HMG Reconstitution Calculator

Yes. Human menopausal gonadotropin (menotropins; Menopur and generics) is US-approved for ovulation induction and controlled ovarian stimulation in assisted reproduction; a 2026 US RCT confirmed the prefilled pen is non-inferior to the approved powder formulation (ongoing pregnancy 45.0% vs 42.7%). It is prescription-only; use without ultrasound/estradiol monitoring is unsafe (practitioner consensus).

HMG is extracted from the urine of postmenopausal women and supplies both FSH and LH activity. In highly purified HMG, most "LH activity" is hCG of placental origin: β-hCG constitutes 18–47% of gonadotropin content vs only traces of β-LH (0.9–1.2%), alongside roughly 20–30% non-gonadotropin protein impurities (mass spectrometry).

Subcutaneous is the standard route. An RCT (n=125) found SC highly purified HMG caused significantly fewer injection-site reactions than SC Repronex. The liquid prefilled pen is bioequivalent to reconstituted powder (FSH AUC ratio 1.12, Cmax 1.17 (90% CI within 0.80–1.25) ), with clinical non-inferiority (8.2 vs 6.6 fertilized oocytes) and fewer mild injection-site reactions.

Dosing is response-guided, not body-weight-based. ART: start 225 IU/day for the first 5 days, then adjust. Ovulation induction: 75 IU from cycle day 2 with step-up increments from day 9. Hypogonadotropic hypogonadism (IVF): low-dose hCG 50–300 IU/day plus daily HMG; mean total HMG ~2,960 IU over ~13 days of stimulation.

Cochrane review (59 RCTs, 18,119 women): versus HMG/HP-hMG, rFSH produces lower live birth (OR 0.83) and clinical pregnancy (OR 0.87), but higher OHSS risk (OR 1.42); moderate-certainty evidence. Conversely, a 2:1 rFSH:rLH combination retrieved 1.43 more oocytes/cycle and 18% higher clinical pregnancy than HP-hMG alone in a mixed-design meta-analysis. Real-world data: rFSH+HP-hMG matched rFSH pregnancy rates despite worse prognostic baseline, with lower OHSS in frozen-transfer patients.

HMG drives follicle growth (FSH plus supporting LH/hCG activity); hCG is an LH mimic used as the ovulation trigger or as low-dose daily LH support during stimulation. As stimulation adjuncts, hMG vs low-dose hCG give comparable live birth after fresh (42% vs 49%) and frozen (46% vs 53%) transfer. In hypogonadotropic patients, higher daily hCG doses shorten HMG duration (14.8→13.0 days) without improving embryo quality.

Yes, for hypogonadotropic hypogonadism, not as a general fertility aid. In 112 CHH men, hCG plus either hMG or rFSH produced detectable sperm in 85.7%; pregnancy rates were 38.6% (hMG) vs 51.2% (rFSH), not statistically different (retrospective). In adolescents, hCG/hMG beat GnRH-pump therapy for penile growth at 3 months (6.9 vs 5.1 cm) and testosterone at 9–12 months (observational). Typical regimens pair hCG 1,000–5,000 IU 2–3×/week with hMG 75–150 IU 2–3×/week (practitioner consensus).

Primary risks are ovarian hyperstimulation syndrome (OHSS), multiple pregnancy, and thrombosis. OHSS can occur even without an exogenous trigger: endogenous pregnancy hCG produced severe pleural effusion requiring 4,700 mL drainage in one case. OHSS risk is nonetheless lower with HMG than rFSH (OR 1.42). Multiple pregnancy remains a recognized risk of gonadotropin stimulation (practitioner consensus). Arterial/venous thrombotic events are reported, including bioprosthetic valve thrombosis. Mitigation: lowest effective dose, cycle monitoring, and GnRH-agonist trigger in high responders (practitioner consensus).