HMG
human menopausal gonadotropin / menotropins
HMG (human menopausal gonadotropin / menotropins) is a hormonal & sexual research compound. Purified gonadotropin preparation carrying both FSH and LH activity. HCG, already in the Vault, mimics LH alone — HMG brings the FSH arm as well, which is the half that acts on Sertoli cells and spermatogenesis rather than on testosterone output.
HMG quick facts
| Route | Subq or IM |
| Frequency | 3x Weekly |
| Half-life | FSH component ~30-40 hrs |
| Forms | Injectable |
| Evidence level | Approved (fertility); human |
Sits directly beside HCG and answers a different question. Dosed in international units, not milligrams — a unit error here is an order of magnitude, and the reconstitution calculator will not catch it because IU and mg are not convertible without the preparation's specific activity. The 75-150 IU range is the approved one; the 3x-weekly cadence is Cam's protocol rather than the daily schedule used in fertility medicine.
How HMG works
Purified gonadotropin preparation carrying both FSH and LH activity. HCG, already in the Vault, mimics LH alone — HMG brings the FSH arm as well, which is the half that acts on Sertoli cells and spermatogenesis rather than on testosterone output.
Proposed benefits
Researched for libido, hormonal signaling and reproductive / sexual function.
Where to get HMG
Buy HMG at Disguised Alpha →Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for HMG
Graded by what exists behind each claim.
✅ Clinically validated
- Approved and long-used in fertility medicine, typically 75-150 IU under monitoring. Menotropins are purified from postmenopausal urine and carry both FSH and LH activity. The IU range here is the approved one; the 3x-weekly cadence is protocol practice, not the daily schedule the fertility approvals were written around.
- Dosed in international units, never in milligrams. IU and mg are not interconvertible without the preparation's specific activity, so the reconstitution calculator cannot catch a unit error here — and a unit error is an order of magnitude.
📊 Correlative data
- Decades of use in assisted reproduction, always with monitoring. The known hazard of the class is ovarian hyperstimulation in women; in men the practical issue is that the FSH arm is what supports spermatogenesis.
🧪 Theoretical / extrapolated
- HCG mimics LH alone. HMG brings the FSH arm as well — the half acting on Sertoli cells rather than on testosterone output. That is the whole reason it sits beside HCG rather than replacing it.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What HMG actually does
The testis runs on two hormones acting on two different cells, and the whole point of this preparation is that it supplies the one hCG does not. Luteinizing hormone binds the LHCGR on Leydig cells in the interstitium; the receptor is Gs-coupled, cyclic AMP rises, protein kinase A activates steroidogenic acute regulatory protein, cholesterol is moved into the mitochondrion, and CYP11A1 starts the steroid pathway that ends in testosterone. Follicle-stimulating hormone binds FSHR on Sertoli cells inside the seminiferous tubule; the same second messenger, an entirely different program — androgen-binding protein, inhibin B, and the nursing environment that developing germ cells require.
So FSH does not raise testosterone, and that is not a limitation. It is the division of labor. hCG mimics LH and produces intratesticular testosterone Coviello 2005. hMG brings the Sertoli arm. A page that describes hMG as “stronger hCG” has misread the receptor biology: they act on different cells, produce different products, and are measured by different tests.
The cleanest demonstration of that split is a single patient. A man with suspected isolated FSH deficiency — normal testosterone, and therefore an intact LH-Leydig axis — was treated with 150 units of hMG three times weekly. Sperm concentration went from 2.5 million per mL with under 1% motility to 264 million per mL with 12% motility after three months Sugie 2023. One case, and it is the experiment nature ran: hold the LH arm constant, add FSH, and see what changes. What changed was spermatogenesis, by two orders of magnitude.
And the unit problem, which is chemistry rather than carelessness. Gonadotropins are dosed in international units because they are dosed by biological activity measured against an international reference standard, not by mass. A milligram of protein is a milligram; an international unit is a defined amount of effect. There is no conversion between them without knowing the specific activity of that particular preparation, which differs between products and between lots. That is why a reconstitution calculator built for milligram peptides cannot help here — not because it is badly written, but because the two quantities are not the same kind of number.
Cell, rodent, human — and where it stops
Step one, human, immediately — this is a licensed medicine and there is no rodent step to cross. The relevant literature is decades of reproductive endocrinology in men and women with hypogonadotropic hypogonadism, which is the condition the drug exists for Salvio 2024.
Step two, the numbers, and they are the strongest evidence in this cohort for combining the two arms rather than using one. A systematic review and meta-analysis covering 103 studies and 5,328 patients found gonadotropins produced significant increases in testicular volume, penile size and testosterone in over 98% of analyses. The decisive comparison is on spermatogenesis: 86% (95% CI 82–91%) with hCG plus FSH, against 40% (95% CI 25–56%) with hCG alone Alexander 2024. Adding the FSH arm roughly doubles the proportion of men who achieve spermatogenesis. That single comparison is the entire case for this compound and it belongs on the page in numbers.
Step three, the comparator nobody in this space considers. A systematic review and meta-analysis compared pulsatile gonadotropin-releasing hormone therapy against gonadotropin therapy for spermatogenesis in congenital hypogonadotropic hypogonadism Wei 2021. Pulsatile GnRH restores the upstream signal and lets the pituitary make its own LH and FSH in physiological pulses, rather than replacing both downstream. It is a different philosophy and it is in the literature; real-world outcome series with gonadotropins sit alongside it Sahib 2023.
The obstacle, named exactly. Every number above comes from men with hypogonadotropic hypogonadism — men whose pituitary output was absent or very low to begin with. The Vault audience overlaps only partly with that: many are men with suppressed gonadotropins from exogenous androgen use, which is a different starting state with a different Leydig and Sertoli history. The efficacy figures do not automatically transfer, and the honest statement is that the restart literature is far thinner than the hypogonadotropic hypogonadism literature it is usually quoted from. The card's 3x-weekly cadence is likewise not the daily or alternate-day schedule the fertility trials used.
HMG pharmacokinetics — how much of it actually gets in
The card says the FSH component runs ~30–40 hours. That is right, and the reason is a sugar rather than a peptide.
What clears it, and why the two components in one vial have different lifetimes. FSH, LH and hCG are all heterodimeric glycoproteins sharing an identical alpha subunit, with the beta subunit conferring specificity. Their clearance is dominated by their carbohydrate: terminal sialic acid caps protect the molecule from hepatic asialoglycoprotein receptors, while less sialylated isoforms are removed rapidly. hCG carries far more sialic acid than LH, which is why hCG persists for a day or more and pituitary LH is gone in under an hour. Two gonadotropins in the same vial can differ tenfold in half-life for reasons that have nothing to do with the protein and everything to do with its glycosylation. Clearance itself is by hepatic uptake and renal filtration of the intact dimer and its subunits.
The oral barrier. These are 30-plus kilodalton glycoprotein heterodimers. Swallowed, they meet gastric acid, which dissociates the subunits and destroys activity, then pancreatic proteases. Oral bioavailability is effectively zero, first-pass metabolism never becomes relevant, and that is why every gonadotropin in medicine is injected. Subcutaneous and intramuscular routes give comparable bioavailability for these molecules, with subcutaneous absorption slightly slower.
The arithmetic that makes the schedule a real question. With a 30–40 hour half-life, a dose given three times weekly leaves roughly a fifth to a third of the previous dose on board at the next injection, so levels accumulate mildly and trough between doses. Daily dosing — the fertility schedule — produces a far flatter profile. Sertoli cell FSH signaling responds to sustained exposure rather than to peaks, and spermatogenesis takes about 74 days for one cycle plus roughly two weeks of transit. That is why three months is the minimum interval at which any semen measurement means anything, and it is why the case report above measured at three months Sugie 2023.
The unit warning restated as pharmacokinetics. Because potency is defined by bioassay, two vials labeled 75 IU can contain different masses of protein with different isoform profiles and therefore different clearance. A dose in IU is a statement about effect at the reference standard, not about how long the molecule lasts in a person.
What would have to be true, and how you would know it was not
Three predictions with markers and windows. The second is the one that distinguishes this compound from hCG, and the third is the one that argues against how it is usually run.
1. LH & FSH measured on this compound will not mean what they usually mean, and that is a trap worth naming. Exogenous FSH is measured by the same immunoassay as endogenous FSH, so LH & FSH drawn during treatment reports the injection rather than the pituitary. The interpretable draws are before starting and after a washout of at least a week. Prediction: a baseline with low or inappropriately normal gonadotropins is what defines the population in which every efficacy number above was generated Salvio 2024; a baseline with high FSH points at a primary testicular problem, in which case adding more FSH is pushing on a receptor whose downstream cells are the limitation.
2. Total testosterone should barely move, and if it moves a lot the vial is not doing what the label says. FSH acts on Sertoli cells, which do not make testosterone. Draw total testosterone and estradiol at baseline and at 6 weeks. Prediction: testosterone roughly flat on hMG alone, and clearly raised if an hCG-like LH activity is present. That is a genuinely diagnostic pair — it distinguishes a preparation acting through the FSH arm from one acting through the LH arm, using two ordinary tests, in a class where the LH activity of a given preparation is rarely stated.
3. The prediction that cuts against the 3x-weekly protocol: nothing measurable will have changed at 6 weeks, and reading that as failure is the commonest mistake. One spermatogenic cycle is about 74 days. The case that worked measured at three months Sugie 2023, and the meta-analysis endpoints are months out Alexander 2024. So the honest protocol is a semen analysis at baseline and at 3 and 6 months and not in between. A compound whose primary endpoint cannot move for eleven weeks is a compound people abandon at week six for no reason.
What nobody has tested yet
Four questions with no published answer, and they are the ones the Vault audience is actually in.
Nobody has run the FSH-arm question in men recovering from exogenous androgen suppression. The 86%-versus-40% spermatogenesis figure comes from hypogonadotropic hypogonadism Alexander 2024. Whether adding FSH to hCG produces the same doubling in a post-androgen restart is the single most relevant unanswered question for this page's readers, and the trial has not been done.
Nobody has compared three-times-weekly against daily dosing on a semen endpoint. The fertility literature dosed daily or alternate-day. The cadence on this card is neither. Given a 30–40 hour half-life and a receptor that responds to sustained exposure, this is a straightforward pharmacokinetic question with a hard endpoint and no data.
Nobody has published inhibin B trajectories on hMG in this population. Inhibin B is the Sertoli cell's own product and is the closest thing to a direct read-out of whether the FSH arm is engaged — and it moves in weeks rather than in months, which would solve the eleven-week feedback problem above. It is orderable and it is essentially never ordered outside fertility clinics.
Nobody has compared restoring the upstream pulse against replacing both hormones, outside congenital disease. The pulsatile GnRH versus gonadotropin comparison exists for congenital hypogonadotropic hypogonadism Wei 2021. For acquired, reversible suppression — the commoner situation by far — the comparison has never been made.
HMG — its own safety story, not its class's
This preparation's own risks are a dosing-unit error, an estradiol problem and a source problem. The class block below does not carry any of them.
The unit error is the specific hazard here and it is an order-of-magnitude one. Gonadotropins are dosed in international units of biological activity, and there is no conversion to milligrams without the preparation's specific activity. A person accustomed to reconstituting milligram peptides who applies the same arithmetic to a gonadotropin vial can be out by a factor of ten or more in either direction, and no calculator will catch it because the two units are not commensurable. The only safe practice is to work from the vial's own stated IU content and never to convert.
The estradiol problem follows from the mechanism. Anything that increases testicular steroid output increases substrate for aromatase, and aromatization rises with adipose mass. The signs — breast tenderness, water retention, mood change — are the ones people misattribute. Estradiol alongside total testosterone is the pair that separates a real problem from an assumed one, and drawing them together is the whole measure.
Ovarian hyperstimulation is not a male risk and it is the reason this drug is prescription-only. hMG is a fertility medicine, and in women the dose-limiting toxicity is ovarian hyperstimulation syndrome, which can be severe. Any use of a gonadotropin in a woman belongs entirely inside a supervised fertility protocol with ultrasound and estradiol monitoring, and nothing on this page applies to it.
The source problem is unusually acute for this molecule. Menotropins are purified from a biological source and standardized by bioassay. There is no assay a buyer can run to confirm either the identity or the potency of a vial, and unlike a synthetic peptide there is no simple mass-spectrometry answer — a glycoprotein's activity depends on its glycosylation, not just its sequence. A vial of unknown provenance labeled in IU is making a claim about biological activity that nobody has measured. Approved gonadotropins exist and are prescribed; this is education about the pharmacology, not a recommendation for use.
Sources read for this page
- Sugie M, et al. A Case of Suspected Isolated Follicle-Stimulating Hormone (FSH) Deficiency Where Spermatogenesis Was Acquired by Human Menopausal Gonadotropin (hMG). Cureus 2023 · PMID 37065358
- Alexander EC, et al. Gonadotropins for pubertal induction in males with hypogonadotropic hypogonadism: systematic review and meta-analysis. European Journal of Endocrinology 2024 · PMID 38128110
- Wei C, et al. Spermatogenesis of Male Patients with Congenital Hypogonadotropic Hypogonadism Receiving Pulsatile Gonadotropin-Releasing Hormone Therapy Versus Gonadotropin Therapy: A Systematic Review and Meta-Analysis. World Journal of Men's Health 2021 · PMID 32777865
- Salvio G, et al. Hypogonadotropic hypogonadism as a cause of NOA and its treatment. Asian Journal of Andrology 2024 · PMID 39513636
- Sahib BO, et al. Management Outcomes in Males With Hypogonadotropic Hypogonadism Treated With Gonadotropins. Cureus 2023 · PMID 37007338
HMG — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- HMG carries both FSH and LH activity, and the FSH arm is the whole difference from hCG. LH activity acts on Leydig cells and drives testosterone; FSH acts on Sertoli cells and drives spermatogenesis. That is why this sits beside hCG rather than replacing it — it answers the fertility question hCG alone does not.
- Stimulating the gonad raises testosterone and estradiol together, so the aromatization-driven effects arrive as part of the response rather than as a complication of it: gynecomastia, fluid retention, and mood change.
- In women the FSH arm carries a named emergency — ovarian hyperstimulation syndrome. Recruiting several follicles at once produces abdominal distension, pain and vomiting, and in the severe form fluid shifts out of the circulation, the blood concentrates, and the thromboembolic risk becomes real. This is precisely why fertility medicine monitors with ultrasound and serial estradiol instead of dosing to a calendar.
- Multiple follicle recruitment also means multiple gestation, which is a foreseeable outcome of the mechanism rather than a complication of it.
What has actually been reported
- Well characterized — this is an approved fertility drug given under monitoring, so unlike most of this section the human experience is real and documented. Gynecomastia and fluid retention are the common male complaints; OHSS is the serious female one.
How to reduce the risk
Same mechanism as the prediction.
- Do not convert between international units and milligrams. This preparation is dosed in IU, the two units are not interchangeable without the specific activity of the exact preparation in your hand, and the reconstitution calculator cannot bridge them. An error here is an order of magnitude, not a rounding difference.
- Anyone using this to stimulate ovulation needs monitoring rather than a schedule. Abdominal swelling, rapid weight gain or breathlessness in the days after stimulation is an urgent presentation and not a wait-and-see.
- If gynecomastia or fluid retention is the complaint, the lever is the estradiol response, and sensitive E2 is what tells you whether that is actually what is happening before anything is added to manage it.
What it does to your bloodwork
A fact about the assay.
- LH and FSH, total and free testosterone, and sensitive estradiol specifically — this raises E2 more than people expect and a standard estradiol assay is the wrong instrument for reading it.
- If fertility is the reason you are running it, a semen analysis is the outcome measure. Hormones are the process; sperm is the result, and only one of the two answers the question you started with.
Don't run this if
- Any hormone-sensitive cancer, unless an oncologist is directing it — in which case it is their protocol and not one to self-manage.
- Untreated thyroid or adrenal dysfunction, or a pituitary tumor. The axis above the gonad has to be intact for the response to mean anything.
- Unexplained abnormal uterine bleeding, or an ovarian cyst not caused by polycystic ovarian syndrome.
The honest unknown
- The male fertility-restoration use — which is what most people reading this page are doing — is far less characterized than the approved female indication. The mechanism transfers cleanly; the dose schedules, durations and outcome rates do not.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
HMG — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What HMG moves on your bloodwork
Expected direction, not a measured one.
- Complete Blood Count (CBC) with Differential — ↑ expected to rise
Hematocrit and hemoglobin rise — androgens stimulate erythropoiesis. This is the most reliably predictable movement of any compound in the Vault.
What to do: This is the number that decides whether you keep going. Baseline and every 3 months. Dehydration on the draw day inflates it, so hydrate normally or you will chase a false reading. - Total Testosterone — ↑ expected to rise
Expected. Trough vs peak matters enormously — the same protocol reads completely differently depending on when you drew.
What to do: Draw at the same point in the cycle every time or the trend is noise. - LH & FSH — ↓ expected to fall
Suppressed by negative feedback. This is the mechanism, not a side effect — and it is why exogenous androgen shuts down your own production.
What to do: Relevant if fertility matters to you. Worth knowing before, not after. - Estradiol, Sensitive (LC/MS-MS) — ↑ expected to rise
Aromatization converts a fraction to estradiol, and it rises with the androgen. Use the sensitive (LC-MS/MS) assay — the standard immunoassay is unreliable in men and produces numbers people then medicate.
What to do: If you are reading estradiol in a man, the assay choice matters more than the result. - SHBG (Sex Hormone-Binding Globulin) — ↓ expected to fall
Falls with androgen exposure, which raises the free fraction — so free testosterone can climb faster than total.
What to do: Read total and SHBG together; total alone understates what changed. - Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) — ↓ expected to worsen
HDL falls, sometimes markedly. Oral 17-alpha-alkylated compounds do this far more aggressively than injectable esters.
What to do: Baseline and 12 weeks. ApoB is the better long-term read than LDL-C. - PSA (Total + Free + % Free) — ↑ expected to rise
Androgens can raise PSA modestly. It does not create prostate cancer that wasn't there, but it can unmask it.
What to do: Baseline before starting matters — without it, a later number has nothing to be compared against.
- Dose range and how to work up to it
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — HMG in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside HMG
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Total Testosterone | The baseline you can't reconstruct later |
| Free Testosterone | The fraction that does anything — total alone misleads |
| SHBG (Sex Hormone-Binding Globulin) | Explains a normal total sitting on top of a low free |
| Estradiol, Sensitive (LC/MS-MS) | The other half of the ratio, and the source of most symptoms |
| LH & FSH | Separates a testicular problem from a pituitary one |
The “Low T? Rule Out the Reversible Causes First” panel covers these in one order — 11 markers, $211.50 with the discount applied.
Check results you already have → · All 103 markers A–Z
HMG — frequently asked questions
What is HMG?
HMG (human menopausal gonadotropin / menotropins) is a hormonal & sexual research compound. Purified gonadotropin preparation carrying both FSH and LH activity. HCG, already in the Vault, mimics LH alone — HMG brings the FSH arm as well, which is the half that acts on Sertoli cells and spermatogenesis rather than on testosterone output.
Where can I find HMG dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full HMG protocol are available to members inside Skool. This public page covers what HMG is, how it works and the evidence.
What is the half-life of HMG?
HMG has an approximate half-life of FSH component ~30-40 hrs, which is part of what determines how often it's dosed.
What's the evidence behind HMG?
Current evidence level: Approved (fertility); human. HMG is offered for research purposes only and is not an approved medicine.
What HMG is used for
HMG appears under 2 goals in the goal router.
Related Hormonal & Sexual compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.