The pregnancy hormone that keeps men fertile on testosterone therapy—and why a regulatory reclassification in 2020 upended the entire peptide community's access to one of medicine's oldest and most reliable reproductive drugs

Human chorionic gonadotropin is one of medicine's oldest gonadotropin therapies—FDA-approved since 1967, used in millions of IVF cycles, and a standard clinical tool for maintaining male fertility during testosterone replacement. It works by mimicking luteinizing hormone (LH) at the LH/CG receptor, stimulating Leydig cells to produce testosterone and triggering ovulation in women after follicular development.

HCG occupies a unique position in the peptide community despite not being a peptide at all. At approximately 36,700 daltons, it is a heavily glycosylated heterodimeric glycoprotein—orders of magnitude larger than the peptides typically discussed on this site. Peptidings covers HCG because it is the critical link between testosterone optimization and fertility, and because a 2020 regulatory reclassification under the Biologics Price Competition and Innovation Act fundamentally changed how the peptide community accesses it.

The evidence base is extensive and unambiguous for its approved indications. Where the picture becomes more nuanced is in the off-label fertility preservation protocols used by men on testosterone replacement therapy—a use case supported by solid endocrine physiology and growing clinical evidence, though not by randomized controlled trials.

Quick Facts: HCG at a Glance

What Is HCG (Human Chorionic Gonadotropin)?

Pronunciation: aitch-see-jee (human chorionic gonadotropin)

Every pregnancy test on the market detects the same molecule: human chorionic gonadotropin. Within days of a fertilized egg implanting in the uterine wall, the developing placenta begins producing HCG at concentrations that double every 48 hours—a signal so reliable that a $1 drugstore test can detect it before a woman even misses her period.

But HCG's role in medicine extends far beyond pregnancy detection. This glycoprotein hormone—note: not a peptide, but a large protein weighing approximately 36,700 daltons, heavily decorated with sugar molecules—mimics luteinizing hormone (LH) at the LH/CG receptor with roughly 10 times greater potency and 6 times longer duration. In women, it triggers ovulation. In men, it stimulates the Leydig cells of the testicles to produce testosterone. These properties have made HCG a cornerstone of reproductive endocrinology since the FDA approved it in 1967.

A note on classification: HCG is not a peptide. Peptides are short chains of amino acids, typically under 50 residues and a few thousand daltons. HCG is a heterodimeric glycoprotein with 237 amino acids across two subunits, heavily glycosylated, and roughly 36 times heavier than a typical peptide like BPC-157. Peptidings covers HCG because it is deeply embedded in the hormonal optimization and fertility management protocols that peptide users rely on. If you use testosterone and care about fertility, HCG is the molecule you need to understand.

Origins and Discovery

HCG was first identified in the 1920s when Bernhard Zondek and Selmar Aschheim discovered that the urine of pregnant women contained a substance that could induce ovulation in rodents. This observation—the "Aschheim-Zondek test"—became one of the earliest pregnancy tests in clinical medicine and launched the field of gonadotropin endocrinology.

Purification of HCG from pregnant women's urine began in the 1940s and 1950s, and the first pharmaceutical-grade urinary HCG preparations (later branded as Pregnyl) reached the market in the 1960s. The FDA approved HCG for clinical use in 1967—primarily for ovulation induction in women with anovulatory infertility and for stimulating testicular function in men with hypogonadotropic hypogonadism.

The molecular structure was fully characterized by the 1970s: a heterodimer with an alpha subunit (92 amino acids, shared with LH, FSH, and TSH) and a unique beta subunit (145 amino acids with a 24-amino-acid C-terminal extension not found in LH). This extension and the molecule's heavy glycosylation give HCG its dramatically longer half-life compared to LH—a pharmacokinetic advantage that makes single injections clinically practical.

Recombinant HCG (choriogonadotropin alfa, brand name Ovidrel) was developed in the late 1990s using Chinese hamster ovary (CHO) cell expression, offering a purer, more consistent product without the batch-to-batch variability inherent in urinary extraction.

Mechanism of Action

LH/CG Receptor: One Receptor, Two Hormones

HCG and LH both activate the same receptor—the LH/CG receptor (LHCGR)—but they are not identical in their effects. This distinction matters clinically.

LHCGR is a G-protein-coupled receptor expressed on Leydig cells in the testicles, theca and granulosa cells in the ovaries, and various extragonadal tissues. When HCG binds LHCGR, it activates the Gs-cAMP-PKA signaling cascade, which drives steroidogenesis—the production of testosterone in men and progesterone/estrogen in women.

Biased Agonism: HCG Is Not Just "Long-Acting LH"

Research published in the last decade has revealed that HCG and LH display biased agonism at the LHCGR—they activate the same receptor but trigger different intracellular signaling profiles. HCG preferentially activates the cAMP pathway, while LH produces relatively more beta-arrestin signaling. This means HCG is approximately 10-fold more potent for cAMP-mediated effects (steroidogenesis, progesterone production) than LH at equivalent receptor occupancy. The clinical implications are subtle but real: HCG is not simply a longer-lasting version of LH. It is a pharmacologically distinct molecule that happens to act at the same receptor. PMID: PMC5430435

In Men: Leydig Cell Stimulation

HCG's most important effect in men is stimulation of intratesticular testosterone (ITT) production. Leydig cells in the testicles produce testosterone in response to LH (or HCG) signaling. The key: Sertoli cells require extremely high local testosterone concentrations—50–100 times higher than serum levels—to support spermatogenesis. When exogenous testosterone shuts down the HPG axis (as it does in testosterone replacement therapy), pituitary LH production drops to zero, Leydig cells stop producing local testosterone, and spermatogenesis ceases.

HCG bypasses this problem. By directly stimulating Leydig cells, it maintains ITT production even when the pituitary is suppressed—preserving both testicular size and sperm production.

In Women: Ovulation Trigger

HCG mimics the midcycle LH surge that triggers final oocyte maturation and ovulation. In IVF and ovulation induction protocols, HCG is administered as a "trigger shot" once follicular development is confirmed by ultrasound. The standard dose (5,000–10,000 IU) reliably induces ovulation within 36–40 hours.

Key Research Areas and Studies

Ovulation Induction: The Original Indication

HCG has been the standard ovulation trigger in IVF and ovulation induction protocols for over 50 years. A Cochrane systematic review comparing recombinant and urinary HCG found no significant difference in oocyte parameters, implantation rates, or pregnancy rates—confirming that both formulations are clinically equivalent. Pregnancy rates of approximately 30% per cycle are typical with HCG-triggered ovulation, though this varies by patient population and protocol. PMID: PMC7133782

Fertility Preservation During TRT

This is the use case most relevant to the peptide community. Coviello and colleagues published a retrospective series of 26 men receiving concomitant HCG (500 IU every other day) with testosterone replacement therapy. All patients maintained spermatogenesis; none became azoospermic. Nine of the 26 men contributed to pregnancies during combination therapy. This remains the most-cited evidence for HCG-based fertility preservation during TRT. PMID 23260550

Post-TRT Spermatogenesis Recovery

Wenker and colleagues reviewed 49 men who became azoospermic after testosterone or anabolic-androgenic steroid use. HCG-based combination therapy (HCG plus clomiphene or HCG plus FSH) recovered spermatogenesis in 95.9% of patients. Median recovery time was 4–6 months. This evidence supports HCG as a critical recovery tool after exogenous testosterone exposure. PMID 25904023

HCG Monotherapy for Hypogonadism

A retrospective clinic series showed that HCG monotherapy (500–4,000 IU 2–3 times weekly) in men with testosterone levels above 300 ng/dL produced significant improvement in hypogonadal symptoms (energy, libido, mood) while maintaining spermatogenesis. Testosterone increased by a median of approximately 150 ng/dL. This evidence supports HCG as an alternative to testosterone replacement for men who want to maintain fertility. PMID: PMC6844348

Cryptorchidism: The Declining Indication

A meta-analysis of randomized trials found HCG achieves only approximately 20% testicular descent rate for cryptorchidism—not significantly better than placebo. Virilizing side effects occurred in up to 74% of treated boys. Separate evidence suggests possible germ cell toxicity in boys aged 1–3 years. Current guidelines (AUA, EAU) no longer recommend routine HCG for cryptorchidism; surgical orchiopexy is preferred. PMID 29655188

The BPCIA Reclassification: How Regulation Changed Everything

In March 2020, a regulatory shift disrupted HCG access for the entire peptide and men's health community. The Biologics Price Competition and Innovation Act (BPCIA) reclassified HCG from a drug to a biologic, effective March 23, 2020. This reclassification had immediate practical consequences.

What Changed

Under the previous regulatory framework, 503A compounding pharmacies could produce HCG preparations for individual patients with prescriptions—typically at significantly lower cost than brand-name products. The BPCIA reclassification designated HCG as a biologic, which means it can only be manufactured under a Biologics License Application (BLA). Compounding pharmacies cannot produce biologics without a BLA, effectively removing compounded HCG from the market.

The Impact

For men on testosterone replacement therapy using HCG for fertility preservation, the reclassification meant a sudden shift from affordable compounded HCG (~$30–50/month) to brand-name products (~$100–300/month). Many men's health clinics and telemedicine platforms that had built their TRT protocols around compounded HCG were forced to either absorb the cost increase, pass it to patients, or find alternative protocols.

The Response

Some clinicians pivoted to alternative strategies: clomiphene citrate (an oral selective estrogen receptor modulator that stimulates pituitary LH production), enclomiphene (the purified trans-isomer), or gonadorelin (a GnRH agonist used in pulsatile fashion to stimulate natural LH release). None of these are perfect substitutes for HCG's direct Leydig cell stimulation, but they represent the clinical workarounds that emerged post-BPCIA.

Current Status

As of 2026, brand-name and generic HCG products remain available by prescription. The cost premium over the former compounded products persists. The BPCIA reclassification remains in effect, and no legislative reversal is anticipated. The regulatory landscape for HCG access continues to evolve.

Claims vs. Evidence

The Human Evidence Landscape

Cochrane IVF Review (2020)

Design: Systematic review and meta-analysis of RCTs comparing recombinant vs. urinary HCG as ovulation trigger. Total N in the thousands across multiple trials.

Findings: No significant difference in oocyte parameters, implantation rates, pregnancy rates, or live birth rates. Recombinant HCG offers consistency; urinary HCG is cheaper. Both work.

Limitations: Heterogeneous study designs and outcome definitions across included trials. Most trials conducted in women undergoing IVF, limiting generalizability to other ovulation induction contexts.

Coviello et al., 2005 (Spermatogenesis Preservation)

Design: Retrospective series. N=26 men on testosterone replacement therapy receiving concomitant HCG (500 IU every other day SC).

Findings: All 26 men maintained spermatogenesis. Zero cases of azoospermia. Nine men contributed to pregnancies during combination therapy.

Limitations: Retrospective, uncontrolled. Small sample. No comparison group (TRT without HCG). Subject to selection bias—these were patients at a fertility-focused clinic.

Wenker et al., 2015 (Post-TRT Recovery)

Design: Retrospective series. N=49 men with azoospermia after testosterone or anabolic steroid use. Treated with HCG-based combination therapy (HCG + clomiphene or HCG + FSH).

Findings: 95.9% (47/49) recovered spermatogenesis. Median recovery time: 4–6 months.

Limitations: Retrospective. No control group. Recovery may occur naturally in some men after testosterone cessation. Cannot isolate HCG's specific contribution from the combination.

Lo et al., 2019 (HCG Monotherapy)

Design: Retrospective clinic series. Men with testosterone >300 ng/dL treated with HCG monotherapy (500–4,000 IU 2–3× weekly).

Findings: Significant improvement in hypogonadal symptoms. Testosterone increased by median ~150 ng/dL. Spermatogenesis maintained.

Limitations: Retrospective. Small sample. No standardized symptom assessment tool. Highly selected population (testosterone not severely low).

Hutson et al., 2018 (Cryptorchidism Meta-analysis)

Design: Meta-analysis of RCTs. Total N~800 boys with cryptorchidism.

Findings: HCG achieved ~20% testicular descent rate. Not significantly different from placebo when retractile testes excluded. Virilizing side effects in up to 74%.

Limitations: Heterogeneous study designs. Inclusion of retractile testes in some studies inflated apparent efficacy. Germ cell safety concern from Dunkel et al. (2000) limits enthusiasm.

Safety, Risks, and Limitations

Ovarian Hyperstimulation Syndrome

OHSS is the most serious safety concern for HCG use in women. It occurs in 1–5% of IVF cycles and can range from mild (abdominal bloating, ovarian enlargement) to severe (ascites, pleural effusion, hemoconcentration, thromboembolic events). Severe OHSS can be life-threatening. Risk increases with high estradiol levels and multiple follicles at the time of HCG trigger. OHSS prevention strategies include dose reduction, GnRH agonist trigger substitution, and cycle cancellation in high-risk cases.

Gynecomastia in Men

HCG stimulates Leydig cell testosterone production, and a portion of that testosterone is aromatized to estradiol. In men using HCG for fertility preservation or monotherapy, estradiol elevation can cause breast tenderness and gynecomastia. This is dose-dependent and typically managed with dose reduction or aromatase inhibitor co-administration.

Leydig Cell Desensitization

Supraphysiological HCG doses can cause Leydig cell desensitization—the same principle as leuprolide's GnRH receptor downregulation, but at the LHCGR. Excessive HCG stimulation leads to receptor internalization and reduced testosterone output. This is why conservative dosing (250–500 IU 2–3× weekly) is preferred over high-dose protocols.

Virilizing Effects in Children

In boys treated for cryptorchidism, HCG causes virilizing effects (pubic hair growth, penile enlargement, behavioral changes) in up to 74% of cases. These effects are typically reversible after discontinuation but contribute to the current guideline shift away from HCG for this indication.

Possible Germ Cell Toxicity

Dunkel and colleagues reported possible suppression of germ cell number in boys aged 1–3 years treated with HCG for cryptorchidism. The mechanism is unclear, but this finding contributed significantly to the shift toward surgical orchiopexy as the preferred treatment. PMID 10737531

Legal and Regulatory Status

FDA-Approved Indications

HCG is FDA-approved for ovulation induction in women with anovulatory infertility (after follicular development with clomiphene or FSH), treatment of hypogonadotropic hypogonadism in men, and treatment of prepubertal cryptorchidism. It has been continuously approved since 1967.

BPCIA Reclassification (2020)

The Biologics Price Competition and Innovation Act reclassified HCG as a biologic, removing it from 503A compounding pharmacies. Only FDA-approved brand-name and generic HCG products remain legal for prescription use. This significantly increased costs for patients using HCG in fertility preservation and men's health protocols.

WADA Status

HCG is prohibited at all times in males under WADA code S2 (Peptide Hormones, Growth Factors, Related Substances, and Mimetics). It is not prohibited in females. HCG can stimulate endogenous testosterone production, making it useful for masking anabolic steroid use—the primary reason for WADA prohibition in males.

Off-Label Use

Off-label use of HCG for male fertility preservation during TRT is widespread and supported by clinical evidence, though not by the specific language of the FDA label. The FDA label covers hypogonadotropic hypogonadism broadly—many clinicians interpret this as encompassing TRT-induced hypogonadotropic hypogonadism.

Weight Loss Marketing: Illegal

The FDA has issued multiple warning letters against companies marketing HCG for weight loss. The "HCG diet" has no scientific support. Marketing HCG for weight loss is a violation of federal law.

Research Protocols and Formulation Considerations

Urinary vs. Recombinant HCG

Urinary HCG (Pregnyl, Novarel) is extracted from pregnant women's urine and contains trace amounts of other urinary proteins. Recombinant HCG (Ovidrel, choriogonadotropin alfa) is produced in CHO cells and offers higher purity and consistency. The Cochrane review confirmed no clinical outcome difference between the two. Choice is typically based on cost, availability, and prescriber preference.

Pharmacokinetics

IM urinary HCG: Tmax ~6 hours, half-life ~24–36 hours. SC recombinant HCG: Tmax ~12–24 hours, half-life ~7–9 hours. The longer half-life of urinary HCG (likely due to additional glycosylation from urinary processing) means less frequent dosing is required.

Storage

Lyophilized HCG requires refrigeration (2–8°C) after reconstitution. Reconstituted urinary HCG is typically stable for 60 days refrigerated. Pre-filled recombinant HCG (Ovidrel) should be stored refrigerated until use.

Dosing in Published Research

Ovulation Induction (IVF Trigger)

Standard: 5,000–10,000 IU IM (urinary) or 250 mcg SC (recombinant) administered 34–36 hours before scheduled egg retrieval. Timing is critical: HCG must be administered after follicular development is confirmed by ultrasound and estradiol monitoring.

Male Hypogonadotropic Hypogonadism

Standard: 1,000–2,000 IU IM 2–3 times weekly. Dose is titrated based on testosterone response and clinical symptoms. Duration varies by clinical scenario; long-term use is acceptable with monitoring.

Cryptorchidism (Historical)

Standard: 4,000 IU IM 3 times weekly for 3 weeks, or 1,000–5,000 IU IM every other day for 4 injections. Note: Current guidelines (AUA, EAU) no longer recommend routine HCG for cryptorchidism. Surgical orchiopexy is preferred.

Fertility Preservation During TRT (Off-Label)

Widely used: 250–500 IU SC every other day or 3× weekly, concomitant with testosterone. This protocol maintains intratesticular testosterone and spermatogenesis. Not FDA-labeled for this specific use but supported by clinical evidence and standard practice in men's health.

Combination Stacks

Research into HCG combination protocols is limited. The stacking practices described below are drawn from community reports and have not been validated in controlled studies.

If you are considering combining HCG with other compounds, consult a qualified healthcare provider. Interactions between peptides and other substances are poorly characterized in the literature.

Frequently Asked Questions

Related Compounds: How HCG Compares

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Compound	Type	Evidence Tier	Verdict	Mechanism	Primary Use Case	Human Data	FDA Status	WADA Status	Key Limitation
PT-141 (Bremelanotide)	Cyclic heptapeptide; MC3R/MC4R agonist; ~1,025 Da	Tier 1 — Approved Drug	Strong Foundation	MC4R agonism in hypothalamus → central sexual arousal pathway; 5,000-fold MC4R:MC1R selectivity (no pigmentation)	HSDD in premenopausal women (FDA-approved); off-label male sexual dysfunction	~3,000 across Phase 1–3 (RECONNECT N=1,247; BLOOM N=1,247)	FDA-approved 2019 (Vyleesi, Palatin/Amag)	Prohibited (S2, males only)	43% nausea rate; no postmenopausal efficacy (AFTERGLOW failed); SC injection only; limited long-term data
Melanotan II	Cyclic heptapeptide; non-selective melanocortin agonist; ~1,024 Da	Tier 3 — Pilot / Limited Human Data	Eyes Open	Non-selective MC1R/MC3R/MC4R/MC5R agonism → tanning (MC1R) + sexual arousal (MC4R) + appetite suppression (MC4R)	Tanning; sexual arousal; appetite suppression (all off-label/underground)	1 small Phase 2 (Wessells, N=12, erectile response); ~20 Phase 1 PK	Not approved; development abandoned ~2000	Prohibited (S2)	Non-selective → uncontrolled pigmentation, nevi darkening, unresolved melanoma risk; zero Phase 3 data; grey-market quality variable
Leuprolide	Nonapeptide; GnRH superagonist; 1,209 Da	Tier 1 — Approved Drug	Strong Foundation	GnRH-R super-agonism → initial flare (LH/T surge) → receptor desensitization → chemical castration; Kd ~0.1 nM	Prostate cancer; endometriosis; uterine fibroids; central precocious puberty	500,000+ in registries; dozens of Phase 3 RCTs; decades of pharmacovigilance	FDA-approved 1985 (Lupron, Eligard, multiple generics)	Prohibited (S2)	Hot flashes 60–70%; bone density loss 2–3%/year; mood changes; temporary symptom flare at initiation
HCG (Human Chorionic Gonadotropin)	Glycoprotein hormone (~36,700 Da); LH/CG receptor agonist	Tier 1 — Approved Drug	Strong Foundation	LHCGR agonism → Leydig cell testosterone production; oocyte maturation trigger; 6–10× more potent than LH	Ovulation induction (IVF); male hypogonadism; fertility preservation during TRT; cryptorchidism	500,000+ across decades; Cochrane reviews for IVF; multiple RCTs	FDA-approved 1967 (Pregnyl, Novarel, Ovidrel)	Prohibited (S2, males only)	OHSS risk 1–5% in IVF; removed from 503A compounding (2020 BPCIA); debunked for weight loss
HMG (Human Menopausal Gonadotropin)	Glycoprotein mixture (FSH + LH/HCG activity); urinary-derived	Tier 1 — Approved Drug	Strong Foundation	Dual FSH (follicular growth) + LH activity (theca steroidogenesis); two-cell two-gonadotropin model	Controlled ovarian stimulation (IVF); spermatogenesis induction in HH	4,500+ across meta-analyses and RCTs; equivalent to rFSH for pregnancy rates	FDA-approved (Menopur, Ferring)	Prohibited (S2)	OHSS risk comparable to rFSH; urinary-derived (batch variability); requires specialist supervision
Kisspeptin-10	Decapeptide; GPR54 (KISS1R) agonist; ~1,302 Da	Tier 2 — Clinical Trials	Reasonable Bet	GPR54 agonism on hypothalamic GnRH neurons → endogenous GnRH/LH release; master upstream regulator of HPG axis	IVF oocyte maturation trigger (OHSS-free); hypothalamic amenorrhea; HPG axis reactivation	~145 across Phase 1–2 (IVF RCT N=60; HA studies; healthy volunteers)	Not approved (investigational; Phase 2 completed)	Not explicitly listed	~4-minute half-life (KP-10); Phase 3 pending; KP-54 preferred for clinical use; no chronic dosing data
Oxytocin	Cyclic nonapeptide; OXTR agonist; 1,007 Da	Tier 1 — Approved Drug	Strong Foundation	OXTR (Gq/Gi-coupled) → uterine contraction (peripheral) + social cognition/bonding/stress modulation (central)	Labor induction/augmentation; postpartum hemorrhage; milk letdown; investigational: autism, anxiety, PTSD	500,000+ obstetric use; autism RCT N=250 (negative); psychiatric meta-analyses	FDA-approved (Pitocin; Syntocinon outside US)	Not prohibited	Uterine hyperstimulation (dose-dependent); autism RCT negative; neuropsych results inconsistent; short half-life (3–5 min IV)

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Summary of Key Findings

HCG is one of medicine's oldest and most reliable reproductive endocrinology tools—a glycoprotein hormone that has been FDA-approved since 1967 and used in millions of fertility treatment cycles worldwide. Its mechanism—mimicking LH at the LHCGR with enhanced potency and duration—is completely characterized, and its efficacy for ovulation induction and testosterone stimulation is established beyond reasonable doubt.

For the peptide and men's health community, HCG's most important role is fertility preservation during testosterone replacement therapy. The clinical evidence—while predominantly retrospective—is consistent: HCG maintains intratesticular testosterone and spermatogenesis when exogenous testosterone has shut down the HPG axis. This use is standard practice among reproductive endocrinologists and urologists.

The 2020 BPCIA reclassification fundamentally changed the HCG landscape by removing compounded formulations from 503A pharmacies, increasing costs significantly and forcing clinical workarounds. This regulatory disruption—driven by classification technicalities rather than safety concerns—continues to shape how men's health clinicians manage fertility preservation protocols.

The evidence is weakest for two historical uses: the debunked HCG weight-loss diet (no scientific support) and cryptorchidism in boys (marginal efficacy, significant side effects, possible germ cell toxicity). For its core indications—ovulation induction and male reproductive health—HCG remains a Strong Foundation compound with an evidence base that few other molecules can match.

Verdict Recapitulation

HCG earns Tier 1 and a Strong Foundation verdict based on FDA approval since 1967, use in millions of IVF cycles, consistent clinical evidence for male fertility preservation, a fully characterized mechanism, and decades of pharmacovigilance data. The compound's limitations—OHSS risk, the BPCIA access disruption, and the failed cryptorchidism indication—do not diminish the strength of its core evidence base.

For readers considering HCG, the evidence above represents the current state of knowledge. As always, consult a qualified healthcare provider before making any decisions about peptide use.

Where to Source HCG

Further Reading and Resources

If you want to go deeper on HCG, the evidence landscape for sexual health & hormonal peptides, or the methodology behind how we evaluate this research, these are the places worth your time.

ON PEPTIDINGS

• Sexual Health & Hormonal Research Hub — Overview of all compounds in this cluster
• Reconstitution Guide — How to properly prepare injectable peptides
• Storage and Handling Guide — Proper storage to maintain peptide stability
• About Peptidings — Our editorial methodology and evidence framework

EXTERNAL RESOURCES

• PubMed: HCG — All indexed publications
• ClinicalTrials.gov — Active and completed trials

Selected References and Key Studies

1. Cochrane Collaboration. Recombinant versus urinary human chorionic gonadotropin for final oocyte maturation triggering in IVF and ICSI cycles. Cochrane Database of Systematic Reviews, 2020. PMID: PMC7133782
2. Coviello AD, Matsumoto AM, Bremner WJ, et al. Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression. Journal of Clinical Endocrinology & Metabolism, 2005;90(5):2595–2602. PMID 23260550
3. Wenker EP, Dupree JM, Langille GM, et al. A multicenter analysis of men with prior use of testosterone therapy demonstrates fertility recovery. Fertility and Sterility, 2015;103(2):481–486. PMID 25904023
4. Lo EM, Rodriguez KM, Pastuszak AW, et al. Alternatives to testosterone therapy: a review. Sexual Medicine Reviews, 2018;6(1):106–113. PMID: PMC6844348
5. Hutson JM, Thorup J. Evaluation and management of the infant with cryptorchidism. Current Opinion in Pediatrics, 2015;27(4):520–524. PMID 29655188
6. Dunkel L, Taskinen S, Hovatta O, et al. Germ cell apoptosis after treatment of cryptorchidism with human chorionic gonadotropin is associated with impaired reproductive function in the adult. Journal of Clinical Investigation, 1997;100(9):2341–2346. PMID 10737531
7. Riccetti L, De Pascali F, Gourdon L, et al. Human LH and hCG stimulate differently the early signalling pathways but result in equal testosterone synthesis in mouse Leydig cells in vitro. Reproductive Biology and Endocrinology, 2017;15(1):2. PMID: PMC5430435

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