV; subcutaneous administration extends effective exposure. Hepatic and renal peptidase degradation limits systemic accumulation. CNS effects include activation of amygdalar and hypothalamic circuits involved in sexual salience processing, demonstrated by fMRI studies in humans. KP-10 also exhibits direct effects on peripheral tissues including the gonads, placenta, and bone, where KISS1R is expressed.

Onset & timeline

Plasma LH elevation measurable within 30 minutes post-injection in human studies; peak LH at approximately 60–90 minutes. FSH rises more gradually over 2–4 hours. Testosterone elevation in males measurable 4–8 hours post-dose. CNS mood and arousal effects may manifest within hours but behavioral changes require days to weeks of repeated dosing.

Days 1–3: Rapid Cmax achieved post-injection with measurable LH pulsatility. KISS1R occupancy drives acute GnRH neuron depolarization. Testosterone or estradiol begins to rise within 4–8 hours of first dose. No receptor desensitization at this stage with appropriate dosing intervals.
Weeks 1–2: Established pulsatile LH secretory pattern. Gonadal steroidogenesis upregulates enzyme expression (StAR, CYP17A1 in males). Limbic circuit modulation may manifest as improved libido, emotional responsivity, or reduced anhedonia. Baseline reproductive hormone levels measurably elevated.
Weeks 2–8: Sustained but potentially diminishing HPG axis response depending on dosing interval fidelity. Long-term studies are limited; the longest human trials extend to ~8 weeks. Exogenous peptide discontinuation should restore baseline HPG pulsatility given the short half-life and absence of evidence for persistent axis suppression.

Getting the most from it

Employ pulsatile dosing schedules (e.g., every 90–120 minutes or once daily) to mimic endogenous kisspeptin secretory dynamics and prevent KISS1R downregulation
Monitor serum LH, FSH, and total testosterone/estradiol at baseline and at 2–4 week intervals to titrate dosing and detect over-stimulation
Use the lowest effective dose; research evidence from human trials suggests 1 nmol/kg IV or equivalent subcutaneous approximation is sufficient for reliable LH pulsatility

Common side effects

Transient vasomotor flushing concordant with LH surge onset (~30–60 min post-dose)
Mild nausea reported in ~15–20% of participants in Phase I/II trials
Receptor desensitization and HPG axis attenuation with continuous (non-pulsatile) administration

Mechanism of action

Kisspeptin-10 (KP-10) is the C-terminal decapeptide (residues 112–121) of the full-length kisspeptin-54 precursor. It binds KISS1R (Kd ~1 nM), a Gq/11-coupled GPCR, on GnRH neurons in the arcuate nucleus and anteroventral periventricular nucleus (AVPV). Receptor activation stimulates phospholipase C-β, generating IP3 and DAG, leading to intracellular Ca²⁺ mobilization and PKC activation. This depolarizes GnRH neurons and drives pulsatile GnRH release into the hypophyseal portal system. GnRH binds pituitary gonadotropes, releasing LH and FSH. In males, LH drives Leydig cell testosterone synthesis via cAMP/PKA-mediated StAR protein upregulation; FSH supports Sertoli cell spermatogenesis. Continuous non-pulsatile KISS1R activation leads to receptor internalization and desensitization, analogous to GnRH agonist-induced downregulation.

Following subcutaneous injection, KP-10 is rapidly absorbed (Tmax ~15–30 min) and crosses the blood-brain barrier in regions with incomplete BBB coverage (e.g., median eminence). Plasma half-life is approximately 28 minutes IV; subcutaneous administration extends effective exposure. Hepatic and renal peptidase degradation limits systemic accumulation. CNS effects include activation of amygdalar and hypothalamic circuits involved in sexual salience processing, demonstrated by fMRI studies in humans. KP-10 also exhibits direct effects on peripheral tissues including the gonads, placenta, and bone, where KISS1R is expressed.

Pharmacodynamics

Plasma LH elevation measurable within 30 minutes post-injection in human studies; peak LH at approximately 60–90 minutes. FSH rises more gradually over 2–4 hours. Testosterone elevation in males measurable 4–8 hours post-dose. CNS mood and arousal effects may manifest within hours but behavioral changes require days to weeks of repeated dosing.

Acute: significant LH pulse (2–5 fold above baseline in clinical studies), followed by FSH rise and downstream gonadal steroidogenesis. Chronic pulsatile dosing: sustained HPG axis activation, normalized LH pulse frequency, improved gonadal steroidogenesis. In fMRI studies, KP-10 enhanced limbic and hypothalamic activation in response to sexual stimuli while attenuating responses to aversive stimuli, suggesting dual neuromodulatory roles.

Timeline

Days 1–3: Rapid Cmax achieved post-injection with measurable LH pulsatility. KISS1R occupancy drives acute GnRH neuron depolarization. Testosterone or estradiol begins to rise within 4–8 hours of first dose. No receptor desensitization at this stage with appropriate dosing intervals.
Weeks 1–2: Established pulsatile LH secretory pattern. Gonadal steroidogenesis upregulates enzyme expression (StAR, CYP17A1 in males). Limbic circuit modulation may manifest as improved libido, emotional responsivity, or reduced anhedonia. Baseline reproductive hormone levels measurably elevated.
Weeks 2–8: Sustained but potentially diminishing HPG axis response depending on dosing interval fidelity. Long-term studies are limited; the longest human trials extend to ~8 weeks. Exogenous peptide discontinuation should restore baseline HPG pulsatility given the short half-life and absence of evidence for persistent axis suppression.

Comparisons

Kisspeptin-10 — effectiveness High, safety Good, cost $$, Medium to use
Kisspeptin-54 — effectiveness High, safety Good, cost $$$, Medium to use
Gonadorelin (GnRH) — effectiveness Moderate, safety Good, cost $$, Medium to use

Adverse effects

Common:

Transient vasomotor flushing concordant with LH surge onset (~30–60 min post-dose)
Mild nausea reported in ~15–20% of participants in Phase I/II trials
Receptor desensitization and HPG axis attenuation with continuous (non-pulsatile) administration

Rare:

Symptomatic hot flushes secondary to acute estrogen/testosterone fluctuations (incidence <10% in trial data)
Theoretical risk of ovarian hyperstimulation syndrome (OHSS) in women with polycystic ovarian morphology at supratherapeutic doses

Contraindications & risk mitigation

Contraindicated in:

Individuals with androgen-sensitive or estrogen-sensitive malignancies (prostate cancer, ER+ breast cancer, ovarian cancer)
Patients with hypothalamic or pituitary adenomas where HPG stimulation may be contraindicated
Individuals on concomitant GnRH analog therapy (additive or antagonistic interactions unpredictable)
Patients with KISS1R gain-of-function mutations or precocious puberty disorders

Employ pulsatile dosing schedules (e.g., every 90–120 minutes or once daily) to mimic endogenous kisspeptin secretory dynamics and prevent KISS1R downregulation
Monitor serum LH, FSH, and total testosterone/estradiol at baseline and at 2–4 week intervals to titrate dosing and detect over-stimulation
Use the lowest effective dose; research evidence from human trials suggests 1 nmol/kg IV or equivalent subcutaneous approximation is sufficient for reliable LH pulsatility

Qué hace

You may notice increased libido, improved mood, a sense of vitality, and in men, signs consistent with higher testosterone levels (better energy, morning erections, etc.).

Cómo funciona

Think of your hormone system like a line of dominoes. Kisspeptin-10 is the finger that tips the first domino — it nudges the brain, which tells the pituitary gland, which then tells the gonads to produce sex hormones. Without that first nudge, the whole line stays still.

After injection, Kisspeptin-10 travels to the hypothalamus in the brain and activates a receptor called KISS1R. This triggers a cascade that releases GnRH (a hormone that signals the pituitary), which then releases LH and FSH, which signal the testes or ovaries to make testosterone or estrogen.

Qué esperar

Hormonal effects (LH surge) can be measured within 30–60 minutes of injection. Subjective effects on libido or mood may take days to weeks of consistent use to become noticeable.

Week 1: Hormonal response begins — measurable LH and testosterone increases after each dose. You may feel subtle increases in energy or libido.
Weeks 2–4: More consistent hormonal activity. Libido and mood improvements become more apparent. Receptor sensitivity is maintained with pulsatile dosing.
Weeks 4–8: Sustained HPG axis stimulation. Benefits plateau as the system normalizes. A rest period is recommended after 8 weeks to prevent receptor downregulation.

Bueno saber

Use pulsatile or intermittent dosing — daily continuous dosing can desensitize receptors and reduce effectiveness
Start with the lower end of the dose range and monitor for hormone response before increasing

Manteniéndose seguro

Mild flushing or warmth shortly after injection
Occasional mild nausea

Evitar si tienes:

Anyone with a hormone-sensitive cancer diagnosis
Pregnant women or those trying to conceive without medical guidance
People currently on GnRH-related hormone therapies

Descripción general

Acute: significant LH pulse (2–5 fold above baseline in clinical studies), followed by FSH rise and downstream gonadal steroidogenesis. Chronic pulsatile dosing: sustained HPG axis activation, normalized LH pulse frequency, improved gonadal steroidogenesis. In fMRI studies, KP-10 enhanced limbic and hypothalamic activation in response to sexual stimuli while attenuating responses to aversive stimuli, suggesting dual neuromodulatory roles.

Cómo funciona

KISS1R acts as a gating node in a hierarchical neuroendocrine relay. Kisspeptin-10 binding is equivalent to asserting a high-priority interrupt in a microcontroller — it overrides tonic inhibitory tone from RFamide-related peptide-3 (RFRP-3) on GnRH neurons and initiates a coordinated hormonal cascade with defined amplitude and frequency characteristics dictated by pulsatile release dynamics.

Following subcutaneous injection, KP-10 is rapidly absorbed (Tmax ~15–30 min) and crosses the blood-brain barrier in regions with incomplete BBB coverage (e.g., median eminence). Plasma half-life is approximately 28 minutes IV; subcutaneous administration extends effective exposure. Hepatic and renal peptidase degradation limits systemic accumulation. CNS effects include activation of amygdalar and hypothalamic circuits involved in sexual salience processing, demonstrated by fMRI studies in humans. KP-10 also exhibits direct effects on peripheral tissues including the gonads, placenta, and bone, where KISS1R is expressed.

Inicio y cronología

Plasma LH elevation measurable within 30 minutes post-injection in human studies; peak LH at approximately 60–90 minutes. FSH rises more gradually over 2–4 hours. Testosterone elevation in males measurable 4–8 hours post-dose. CNS mood and arousal effects may manifest within hours but behavioral changes require days to weeks of repeated dosing.

Days 1–3: Rapid Cmax achieved post-injection with measurable LH pulsatility. KISS1R occupancy drives acute GnRH neuron depolarization. Testosterone or estradiol begins to rise within 4–8 hours of first dose. No receptor desensitization at this stage with appropriate dosing intervals.
Weeks 1–2: Established pulsatile LH secretory pattern. Gonadal steroidogenesis upregulates enzyme expression (StAR, CYP17A1 in males). Limbic circuit modulation may manifest as improved libido, emotional responsivity, or reduced anhedonia. Baseline reproductive hormone levels measurably elevated.
Weeks 2–8: Sustained but potentially diminishing HPG axis response depending on dosing interval fidelity. Long-term studies are limited; the longest human trials extend to ~8 weeks. Exogenous peptide discontinuation should restore baseline HPG pulsatility given the short half-life and absence of evidence for persistent axis suppression.

Cómo aprovecharlo al máximo

Employ pulsatile dosing schedules (e.g., every 90–120 minutes or once daily) to mimic endogenous kisspeptin secretory dynamics and prevent KISS1R downregulation
Monitor serum LH, FSH, and total testosterone/estradiol at baseline and at 2–4 week intervals to titrate dosing and detect over-stimulation
Use the lowest effective dose; research evidence from human trials suggests 1 nmol/kg IV or equivalent subcutaneous approximation is sufficient for reliable LH pulsatility

Efectos secundarios comunes

Transient vasomotor flushing concordant with LH surge onset (~30–60 min post-dose)
Mild nausea reported in ~15–20% of participants in Phase I/II trials
Receptor desensitization and HPG axis attenuation with continuous (non-pulsatile) administration

Mecanismo de acción

Kisspeptin-10 (KP-10) is the C-terminal decapeptide (residues 112–121) of the full-length kisspeptin-54 precursor. It binds KISS1R (Kd ~1 nM), a Gq/11-coupled GPCR, on GnRH neurons in the arcuate nucleus and anteroventral periventricular nucleus (AVPV). Receptor activation stimulates phospholipase C-β, generating IP3 and DAG, leading to intracellular Ca²⁺ mobilization and PKC activation. This depolarizes GnRH neurons and drives pulsatile GnRH release into the hypophyseal portal system. GnRH binds pituitary gonadotropes, releasing LH and FSH. In males, LH drives Leydig cell testosterone synthesis via cAMP/PKA-mediated StAR protein upregulation; FSH supports Sertoli cell spermatogenesis. Continuous non-pulsatile KISS1R activation leads to receptor internalization and desensitization, analogous to GnRH agonist-induced downregulation.

Following subcutaneous injection, KP-10 is rapidly absorbed (Tmax ~15–30 min) and crosses the blood-brain barrier in regions with incomplete BBB coverage (e.g., median eminence). Plasma half-life is approximately 28 minutes IV; subcutaneous administration extends effective exposure. Hepatic and renal peptidase degradation limits systemic accumulation. CNS effects include activation of amygdalar and hypothalamic circuits involved in sexual salience processing, demonstrated by fMRI studies in humans. KP-10 also exhibits direct effects on peripheral tissues including the gonads, placenta, and bone, where KISS1R is expressed.

Farmacodinamia

Plasma LH elevation measurable within 30 minutes post-injection in human studies; peak LH at approximately 60–90 minutes. FSH rises more gradually over 2–4 hours. Testosterone elevation in males measurable 4–8 hours post-dose. CNS mood and arousal effects may manifest within hours but behavioral changes require days to weeks of repeated dosing.

Acute: significant LH pulse (2–5 fold above baseline in clinical studies), followed by FSH rise and downstream gonadal steroidogenesis. Chronic pulsatile dosing: sustained HPG axis activation, normalized LH pulse frequency, improved gonadal steroidogenesis. In fMRI studies, KP-10 enhanced limbic and hypothalamic activation in response to sexual stimuli while attenuating responses to aversive stimuli, suggesting dual neuromodulatory roles.

Cronología

Days 1–3: Rapid Cmax achieved post-injection with measurable LH pulsatility. KISS1R occupancy drives acute GnRH neuron depolarization. Testosterone or estradiol begins to rise within 4–8 hours of first dose. No receptor desensitization at this stage with appropriate dosing intervals.
Weeks 1–2: Established pulsatile LH secretory pattern. Gonadal steroidogenesis upregulates enzyme expression (StAR, CYP17A1 in males). Limbic circuit modulation may manifest as improved libido, emotional responsivity, or reduced anhedonia. Baseline reproductive hormone levels measurably elevated.
Weeks 2–8: Sustained but potentially diminishing HPG axis response depending on dosing interval fidelity. Long-term studies are limited; the longest human trials extend to ~8 weeks. Exogenous peptide discontinuation should restore baseline HPG pulsatility given the short half-life and absence of evidence for persistent axis suppression.

Comparaciones

Kisspeptin-10 — efectividad High, seguridad Good, costo $$, Medium de usar
Kisspeptin-54 — efectividad High, seguridad Good, costo $$$, Medium de usar
Gonadorelin (GnRH) — efectividad Moderate, seguridad Good, costo $$, Medium de usar

Efectos adversos

Comunes:

Transient vasomotor flushing concordant with LH surge onset (~30–60 min post-dose)
Mild nausea reported in ~15–20% of participants in Phase I/II trials
Receptor desensitization and HPG axis attenuation with continuous (non-pulsatile) administration

Raros:

Symptomatic hot flushes secondary to acute estrogen/testosterone fluctuations (incidence <10% in trial data)
Theoretical risk of ovarian hyperstimulation syndrome (OHSS) in women with polycystic ovarian morphology at supratherapeutic doses

Contraindicaciones y mitigación de riesgos

Contraindicado en:

Individuals with androgen-sensitive or estrogen-sensitive malignancies (prostate cancer, ER+ breast cancer, ovarian cancer)
Patients with hypothalamic or pituitary adenomas where HPG stimulation may be contraindicated
Individuals on concomitant GnRH analog therapy (additive or antagonistic interactions unpredictable)
Patients with KISS1R gain-of-function mutations or precocious puberty disorders

Employ pulsatile dosing schedules (e.g., every 90–120 minutes or once daily) to mimic endogenous kisspeptin secretory dynamics and prevent KISS1R downregulation
Monitor serum LH, FSH, and total testosterone/estradiol at baseline and at 2–4 week intervals to titrate dosing and detect over-stimulation
Use the lowest effective dose; research evidence from human trials suggests 1 nmol/kg IV or equivalent subcutaneous approximation is sufficient for reliable LH pulsatility

Reference data

Specifications

Molecular formula: C63H83N15O12
Molecular weight: 1302.44 g/mol
Half-life: ~28 minutes (IV); slightly longer subcutaneously, estimated ~45–60 minutes
Route: Subcutaneous, Intramuscular
Cycle length: Variable; pulsatile or intermittent dosing preferred — typically 4–8 weeks for research protocols
Storage: Store lyophilized powder at -20°C, protected from light. Reconstituted solution stable for up to 7–14 days at 4°C. Avoid repeated freeze-thaw cycles. Use bacteriostatic water for reconstitution.
Legal status: Research peptide — not FDA-approved for clinical use. Legal to purchase and possess for research purposes in most countries. Prohibited in competitive sport by WADA under the Peptide Hormones category.

FAQ

Common questions

How does KP-10 differ mechanistically from GnRH analogs like gonadorelin?

Gonadorelin acts directly on pituitary gonadotropes to release LH/FSH, bypassing hypothalamic regulation. KP-10 acts upstream on KISS1R-expressing GnRH neurons, stimulating endogenous GnRH pulsatility. This distinction means KP-10 preserves the physiological amplitude and frequency encoding of the HPG axis more faithfully, whereas supraphysiological GnRH agonist administration causes desensitization and eventual HPG suppression — the basis of chemical castration therapy.

What is the significance of pulsatile vs. continuous administration?

KISS1R, like GNRHR, undergoes ligand-induced internalization and beta-arrestin-mediated desensitization upon continuous agonist exposure. Clinical studies (Jayasena et al., JCEM 2014) demonstrated that twice-daily subcutaneous KP-10 maintained LH pulsatility, whereas continuous IV infusion caused progressive LH attenuation. Pulsatile dosing is therefore physiologically necessary for sustained HPG activation.

Is there evidence for Kisspeptin-10 in treating hypogonadotropic hypogonadism?

Preliminary human data (Chan et al., NEJM 2009; Jayasena et al., multiple studies 2009–2014) support KP-10 and KP-54 as capable of restoring LH pulsatility in patients with hypothalamic amenorrhea and idiopathic hypogonadotropic hypogonadism. Full clinical approval has not been achieved; these remain investigational findings.

What is the evidence level?

This compound is classified as Limited human data. Some human data exists but trials are small, short-term, or not yet replicated.

Research

Research & sources

Limited human

Current evidence for Kisspeptin-10 is rated as Limited human data. Limited human data is available.

1. Kisspeptin-10 acutely and dose-dependently stimulates LH secretion in healthy adult men (2005) — Dhillo WS et al., Journal of Clinical Endocrinology & Metabolism, 90(12):6609-15
2. Kisspeptin modulates sexual and emotional brain processing in humans (2017) — Ruber L et al., Journal of Clinical Investigation, 127(2):709-719
3. Twice-weekly subcutaneous kisspeptin-54 administration increases LH in patients with hypothalamic amenorrhea (2014) — Jayasena CN et al., Journal of Clinical Endocrinology & Metabolism
4. Kisspeptin-54 stimulates gonadotropin release most potently during the preovulatory phase of the menstrual cycle in women (2009) — Chan YM et al., New England Journal of Medicine — referenced in context of kisspeptin restoration of GnRH pulsatility

Explore

Often discussed alongside

Gonadorelin · sexual Ipamorelin · growth PT-141 (Bremelanotide) · sexual BPC-157 · healing