The placenta makes a hormone so similar to the pituitary’s luteinising hormone that both activate the same receptor on the ovary and testis. That overlap is why hCG is studied.
hCG · Placental LH-receptor glycoprotein hormone
The ovaries and testes are told to make their hormones by luteinising hormone from the pituitary. In pregnancy, the placenta sends its own version, hCG, which activates the same receptor for longer. Researchers and clinicians use that overlap to act directly on the gonads when the pituitary signal is absent or needs a timed push. The evidence is human, from decades of fertility medicine.
Human chorionic gonadotropin, hCG, is a glycoprotein hormone, a protein with attached sugar chains, rather than a short peptide. It has two subunits. The alpha subunit is shared with luteinising hormone (LH), follicle-stimulating hormone and thyroid-stimulating hormone; the beta subunit is specific to hCG and closely resembles the beta subunit of LH (Cole, 2010).
That resemblance is the mechanism. Both LH and hCG bind and activate the same receptor, the LH/CG receptor, on cells of the ovary and testis, which respond by making progesterone or testosterone (Ascoli et al., 2002). hCG carries more sugar chains and stays in the blood far longer than LH, so one exposure produces a prolonged signal. In pregnancy this keeps the corpus luteum making progesterone until the placenta takes over; it is also the molecule detected by pregnancy tests. hCG is produced either by purification from the urine of pregnant women or by recombinant DNA technology; the two are not identical in their sugar chains.
Because hCG acts directly on the gonads, it is used where the pituitary signal is missing or where a single timed surge is wanted. In assisted reproduction, an hCG injection substitutes for the natural LH surge to trigger final egg maturation before retrieval. A Cochrane review pooled randomised trials in women undergoing IVF or ICSI comparing recombinant with urinary hCG for this purpose, measuring live births, ongoing pregnancies and ovarian hyperstimulation, and found no clear difference between the two sources (Youssef et al., 2016). In men with hypogonadotropic hypogonadism, a lack of pituitary drive to the testes, hCG is used clinically to stimulate testosterone production and, with FSH, sperm production.
In Australia, hCG is a Schedule 4 prescription medicine, and registered hCG products are used for these fertility indications. The same testosterone-stimulating action is why hCG is prohibited in sport: the 2026 WADA Prohibited List places chorionic gonadotrophin under S2.2.1, testosterone-stimulating peptides in males, prohibited at all times, in and out of competition. The Cole review also surveys proposed non-reproductive actions of hCG and hCG-related molecules; these remain largely laboratory findings.
Urinary and recombinant hCG differ in their sugar chains and in the isoforms present, so identity matters when reading a study; the pooled fertility evidence found them comparable for egg-maturation triggering, but that finding is specific to that use. Clinical evidence concerns registered products used under specialist supervision in defined fertility settings and does not transfer to other purposes or to non-registered material. Proposed roles of hCG variants outside reproduction come mainly from cell studies. Prolonged LH receptor stimulation also has known consequences, including ovarian hyperstimulation in women and suppression of the pituitary signal in men, which the fertility literature documents rather than ignores.
Human chorionic gonadotrophin is listed in Schedule 4 (prescription only) of the Australian Poisons Standard (June 2026), except in pregnancy test kits, and registered hCG medicines are used in Australian fertility care; the material supplied by Pulse is not a registered medicine. In sport, chorionic gonadotrophin is prohibited at all times, in and out of competition, under S2.2.1 of the 2026 WADA Prohibited List (testosterone-stimulating peptides in males).
Sources and status checked 2026-09-22
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