HCG

What HCG is and how it works

Human chorionic gonadotropin is a glycoprotein hormone made by the placenta. It is built from two subunits: an alpha subunit essentially identical to the alpha subunit of luteinizing hormone, follicle-stimulating hormone and thyroid-stimulating hormone, and a beta subunit whose amino acid sequence is its own. The approved urinary-derived product is obtained from human pregnancy urine and standardized by a biological assay, which is why its strengths are expressed in units rather than in milligrams.

It acts at the luteinizing hormone/chorionic gonadotropin receptor. In men that means stimulating the Leydig cells of the testis to produce androgen; in women it substitutes for the mid-cycle luteinizing hormone surge that triggers ovulation. That single mechanism is the reason one molecule turns up in fertility clinics, in paediatric endocrinology, and in discussions about testosterone therapy — and the reason none of those literatures transfers to any of the others.

Four boundaries decide what a given study can be read to say. The first is formulation. The urinary-derived hormone and recombinant choriogonadotropin alfa are separate licensed products with separate applications, separate routes and separate unit systems. A randomized crossover pharmacokinetic study in 26 healthy women, which gave 10,000 IU of a highly purified urinary product against 250 µg of the recombinant one and recorded that 250 µg corresponds to 6,500 IU, found half-lives that were very similar — 36.77 ± 5.11 hours against 38.63 ± 6.08 hours — but did not demonstrate bioequivalence: the upper 90% confidence limits for exposure were 130.21% and 128.51% against a 125% threshold, and peak concentration was about 50% higher for the urinary product. The authors, one an employee of the sponsor and two employed by the contract research organization the sponsor paid, argued the difference is not clinically relevant.^[18] The second boundary is luteinizing hormone itself, which acts at the same receptor but circulates with a far shorter half-life; no figure for it is quoted here because no primary source for one was checked. The third is menotropins and follicle-stimulating hormone, which are different biologics — in the male hypogonadism trials described below, FSH is added to hCG rather than substituted for it. The fourth is route: the approved labeling of the urinary product permits intramuscular use only, while a randomized study in 24 healthy young men given 5,000 IU by each route found the peak significantly delayed and the serum half-life significantly prolonged after subcutaneous injection, with testosterone, luteinizing hormone and follicle-stimulating hormone responses identical.^[19]

This page carries a "Human RCT evidence" stamp. That describes the tier of evidence that exists, not whether the compound does what a reader came here hoping. Randomized human trials exist in several of its claim areas, and in the area most readers arrive asking about — weight loss — they are uniformly negative.

What the research actually shows

The weight-loss literature is randomized, old, and negative. A criteria-based meta-analysis traced 8 controlled and 16 uncontrolled trials, scored them on study population, intervention, measurement and analysis, and found methodological scores from 16 to 73 out of 100. Of the 12 studies scoring 50 or more, exactly one reported the hormone a useful adjunct; the authors concluded that there is no scientific evidence that it is effective in the treatment of obesity, that it does not bring about weight loss or fat redistribution, and that it does not reduce hunger.^[1] The individual trials behind that hold up on their own. A 32-day randomized double-blind study in 51 women set out specifically to reproduce the earlier positive result that had made the idea popular, and found no significant difference between arms in number of injections received, weight loss, percent of weight loss, hip or waist circumference, weight loss per injection, or hunger ratings.^[2] An inpatient study removed diet adherence as an explanation altogether by admitting the participants: six hospitalized women on 500-calorie diets received 125 IU intramuscularly daily for 30 days and five received diluent, and mean weight loss, skinfold thickness and body measurements were not different between them.^[3] A 1990 randomized trial gave 40 women with a body mass index above 30 the same 5,000 kJ diet with daily injections six days a week for six weeks and reported no advantage on any variable recorded; a PubMed search on 1 September 2026 for ("chorionic gonadotropin"[tiab] OR hCG[tiab]) AND obesity[tiab] AND randomized controlled trial[pt] AND ("1991"[dp]:"2026"[dp]) returned 3 records, none of them a trial of this hormone for obesity, so that 1990 trial is the most recent one those searches located.^[4]

In assisted reproduction it works, and the trade-off is measurable in both directions. A Cochrane review of 17 randomized trials in 1,847 women compared triggering with a gonadotropin-releasing hormone agonist against hCG. The agonist was associated with a lower live birth rate (OR 0.47, 95% CI 0.31 to 0.70; five trials, 532 women, moderate-quality evidence) and with a lower rate of ovarian hyperstimulation syndrome (OR 0.15, 95% CI 0.05 to 0.47; eight trials, 989 women, moderate-quality evidence) — which the authors summarized as preventing the syndrome to the detriment of the live birth rate.^[6] A 2025 network meta-analysis of 12 randomized trials in 1,931 predicted healthy responders found no significant difference in clinical pregnancy between the two (RR 1.13, 95% CI 0.80 to 1.60). Its authors describe the syndrome as significantly less frequent with the agonist, but the interval they print for that comparison is RR 0.56, 95% CI 0.19 to 1.75, which crosses 1; the interval is reported here as printed.^[7] A separate meta-analysis locates the driver precisely: in high-risk women given no luteal phase support the pooled incidence of severe cases was 0% (95% CI 0.0 to 0.0; 983 women), and adding hCG back to standard luteal support brought it to 1% (95% CI 0.0 to 2.0; 707 women).^[9]

The trigger amount has been tested rather than assumed. A double-blinded randomized noninferiority trial in 105 women met its primary endpoint: an alternative 1,500 IU trigger given with 450 IU of follicle-stimulating hormone was noninferior to a standard 5,000 or 10,000 IU trigger for oocyte competence, with a relative risk of 0.91 against a prespecified 0.8 margin. Live birth per randomized participant was 48.1% against 62.7% (RR 0.73, 95% CI 0.48 to 1.11).^[8]

In male hypogonadotropic hypogonadism the published trials are open-label. A Phase III multicentre single-arm study pretreated 23 azoospermic men with the hormone alone for 16 weeks; the 18 whose testosterone normalized while they remained azoospermic entered a 52-week phase with a long-acting FSH analog added, after which mean testicular volume rose from 8.6 to 17.8 mL and 14 of them, 77.8%, reached a sperm count of at least 1 million per mL. Sixteen weeks of the hormone by itself normalized testosterone in that cohort without producing sperm. The author group includes employees of the sponsor.^[10] A prospective uncontrolled study in 14 adolescent males reported normal sexual maturation in all of them and sperm production in 4 of 5 and 3 of 3 patients assessed, on 1,000 to 1,500 IU intramuscularly with FSH every alternate day.^[11]

The testosterone-adjunct question rests on a randomized trial that measured a hormone rather than fertility. A PubMed search on 1 September 2026 for ("chorionic gonadotropin"[tiab] OR hCG[tiab]) AND "testosterone replacement"[tiab] AND randomized controlled trial[pt] returned zero records against 62 for the same query without the publication-type filter; the randomized study described next is titled and indexed under different terms. Twenty-nine men with normal reproductive physiology were given 200 mg of testosterone enanthate weekly with either saline or 125, 250 or 500 IU every other day for three weeks, and intratesticular testosterone was measured in testicular fluid obtained by percutaneous aspiration. In the placebo arm that concentration fell by 94%. It rose linearly with dose (P < 0.001), finishing 25% below baseline at 125 IU, 7% below at 250 IU and 26% above at 500 IU. The authors stated in the same paragraph that determining the intratesticular testosterone threshold required to maintain spermatogenesis in man would take a further study.^[12] The semen-parameter evidence is a retrospective chart review of 26 hypogonadal men given 500 IU intramuscularly every other day alongside testosterone therapy, with a mean follow-up of 6.2 months: no change in semen parameters, no patient becoming azoospermic, 9 of 26 contributing to a pregnancy, and an authors' conclusion phrased as "may preserve fertility".^[13] A retrospective series of 28 men switched to the hormone as monotherapy found no significant change in mean hormone levels including testosterone across the whole cohort and a significant fall in haematocrit in the 15 men with paired values.^[14]

In undescended testes the meta-analyses disagree. One restricted to seven randomized trials of low overall quality concluded the hormone is no more effective than placebo; its hCG-versus-placebo risk ratio of 7.74 carried a 95% CI of 0.14 to 425.72 across two trials and 31 boys, and no significant difference was found against gonadotropin-releasing hormone in either unilateral or bilateral disease.^[15] An earlier and much larger review of 33 publications covering 3,282 boys reported success in randomized trials of 19% (95% CI 13 to 25) against 4% (95% CI 2 to 6) for placebo, with the authors' own caveats that data about the effect are scanty and that nonrandomized trials overestimated it.^[16]

Where the evidence is weak

The use most readers arrive for is the one the searches behind this page found least evidence for. A PubMed search on 1 September 2026 for ("chorionic gonadotropin"[tiab] OR hCG[tiab]) AND "testosterone replacement"[tiab] AND randomized controlled trial[pt] returned zero records, while the same query without the publication-type filter returned 62 — the absence is of the study design, not of the topic. What exists is one 3-week randomized study in healthy volunteers measuring a hormone concentration inside the testis, whose own authors said it did not establish the concentration needed to sustain sperm production, plus two small retrospective series.^[12][13]

Nor is there long-term safety data for that use. A PubMed search on 1 September 2026 for ("chorionic gonadotropin"[tiab] OR hCG[tiab]) AND ("testosterone replacement"[tiab] OR "testosterone therapy"[tiab]) AND ("long-term"[tiab] OR safety[tiab]) AND (cohort studies[mh] OR randomized controlled trial[pt]) returned 3 records, none of which is a long-term safety study in this population, against 222 for the same query shape run against testosterone. One of the retrospective series says so in its own words: no data are available regarding the long-term efficacy and safety of monotherapy in men with a history of exogenous testosterone use.^[14]

Sexual-function outcomes were searched for and not found. A PubMed search on 1 September 2026 for ("chorionic gonadotropin"[tiab] OR hCG[tiab]) AND ("sexual desire"[tiab] OR libido[tiab] OR "erectile"[tiab]) AND randomized controlled trial[pt] returned zero records, while the same query shape run against testosterone on the same date returned 290 — so the absence is of trials of this hormone rather than of a working search. That is worth stating plainly on a page filed under sexual health: the reproductive-endocrine claims here are about hormone concentrations, ovulation and sperm counts, and none of them is a claim about desire.

The oral and sublingual products have no trial evidence the searches behind this page could find. A PubMed search on 1 September 2026 for ("oral hCG"[tiab] OR "sublingual hCG"[tiab] OR "homeopathic hCG"[tiab]) AND (trial[tiab] OR randomized[tiab]) returned zero records. What the same searches did return is a single case report of a serious event after sublingual use.^[5]

The negative weight-loss literature is genuinely old. A PubMed search on 1 September 2026 for ("chorionic gonadotropin"[tiab] OR hCG[tiab]) AND obesity[tiab] AND (systematic review[pt] OR meta-analysis[pt]) AND ("1996"[dp]:"2026"[dp]) returned 2 records, neither about this hormone and obesity, and a ClinicalTrials.gov query on the same date for obesity with chorionic gonadotropin as the intervention returned 6 studies, none of them an interventional trial for weight loss, against 330 for the same query shape with a currently-marketed weight-loss drug. Age is a fair criticism of that literature; it is not a reason to expect a different answer, and the trials that exist are consistent with each other.^[1]

Design and sponsorship limits run through the rest. The male hypogonadism trials are single-arm or uncontrolled and one is authored in part by the sponsor's employees;^[10] the pharmacokinetic comparison is authored by a sponsor employee and by staff of the contract research organization the sponsor paid;^[18] the inpatient obesity study is typed by PubMed as a controlled clinical trial rather than a randomized one and enrolled 11 women in total;^[3] and the cryptorchidism evidence is thin enough that one meta-analysis reported a confidence interval spanning three orders of magnitude.^[15]

One approved indication runs against current specialist consensus. A Nordic multidisciplinary consensus concluded that surgery is generally preferred to hormonal treatment for undescended testes, recorded that 15 to 20% of retained testes descend on hormones with one-fifth of those re-ascending, and stated that treatment may be harmful to future spermatogenesis through increased germ-cell apoptosis.^[17]

Legal and regulatory status

HCG is FDA-approved, and the approval is narrow in a way that matters more here than on almost any other page in this library. Every currently approved product is licensed under a biologics license application; there is no new drug application for chorionic gonadotropin in Drugs@FDA. Three urinary-derived injectable products were in prescription marketing status when Drugs@FDA was checked on 1 September 2026 — BLA 017067 held by Fresenius Kabi, original approval 5 March 1973; BLA 017016 held by Ferring, original approval 15 January 1974; and BLA 017692, PREGNYL, held by Organon, original approval 20 October 1976 — alongside BLA 021149, OVIDREL, held by EMD Serono, original approval 20 September 2000, which is choriogonadotropin alfa, a recombinant product supplied in a prefilled syringe for subcutaneous use only and indicated only for final follicular maturation and ovulation induction in women. Several other applications, including five abbreviated applications, are in discontinued status. A National Drug Code directory query on 1 September 2026 for records whose active-ingredient name is CHORIONIC GONADOTROPIN returned ten, and not one of them is a finished prescription product. Eight are registered as bulk ingredient, six of those explicitly as bulk ingredient for human prescription compounding; the other two are unapproved homeopathic over-the-counter oral products, and they are taken up under enforcement below. An ingredient registration is not an approval, and neither is a homeopathic listing. The other half of that result matters as much: the licensed injectables named above are in the same directory with their BLA numbers attached, and they fall outside this particular query for a listing reason rather than a regulatory one — every urinary-derived prescription product is listed as a kit, whose product record carries no active-ingredient entry of its own, and the recombinant product is listed under the ingredient name choriogonadotropin alfa. The count is a fact about one query, not a census of the molecule.

The approved indications, verbatim from current labeling, are three and only three: prepubertal cryptorchidism not due to anatomical obstruction; selected cases of hypogonadotropic hypogonadism, meaning hypogonadism secondary to a pituitary deficiency, in males; and induction of ovulation and pregnancy in the anovulatory, infertile woman in whom the cause of anovulation is secondary and not due to primary ovarian failure, and who has been appropriately pretreated with human menotropins. The route is stated in the labeling as intramuscular use only. Weight loss is not among the indications, and neither is anything to do with testosterone therapy in men who do not have hypogonadotropic hypogonadism.

The labeling says so itself, in capitals, and it is important to name the sections the text actually comes from. The first paragraph of INDICATIONS AND USAGE reads: "HCG HAS NOT BEEN DEMONSTRATED TO BE EFFECTIVE ADJUNCTIVE THERAPY IN THE TREATMENT OF OBESITY. THERE IS NO SUBSTANTIAL EVIDENCE THAT IT INCREASES WEIGHT LOSS BEYOND THAT RESULTING FROM CALORIC RESTRICTION, THAT IT CAUSES A MORE ATTRACTIVE OR ''NORMAL'' DISTRIBUTION OF FAT, OR THAT IT DECREASES THE HUNGER AND DISCOMFORT ASSOCIATED WITH CALORIE-RESTRICTED DIETS." The last sentence of CLINICAL PHARMACOLOGY reads: "HCG HAS NO KNOWN EFFECT ON FAT MOBILIZATION, APPETITE OR SENSE OF HUNGER, OR BODY FAT DISTRIBUTION." Neither statement is a boxed warning, and this page will not call it one. A boxed warning is a specific labeling artifact carried in its own coded section; the structured product label for the marketed urinary product, checked on 1 September 2026, contains no such section and the openFDA record for it carries no boxed-warning field, verified in the same session against a control product whose boxed-warning field is populated. The label's actual WARNINGS section is about co-administration with menotropins and names ovarian hyperstimulation, rupture of ovarian cysts with resultant hemoperitoneum, multiple births and arterial thromboembolism, plus anaphylaxis and other hypersensitivity reactions reported with urinary-derived products. Its contraindications are precocious puberty, prostatic carcinoma or other androgen-dependent neoplasm, and prior allergic reaction. No federal regulation is cited here as the source of the obesity statements: a search for one was run and returned nothing relevant, so the honest position is that the statements are labeling text and this page asserts nothing about their statutory basis.

Enforcement is a real and separate strand, and it was warning letters and litigation rather than recalls. An FDA consumer update, current as of 13 July 2020, advises consumers to avoid weight-loss products claiming to contain the hormone, states that it is not approved for use without a prescription for any purpose and is not approved for weight loss, and quotes the director of FDA's Office of Unapproved Drugs and Labeling Compliance saying that any loss is from severe calorie restriction, not from the HCG. A Federal Register notice of 13 March 2025 — an FDA final debarment order, and therefore the most current agency statement located — records verbatim that "FDA has not approved any HCG-containing products for weight loss, nor for any purpose without a prescription." The Federal Trade Commission brought a federal court action over health claims for oral weight-loss drops in the District of Arizona under civil action number 2:14-cv-00015-NVW. What could not be verified in this session is the individual set of joint FDA/FTC warning letters often described as accompanying that campaign: the agency page that carried them returned HTTP 404 on 1 September 2026, so their number and recipients are neither asserted nor denied here. Oral products of this kind remain registered, and they are the only finished products the ingredient query above returns at all. Both are over-the-counter oral preparations from a single labeler, one a spray and one a liquid, and the directory categorizes each as unapproved homeopathic — the drops-and-sprays category the consumer update is written about. Their labels, effective in July 2026, declare the hormone as an active ingredient at homeopathic dilutions between 8X and 60X, which are dilution factors of one part in a hundred million and one part in 10⁶⁰ respectively — that is the analytical reason such products are not comparable to an injected hormone, and it is a labeling fact rather than a dosing comparison. Their stated indications are labeling facts too, and both are weight-loss claims: one label reads "May help to release stored fat for consumption by the body", the other "Detox, appetite control, supports normal fat loss and normal muscle building when used in conjunction with the HCG program". Both listings carry a marketing end date of 31 August 2026 and were still returned by the directory on 1 September 2026; whether that reflects a withdrawal or a routine listing expiry is not something the record settles, and this page asserts neither. A published case report of a serious event after sublingual use notes that the marketed drops, lozenges and pellets have no evidence-based efficacy and safety standard behind them.^[5]

Compounding. Checked on 1 September 2026, chorionic gonadotropin does not appear anywhere in FDA's 503A bulk drug substance nomination category lists, in the document self-dated Updated May 14, 2026, nor in the 503B outsourcing facility bulks list self-dated Updated March 21, 2025, nor on FDA's separate page listing bulk drug substances used in compounding that may present significant safety risks, whose content is stamped current as of 22 April 2026 and which does name several other research peptides. Each of those three null results was run alongside in-document positive controls that returned hits.

Anti-doping. The 2026 World Anti-Doping Agency International Standard Prohibited List, in force from 1 January 2026, was retrieved on 1 September 2026 from the WADA-hosted document linked by the USADA prohibited-list page. Chorionic gonadotropin is named on it. Section S2, "PEPTIDE HORMONES, GROWTH FACTORS, RELATED SUBSTANCES, AND MIMETICS", is "PROHIBITED AT ALL TIMES (IN- AND OUT-OF-COMPETITION)" and states that "All prohibited substances in this class are non-Specified Substances". Within it, S2.2 covers peptide hormones and their releasing factors, and S2.2.1 is headed "Testosterone-stimulating peptides in males including, but not limited to:" and lists "chorionic gonadotrophin (CG)" as its first entry. The heading's scope clause — "in males" — is part of the entry and is transcribed here rather than paraphrased; the List spells the substance "gonadotrophin". It is not on the 2026 Monitoring Program, whose only entry on this axis reads "In and Out-of-Competition: Gonadotrophin-releasing hormone (GnRH) analogues in females under 18 years only", and monitoring is not prohibition in any case. The List is reissued annually, so the position above is dated rather than standing, and anyone in a tested sport checks the current year's document rather than this page.

PHL does not sell peptides, does not prescribe, and does not tell anyone where to obtain anything.

Questions to bring to a provider

The useful conversation depends entirely on which of this molecule's several unrelated uses is actually on the table, so it starts by naming that. Questions worth raising:

• If weight loss is the goal, what does it mean that the approved labeling itself says the hormone has not been demonstrated effective for obesity, and that the randomized trials behind that statement found no difference from placebo in weight, circumference or hunger?^[1][2]
• If the goal is preserving fertility while on testosterone therapy, what is the actual evidence base — a 3-week randomized study measuring a hormone concentration in healthy volunteers, and a retrospective review of 26 men — and what would count as an answer before starting?^[12][13]
• What semen analysis, testosterone, oestradiol and haematocrit monitoring would be in place, and at what intervals, given that the safety numbers this page could find in that population come from small uncontrolled series?^[14]
• Precocious puberty, prostatic carcinoma or another androgen-dependent neoplasm, and a prior allergic reaction are labeled contraindications. Where does the current history sit relative to those?
• In a fertility context, how is ovarian hyperstimulation risk being assessed, and what does the trigger choice trade off — given that substituting an agonist lowers that risk and also lowers the live birth rate?^[6]
• If the question concerns a child with an undescended testis, how does the treating team weigh an approved hormonal indication against a specialist consensus that prefers surgery and raises a germ-cell concern?^[17]
• Is the product under discussion the licensed urinary-derived injectable, the recombinant one, or an oral or sublingual preparation — and does everyone in the conversation know which, given that they are not the same thing?^[18]

A drug can be genuinely effective for three narrow reproductive purposes and genuinely useless for the thing most people have heard about it. Both halves of that sentence are supported by randomized evidence, and keeping them apart is most of what this page is for.