HCG

The HCG evidence base cited here is 5 sources — 2 clinical, 1 review, 1 regulatory. Its strongest evidence is human — 2 clinical studies, most recently 2019 ("Human Chorionic Gonadotropin Monotherapy for the Treatment of Hypogonada…"). Regulatory status: FDA-approved.

• HCG is a large (~37 kDa) glycoprotein hormone — the second big glycoprotein in this collection alongside follistatin — naturally produced by the placenta. It is a genuine FDA-approved drug for specific indications.
• It activates LH receptors: in men it stimulates testicular testosterone production (used to maintain testicular function and fertility during TRT and to treat hypogonadism/cryptorchidism); in women it triggers final oocyte maturation/ovulation.
• It has real clinical-trial backing across fertility and cryptorchidism uses — unlike most research peptides — though many bodybuilding/TRT-adjunct uses are off-label.

Human chorionic gonadotropin (HCG) is a glycoprotein hormone of pregnancy that mimics luteinizing hormone (LH). Pharmaceutically it is either urinary-derived (e.g. Pregnyl, Novarel) or recombinant (Ovidrel), and it is FDA-approved for hypogonadism, infertility, and cryptorchidism. In TRT practice it is widely used to keep the testes functioning while exogenous testosterone suppresses the natural signal.

It is a regulated hormone drug; everything below is research/clinical context, not medical guidance.

HCG is a heterodimeric glycoprotein (~36,700 Da) made of two non-covalently linked subunits: an alpha subunit identical to that of LH, FSH, and TSH, and a unique beta subunit that gives HCG its specific activity. The beta subunit carries a 24-amino-acid C-terminal extension not found in LH, and the molecule is heavily glycosylated (~30% carbohydrate), which extends its half-life and shapes receptor binding.

That heavy glycosylation also explains why urinary-derived and recombinant versions differ slightly — their glycosylation patterns aren't identical.

HCG binds and activates LH receptors. On testicular Leydig cells that drives testosterone (and some estrogen) biosynthesis — which is why it preserves testicular size and intratesticular testosterone (and therefore fertility) during testosterone-replacement therapy that would otherwise shut the testes down. In women it acts on ovarian theca cells to stimulate progesterone and triggers the final maturation and release of the egg, which is its role as an ovulation 'trigger shot'.

• Time to peak: ~6–12 hours after injection
• Half-life: ~24–36 hours (≈1.5 days initial)
• Bioavailability ~40–50% via subcutaneous or intramuscular routes; largely cleared within ~7 days

Approved indications have defined dosing; TRT-adjunct and PCT uses are off-label. Figures below are clinical/research context, not guidance.

• TRT adjunct: ~250–500 IU subcutaneously, 2–3× per week (often on days between testosterone injections)
• Hypogonadism monotherapy: ~1,500–2,000 IU IM, 2–3× per week (often with FSH for spermatogenesis)
• Cryptorchidism (pediatric): ~1,000–5,000 IU IM, 2–3× per week for 3–4 weeks (age-dependent)
• Ovulation trigger (female): single ~5,000–10,000 IU (or 250 mcg recombinant) when the lead follicle reaches ~18–20 mm
• PCT: ~1,000–1,500 IU every other day for 2–3 weeks

• Comes lyophilized with a provided diluent; inject diluent slowly down the vial wall, swirl gently (don't shake) until fully clear.
• Calculate concentration (e.g. 5,000 IU in 2 mL = 2,500 IU/mL) and label with date/concentration.
• Refrigerate at 2–8°C after reconstitution and use within ~30–60 days; maintain cold chain for recombinant product. Discard if cloudy, discolored, or particulate.

FDA-approved for specific indications — discuss off-label use with a physician. In men, HCG can cause or worsen gynecomastia by raising estrogen (often managed with an aromatase inhibitor), and high doses can push testosterone/estrogen too high (start low, titrate by labs). In women, ovarian hyperstimulation syndrome (OHSS) is a real risk. It is contraindicated in hormone-sensitive cancers (prostate, breast), can cause headaches/mood swings and fluid retention, may raise thromboembolism risk (caution with clot history), and carries a precocious-puberty risk if misused in children. Long-term use can prompt antibody formation that reduces efficacy.

• Spermatogenesis induction with HCG/FSH (2018 review): the combination induces spermatogenesis in ~70–90% of men with hypogonadotropic hypogonadism.
• Ovulation induction (2017 systematic review): HCG trigger achieves ~15–25% pregnancy per cycle in clomiphene/letrozole protocols, higher with gonadotropin stimulation.
• Cryptorchidism (2014 Cochrane meta-analysis, 1,231 boys): ~25% success for hormonal treatment; surgery is more effective, but HCG/GnRH may have a role in selected cases.

HCG is an FDA-approved prescription drug for hypogonadism, infertility, and cryptorchidism. Other uses (TRT adjunct, PCT, the 'HCG diet') are off-label or, in the case of HCG-for-weight-loss, not supported and previously the subject of FDA action against OTC homeopathic claims. It is also prohibited for male athletes under WADA (it can be used to stimulate endogenous testosterone).

All citations link to the original source (PubMed, journal site, or regulatory filing). Independent research database — no vendor influence on what's cited.