Mechanism

How it works

FSH acts on Sertoli cells in the testes to stimulate spermatogenesis and support sperm maturation, while the LH component (or LH-like activity) acts on Leydig cells via the LH/hCG receptor to stimulate testosterone biosynthesis from cholesterol through the cAMP-PKA signaling cascade. Together, these hormonal signals restore the two-cell, two-gonadotropin system required for full testicular function, including intratesticular testosterone concentrations necessary for normal sperm production. In women, FSH drives follicular recruitment and maturation while LH triggers ovulation and luteinization of the dominant follicle.

Reported in research

Benefits

Restores and maintains spermatogenesis in men with hypogonadotropic hypogonadism or after exogenous androgen suppression
Increases intratesticular testosterone levels, supporting both fertility and testicular volume maintenance
Stimulates follicular development and ovulation induction in anovulatory women undergoing assisted reproduction
Serves as an adjunct to hCG therapy, with FSH component addressing Sertoli cell function that hCG alone cannot fully replicate

Context, not a prescription

Dosing

Typical range: 75 IU FSH/75 IU LH (1 vial) administered 2-3 times per week, or as directed by a fertility specialist (Subcutaneous, Intramuscular)
Cycle length: 8-16 weeks for male fertility restoration; 7-14 days for female ovulation induction cycles
Half-life: FSH component ~24-36 hours; LH component ~20 hours

Safety

Side effects & contraindications

Possible side effects

Injection site pain, redness, or swelling
Ovarian Hyperstimulation Syndrome (OHSS) in women — ranging from mild bloating to severe, life-threatening fluid shifts
Gynecomastia or breast tenderness in men due to elevated estrogen from aromatization
Headache and mood fluctuations
Multiple follicle development and increased risk of multiple gestation in women
Ovarian cysts
Testicular enlargement or discomfort in men

Contraindications

Primary ovarian failure or primary testicular failure (no response to gonadotropin stimulation)
Active sex hormone-sensitive tumors (e.g., prostate cancer, breast cancer, ovarian cancer)
Uncontrolled thyroid or adrenal disorders
Pregnancy
Hypersensitivity to gonadotropins or any component of the preparation
Abnormal uterine bleeding of undetermined origin
Ovarian cysts or enlargement not due to polycystic ovary syndrome

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

In depth

Full profile

What it does

Men may notice increased testicular size, improved energy and libido, and — after several weeks — improved sperm counts. Women typically see ovarian follicle development within a week of a treatment cycle.

How it works

Think of the testes like a factory with two departments: one makes sperm, one makes testosterone. Your brain normally sends two different managers (FSH and LH) to keep both departments running. HMG is like hiring replacement managers when the original ones are absent or blocked.

HMG is injected and travels through the bloodstream directly to the testes (or ovaries in women). It binds to specific receptors on testicular cells, waking them up and telling them to produce sperm and testosterone. In women, it stimulates the ovaries to develop and release eggs.

What to expect

Hormonal changes begin within 24–48 hours of the first injection. Noticeable improvements in testicular volume may appear within 2–4 weeks; sperm production improvements typically take 8–16 weeks.

Week 1: Hormones begin signaling the testes or ovaries. Some users notice slight changes in energy or mild injection site reactions.
Weeks 2-4: Testicular volume may begin to increase in men. In women on a short ovulation induction cycle, follicles are developing and ready for trigger by end of week 2.
Weeks 4-16: Sperm parameters (count, motility, morphology) gradually improve over 8–16 weeks in men. Sustained hormonal support maintains intratesticular testosterone. Ongoing monitoring is important.

Good to know

Always use under the supervision of a physician or reproductive endocrinologist
Women undergoing ovulation induction should have regular ultrasound monitoring to prevent OHSS and multiple pregnancies
Men should monitor estrogen levels and use an aromatase inhibitor if needed

Staying safe

Soreness or redness at the injection site
Mild bloating or discomfort in the lower abdomen
Breast tenderness (men and women)
Headaches

Avoid if you have:

People with hormone-sensitive cancers (prostate, breast, ovarian)
Women who are pregnant
Anyone with severe untreated thyroid or adrenal conditions
People with primary gonadal failure (testes/ovaries that don't respond to hormones)

Overview

Biochemically: rising inhibin B, intratesticular testosterone, and eventual improvement in sperm concentration, total motility, and morphology (WHO criteria). Clinically: testicular volume increases (measurable by orchidometer), improved semen analysis parameters, and in women, rising estradiol and follicular growth on transvaginal ultrasound.

How it works

If the hypothalamic-pituitary-gonadal (HPG) axis is a command hierarchy, HMG bypasses the headquarters (hypothalamus and pituitary) entirely and delivers direct operational orders to the field units (Sertoli and Leydig cells), activating parallel but coordinated production lines for sperm and testosterone simultaneously.

Following subcutaneous or intramuscular injection, FSH and LH are absorbed into systemic circulation and distribute to gonadal tissue. FSH has a longer half-life (~24–36h) due to higher sialic acid content on glycan chains, which reduces receptor-mediated clearance. LH is cleared more rapidly (~20h). Bioavailability via subQ is approximately 70–75% for FSH. In men on exogenous androgens, gonadotropin suppression is reversed at the gonadal level, allowing intratesticular testosterone to recover even in the presence of exogenous testosterone-mediated pituitary suppression.

Onset & timeline

FSH receptor upregulation on Sertoli cells occurs within 24 hours of the first dose; measurable increases in serum inhibin B (a Sertoli cell activity marker) typically occur within 1–2 weeks. Sperm appear in ejaculate improvements (if azoospermic) may take 3–6 months due to the 74-day spermatogenic cycle duration.

Days 1-7: FSH and LH receptors on Sertoli and Leydig cells are occupied and activated. cAMP rises within hours. Steroidogenesis begins upregulating; early inhibin B increases measurable by Day 5–7 in responsive men.
Weeks 1-4: Leydig cell hypertrophy and increased CYP17A1 expression drive rising intratesticular testosterone. Testicular volume increases measurably. In women on a 10–14 day stimulation cycle, dominant follicle selection occurs by Day 7–10 with trigger-ready follicles by Day 10–14.
Weeks 4-16: Spermatogonial proliferation through to spermatid elongation progresses over the full 74-day spermatogenic cycle. Meaningful semen analysis improvement typically documented at 12 and 16 weeks. Continued FSH stimulation is required to maintain Sertoli cell support throughout.

Getting the most from it

Monitor serum estradiol, inhibin B, LH, FSH, and testosterone every 2–4 weeks in men; adjust dose to maintain physiological ranges
In women, mandate transvaginal ultrasound follicle monitoring with estradiol assays to trigger ovulation only when 1–2 dominant follicles reach 17–18mm; cancel cycle if >3 large follicles (OHSS risk)
Co-administer a low-dose aromatase inhibitor (e.g., anastrozole 0.5–1mg/week) in men with estrogen excess symptoms
Initiate at the lowest effective dose (75 IU 2x/week) and titrate based on response biomarkers

Common side effects

Injection site reactions: erythema, induration (subQ >IM in frequency)
Gynecomastia/breast tenderness in men secondary to peripheral aromatization of elevated intratesticular testosterone to estradiol
Elevated serum estradiol requiring aromatase inhibitor co-administration in some men
Mild OHSS in women: bloating, pelvic discomfort, mild ascites (Grade 1–2)

Mechanism of action

HMG delivers exogenous FSH and LH activity (equal 1:1 IU ratio in standard preparations). FSH binds the FSH receptor (FSHR) on Sertoli cells, activating adenylyl cyclase via Gs proteins, elevating cAMP, and activating PKA-dependent transcription of androgen-binding protein (ABP), inhibin B, and GDNF — all critical for spermatogenesis and the blood-testis barrier integrity. The LH component activates the LHCGR on Leydig cells, similarly via cAMP/PKA, upregulating StAR (steroidogenic acute regulatory protein) and CYP11A1 to drive cholesterol import into mitochondria and initiation of the steroidogenic cascade, producing testosterone. This dual stimulation recapitulates the two-cell, two-gonadotropin model essential for intratesticular testosterone concentrations (~50–100x serum levels) required for spermatogenesis completion at the level of spermatid maturation.

Following subcutaneous or intramuscular injection, FSH and LH are absorbed into systemic circulation and distribute to gonadal tissue. FSH has a longer half-life (~24–36h) due to higher sialic acid content on glycan chains, which reduces receptor-mediated clearance. LH is cleared more rapidly (~20h). Bioavailability via subQ is approximately 70–75% for FSH. In men on exogenous androgens, gonadotropin suppression is reversed at the gonadal level, allowing intratesticular testosterone to recover even in the presence of exogenous testosterone-mediated pituitary suppression.

Pharmacodynamics

FSH receptor upregulation on Sertoli cells occurs within 24 hours of the first dose; measurable increases in serum inhibin B (a Sertoli cell activity marker) typically occur within 1–2 weeks. Sperm appear in ejaculate improvements (if azoospermic) may take 3–6 months due to the 74-day spermatogenic cycle duration.

Biochemically: rising inhibin B, intratesticular testosterone, and eventual improvement in sperm concentration, total motility, and morphology (WHO criteria). Clinically: testicular volume increases (measurable by orchidometer), improved semen analysis parameters, and in women, rising estradiol and follicular growth on transvaginal ultrasound.

Timeline

Days 1-7: FSH and LH receptors on Sertoli and Leydig cells are occupied and activated. cAMP rises within hours. Steroidogenesis begins upregulating; early inhibin B increases measurable by Day 5–7 in responsive men.
Weeks 1-4: Leydig cell hypertrophy and increased CYP17A1 expression drive rising intratesticular testosterone. Testicular volume increases measurably. In women on a 10–14 day stimulation cycle, dominant follicle selection occurs by Day 7–10 with trigger-ready follicles by Day 10–14.
Weeks 4-16: Spermatogonial proliferation through to spermatid elongation progresses over the full 74-day spermatogenic cycle. Meaningful semen analysis improvement typically documented at 12 and 16 weeks. Continued FSH stimulation is required to maintain Sertoli cell support throughout.

Comparisons

HMG (Menotropins) — effectiveness Very High, safety Moderate, cost $$$, Medium to use
Recombinant FSH (rFSH) — effectiveness High, safety Good, cost $$$$, Medium to use
hCG — effectiveness High, safety Good, cost $$, Medium to use

Adverse effects

Common:

Injection site reactions: erythema, induration (subQ >IM in frequency)
Gynecomastia/breast tenderness in men secondary to peripheral aromatization of elevated intratesticular testosterone to estradiol
Elevated serum estradiol requiring aromatase inhibitor co-administration in some men
Mild OHSS in women: bloating, pelvic discomfort, mild ascites (Grade 1–2)

Rare:

Severe OHSS (Grade 3) in women: massive ascites, pleural effusion, hemoconcentration, thromboembolic events — incidence ~1–2% in IVF cycles with careful monitoring
Antibody formation to urinary-derived gonadotropins (rare, estimated <1% with modern purified preparations)
Testicular torsion risk theoretically increased with rapid testicular enlargement (very rare case reports)

Contraindications & risk mitigation

Contraindicated in:

Men with primary hypogonadism (Klinefelter syndrome, bilateral orchidectomy) — no functional gonadal tissue to respond
Active sex hormone-sensitive malignancies (prostate carcinoma, hormone-receptor positive breast cancer)
Women with uncontrolled PCOS at high OHSS risk without ultrasound monitoring capability
Patients with active thromboembolic disease or hereditary thrombophilias without anticoagulation management
Uncontrolled hypothyroidism or hyperprolactinemia (will blunt response)

Monitor serum estradiol, inhibin B, LH, FSH, and testosterone every 2–4 weeks in men; adjust dose to maintain physiological ranges
In women, mandate transvaginal ultrasound follicle monitoring with estradiol assays to trigger ovulation only when 1–2 dominant follicles reach 17–18mm; cancel cycle if >3 large follicles (OHSS risk)
Co-administer a low-dose aromatase inhibitor (e.g., anastrozole 0.5–1mg/week) in men with estrogen excess symptoms
Initiate at the lowest effective dose (75 IU 2x/week) and titrate based on response biomarkers

Qué hace

Men may notice increased testicular size, improved energy and libido, and — after several weeks — improved sperm counts. Women typically see ovarian follicle development within a week of a treatment cycle.

Cómo funciona

Think of the testes like a factory with two departments: one makes sperm, one makes testosterone. Your brain normally sends two different managers (FSH and LH) to keep both departments running. HMG is like hiring replacement managers when the original ones are absent or blocked.

HMG is injected and travels through the bloodstream directly to the testes (or ovaries in women). It binds to specific receptors on testicular cells, waking them up and telling them to produce sperm and testosterone. In women, it stimulates the ovaries to develop and release eggs.

Qué esperar

Hormonal changes begin within 24–48 hours of the first injection. Noticeable improvements in testicular volume may appear within 2–4 weeks; sperm production improvements typically take 8–16 weeks.

Week 1: Hormones begin signaling the testes or ovaries. Some users notice slight changes in energy or mild injection site reactions.
Weeks 2-4: Testicular volume may begin to increase in men. In women on a short ovulation induction cycle, follicles are developing and ready for trigger by end of week 2.
Weeks 4-16: Sperm parameters (count, motility, morphology) gradually improve over 8–16 weeks in men. Sustained hormonal support maintains intratesticular testosterone. Ongoing monitoring is important.

Bueno saber

Always use under the supervision of a physician or reproductive endocrinologist
Women undergoing ovulation induction should have regular ultrasound monitoring to prevent OHSS and multiple pregnancies
Men should monitor estrogen levels and use an aromatase inhibitor if needed

Manteniéndose seguro

Soreness or redness at the injection site
Mild bloating or discomfort in the lower abdomen
Breast tenderness (men and women)
Headaches

Evitar si tienes:

People with hormone-sensitive cancers (prostate, breast, ovarian)
Women who are pregnant
Anyone with severe untreated thyroid or adrenal conditions
People with primary gonadal failure (testes/ovaries that don't respond to hormones)

Descripción general

Biochemically: rising inhibin B, intratesticular testosterone, and eventual improvement in sperm concentration, total motility, and morphology (WHO criteria). Clinically: testicular volume increases (measurable by orchidometer), improved semen analysis parameters, and in women, rising estradiol and follicular growth on transvaginal ultrasound.

Cómo funciona

If the hypothalamic-pituitary-gonadal (HPG) axis is a command hierarchy, HMG bypasses the headquarters (hypothalamus and pituitary) entirely and delivers direct operational orders to the field units (Sertoli and Leydig cells), activating parallel but coordinated production lines for sperm and testosterone simultaneously.

Following subcutaneous or intramuscular injection, FSH and LH are absorbed into systemic circulation and distribute to gonadal tissue. FSH has a longer half-life (~24–36h) due to higher sialic acid content on glycan chains, which reduces receptor-mediated clearance. LH is cleared more rapidly (~20h). Bioavailability via subQ is approximately 70–75% for FSH. In men on exogenous androgens, gonadotropin suppression is reversed at the gonadal level, allowing intratesticular testosterone to recover even in the presence of exogenous testosterone-mediated pituitary suppression.

Inicio y cronología

FSH receptor upregulation on Sertoli cells occurs within 24 hours of the first dose; measurable increases in serum inhibin B (a Sertoli cell activity marker) typically occur within 1–2 weeks. Sperm appear in ejaculate improvements (if azoospermic) may take 3–6 months due to the 74-day spermatogenic cycle duration.

Days 1-7: FSH and LH receptors on Sertoli and Leydig cells are occupied and activated. cAMP rises within hours. Steroidogenesis begins upregulating; early inhibin B increases measurable by Day 5–7 in responsive men.
Weeks 1-4: Leydig cell hypertrophy and increased CYP17A1 expression drive rising intratesticular testosterone. Testicular volume increases measurably. In women on a 10–14 day stimulation cycle, dominant follicle selection occurs by Day 7–10 with trigger-ready follicles by Day 10–14.
Weeks 4-16: Spermatogonial proliferation through to spermatid elongation progresses over the full 74-day spermatogenic cycle. Meaningful semen analysis improvement typically documented at 12 and 16 weeks. Continued FSH stimulation is required to maintain Sertoli cell support throughout.

Cómo aprovecharlo al máximo

Monitor serum estradiol, inhibin B, LH, FSH, and testosterone every 2–4 weeks in men; adjust dose to maintain physiological ranges
In women, mandate transvaginal ultrasound follicle monitoring with estradiol assays to trigger ovulation only when 1–2 dominant follicles reach 17–18mm; cancel cycle if >3 large follicles (OHSS risk)
Co-administer a low-dose aromatase inhibitor (e.g., anastrozole 0.5–1mg/week) in men with estrogen excess symptoms
Initiate at the lowest effective dose (75 IU 2x/week) and titrate based on response biomarkers

Efectos secundarios comunes

Injection site reactions: erythema, induration (subQ >IM in frequency)
Gynecomastia/breast tenderness in men secondary to peripheral aromatization of elevated intratesticular testosterone to estradiol
Elevated serum estradiol requiring aromatase inhibitor co-administration in some men
Mild OHSS in women: bloating, pelvic discomfort, mild ascites (Grade 1–2)

Mecanismo de acción

HMG delivers exogenous FSH and LH activity (equal 1:1 IU ratio in standard preparations). FSH binds the FSH receptor (FSHR) on Sertoli cells, activating adenylyl cyclase via Gs proteins, elevating cAMP, and activating PKA-dependent transcription of androgen-binding protein (ABP), inhibin B, and GDNF — all critical for spermatogenesis and the blood-testis barrier integrity. The LH component activates the LHCGR on Leydig cells, similarly via cAMP/PKA, upregulating StAR (steroidogenic acute regulatory protein) and CYP11A1 to drive cholesterol import into mitochondria and initiation of the steroidogenic cascade, producing testosterone. This dual stimulation recapitulates the two-cell, two-gonadotropin model essential for intratesticular testosterone concentrations (~50–100x serum levels) required for spermatogenesis completion at the level of spermatid maturation.

Following subcutaneous or intramuscular injection, FSH and LH are absorbed into systemic circulation and distribute to gonadal tissue. FSH has a longer half-life (~24–36h) due to higher sialic acid content on glycan chains, which reduces receptor-mediated clearance. LH is cleared more rapidly (~20h). Bioavailability via subQ is approximately 70–75% for FSH. In men on exogenous androgens, gonadotropin suppression is reversed at the gonadal level, allowing intratesticular testosterone to recover even in the presence of exogenous testosterone-mediated pituitary suppression.

Farmacodinamia

FSH receptor upregulation on Sertoli cells occurs within 24 hours of the first dose; measurable increases in serum inhibin B (a Sertoli cell activity marker) typically occur within 1–2 weeks. Sperm appear in ejaculate improvements (if azoospermic) may take 3–6 months due to the 74-day spermatogenic cycle duration.

Biochemically: rising inhibin B, intratesticular testosterone, and eventual improvement in sperm concentration, total motility, and morphology (WHO criteria). Clinically: testicular volume increases (measurable by orchidometer), improved semen analysis parameters, and in women, rising estradiol and follicular growth on transvaginal ultrasound.

Cronología

Days 1-7: FSH and LH receptors on Sertoli and Leydig cells are occupied and activated. cAMP rises within hours. Steroidogenesis begins upregulating; early inhibin B increases measurable by Day 5–7 in responsive men.
Weeks 1-4: Leydig cell hypertrophy and increased CYP17A1 expression drive rising intratesticular testosterone. Testicular volume increases measurably. In women on a 10–14 day stimulation cycle, dominant follicle selection occurs by Day 7–10 with trigger-ready follicles by Day 10–14.
Weeks 4-16: Spermatogonial proliferation through to spermatid elongation progresses over the full 74-day spermatogenic cycle. Meaningful semen analysis improvement typically documented at 12 and 16 weeks. Continued FSH stimulation is required to maintain Sertoli cell support throughout.

Comparaciones

HMG (Menotropins) — efectividad Very High, seguridad Moderate, costo $$$, Medium de usar
Recombinant FSH (rFSH) — efectividad High, seguridad Good, costo $$$$, Medium de usar
hCG — efectividad High, seguridad Good, costo $$, Medium de usar

Efectos adversos

Comunes:

Injection site reactions: erythema, induration (subQ >IM in frequency)
Gynecomastia/breast tenderness in men secondary to peripheral aromatization of elevated intratesticular testosterone to estradiol
Elevated serum estradiol requiring aromatase inhibitor co-administration in some men
Mild OHSS in women: bloating, pelvic discomfort, mild ascites (Grade 1–2)

Raros:

Severe OHSS (Grade 3) in women: massive ascites, pleural effusion, hemoconcentration, thromboembolic events — incidence ~1–2% in IVF cycles with careful monitoring
Antibody formation to urinary-derived gonadotropins (rare, estimated <1% with modern purified preparations)
Testicular torsion risk theoretically increased with rapid testicular enlargement (very rare case reports)

Contraindicaciones y mitigación de riesgos

Contraindicado en:

Men with primary hypogonadism (Klinefelter syndrome, bilateral orchidectomy) — no functional gonadal tissue to respond
Active sex hormone-sensitive malignancies (prostate carcinoma, hormone-receptor positive breast cancer)
Women with uncontrolled PCOS at high OHSS risk without ultrasound monitoring capability
Patients with active thromboembolic disease or hereditary thrombophilias without anticoagulation management
Uncontrolled hypothyroidism or hyperprolactinemia (will blunt response)

Monitor serum estradiol, inhibin B, LH, FSH, and testosterone every 2–4 weeks in men; adjust dose to maintain physiological ranges
In women, mandate transvaginal ultrasound follicle monitoring with estradiol assays to trigger ovulation only when 1–2 dominant follicles reach 17–18mm; cancel cycle if >3 large follicles (OHSS risk)
Co-administer a low-dose aromatase inhibitor (e.g., anastrozole 0.5–1mg/week) in men with estrogen excess symptoms
Initiate at the lowest effective dose (75 IU 2x/week) and titrate based on response biomarkers

Reference data

Specifications

Molecular formula: Complex glycoprotein mixture (FSH: ~34 kDa heterodimer; LH: ~28 kDa heterodimer)
Molecular weight: FSH ~34,000 Da; LH ~28,000 Da
Half-life: FSH component ~24-36 hours; LH component ~20 hours
Route: Subcutaneous, Intramuscular
Cycle length: 8-16 weeks for male fertility restoration; 7-14 days for female ovulation induction cycles
Storage: Unreconstituted lyophilized powder: store at 2–8°C (refrigerated) or up to 25°C away from light for short periods. Once reconstituted with sterile water or bacteriostatic water, use within 28 days if refrigerated at 2–8°C. Never freeze reconstituted solution. Protect from light.
Legal status: Prescription-only medication in the United States (FDA-approved for fertility indications), EU, and most countries. Off-label use for male fertility restoration and TRT-adjunct is common under physician supervision. Not approved for performance enhancement use.

FAQ

Common questions

Why is HMG superior to hCG monotherapy for sperm production?

hCG provides only LH-like activity (LHCGR agonism), which is sufficient to stimulate Leydig cell testosterone production but insufficient alone to drive the full spermatogenic program. Sertoli cells require FSH receptor activation for ABP secretion, GDNF production, and maintenance of the blood-testis barrier. Studies (e.g., Bouloux et al., 2002, Human Reproduction) demonstrate that FSH addition to hCG significantly improves sperm counts and pregnancy rates in hypogonadotropic hypogonadism over hCG alone.

What distinguishes urinary HMG from recombinant FSH (rFSH)?

Urinary HMG (menotropins) contains both FSH and LH activity from postmenopausal urine, including urinary LH and trace hCG. Highly purified HMG (HP-HMG) contains FSH plus a standardized amount of hCG-driven LH activity. Recombinant FSH (follitropin alfa/beta) provides pure FSH with no LH activity. Clinical evidence (e.g., Cochrane reviews on ART) suggests HP-HMG may have marginally better live birth rates per cycle start in IVF compared to rFSH, possibly due to the LH activity component.

What is the evidence level?

This compound is classified as Clinical evidence. Randomized controlled trial data in humans exists and supports use in specific contexts.

Research

Research & sources

Clinical evidence

Current evidence for Human Menopausal Gonadotropin (HMG) is rated as Clinical evidence. Human clinical evidence supports the reported effects.

1. Bouloux PM et al. — First International Norditropin Study Group. Induction of spermatogenesis by recombinant follicle-stimulating hormone in azoospermic men with hypogonadotropic hypogonadism (2002) — Human Reproduction, 17(11):2835–2843
2. Cochrane Review: Urinary gonadotrophins versus recombinant gonadotrophins for ovarian stimulation in IVF/ICSI cycles (2017) — Cochrane Database of Systematic Reviews, CD005354
3. Liu PY, Baker HW — Gonadotropin therapy in males: pathophysiology and evidence base (2009) — Asian Journal of Andrology, 11(1):3–14

Explore

Often discussed alongside

Human Chorionic Gonadotropin (HCG) · sexual Gonadorelin · sexual