HMG (Gonadotropină Menopauză Umană / Menotropină) — Grad de cercetare

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What Is HMG (Menotropin)?

HMG — Human Menopausal Gonadotropin, also known as menotropin (CAS 61489-71-2) — is a urinary-derived glycoprotein-hormone preparation containing equal amounts of LH (luteinising hormone) and FSH (follicle-stimulating hormone) bioactivity, standardised at 75 IU of each per vial. It is purified by ion-exchange and gel-filtration chromatography from the pooled urine of postmenopausal women, who have naturally elevated pituitary gonadotropin output (LH and FSH typically 50–100+ mIU/mL each) due to the loss of ovarian negative-feedback inhibition that accompanies menopause.

The “menopausal” in the name refers to this source: postmenopausal urine is the most concentrated natural source of LH and FSH available for industrial-scale purification, and hMG has been produced from this source since the early 1960s (the original Cesare Serono-developed Pergonal preparation). The compositional refinement of hMG has evolved substantially over the decades — earlier preparations had highly variable LH:FSH ratios and significant protein-impurity loads; modern preparations (the basis of our research-grade material) are standardised at 75:75 IU bioactivity per vial with ≥99% HPLC purity.

hMG is the canonical dual-gonadotropin pharmacological tool. Where HCG selectively activates the LHCGR, where pure-LH (recombinant Luveris) selectively activates the LHCGR at physiological half-life, where pure-FSH (recombinant Gonal-F / Puregon) selectively activates the FSHR, hMG activates both receptors simultaneously at a fixed 1:1 ratio. The two receptors are expressed on different cell populations within the gonad — LHCGR on Leydig cells / theca cells / luteinised granulosa / corpus luteum; FSHR on Sertoli cells / mural granulosa — so dual activation produces a complete physiological gonadotropin stimulus that more closely mimics endogenous mid-cycle pituitary output than either receptor activated alone.

A research-relevant nuance: HCG co-purification. Published compositional analyses of urinary-derived hMG preparations report that the bulk of the in-vivo LH-receptor bioactivity is actually attributable to trace HCG co-purified from postmenopausal urine — approximately 95% of LH-receptor-mediated bioactivity by some analyses (Wolfenson et al., 2005). This is because HCG and LH bind the same LHCGR with similar affinity, but HCG has 33–37 h plasma half-life versus LH’s ~20 min, so even small HCG amounts dominate the cumulative in-vivo LH-equivalent signal. This is part of why hMG produces sustained Leydig-cell stimulation despite the nominal “LH activity” of LH itself being short-lived. For research protocols where this distinction matters (pure-LH pharmacology vs HCG-contaminated mixed-LH signal), recombinant LH (Luveris) is the cleaner tool; for protocols where dual LHCGR + FSHR activation at physiological 1:1 ratio is the goal, hMG is the canonical reference.

Mechanism of Action — Dual LHCGR + FSHR Activation

hMG’s mechanism is the dual sum of its two component activities, both well-characterised in endocrine pharmacology:

• LH (and co-purified HCG) → LHCGR activation — The LH component (and the trace HCG that co-purifies from postmenopausal urine) binds the LH/CG receptor on Leydig cells (testis) and theca / granulosa / luteal cells (ovary). Gs-coupling raises cAMP, activates PKA, upregulates StAR-mediated mitochondrial cholesterol transport, and induces CYP11A1 / CYP17A1 / 3β-HSD / 17β-HSD steroidogenic enzymes — driving de-novo testosterone biosynthesis (male) or androstenedione biosynthesis (female).
• FSH → FSHR activation — The FSH component binds the FSH receptor on Sertoli cells (testis) and mural granulosa cells (ovary). FSHR is also Gs-coupled, but its downstream programme is distinct: in Sertoli cells FSHR activation drives androgen-binding protein (ABP), inhibin B, and the structural support programme that sustains spermatogenesis; in granulosa cells FSHR activation drives CYP19A1 (aromatase), converting theca-cell-derived androgens to oestrogens, and promotes follicular maturation through the antral and pre-ovulatory stages.
• Combined two-cell two-gonadotropin model — The classical endocrine framework. In the male testis, LH-stimulated Leydig cells produce testosterone, which diffuses into adjacent Sertoli cells where FSH-induced androgen-binding protein and Sertoli-cell metabolic machinery convert it into the high-intratesticular-testosterone microenvironment that spermatogenesis requires. In the female ovary, LH-stimulated theca cells produce androgens, which diffuse into adjacent granulosa cells where FSH-induced aromatase converts them into oestrogens. The two-cell two-gonadotropin model is the canonical framework, and hMG is the canonical pharmacological tool for engaging both halves of it simultaneously.
• Receptor desensitization and tachyphylaxis — Both LHCGR and FSHR undergo arrestin-mediated desensitization after sustained agonist exposure. Repeated high-dose hMG dosing can produce receptor downregulation — a well-documented phenomenon in published gonadotropin-pharmacology research relevant to chronic-dosing protocols.
• Hypothalamic-pituitary feedback — As with HCG, hMG-driven gonadal steroid output feeds back to the hypothalamus and pituitary to suppress endogenous GnRH and LH/FSH secretion. In the context of HPG-suppression research (testosterone replacement, AAS exposure, pharmacological GnRH antagonism), hMG bypasses the hypothalamic-pituitary blockade by acting directly at the gonadal receptors — preserving both Leydig-cell function (LH side) and Sertoli-cell / spermatogenesis-support function (FSH side) simultaneously, which is what distinguishes hMG from pure-HCG protocols in this research context.

The pharmacokinetic profile of hMG broadly mirrors that of its components: FSH activity persists with 30–40 h terminal half-life, LH-equivalent activity is dominated by the long-half-life co-purified HCG (33–37 h), and the combined preparation produces sustained 24–72 h dual gonadotropin stimulation per dose. Typical research-protocol dosing is 75–225 IU SC daily in rodent or human-subject research — equivalent to 1–3 vials of the 75 IU strength.

Published Research Applications

hMG is used in laboratory research contexts that investigate:

• Gonadotropin pharmacology — the canonical dual-receptor reference — most-cited dual LHCGR + FSHR agonist in published gonadotropin research; standard reference compound for dissecting LH-only vs FSH-only vs combined gonadotropin signalling
• Spermatogenesis induction research — in hypogonadotropic-hypogonadism rodent models, hMG (with or without supplementary HCG) is the canonical tool for inducing spermatogenesis by restoring both Leydig-cell testosterone production and Sertoli-cell FSH support; standard research-protocol cycle is 75–150 IU SC three times per week for 6–24 months in clinical-translational research
• Female ovarian-stimulation research — the historical foundation tool of in-vitro fertilisation research; hMG drives follicular development through the antral and pre-ovulatory stages in published ovulation-induction protocols, typically combined with HCG as ovulation trigger; widely used in research on polycystic ovary syndrome (PCOS), unexplained infertility, and assisted reproductive technologies
• Two-cell two-gonadotropin model research — the canonical framework of gonadal steroidogenesis pharmacology; hMG is the standard tool for activating both halves of the model simultaneously; published Sertoli-Leydig co-culture and theca-granulosa co-culture research uses hMG to recapitulate the physiological dual-receptor stimulus
• HPG-axis suppression-recovery research — in published research models where endogenous LH/FSH has been suppressed (by exogenous testosterone, AAS exposure, or GnRH antagonism), hMG preserves both Leydig-cell function and Sertoli-cell function by direct gonadal receptor activation — distinguishing it from HCG-only protocols which preserve only LH-side function and risk Sertoli-cell atrophy
• Comparative pharmacology vs pure-LH / pure-FSH / HCG — published head-to-head comparisons of hMG vs recombinant LH (Luveris), recombinant FSH (Gonal-F / Puregon), recombinant HCG (Ovidrel), and various combinations are extensive; hMG is the urinary-derived 1:1 mixed reference against which all of these are benchmarked
• Follicular development and granulosa-cell biology — published ex-vivo follicular culture and primary granulosa-cell research uses hMG to drive simultaneous theca-cell androgen production and granulosa-cell aromatase induction — the most physiologically relevant in-vitro stimulus available
• Corpus-luteum biology — sustained LHCGR activation by the LH component (and co-purified HCG) maintains corpus-luteum function and progesterone production; used in research on the luteal phase and luteo-placental transition

For broader context on HPG-axis and reproductive-system research peptides in this catalogue, see HCG (Human Chorionic Gonadotropin) (pure LHCGR agonist — direct comparison; LH-side activity only), Kisspeptină-10 (the upstream hypothalamic Kiss1R agonist — drives endogenous GnRH pulsatility), PT-141 (Bremelanotide) (melanocortin-receptor pharmacology — sexual-function research), and Oxitocină Acetat (posterior pituitary peptide hormone). Browse the full research peptides & compounds catalog.

Available Strengths and Concentrations

MedsBase stocks HMG (urinary-extracted menotropin) in a single lyophilized vial strength calibrated to the standard 1:1 LH:FSH bioactivity unit. The vial is available in 10-vial or 20-vial pack formats:

The 75:75 IU vial is the international-reference dose unit and the format used in essentially all published gonadotropin research and clinical practice. Multiple-vial dosing (150 IU, 225 IU per administration) is standard for higher-dose protocols. The 20-vial pack is the more economical purchase per-IU for extended-cycle or multi-cohort protocols.

How It Compares — HMG vs HCG

HCG and hMG are the two urinary-derived gonadotropin preparations in this catalogue, and they target the gonadotropin-receptor system in mechanistically distinct ways. HCG is a pure LH/CG receptor agonist — Leydig-cell / theca-cell activation only. hMG is the dual LH + FSH preparation — engages both halves of the two-cell two-gonadotropin model simultaneously. The choice between them in research depends on whether the protocol needs LH-side activation alone or combined LH-side + FSH-side activation.

For research focused on dual LHCGR + FSHR activation, spermatogenesis induction, or the canonical two-cell two-gonadotropin model, hMG is the standard reference compound. For research focused on Leydig-cell-only stimulation, ovulation triggering, or HCG-specific LHCGR pharmacology, HCG is the more targeted tool. See also Kisspeptină-10 for upstream hypothalamic Kiss1R / GnRH-pulsatility research.

Storage and Reconstitution

Before reconstitution: store lyophilized vials refrigerated at 2–8 °C in original packaging for short-term working stock. For long-term storage, freeze unopened vials at −20 °C (stable ≥36 months at −20 °C; ≥18 months at 2–8 °C). The lyophilized cake is mannitol- or lactose-stabilised and is reasonably tolerant of brief room-temperature exposure during handling, but should be returned to refrigeration promptly. Protect from light.

Reconstitution procedure: for each 75 IU vial, inject 1.0 mL of bacteriostatic water down the side wall of the vial (not directly onto the lyophilized cake) — this yields a working stock of 75 IU LH + 75 IU FSH per mL. For research protocols that need higher concentrations (multi-vial pooling for higher single-dose), reconstitute 2–3 vials with the same 1.0 mL diluent total to give 150–225 IU/mL. Swirl gently to dissolve — do not shake, do not vortex. High-shear mixing dissociates the α/β heterodimers of both LH and FSH components and destroys gonadotropin-receptor bioactivity. The mannitol-based lyophilization cake typically dissolves within 30–60 seconds with gentle swirling.

Critical storage rules for reconstituted material: once reconstituted, store at 2–8 °C and use within 30 days. Do not freeze reconstituted hMG — freeze-thaw cycles dissociate the LH and FSH α/β heterodimers (the same physical-chemistry constraint as HCG) and irreversibly destroy bioactivity. Protect from light. Discard if cloudiness, particulates, or marked colour change appears. For research protocols requiring multiple aliquots, prepare aliquots at the time of reconstitution and store at 2–8 °C separately rather than freezing.

Întrebări frecvente

What is the difference between HMG and HCG?

HCG is a pure LH/CG-receptor agonist — single glycoprotein hormone (CAS 9002-61-3) that binds and activates only the LHCGR on Leydig / theca / granulosa / luteal cells. hMG is a 1:1 mixture of LH and FSH bioactivity — distinct glycoprotein hormones (combined CAS 61489-71-2) that bind both the LHCGR (LH side) and the FSHR (FSH side). The clinical and research consequence is that hMG produces dual-receptor stimulation that engages both halves of the two-cell two-gonadotropin model (Leydig + Sertoli in males; theca + granulosa in females), where HCG produces single-receptor stimulation of the LHCGR side only.

What is the HCG co-purification in hMG, and why does it matter for research?

Published compositional analyses of urinary-derived hMG preparations report that approximately 95% of the in-vivo LH-receptor-mediated bioactivity is actually attributable to trace HCG co-purified from postmenopausal urine, rather than to LH itself (Wolfenson et al., 2005). This is because HCG and LH bind the same LHCGR with similar affinity, but HCG has 33–37 h plasma half-life vs LH’s ~20 min — so even small amounts of co-purified HCG dominate the cumulative in-vivo LH-equivalent signal. For research protocols where this distinction matters (e.g., comparing pure-LH pharmacology vs HCG-contaminated mixed-LH signal), recombinant LH (Luveris) is the cleaner tool. For protocols where dual LHCGR + FSHR activation at fixed 1:1 ratio is the goal, hMG is the canonical reference.

Why is hMG sourced from postmenopausal women’s urine?

Postmenopausal women lose ovarian negative-feedback inhibition of the hypothalamic-pituitary axis, which raises pituitary LH and FSH output dramatically — typical postmenopausal serum LH and FSH are 50–100+ mIU/mL each, an order of magnitude higher than premenopausal values. Both hormones are then renally cleared into urine in concentrated form. Pooled postmenopausal urine is therefore the most concentrated natural source of LH + FSH for industrial-scale extraction. The hMG industry was built on this insight in the early 1960s (Pergonal was the original Serono preparation) and continues today, though much of the clinical market has shifted to recombinant pure-LH and pure-FSH preparations.

What published dose ranges have been used in research?

Single-dose research-protocol use is typically 75–225 IU SC per administration (1–3 vials of the 75 IU strength), with 3×/week or daily dosing in chronic protocols. Spermatogenesis-induction protocols in published hypogonadotropic-hypogonadism research typically use 75–150 IU 3×/week for 6–24 months in combination with HCG (the HCG provides additional Leydig-cell stimulation). In-vitro Sertoli-cell or granulosa-cell culture protocols typically use 1–10 IU/mL in growth medium. Researchers should consult primary literature appropriate to the species, model, and endpoint.

What is the difference between hMG and pure recombinant FSH (Gonal-F / Puregon)?

Pure recombinant FSH (follitropin alfa / Gonal-F; follitropin beta / Puregon; produced in CHO cells from cloned FSH α and β cDNAs) contains doar FSH bioactivity — no LH, no HCG. hMG contains both LH and FSH bioactivity at 1:1 ratio (plus trace HCG). For research protocols that need pure FSHR activation isolated from LHCGR signalling, recombinant FSH is the correct tool. For protocols that need combined dual-receptor activation at physiological ratio, hMG is the correct tool. Published head-to-head trials in ovarian-stimulation research have compared the two with broadly equivalent follicular-development endpoints but with subtly different oestradiol-response profiles (hMG tends to produce slightly higher mid-cycle oestradiol due to the LH-side androgen substrate it provides for granulosa-cell aromatase).

Why can’t reconstituted hMG be frozen?

The same reason as HCG — both LH and FSH are heterodimers of two non-covalently associated subunits (α + β each). The α/β interaction is stable in the lyophilized cake (no water to disrupt the interaction) and stable in refrigerated aqueous solution at 2–8 °C (kinetics of dissociation are slow at low temperature). But ice-crystal formation during freezing physically pulls the subunits apart, and they re-associate only inefficiently on thawing. The result is that frozen-and-thawed hMG retains a large fraction of immunoreactivity but loses a large fraction of bioactivity. Lyophilized hMG can be frozen and is stable at −20 °C; reconstituted hMG cannot.

What is the WADA regulatory status of hMG?

hMG / menotropin is on the World Anti-Doping Agency (WADA) Prohibited List under class S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). It is prohibited at all times — both in-competition and out-of-competition — for male athletes. Researchers conducting human-subject research with hMG need to be aware of this regulatory status. For laboratory in-vitro and rodent in-vivo research the WADA status is informational only.

How does this research-grade hMG compare with the branded clinical preparations (Menopur, Menogon, Repronex)?

The branded clinical preparations are urinary-extracted menotropin (Menopur, Menogon, Repronex; the historical Pergonal preparation has been largely discontinued) packaged under various manufacturer SKUs for clinical use in assisted reproductive technologies. The research-grade hMG supplied here is the same urinary-extracted preparation at ≥99% HPLC purity, supplied without a clinical-use label and intended for laboratory research only. Researchers seeking clinical-use menotropin should obtain it through a clinical supply chain; researchers seeking research-grade material for in-vitro receptor pharmacology, rodent in-vivo work, or other laboratory applications can use the material supplied here.

Can hMG be combined with HCG, Kisspeptin-10, or testosterone in research protocols?

Yes — these compounds target different layers of the HPG axis and are commonly combined in published research. The most-published combinations are hMG + HCG (the standard clinical and research protocol for spermatogenesis induction in hypogonadotropic-hypogonadism models — hMG provides FSH-side support, additional HCG provides supplemental LH-side stimulation); hMG + Kisspeptină-10 (upstream + downstream dissection — kisspeptin drives endogenous GnRH while hMG provides direct gonadal stimulation); hMG + exogenous testosterone (for HPG-suppression-recovery research, where the testosterone suppresses endogenous LH/FSH and hMG bypasses the suppression by acting directly at the gonad). Reconstitute each separately and follow each compound’s specific storage rules — neither hMG nor HCG should be frozen reconstituted.

Other Research Peptides for HPG-Axis and Reproductive Research

• HCG (Human Chorionic Gonadotropin) — Pure LH/CG-receptor agonist — direct comparison; LH-side activity only
• Kisspeptină-10 — Hypothalamic Kiss1R agonist — upstream HPG-axis regulator, drives GnRH pulsatility
• PT-141 (Bremelanotide) — Melanocortin-4 receptor agonist — sexual-function research
• Oxitocină Acetat — Posterior pituitary nonapeptide — reproductive and social-bonding research
• Tesamorelin — GHRH analogue — different endocrine axis, commonly co-studied
• Apă BAC (Apă bacteriostatică) — Required for reconstituting any lyophilized vial — sterile, 0.9% benzyl-alcohol-preserved diluent

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