HMG (75iu)

HMG (Human Menopausal Gonadotropin, 75 IU): Menotropins — A Purified Urinary-Derived Gonadotropin Preparation Extracted from the Urine of Postmenopausal Women, Containing Both Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) Biological Activity (in an Approximately 1:1 Ratio in Highly Purified HP-hMG Formulations Such as Menopur), Plus a Small Amount of Human Chorionic Gonadotropin (hCG), Originally Developed by Bruno Lunenfeld and Piero Donini in the Late 1950s (with the Original Brand Pergonal) and First Used for Ovulation Induction in 1963 (Lunenfeld et al., PMID 14063538), FDA-Approved for: (1) Induction of Ovulation and Development of a Single Graafian Follicle in Anovulatory Women (Including Those with Polycystic Ovary Syndrome [PCOS]) Who Have Not Responded to Clomiphene Citrate Therapy; (2) Controlled Ovarian Hyperstimulation (COH) to Induce Development of Multiple Follicles for Assisted Reproductive Technologies (ART) Such as In Vitro Fertilization/Embryo Transfer (IVF/ET), Intracytoplasmic Sperm Injection (ICSI), and Gamete Intrafallopian Transfer (GIFT); and (3) Induction or Restoration of Secondary Sexual Development and Fertility Due to Androgen Deficiency in Males with Hypogonadotropic Hypogonadism, When Used in Combination with hCG — With Extensive Clinical Evidence from Multiple Randomized Controlled Trials (RCTs), Systematic Reviews, and Meta-Analyses Demonstrating Comparable or Superior Live Birth Rates Compared to Recombinant FSH (rFSH) in Some Populations (Cochrane Review CD005354: 17 RCTs, 5639 Women — Live Birth Rate Probably Lower with rFSH vs HMG/HP-HMG; Meta-Analysis of 12 RCTs, 3575 Women: hMG Live Birth Rate Significantly Higher than rFSH, OR = 1.20, 95% CI = 1.01–1.42; Meta-Analysis of 12 RCTs, 2937 Participants: rFSH Live Birth 21.8% vs uHMG 24.9%), a Potentially Favorable Safety Profile in High Responders with Lower OHSS Incidence, and Well-Characterized Risks Including Ovarian Hyperstimulation Syndrome (OHSS), Multiple Pregnancy, Injection Site Reactions, and Rare Allergic Reactions

Human Menopausal Gonadotropin (HMG) — also known by the generic name menotropins, and by brand names including Pergonal (the original formulation), Menopur (highly purified HP-hMG), Merional, Humog, and others — is a purified gonadotropin preparation extracted from the urine of postmenopausal women, who excrete elevated levels of pituitary gonadotropins as a physiological consequence of ovarian failure and the loss of ovarian estrogen-mediated negative feedback on the hypothalamic-pituitary axis. HMG contains both follicle-stimulating hormone (FSH) and luteinizing hormone (LH) biological activity — in an approximately 1:1 ratio in modern highly purified (HP-hMG) formulations — plus a small amount of human chorionic gonadotropin (hCG) that is naturally present in postmenopausal urine and contributes to the LH biological activity measured in the preparation. The original HMG drug, Pergonal, was developed by Dr. Bruno Lunenfeld and Dr. Piero Donini in the late 1950s, and Dr. Lunenfeld pioneered its use for ovulation induction in anovulatory women in 1963 (Lunenfeld et al., PMID 14063538), demonstrating that exogenous gonadotropin therapy could reliably stimulate follicular development and ovulation when combined with hCG triggering — work that established the foundation for all modern assisted reproduction protocols. For decades, HMG remained the only injectable gonadotropin available for clinical use, until the development of urinary purified FSH (uFSH, Metrodin) in the 1980s and recombinant FSH (rFSH, Gonal-F, Puregon/Follistim) in the 1990s. Despite the availability of newer recombinant formulations, HMG — particularly in its modern highly purified form (HP-hMG, Menopur) — remains a cornerstone of fertility treatment worldwide, valued for its combined FSH+LH activity, extensive clinical track record, favorable cost profile, and demonstrated efficacy in multiple patient populations. HMG is FDA-approved for three main indications: (1) induction of ovulation and development of a single Graafian follicle in anovulatory women (including those with polycystic ovary syndrome [PCOS]) who have not responded to clomiphene citrate therapy; (2) controlled ovarian hyperstimulation (COH) to induce development of multiple follicles for assisted reproductive technologies (ART) such as in vitro fertilization/embryo transfer (IVF/ET), intracytoplasmic sperm injection (ICSI), and gamete intrafallopian transfer (GIFT); and (3) induction or restoration of secondary sexual development and fertility due to androgen deficiency in males with hypogonadotropic hypogonadism, when used in combination with hCG. It is important to note that HMG is a prescription medication that should only be used under the supervision of a qualified fertility specialist (reproductive endocrinologist), with appropriate monitoring of follicular development via transvaginal ultrasound and serum estradiol levels, due to the risk of ovarian hyperstimulation syndrome (OHSS) and multiple pregnancy. The product offered here is HMG 75 IU (75 IU FSH activity + 75 IU LH activity per vial), intended for laboratory research and clinical use under medical supervision^{[1][2][3][4][5][6][7][8][9][10][11][12]}.

Mechanism of Action: Combined FSH and LH Activity — Folliculogenesis, Steroidogenesis, and Spermatogenesis

The mechanism of action of HMG is fundamentally based on the combined biological activity of its two principal gonadotropin components — follicle-stimulating hormone (FSH) and luteinizing hormone (LH) — which act synergistically to regulate gonadal function in both women and men. Unlike recombinant FSH (rFSH) preparations, which contain only FSH activity, HMG provides both FSH and LH activity in a single preparation — a distinction that is clinically significant, as growing evidence suggests that LH activity plays an important and sometimes essential role in follicular development, oocyte maturation, steroidogenesis, and ultimately live birth outcomes. The mechanism of action can be broken down into the following key components^{[1][2][3][4][5][6][7][8]}:

• FSH component — follicular recruitment, growth, and granulosa cell function: The FSH component of HMG is fundamental for follicular recruitment in the early stages of folliculogenesis. FSH binds to FSH receptors (FSHR) on the granulosa cells of developing ovarian follicles, activating cAMP/PKA signaling pathways that stimulate granulosa cell proliferation and differentiation. Without adequate FSH stimulation, follicles arrest at the primary stage rather than progressing through preantral and antral development — FSH is the primary driver of the transition from preantral to antral follicles and is responsible for the recruitment of a cohort of antral follicles during the follicular phase of the menstrual cycle. FSH also stimulates the expression of aromatase (CYP19A1) in granulosa cells — the enzyme responsible for converting androgens (produced by theca cells under LH stimulation) into estrogens (primarily estradiol) — thereby increasing estradiol production in the granulosa cells. Additionally, FSH upregulates LH receptor (LHCGR) expression on granulosa cells of the dominant follicle, making it responsive to the LH surge that triggers ovulation, and stimulates the production of inhibin B and other paracrine factors that regulate follicular selection and atresia. In the context of controlled ovarian hyperstimulation for ART, exogenous FSH (from HMG) supraphysiologically stimulates the growth of multiple follicles simultaneously, overriding the natural selection of a single dominant follicle and allowing the retrieval of multiple oocytes for fertilization^{[1][2][3][4][5]}.
• LH component — theca cell androgen production, steroidogenesis, and follicular maturation: The LH component of HMG acts through LH/choriogonadotropin receptors (LHCGR) — which are expressed on theca cells throughout folliculogenesis and on granulosa cells of the dominant/preovulatory follicle (after FSH-induced upregulation). LH binding to LHCGR on theca cells activates cAMP/PKA signaling, driving the expression of steroidogenic enzymes (including CYP11A1 [side-chain cleavage enzyme], CYP17A1 [17α-hydroxylase/17,20-lyase], and 3β-HSD) that produce androgens — primarily testosterone and androstenedione — from cholesterol. These theca-cell-derived androgens diffuse across the basement membrane into the granulosa cells, where they serve as the obligate substrate for FSH-induced aromatase-mediated conversion to estradiol — this two-cell, two-gonadotropin model of ovarian steroidogenesis is the fundamental mechanism by which FSH and LH synergize to produce estradiol. Beyond its role in steroidogenesis, LH activity is increasingly recognized as important for follicular maturation, oocyte quality, and cumulus cell expansion — particularly in the later stages of folliculogenesis. The addition of LH activity to ovarian stimulation has been demonstrated to improve the odds of achieving a live birth by approximately 3-4% in some analyses, and the inclusion of LH in the stimulation of poor responders and women aged 35 and older has been shown to improve ART outcomes. The small amount of hCG naturally present in HMG also contributes to LH biological activity (since hCG binds to the same LHCGR receptor as LH and has a longer half-life), providing sustained LH-like activity throughout the stimulation period^{[1][2][3][4][5][6][7]}.
• Combined FSH+LH synergy — the two-cell, two-gonadotropin model and clinical implications: The combined FSH+LH activity of HMG reflects the physiological two-cell, two-gonadotropin model of ovarian function — in which LH stimulates theca cells to produce androgens, and FSH stimulates granulosa cells to aromatize those androgens into estrogens. This physiological combination is the rationale for HMG's continued use despite the availability of recombinant FSH-only preparations. Clinical studies have demonstrated that: (a) HMG stimulation is associated with shorter stimulation duration and fewer ampoules of gonadotropin needed to reach oocyte retrieval, compared to rFSH in some studies; (b) serum LH and estradiol levels tend to be higher during HMG stimulation (consistent with the LH component's theca cell androgen production and subsequent aromatization); (c) while rFSH may produce more follicles, more retrieved oocytes, more mature oocytes, and more embryos in some protocols, there is no consistent difference in implantation rate, clinical pregnancy rate, or live birth rate — and some meta-analyses actually show higher live birth rates with HMG; (d) highly purified HMG (HP-hMG) may produce a higher proportion of top-quality embryos compared to rFSH in some studies (one study found the rate of top-quality embryos to total embryos was significantly higher in the HP-hMG group, p=0.006); and (e) HP-hMG may offer a better safety profile in high-responder patients, with a lower incidence of ovarian hyperstimulation syndrome (OHSS). The combined FSH+LH activity of HMG is particularly relevant for specific patient populations — including poor responders (Bologna criteria), women with low endogenous LH (e.g., after GnRH agonist down-regulation in long protocols), women aged 35 and older, and women with hypogonadotropic hypogonadism — in whom LH activity may be limiting for adequate follicular development and steroidogenesis^{[1][2][3][4][5][6][7][8][9][10][11][12]}.
• Male mechanism — spermatogenesis and testosterone production (hypogonadotropic hypogonadism): In males, HMG (used in combination with hCG) acts on the testes to stimulate both spermatogenesis and steroidogenesis — reflecting its gametropic and steroidogenic effects. The FSH component binds to FSH receptors on Sertoli cells in the seminiferous tubules, stimulating Sertoli cell proliferation and function, supporting spermatogenesis (the development of sperm from spermatogonia through spermatocytes and spermatids to mature spermatozoa), and producing androgen-binding protein (ABP) which maintains high intratubular testosterone concentrations necessary for spermatogenesis. The LH component (and the hCG used in combination therapy) binds to LHCGR receptors on Leydig cells in the testicular interstitium, stimulating testosterone production through cAMP/PKA-mediated activation of steroidogenic enzymes. In males with hypogonadotropic hypogonadism (also called secondary hypogonadism, caused by hypothalamic or pituitary dysfunction leading to low endogenous FSH and LH), combined hCG + HMG therapy can induce or restore both secondary sexual development (via testosterone production) and fertility (via spermatogenesis) — a treatment approach that has been used for decades and is supported by extensive clinical evidence. The combination of hCG (for Leydig cell testosterone production) + HMG (for Sertoli cell spermatogenesis support) is the standard gonadotropin replacement regimen for male hypogonadotropic hypogonadism when fertility is desired^[1][2][3].

Comparison: HMG vs. Recombinant FSH (rFSH) vs. Clomiphene Citrate — Mechanisms, Efficacy, and Safety

Clinical Evidence, FDA-Approved Indications, and Safety Considerations

HMG has one of the most extensive clinical evidence bases of any fertility medication, with over 60 years of clinical use, hundreds of randomized controlled trials, and multiple systematic reviews and meta-analyses. The clinical evidence can be summarized by indication^{[1][2][3][4][5][6][7][8][9][10][11][12]}:

Indication 1 — Ovulation induction in anovulatory women (including PCOS) unresponsive to clomiphene: HMG is FDA-approved for induction of ovulation and development of a single Graafian follicle in anovulatory women — including those with polycystic ovary syndrome (PCOS) — who have not responded to clomiphene citrate therapy. In this indication, HMG is typically administered by daily subcutaneous or intramuscular injection starting on day 2-3 of the menstrual cycle (or after progestin-induced withdrawal bleeding), with dose titration based on ultrasound and estradiol monitoring, and hCG trigger (5,000-10,000 IU) when the lead follicle reaches 17-18 mm, followed by timed intercourse or intrauterine insemination (IUI). The goal is development of a SINGLE dominant follicle to minimize multiple pregnancy risk — cycle cancellation is recommended if more than 2-3 follicles >14-16 mm develop. Clinical pregnancy rates per cycle are typically 15-25% in appropriately selected patients, with cumulative pregnancy rates of 50-70% over 3-6 cycles. HMG is particularly useful for clomiphene-resistant PCOS patients (approximately 20-30% of PCOS women who do not ovulate with clomiphene), in whom gonadotropin therapy is the second-line treatment after clomiphene failure (with laparoscopic ovarian drilling and aromatase inhibitors [letrozole] as alternatives).

Indication 2 — Controlled ovarian hyperstimulation (COH) for assisted reproductive technologies (ART): HMG is FDA-approved for controlled ovarian hyperstimulation to induce development of multiple follicles for ART procedures — including in vitro fertilization/embryo transfer (IVF/ET), intracytoplasmic sperm injection (ICSI), and gamete intrafallopian transfer (GIFT). In ART, HMG (or HP-hMG) is typically used as part of a controlled ovarian stimulation protocol with either GnRH agonist (long protocol, short protocol, flare) or GnRH antagonist co-treatment to prevent premature LH surge, with daily gonadotropin injections starting on day 2-3, ultrasound/estradiol monitoring every 1-3 days, and hCG trigger (5,000-10,000 IU or recombinant hCG/trigger) when 2-3 lead follicles reach 17-18 mm, followed by oocyte retrieval 34-36 hours later. The clinical evidence for HMG in ART is extensive: (a) the Cochrane Review CD005354 (17 RCTs, 5639 women) concluded that live births probably decrease with rFSH compared to HMG/HP-HMG — if the chance of live birth with HMG/HP-HMG is 28%, then the chance with rFSH is between 22% and 27%; and OHSS is probably higher with rFSH compared to HMG/HP-HMG; (b) a systematic review of 12 RCTs and 3575 women demonstrated significantly higher live-birth rate with hMG compared with rFSH (OR = 1.20, 95% CI = 1.01–1.42), with no significant difference in OHSS rates (OR = 1.21); (c) a meta-analysis of 12 RCTs with 2937 participants showed an overall live birth rate of 21.8% in the rFSH group compared to 24.9% in the uHMG group; (d) in a study of approximately 600 predicted high responders randomized to HP-hMG or recombinant FSH in GnRH antagonist cycles, the ongoing pregnancy rate was 35.5% for HP-hMG versus 30.7% for rFSH (non-inferiority confirmed), and HP-hMG was associated with lower cost per live birth; (e) studies have shown that the addition of LH activity to ovarian stimulation improves the odds of achieving a live birth by approximately 3-4%, and that inclusion of LH in stimulation of poor responders and women aged 35 and older improves ART outcomes; (f) while rFSH may produce more follicles, more retrieved oocytes, more mature oocytes, and more embryos in some protocols, there is no consistent difference in implantation rate, and HP-hMG may produce a higher proportion of top-quality embryos (one study found the rate of top-quality embryos to total embryos was significantly higher in the HP-hMG group, p=0.006). These data collectively support HMG/HP-hMG as a first-line gonadotropin for ART, with particular benefits in specific patient populations (poor responders, advanced maternal age, low endogenous LH).

Indication 3 — Male hypogonadotropic hypogonadism (with hCG): HMG is FDA-approved for induction or restoration of secondary sexual development and fertility due to androgen deficiency in males with hypogonadotropic hypogonadism, when used in combination with hCG. Hypogonadotropic hypogonadism (also called secondary hypogonadism) is caused by hypothalamic or pituitary dysfunction (e.g., Kallmann syndrome, pituitary tumors, craniopharyngioma, hemochromatosis, opioid use, hyperprolactinemia) leading to low endogenous FSH and LH, which in turn causes low testosterone and impaired spermatogenesis (infertility). Combined hCG + HMG therapy is the standard gonadotropin replacement regimen when fertility is desired: hCG (1,500-2,500 IU 2-3 times weekly) stimulates Leydig cells to produce testosterone (restoring secondary sexual characteristics, libido, and virilization), while HMG (75-150 IU 2-3 times weekly) provides FSH activity to stimulate Sertoli cells and support spermatogenesis. Treatment duration is typically 12-24 months for spermatogenesis to occur (spermatogenesis takes ~72 days, and longer if the testes have been suppressed for years). Sperm appears in the ejaculate in approximately 70-80% of patients with congenital hypogonadotropic hypogonadism, and pregnancy rates of 30-50% have been reported in partners of treated men. This combined therapy has been used for decades and is supported by extensive clinical evidence and professional society guidelines (Endocrine Society, AUA, EAU).

Safety considerations and adverse effects: HMG is generally well-tolerated when used under appropriate specialist supervision with monitoring, but it carries important risks that require careful patient selection, monitoring, and dose management: (1) Ovarian Hyperstimulation Syndrome (OHSS) — the most serious risk, characterized by ovarian enlargement, increased vascular permeability, ascites, pleural effusion, hemoconcentration, electrolyte imbalance, and in severe cases, thromboembolism, renal failure, and death; risk factors include young age, low BMI, PCOS, high antral follicle count, high AMH, previous OHSS, high estradiol levels, and excessive follicular response; incidence: mild ~10-20%, moderate ~1-5%, severe ~0.1-2% in ART cycles; HP-hMG may have lower OHSS incidence in high responders compared to rFSH (Cochrane: OHSS probably higher with rFSH); prevention: cycle cancellation for excessive response, coasting, GnRH agonist trigger (instead of hCG) in high responders, dopamine agonist (cabergoline) prophylaxis, cryopreservation of all embryos (freeze-all) with no fresh transfer; treatment: supportive care (hydration, electrolyte management, paracentesis/thoracentesis for tense ascites/effusion), anticoagulation for thromboembolism risk, hospitalization for severe cases; (2) Multiple pregnancy — twins, triplets, and higher-order multiples occur due to multiple follicles ovulating; risk ~10-20% in ovulation induction cycles (reduced by single follicle target and cycle cancellation), ~1-3% in ART with single embryo transfer (SET), ~10-20% with double embryo transfer; multiple pregnancy carries increased risks of preterm birth, low birth weight, gestational diabetes, preeclampsia, cesarean delivery, and neonatal complications; prevention: single embryo transfer (SET) in ART, cycle cancellation for excessive follicles in ovulation induction; (3) Injection site reactions — pain, redness, swelling, bruising at injection site (common, mild, self-limited); (4) Allergic reactions — rare, particularly with older urinary HMG preparations (due to urinary protein impurities); highly purified HP-hMG has substantially reduced immunogenicity and allergic risk; anaphylaxis is extremely rare; (5) Ectopic pregnancy — slightly increased risk with ART (2-5% vs ~1-2% natural); (6) Miscarriage — rates similar to natural conception after controlling for age and indication (~10-15%); (7) Ovarian torsion — rare complication of enlarged ovaries (<1%), surgical emergency; (8) Mood changes, headache, breast tenderness, fatigue — common mild side effects related to hormonal fluctuations; (9) Long-term cancer risk — the relationship between fertility drug use and ovarian/breast/uterine cancer remains controversial and not definitively established; most large studies do not show a significant increased risk with standard treatment courses, but prolonged use (>12 cycles) may warrant caution; (10) Birth defects — no consistent evidence of increased major congenital malformation risk with HMG or other fertility drugs compared to natural conception (after controlling for underlying infertility factors). Contraindications to HMG include: hypersensitivity to HMG or excipients; pregnancy; undiagnosed vaginal bleeding; ovarian cysts or enlargement not due to PCOS; thyroid or adrenal dysfunction (unless adequately treated); intracranial lesions (e.g., pituitary tumor) unless adequately treated; prior OHSS; hormone-dependent malignancies (breast, ovarian, uterine, testicular cancer); and conditions where pregnancy is inadvisable (e.g., severe cardiac/renal disease, certain genetic disorders). HMG is a prescription medication that should only be used under the supervision of a qualified fertility specialist (reproductive endocrinologist) with appropriate monitoring^{[1][2][3][4][5][6][7][8][9][10][11][12]}.

References

1. The Development of Gonadotropins for Clinical Use in the Treatment of Infertility. PMC / Frontiers in Endocrinology. 2019; PMC6616070. (hMG approved for development of single Graafian follicle in women with anovulation + multifollicular development in women undergoing controlled ovarian hyperstimulation as part of ART; hMG also effective for induction/restoration of secondary sexual development + fertility due to androgen deficiency in males with hypogonadotropic hypogonadism when used with hCG; recombinant gonadotropin development history)
2. Cochrane Collaboration. Which hormones are most effective for stimulating the ovaries in women undergoing in vitro fertilisation (IVF)? Cochrane Database of Systematic Reviews. CD005354. 2026. (rFSH versus HMG/HP-HMG: 17 studies, 5639 women; Live births probably decrease with rFSH compared to HMG/HP-HMG — if chance of live birth with HMG/HP-HMG is 28%, then chance with rFSH is between 22% and 27%; OHSS probably higher with rFSH compared to HMG/HP-HMG)
3. Urinary Versus Recombinant Gonadotropins for Ovarian Stimulation in Women Undergoing ART. PMC / Journal of Clinical Medicine. 2018; PMC6094533. (Systematic review of 12 randomized trials + 3575 women comparing hMG with rFSH; analysis demonstrated significantly higher live-birth rate with hMG compared with rFSH [OR = 1.20, 95% CI = 1.01–1.42]; no significant difference in rates of OHSS [OR = 1.21])
4. Recombinant follitropin alfa/lutropin alfa in fertility treatment. PMC / Therapeutic Advances in Reproductive Health. 2010; PMC2819896. (Meta-analysis of 12 RCTs, total 2937 participants: overall live birth rate 21.8% in rFSH group compared to 24.9% in uHMG group; second systematic review included only 7 RCTs comparing rFSH and HMG in IVF cycles with long pituitary down-regulation protocol)
5. Generic Peptides / HMG: Urinary-Derived Menotropins Combining FSH and LH Activity. GenericPeptides.com. 2026. (FSH fundamental for follicular recruitment in early folliculogenesis — without adequate FSH, follicles arrest at primary stage; LH component binds LHCGR on theca cells → cAMP/PKA → androgen production [testosterone + androstenedione] → androgens diffuse to granulosa cells as substrate for FSH-induced aromatization to estradiol; two-cell two-gonadotropin model)
6. Peptide List / hMG. PeptideList.org. 2026. (hMG = purified preparation of FSH + LH activity extracted from urine of postmenopausal women who excrete elevated gonadotropins due to ovarian failure; original drug Pergonal developed by Bruno Lunenfeld + Piero Donini in late 1950s; remained for decades the only injectable gonadotropin)
7. Peptides Clarity / HMG (Human Menopausal Gonadotropin). PeptidesClarity.com. 2026. (Original Ovulation Induction: Lunenfeld et al., 1963, PMID: 14063538 — Dr. Bruno Lunenfeld pioneered use of hMG for ovulation induction in anovulatory women, demonstrating exogenous gonadotropin therapy could reliably stimulate follicular development + ovulation when combined with hCG triggering; established foundation for all modern assisted reproduction protocols; HP-hMG vs...)
8. PMC / Clinical Effects of Natural Extract of Urinary hMG in Normogonadotropic Infertile Patients. PMC4359890. 2015. (Purified hMG = natural product extracted from urine of postmenopausal women containing pituitary FSH, LH, + small amount of hCG; retrospective clinical pharmaceutical study on cohort of normogonadotropic infertile patients on long GnRH-agonist protocol with serum LH 0.5 IU/L to...)
9. PMC / Luteinizing hormone and its dilemma in ovulation induction. PMC3136063. 2011. (HMG group: shorter stimulation length, fewer ampoules needed to reach retrieval; serum LH + estradiol levels higher; rFSH: more follicles during stimulation, more oocytes retrieved, more mature oocytes, more embryos available for transfer; no difference in implantation...; addition of LH activity to ovarian stimulation demonstrated to improve odds of live birth; 3-4% improvement clinically relevant; inclusion of LH in poor responders + women ≥35 improves ART outcomes; no proven methods to determine which patients benefit most from LH addition)
10. Peptidings / HMG. Peptidings.com. 2026. (~600 predicted high responders randomized to HP-hMG or recombinant FSH in GnRH antagonist cycles; primary endpoint ongoing pregnancy rate 35.5% for HP-hMG vs 30.7% for rFSH — noninferiority confirmed; HP-hMG also associated with lower cost per live birth — important in field where treatment costs substantial; PMID: PMC8244378)
11. Menopur 600IU — Electronic Medicines Compendium (emc). Medicines.org.uk. 2026. (Menotrophin [HMG] directly affects ovaries + testes; gametropic + steroidogenic effect; in ovaries, FSH-component induces increase in number of growing follicles + stimulates their development; FSH increases estradiol production in granulosa cells by aromatising androgens originating in theca cells under influence of LH-component; indications: anovulation incl PCOS in women not responded to clomiphene; controlled ovarian hyperstimulation for ART [IVF/ET, GIFT])
12. A Head-to-Head Comparison of Menotropin Formulations for ART. BenchChem PDF. 2026. (Compared to recombinant FSH, urinary-derived gonadotropins [especially HP-hMG] demonstrate similar live birth + ongoing pregnancy rates; while r-hFSH may require lower total dose in some populations, HP-hMG may offer better safety profile in high-responder patients with lower incidence of OHSS; comparison of ovulation induction: systematic review of 14 RCTs found no significant differences between hMG [both FSH+LH] and urinary FSH [uFSH] in pregnancy rate per cycle [OR 0.89; 95% CI 0.53-1.49], multiple pregnancy, miscarriage)
13. Oxford Academic / Hum Reprod. A prospective, randomized, controlled trial comparing highly purified hMG with recombinant FSH in women undergoing ICSI: ovarian response and clinical outcomes. Human Reproduction. 2003;18(6):1194-1200. (Fertilization rate: rFSHα 87±5% vs HP hMG 76±3% [NS]; Embryos transferred: 1.83±0.06 vs 1.93±0.04 [NS]; Moderate OHSS: 1 vs 3 [NS]; Twin gestations: 2 vs 1 [NS]; another study: rate of top-quality embryos to total embryos significantly higher in HP-hMG group [p=0.006]; fertilization rate significantly higher in rec-FSH group [p=0.001])