Menotropins (hMG)

What Is Menotropins (hMG)?

Menotropins, also called human menopausal gonadotropin (hMG), is a urine-derived preparation containing both follicle-stimulating hormone (FSH) and luteinizing hormone (LH) activity.^[1] It is extracted from the urine of postmenopausal women, whose pituitary glands secrete high levels of both gonadotropins.

hMG is one of the oldest gonadotropin preparations used in reproductive medicine. Most published research on it comes from clinical studies of controlled ovarian stimulation in assisted reproduction and from studies in men with hypogonadotropic hypogonadism, a condition marked by inadequate pituitary gonadotropin secretion.^[1][2]

Because hMG supplies two hormones at once, much of the literature compares it with recombinant FSH (rFSH), which provides FSH activity alone, to ask whether the added LH activity changes hormonal profiles or outcomes.^[1][3]

Chemical Structure and Molecular Identity

Menotropins is not a single molecule but a mixture of glycoprotein hormones purified from urine, so it has no single sequence, formula or molecular weight. Its activity comes from FSH and LH, both heterodimeric glycoproteins that share a common alpha subunit and differ in their hormone-specific beta subunits.

PubChem has no compound record for menotropins, and this page does not list a formula, molecular weight or CAS number. Gonadotropins are protein hormones central to the endocrine system that regulates growth, sexual development and reproductive function.^[3] Preparations like hMG are characterized by their measured biological activity rather than by small-molecule identifiers.

Purity grades

Most recent studies use highly purified hMG (HP-hMG), a urine-derived preparation that retains both FSH and LH activity.^[1] Researchers distinguish it from recombinant FSH, which supplies FSH activity alone and has been compared with hMG in many randomized trials.^[3]

Research History and Development

hMG was a foundation of early ovulation induction and in vitro fertilization, and its research history tracks the evolution of stimulation protocols from the 1980s onward. A 1992 review described how protocols for oocyte retrieval evolved from clomiphene citrate combined with hMG, to hMG alone, and then to hMG combined with a gonadotropin-releasing hormone agonist (GnRH-a).^[4]

According to that review, clomiphene was largely abandoned in this setting after studies linked its antiestrogen effect to reduced implantation. The GnRH-a was added to keep LH low late in follicular development and prevent premature ovulation, and the long GnRH-a/hMG approach became the most common preparation for oocyte retrieval at the time.^[4]

With the arrival of recombinant FSH, research shifted toward head-to-head comparisons of urinary hMG with rFSH, later including highly purified hMG.^[3][5] In parallel, hMG was studied together with hCG to induce testicular development and sperm production in men with secondary hypogonadism.^[6]

More recent work tests hMG in specific patient groups, such as predicted high responders and women with poor ovarian reserve, and in combination with the aromatase inhibitor letrozole.^[5][7][8]

Mechanisms Studied in Research

hMG acts through the FSH and LH receptors, supplying both gonadotropin signals that the pituitary normally provides. In the ovary, FSH drives follicle growth and LH supports androgen production that feeds estradiol synthesis; in the testis, FSH acts on Sertoli cells and LH stimulates testosterone production by Leydig cells.

The LH component is what distinguishes hMG from rFSH. A 2018 review reported that highly purified hMG produces a different endocrine profile than rFSH during ovarian stimulation, in terms of serum FSH, androgens and estradiol. The same review noted that, compared with rFSH, it was associated with a less pronounced follicular response and a lower risk of ovarian overstimulation.^[1]

Male hypogonadotropic hypogonadism

In men with hypogonadotropic hypogonadism, testosterone alone promotes virilization but not testicular growth or spermatogenesis. Gonadotropin regimens, including those using hMG, are studied because they stimulate the testis directly.^[2] A 1998 case series of 42 men reported that bilateral testicular volume doubled within 5 to 12 months on combined hCG/hMG or pulsatile GnRH.^[6]

Key Findings From Published Studies

Clinical studies generally find hMG comparable to rFSH on pregnancy and live birth outcomes, with differences in oocyte yield and adverse event rates depending on the population studied. All findings below come from human studies.

Comparisons with recombinant FSH

• High responders: in a randomized, assessor-blinded noninferiority trial of 620 women with high antimüllerian hormone levels, ongoing pregnancy after fresh transfer was 35.5% with HP-hMG and 30.7% with rFSH, meeting noninferiority. Ovarian hyperstimulation syndrome occurred in 9.7% versus 21.4%, and cumulative early pregnancy loss in 14.5% versus 25.5%. Cumulative live birth rates were similar at 50.6% and 51.5%.^[5]
• Poor ovarian reserve: a retrospective cohort of 165 patients found no significant differences between HP-hMG and rFSH in oocyte numbers, top-quality embryos, clinical pregnancy or live birth. Serum estradiol and progesterone levels, endometrial thickness and stimulation duration also did not differ.^[7]
• Oocyte yield: a 2015 systematic review found a higher mean number of oocytes per cycle with rFSH in 10 of 13 randomized trials, at a similar cost per oocyte.^[3]
• Overall profile: a 2018 review concluded that highly purified hMG gave pregnancy rates similar to rFSH in IVF/ICSI despite a lower oocyte yield, and improved some aspects of embryo quality in IVF but not ICSI.^[1]

Combination with letrozole

In a randomized trial of 174 women with polycystic ovary syndrome, ovulation rates were identical (85.1%) whether a lower or higher letrozole dose preceded hMG, and ongoing pregnancy rates did not differ significantly. The lower-dose arm had a higher monofollicular development rate (67.8% vs 46.0%).^[8] In a retrospective analysis of 526 intrauterine insemination cycles, hMG plus letrozole was associated with higher clinical pregnancy (24.8% vs 14.8%) and live birth rates (19.9% vs 11.2%) than hMG alone.^[9]

Men with hypogonadotropic hypogonadism

A 2024 meta-analysis of 103 studies covering 5,328 patients found hMG used in 40.8% of studies. Across gonadotropin regimens, testicular volume, penile size and testosterone increased significantly in over 98% of analyses, though heterogeneity was high.^[2] In the 1998 series, sperm appeared in the ejaculate in 54 of 57 treatment courses.^[6]

Because hMG is a biological mixture whose FSH and LH content varies by purification, researchers typically rely on batch-specific activity assays and purity data to characterize any preparation.

Because hMG is a biological mixture whose FSH and LH content varies by purification, researchers typically rely on batch-specific activity assays and purity data.

Regulatory and Research Status

Menotropins is an FDA-approved prescription drug, regulated in the United States as a biological product, and highly purified urinary hMG remains in clinical use internationally. It is referred to here only by its generic name. Its approved uses fall within reproductive medicine, and it is available only by prescription.

Research continues to define where hMG fits relative to recombinant gonadotropins, particularly in subgroups such as high responders and patients with poor ovarian reserve, and in combination with oral agents such as letrozole.^[5][7][8] The 2024 meta-analysis of male pubertal induction noted substantial heterogeneity in treatment approaches across studies, leaving open questions about optimal regimens.^[2]

This page summarizes published research for reference purposes and does not provide guidance on human use.