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Peptide Database

Reference entry

HCG (Human Chorionic Gonadotropin)

Human Chorionic Gonadotropin · LH Receptor Agonist

Overview

HCG is a glycoprotein hormone naturally produced by the placenta during pregnancy that binds LH receptors to stimulate testosterone and estrogen biosynthesis. FDA-approved for cryptorchidism, hypogonadotropic hypogonadism, and ovulation induction.

Binds to LH receptors on Leydig cells in testes, stimulating testosterone production with a half-life of 24-36 hours, peak levels 6-12 hours post-injection, and 40-50% bioavailability via SubQ or IM routes.

Maintains intratesticular testosterone at baseline during testosterone therapy, preventing atrophy and preserving fertility.

FDA-approved for secondary hypogonadism; combined with FSH for spermatogenesis induction.

Restores testicular function after anabolic steroid cycles.

FDA-approved trigger for follicular maturation; 15-25% pregnancy rate per cycle.

Mechanism

HCG is a glycoprotein hormone naturally produced by the placenta during pregnancy that binds LH receptors to stimulate testosterone and estrogen biosynthesis. FDA-approved for cryptorchidism, hypogonadotropic hypogonadism, and ovulation induction.

Binds to LH receptors on Leydig cells in testes, stimulating testosterone production with a half-life of 24-36 hours, peak levels 6-12 hours post-injection, and 40-50% bioavailability via SubQ or IM routes.

Maintains intratesticular testosterone at baseline during testosterone therapy, preventing atrophy and preserving fertility.

Research areas

  • HCG is a glycoprotein hormone naturally produced by the placenta during pregnancy that binds LH receptors to stimulate testosterone and estrogen biosynthesis. FDA-approved for cryptorchidism, hypogonadotropic hypogonadism, and ovulation induction.
  • Binds to LH receptors on Leydig cells in testes, stimulating testosterone production with a half-life of 24-36 hours, peak levels 6-12 hours post-injection, and 40-50% bioavailability via SubQ or IM routes.
  • Maintains intratesticular testosterone at baseline during testosterone therapy, preventing atrophy and preserving fertility.
  • FDA-approved for secondary hypogonadism; combined with FSH for spermatogenesis induction.
  • Restores testicular function after anabolic steroid cycles.
  • FDA-approved trigger for follicular maturation; 15-25% pregnancy rate per cycle.
  • FDA-approved for prepubertal undescended testes not due to anatomical obstruction; ~25% success rate.

Research notes

  • Gynecomastia (breast tenderness/swelling) due to increased estrogen
  • Headaches, irritability, and mood swings (especially initially)
  • Fluid retention and edema
  • Potential antibody formation with long-term use
  • Signs of gynecomastia (breast tenderness, swelling, nipple sensitivity)
  • Severe or persistent headaches
  • Signs of blood clots (leg swelling/pain, shortness of breath, chest pain)
  • Allergic reactions (rash, hives, difficulty breathing, facial swelling)
  • Severe abdominal pain or bloating in women (possible OHSS)
  • Testicular pain or swelling beyond normal
  • Significant mood changes (depression, aggression, severe irritability)
  • Vision changes
  • Hormone-sensitive cancers (prostate, breast)
  • Pregnancy (except as prescribed)
  • Precocious puberty risk in children
  • Potential antibody formation to HCG with extended use is a theoretical concern, though clinical significance remains unclear. Some users report diminishing HCG effectiveness after months of continuous use. Cycling HCG with breaks or rotation to GnRH analogs may prevent tolerance development.

Pharmacokinetics

  • Binds to LH receptors on Leydig cells in testes, stimulating testosterone production with a half-life of 24-36 hours, peak levels 6-12 hours post-injection, and 40-50% bioavailability via SubQ or IM routes.

References

FAQs

How much HCG is needed to maintain fertility during testosterone replacement therapy?

A landmark clinical study found 250 IU of HCG every other day maintained intratesticular testosterone within 7% of baseline during testosterone therapy, preserving fertility. This low dose is far less than other protocols suggesting HCG is remarkably potent—even minimal doses maintain testicular function when properly timed.

Why does HCG cause gynecomastia if it just stimulates testosterone?

HCG stimulates testosterone production, but testes also express aromatase enzyme that converts testosterone to estrogen. The increased testosterone availability combined with enhanced intratesticular aromatase activity results in elevated estrogen, causing breast tenderness and gynecomastia. Aromatase inhibitors help prevent this side effect.

What's the success rate of HCG for treating cryptorchidism (undescended testes)?

Meta-analysis of HCG in cryptorchidism shows approximately 24% success rate—modest but clinically relevant for select cases. Success is higher for bilateral versus unilateral cryptorchidism. This low success rate led to surgery becoming the standard treatment for most cases, though HCG remains an initial option.