Human menopausal gonadotropin (hMG), also called menotropins, is a fertility drug extracted from the urine of postmenopausal women. It supplies two kinds of hormone activity in equal amounts: follicle-stimulating hormone (FSH), which drives egg and sperm development, and luteinizing hormone (LH) activity, which drives sex-hormone production. The only US product today is Ferring’s Menopur.
In the US, Menopur is approved only for women, to grow multiple egg follicles during in vitro fertilization (IVF). In the UK its label also covers men with hypogonadotropic hypogonadism (low testosterone and absent sperm production caused by pituitary or hypothalamic failure), where it is given together with hCG to start sperm production. Outside medicine it is sometimes grouped with “post cycle therapy” drugs, but the only published evidence we found for its use in men after anabolic steroids is a single case report.
This page summarizes what the FDA and UK labels, clinical trials and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Gonadotropin; urinary mixture with FSH and LH activity |
| Brands / US approval | Menopur (Ferring, 2004; the only marketed US product); earlier Pergonal (1975), Humegon and Repronex, all discontinued |
| Route | Subcutaneous (US label); subcutaneous or intramuscular (UK label) |
| Strength | Vials of 75 IU FSH activity plus 75 IU LH activity |
| Labeled doses | Women in IVF: 225 IU/day to start, maximum 450 IU/day; men (UK label only): 75–150 IU two or three times weekly with hCG |
| Half-life (FSH) | 11–13 h after multiple doses (US label); 30 ± 11 h SC and 27 ± 9 h IM (UK label) |
| Key mechanism fact | The LH activity comes mainly from hCG, not from LH itself |
| US status | Prescription biologic (deemed BLA since March 2020); not a DEA controlled substance |
| WADA status | Contains hCG and LH, both prohibited at all times in males (S2.2.1) |
What it is
The US label describes Menopur as a preparation of gonadotropins with FSH and LH activity, extracted from the urine of postmenopausal women and further purified. Each vial contains 75 IU of FSH activity and 75 IU of LH activity, with lactose, polysorbate 20 and a phosphate buffer as inactive ingredients (Menopur US label). Potency is set by bioassays in rats (ovarian weight gain for FSH, seminal vesicle weight gain for LH) and standardized against World Health Organization international standards. The label notes that hCG is detectable in the product.
The UK label is more explicit about where the LH activity comes from (Menopur UK SmPC):
| Component | Source | Role in the product |
|---|---|---|
| FSH | Urine of postmenopausal women | Provides all of the FSH activity |
| LH | Urine of postmenopausal women (small amounts) | Minor contribution to LH activity |
| hCG | Postmenopausal urine, plus hCG from the urine of pregnant women that “may be added” | The main driver of the LH activity |
In practice, then, a vial of hMG behaves like FSH plus a small dose of hCG. That is the key difference from hCG alone, which supplies LH-like activity with little FSH effect.
What FSH and LH activity do
According to the UK label, hMG acts directly on the ovaries and testes:
- In the ovaries, FSH increases the number of growing follicles. LH activity drives the theca cells to make androgens, which FSH-stimulated granulosa cells convert to estradiol.
- In the testes, FSH matures the Sertoli cells (the “nurse” cells that support developing sperm) and the seminiferous tubules. Sperm production also needs a high androgen level inside the testis, which the label says “can be attained by a prior treatment using hCG.”
Because hMG acts on the gonads themselves, it replaces the pituitary’s signals rather than restarting the pituitary. Drugs that act upstream on the hypothalamus or pituitary, such as clomiphene, enclomiphene and gonadorelin, work differently.
Pharmacokinetics
The two labels report FSH kinetics from different studies in healthy premenopausal women whose own pituitary output had been suppressed. LH could not be modeled; the UK label says the LH data were too sparse.
| Parameter (FSH) | US label, study 2000-03 | UK label |
|---|---|---|
| Regimen | 225 IU once, or 225 IU then 150 IU/day for 6 days | 150 IU/day for 7 days |
| Peak level, multiple doses | 15.0 mIU/mL SC; 12.5 mIU/mL IM | 8.9 IU/L SC; 8.4 IU/L IM (baseline-corrected) |
| Time to peak | 17.9 h SC and 27.5 h IM (single dose); 8–9 h (multiple doses) | Within 7 h |
| Elimination half-life | 11–13 h (multiple doses, SC and IM similar) | 30 ± 11 h SC; 27 ± 9 h IM |
| Excretion | Not described | Mainly via the kidneys |
Sources: Menopur US label; Menopur UK SmPC.
The two half-life estimates differ by more than twofold, and the UK label stresses “great interindividual variability.” Subcutaneous dosing trended toward higher exposure than intramuscular dosing in the US study. Neither label has data in men or in people with kidney or liver impairment.
Approved medical use
United States
Menopur’s only US indication is the development of multiple follicles and pregnancy in ovulatory women as part of an assisted reproductive technology (ART) cycle (Menopur US label). It has no US indication in men.
| Labeled dosing (women in IVF) | Detail |
|---|---|
| Starting dose | 225 IU/day SC, from cycle day 2 or 3, after GnRH agonist pituitary suppression |
| Adjustments | After 5 days, based on ultrasound and estradiol; no more often than every 2 days and no more than 150 IU at a time |
| Maximum | 450 IU/day; no more than 20 days |
| Final step | hCG is given once follicles are mature, and withheld if OHSS risk is high |
United Kingdom
The UK label covers anovulation unresponsive to clomiphene, controlled ovarian stimulation for ART, and hypogonadotropic hypogonadism in men, given with hCG to stimulate sperm production (Menopur UK SmPC). It notes that men with primary testicular failure usually do not respond.
For men, the UK label describes this sequence:
- hCG 1,000–2,000 IU two to three times a week first;
- then hMG 75 or 150 IU (of both FSH and LH activity) two or three times weekly;
- continued for at least 3 or 4 months.
Regulatory status
- Approval history. Drugs@FDA lists four menotropins products: Pergonal (approved August 22, 1975), Humegon (1994), Repronex (1999) and Menopur (October 29, 2004). Only Menopur is still marketed (Drugs@FDA; FDA list of deemed BLAs).
- Biologic since 2020. All four menotropins applications were on FDA’s list of drug approvals “deemed to be” biologics licenses on March 23, 2020 (FDA list of deemed BLAs).
- Not a controlled substance. Menotropins do not appear on the DEA’s list of controlled substances (DEA list) or among the Schedule III anabolic steroids (21 CFR 1308.13). It is a prescription-only drug.
- Sport. The 2026 Prohibited List does not name hMG, but it bans chorionic gonadotrophin (CG) and LH in males at all times as “testosterone-stimulating peptides” (S2.2.1). The S2 class also covers substances with similar biological effects (WADA 2026 Prohibited List). hMG contains both hCG and LH.
What the research shows
IVF: hMG versus recombinant FSH
Most of hMG’s evidence comes from IVF trials comparing it with recombinant FSH (rFSH), which has no LH activity. Three large assessor-blind randomized trials found hMG non-inferior on the primary pregnancy outcome:
| Trial | Design and n | Ongoing pregnancy, hMG vs rFSH | Other results |
|---|---|---|---|
| MERiT (Andersen et al., Hum Reprod 2006) | Assessor-blind RCT, 731 women, long GnRH agonist protocol | 27% vs 22% (OR 1.25, 95% CI 0.89–1.75) | Fewer oocytes with hMG (10.0 vs 11.8) but more top-quality embryos (11.3% vs 9.0%) |
| MEGASET (Devroey et al., Fertil Steril 2012) | Assessor-blind RCT, 749 women, GnRH antagonist protocol, single-blastocyst transfer | 29% vs 27% (intention to treat) | Cumulative live birth 40% vs 38% |
| MEGASET-HR (Witz et al., Fertil Steril 2020) | Assessor-blind RCT, 620 predicted high responders (AMH ≥5 ng/mL) | 35.5% vs 30.7% | OHSS 9.7% vs 21.4%; cumulative live birth 50.6% vs 51.5% |
The US label’s pivotal trial (373 women on Menopur) reported continuing pregnancy in 23% and clinical pregnancy in 26% per cycle, and found Menopur non-inferior to rFSH (Menopur US label).
Pooled evidence has shifted over time:
- The 2011 Cochrane review (42 trials, 9,606 couples) found no clear difference in live birth between rFSH and urinary gonadotropins as a group (OR 0.97, 95% CI 0.87–1.08) (van Wely et al., Cochrane 2011).
- The 2026 update (59 studies, 18,119 women) compared rFSH with hMG specifically. Live birth was probably lower with rFSH (OR 0.83, 95% CI 0.73–0.95; 15 studies, 4,793 participants) and OHSS probably higher (OR 1.42, 95% CI 1.12–1.80; 37 studies), both rated moderate certainty (Berkhout et al., Cochrane 2026). The authors noted that many trials were industry-sponsored.
Inducing sperm production in hypogonadotropic hypogonadism
In men, hMG is used after or alongside hCG. hCG restores testosterone inside the testis; hMG adds the FSH signal. The evidence is from case series and retrospective cohorts, not randomized trials:
| Study | Men | Regimen | Result |
|---|---|---|---|
| Kliesch et al., Eur J Endocrinol 1994 | 26 (33 courses) | hCG 1,000–2,500 IU twice weekly plus hMG 75–150 IU three times weekly, or pulsatile GnRH | Sperm in 30 of 33 courses; pregnancy in 15 of 18 |
| Büchter et al., Eur J Endocrinol 1998 | 42 (57 courses) | hCG/hMG or pulsatile GnRH | Sperm in 54 of 57 courses; pregnancy in 26 of 36; testis volume doubled within 5–12 months |
| Liu et al., Medicine 2016 | 223 azoospermic men with congenital hypogonadotropic hypogonadism | hCG plus hMG | Sperm in 64%, at a median of 15 months; testosterone rose from 0.9 to 15.1 nmol/L |
In the 223-man cohort, sperm counts that were reached (median 11.7 million/mL) were still below WHO reference values, but 19 of the 34 men trying to conceive achieved a pregnancy. Larger starting testis volume and no history of undescended testes predicted earlier success.
Two meta-analyses put this in context:
- Pooling 1,240 men with congenital hypogonadotropic hypogonadism, combination therapy (hCG plus either hMG or recombinant FSH) produced sperm in 66.8% after a weighted mean of 10 months, against 51.9% after 33 months with hCG alone. Heterogeneity was high (I² 86% and 68%) (Pozzi et al., World J Mens Health 2025).
- A 2014 meta-analysis of 44 studies found sperm in the ejaculate in 75% (95% CI 69–81%) of treated men overall (Rastrelli et al., Andrology 2014). The hCG page covers this and later meta-analyses in more detail.
After anabolic steroid use
No controlled trials have tested hMG for recovery after anabolic steroid use. The only specific report found is a single case (Menon, Fertil Steril 2003):
- a bodybuilder who had used seven different anabolic steroids remained azoospermic (no sperm in semen) one year after stopping;
- he received hCG 10,000 IU twice weekly plus hMG 75 IU daily for 3 months;
- semen analyses returned to normal, and the couple conceived 7 months later.
A single case cannot show how often this works or whether recovery would have happened anyway. Larger observational data on post-steroid recovery involve hCG and clomiphene rather than hMG (see the hCG page). As with hCG, hMG drives the testes directly, so it does not show whether the pituitary has recovered.
Side effects and risks
In women: ovarian hyperstimulation and multiple pregnancy
The US label’s warnings center on ovarian stimulation (Menopur US label):
- Ovarian hyperstimulation syndrome (OHSS): a sudden rise in blood-vessel leakiness that moves fluid into the abdomen and chest. It can progress rapidly, peaks about 7–10 days after treatment, and is worse if pregnancy occurs. It occurred in 7.2% of 373 women in the pivotal IVF trial.
- Multiple pregnancy: 35.3% of the 85 pregnancies in that trial were multiple.
- Blood clots and lung complications: thromboembolism, acute respiratory distress syndrome and, rarely, death have been reported with gonadotropins.
- Ovarian torsion, ectopic pregnancy and miscarriage, partly linked to the underlying infertility.
| Adverse reaction (US label, 434 women, IVF/ICSI) | Rate |
|---|---|
| Abdominal pain | 6.7% |
| OHSS | 6.2% |
| Headache | 6.2% |
| Injection site pain and reaction | 3.9% |
| Abdominal cramps | 3.0% |
| Abdomen enlarged | 2.3% |
| Injection site inflammation | 2.3% |
Thrombophlebitis occurred in under 1%. Postmarketing reports include nausea, breast tenderness, acne, rash and hot flushes. The UK label also lists rare allergic reactions, including anaphylaxis (Menopur UK SmPC).
In men
Neither label reports side-effect rates in men. The UK label’s contraindications for men are testicular tumors, prostate cancer, pituitary or hypothalamic tumors, and hypersensitivity to the product. Its LH-like (hCG) component raises testosterone, as the 223-man cohort shows, and hCG also raises estradiol (see the hCG page).
Who should not use it
The US label contraindicates Menopur in women with:
- pregnancy (Pregnancy Category X);
- primary ovarian failure (high FSH);
- uncontrolled thyroid, adrenal or pituitary disease;
- sex-hormone-dependent tumors of the reproductive tract, or pituitary or hypothalamic tumors;
- abnormal uterine bleeding or ovarian cysts or enlargement of unknown cause;
- prior hypersensitivity to menotropins.
Interactions
No drug interaction studies have been done in humans. The UK label expects clomiphene to enhance the follicular response, and notes that a higher hMG dose may be needed after GnRH agonist pituitary suppression.
Key takeaways
- FSH plus hCG from urine. hMG supplies equal FSH and LH activity per vial, and its LH activity comes mostly from hCG.
- A women’s fertility drug in the US. Menopur is FDA-approved only for multiple follicle development in IVF; the UK label adds sperm induction in men with hypogonadotropic hypogonadism.
- Competitive with recombinant FSH in IVF. Three large trials showed non-inferiority, and the 2026 Cochrane review found probably higher live birth and lower OHSS with hMG than with rFSH, at moderate certainty.
- Works with hCG in pituitary failure. In uncontrolled cohorts, hCG plus hMG produced sperm in 64–95% of men or treatment courses, typically after many months.
- Almost no evidence after steroid use. One case report is the extent of it, and like hCG it bypasses rather than restarts the pituitary.
Sources
- Ferring Pharmaceuticals. Menopur (menotropins for injection), prescribing information. DailyMed.
- Ferring Pharmaceuticals Ltd. Menopur 75 IU powder and solvent for solution for injection, Summary of Product Characteristics, revised June 3, 2026. emc.
- Food and Drug Administration. Drugs@FDA: Menopur (menotropins), BLA 021663. FDA.
- Food and Drug Administration. List of approved NDAs for biological products that were deemed to be BLAs on March 23, 2020. FDA.
- Drug Enforcement Administration, Diversion Control Division. Controlled substances, alphabetical order. DEA.
- Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
- World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA 2026 Prohibited List.
- Andersen AN, Devroey P, Arce JC. Clinical outcome following stimulation with highly purified hMG or recombinant FSH in patients undergoing IVF: a randomized assessor-blind controlled trial. Hum Reprod. 2006;21(12):3217–3227. PubMed.
- Devroey P, Pellicer A, Nyboe Andersen A, Arce JC. A randomized assessor-blind trial comparing highly purified hMG and recombinant FSH in a GnRH antagonist cycle with compulsory single-blastocyst transfer. Fertil Steril. 2012;97(3):561–571. PubMed.
- Witz CA, Daftary GS, Doody KJ, et al. Randomized, assessor-blinded trial comparing highly purified human menotropin and recombinant follicle-stimulating hormone in high responders undergoing intracytoplasmic sperm injection. Fertil Steril. 2020;114(2):321–330. PubMed.
- van Wely M, Kwan I, Burt AL, et al. Recombinant versus urinary gonadotrophin for ovarian stimulation in assisted reproductive technology cycles. Cochrane Database Syst Rev. 2011;(2):CD005354. PubMed.
- Berkhout RP, Kostova EB, van Wely M. Recombinant follicle-stimulating hormone (rFSH) versus other recombinant or urinary gonadotropins for ovarian stimulation in assisted reproductive technology cycles. Cochrane Database Syst Rev. 2026;7(7):CD005354. PubMed.
- Kliesch S, Behre HM, Nieschlag E. High efficacy of gonadotropin or pulsatile gonadotropin-releasing hormone treatment in hypogonadotropic hypogonadal men. Eur J Endocrinol. 1994;131(4):347–354. PubMed.
- Büchter D, Behre HM, Kliesch S, Nieschlag E. Pulsatile GnRH or human chorionic gonadotropin/human menopausal gonadotropin as effective treatment for men with hypogonadotropic hypogonadism: a review of 42 cases. Eur J Endocrinol. 1998;139(3):298–303. PubMed.
- Liu Z, Mao J, Wu X, et al. Efficacy and outcome predictors of gonadotropin treatment for male congenital hypogonadotropic hypogonadism: a retrospective study of 223 patients. Medicine (Baltimore). 2016;95(9):e2867. PubMed.
- Pozzi E, Ila V, Petrella F, et al. Evaluating sperm recovery time and efficacy of monotherapy vs. combination therapies in men with congenital hypogonadotropic hypogonadism: a systematic review and meta-analysis. World J Mens Health. 2025;43(3):552–562. PubMed.
- Rastrelli G, Corona G, Mannucci E, Maggi M. Factors affecting spermatogenesis upon gonadotropin-replacement therapy: a meta-analytic study. Andrology. 2014;2(6):794–808. PubMed.
- Menon DK. Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin. Fertil Steril. 2003;79(Suppl 3):1659–1661. PubMed.