hCG: Fertility, Testosterone Support, and How This Glycoprotein Hormone Works

This article is for informational purposes only and does not constitute medical advice. Superpower Health facilitates access to hCG through licensed healthcare providers and pharmacy partners. Always consult a qualified healthcare provider before starting any prescription medication.

Testosterone replacement therapy is widely prescribed for low-T symptoms. It also suppresses the pituitary signals that tell the testes to produce testosterone — and, critically, sperm. For men who want to preserve fertility, maintain testicular size, or eventually restore endogenous production, that suppression is the central problem. hCG addresses it by mimicking the signal that TRT removes.

Human chorionic gonadotropin (hCG) is a glycoprotein hormone with a different purpose in women: it is the hormone of early pregnancy that triggers progesterone production to maintain the uterine lining, and in fertility medicine it serves as a trigger shot to release mature oocytes for IVF. Here is how hCG works for both indications, what the clinical evidence shows, and the regulatory context that every patient considering hCG should understand.

Key Takeaways

• Regulatory Status: FDA-approved; indicated for ovulation induction, assisted reproductive technology, and hypogonadotropic hypogonadism in males
• Research Stage: Approved and marketed; brand-name products Pregnyl, Novarel, and Ovidrel; compounded hCG legally unavailable since March 2020
• Availability: Prescription only; available through Superpower's licensed provider network (brand-name products only)
• Prescribing information: View Pregnyl prescribing information (DailyMed) · View Chorionic Gonadotropin prescribing information (DailyMed)
• How it works: Binds LH receptors in the gonads to stimulate testosterone production and spermatogenesis in men, and ovulation in women.
• What the research shows: Preserves intratesticular testosterone and spermatogenesis during TRT; supports ovulation induction and IVF trigger protocols with established efficacy.
• Not indicated for weight loss: The FDA requires all approved hCG labeling to state that there is no substantial evidence hCG increases weight loss beyond caloric restriction.

What Is hCG?

hCG (human chorionic gonadotropin) is a glycoprotein hormone naturally produced by the placenta during early pregnancy. It is structurally related to luteinizing hormone (LH) — both share the same alpha subunit and bind the same LH/hCG receptor in gonadal tissue. In clinical use, hCG is available as injectable FDA-approved brand-name biologics: Pregnyl, Novarel (powder for reconstitution), and Ovidrel (prefilled syringe, primarily used for fertility). The hormone's ability to mimic LH at the receptor level is the foundation of both its fertility and testosterone-support applications.

How hCG Works in the Body

LH Receptor Agonism in Male Gonadal Tissue

In men, LH is the pituitary signal that drives testosterone production in Leydig cells within the testes. Exogenous testosterone suppresses the hypothalamic-pituitary-gonadal (HPG) axis through negative feedback: the pituitary detects elevated testosterone and reduces LH and FSH secretion. Without LH stimulation, intratesticular testosterone (ITT) falls — and ITT is required for spermatogenesis at concentrations far exceeding serum testosterone levels. hCG binds the LH/hCG receptor on Leydig cells with the same functional result as endogenous LH: it stimulates testosterone synthesis and maintains ITT. A landmark 2010 dose-ranging RCT by Roth and colleagues in the Journal of Clinical Endocrinology and Metabolism studied 37 healthy men with experimentally induced gonadotropin deficiency (via GnRH antagonist acyline) and found that subcutaneous hCG at 0, 15, 60, or 125 IU every other day for 10 days produced dose-dependent increases in intratesticular testosterone — from 77 nmol/L at 0 IU to 923 nmol/L at 125 IU (p < 0.001) — compared with a baseline of approximately 2,508 nmol/L before suppression. This makes hCG a primary tool for preserving testicular function in men on TRT who wish to maintain fertility or testicular volume.

Spermatogenesis Preservation and Restoration

Exogenous testosterone is a preventable cause of male infertility. A foundational 2013 review in Translational Andrology and Urology by Crosnoe, Grober, and colleagues — drawing on an integrated analysis of 30 hormonal male contraception studies — documented that 67% of men recovered to 20 million sperm/mL within 6 months of testosterone discontinuation, 90% within 12 months, and 100% within 24 months, though only 46% returned to their baseline sperm density. The recovery window is not guaranteed, and fertility preservation during treatment is preferable to recovery after the fact. hCG co-administration with testosterone has been shown to maintain spermatogenesis that would otherwise be suppressed. A 2015 case series in the Journal of Sexual Medicine by Wenker, Dupree, and colleagues studied 49 men with testosterone-related azoospermia or severe oligospermia and found that hCG-based combination therapy (3,000 IU subcutaneously every other day, supplemented with clomiphene, tamoxifen, anastrozole, or recombinant FSH) restored spermatogenesis in 47 of 49 men (95.9%), with a mean time to recovery of 4.6 months and a mean first sperm density of 22.6 million/mL. The mechanism is the same: maintaining ITT through LH receptor stimulation preserves the intratesticular environment that spermatogenesis requires.

hCG Monotherapy for Hypogonadism

In addition to adjunct use with TRT, hCG can function as monotherapy for certain presentations of hypogonadism. This approach is particularly relevant for men who want higher testosterone levels without suppressing the HPG axis. A 2022 retrospective study in Cureus by Rainer, Pai, and colleagues followed 28 men (mean age 44 years) with prior exogenous testosterone use receiving hCG monotherapy at 1,000–2,000 IU weekly for a mean of 341 days. In men who had discontinued testosterone before starting hCG (n = 20), total testosterone increased from 307 to 422 ng/dL (p < 0.05), while across the full cohort hematocrit decreased from 45.3% to 44.2% (p < 0.05) with no thromboembolic events — a clinically meaningful safety difference, since elevated hematocrit (erythrocytosis) is a primary safety concern with testosterone therapy. A separate 2022 Cureus study by Zucker, Rainer, Pai, and colleagues studied 31 men with hypogonadal symptoms despite baseline testosterone above 300 ng/dL (median 413 ng/dL) receiving hCG monotherapy at a mean dose of 1,529 IU twice weekly for a mean of 42 weeks. Though median testosterone did not change significantly (413 to 433 ng/dL, p = 0.57), symptomatic improvement was substantial: 86% (19/22) reported improved erectile function and 80% (20/25) reported improved libido, with no thromboembolic events and no significant changes in hematocrit, PSA, or estradiol. For men with hypogonadotropic hypogonadism (secondary hypogonadism where the problem is at the pituitary or hypothalamic level), hCG is particularly well-suited: it bypasses the deficient LH signal directly.

Ovulation Induction and IVF Trigger in Women

In female fertility medicine, hCG serves as an ovulation trigger. The LH surge that naturally triggers oocyte maturation and follicular rupture can be replicated by exogenous hCG administration. In IVF protocols, hCG is injected at a timed interval before oocyte retrieval — typically 34-36 hours before the procedure — to induce final oocyte maturation. A 2023 meta-analysis in the Journal of Assisted Reproduction and Genetics by Hsia, Lee, and colleagues pooled 10 RCTs (N = 1,638; 825 dual trigger vs. 813 hCG-only trigger) and found that dual trigger protocols — combining GnRH agonist with hCG — significantly improved live birth rate (OR 1.61; 95% CI 1.16–2.25) and clinical pregnancy rate (OR 1.48; 95% CI 1.08–2.01) compared to hCG trigger alone in fresh IVF cycles. A 2019 study in Reproductive Biology and Endocrinology by Lin, Wu, and colleagues compared 297 women receiving dual trigger (0.2 mg triptorelin plus 6,500 IU recombinant hCG) with 130 women receiving hCG alone (6,500 IU) in GnRH-antagonist IVF cycles for diminished ovarian reserve (AMH ≤ 1.1 ng/mL), and found significantly higher live birth rates (26.9% vs. 14.5%, p = 0.014), clinical pregnancy rates (33.0% vs. 20.7%, p = 0.035), and fertilization rates (73.1% vs. 58.6%, p = 0.015) in the dual trigger group. hCG is also used for ovulation induction in women with anovulatory cycles, following stimulation with clomiphene or gonadotropins.

What the Research Shows About Effectiveness

Testosterone Levels and Hypogonadism Outcomes

A narrative review spanning 1977–2020 in Expert Review of Endocrinology and Metabolism by Fink, Schoenfeld, and colleagues examined hCG as a treatment approach for secondary hypogonadism, noting that clinical studies using 1,500–5,000 IU two to three times weekly have consistently shown testosterone increases into the eugonadal range (generally 300–1,000 ng/dL) while preserving spermatogenesis — a dual effect that exogenous TRT cannot achieve. A 2021 systematic review in Sexual Medicine Reviews by Raheem and Chen analyzed 25 studies and found that across 5 hCG trials (N = 196, mean age 42 years), mean total testosterone increased from 284.5 to 565.6 ng/dL (p < 0.0001) with concurrent improvement in ADAM symptom scores (28.1 to 30.9, p < 0.0001), confirming that hCG is associated with clinically meaningful improvements in both testosterone levels and hypogonadism symptoms. A 2018 randomized trial in BJU International by Habous, Giona, and colleagues randomized 282 hypogonadal men (mean baseline testosterone 2.31 nmol/L, BMI 30.8) to clomiphene 50 mg daily (n = 95), hCG 5,000 IU twice weekly (n = 94), or the combination (n = 94) for 3 months. All three arms achieved comparable mean testosterone of 5.17 nmol/L (a 223% increase from baseline) with no statistically significant difference between groups, though the combination arm produced superior symptom improvement on the qADAM scale (15.13 vs. 12.73 for clomiphene alone and 11.82 for hCG alone at 3 months, p < 0.01). A 2025 systematic review in Archives of Endocrinology and Metabolism by Hohl and colleagues pooled 10 RCTs (total N = 819) of clomiphene and enclomiphene for male hypogonadism. The single included hCG-comparator trial — Habous 2018 (clomiphene n = 95 vs. hCG 5,000 IU twice weekly n = 94) — reported post-treatment testosterone of approximately 158 ng/dL with clomiphene vs. 134 ng/dL with hCG alone (p < 0.002), though all groups remained below normal reference ranges and the original trial authors concluded the approaches were comparably effective. This is a single-study finding within the review, not a pooled meta-analytic result, and should be interpreted accordingly.

Spermatogenesis Recovery and Fertility Preservation

A 2021 prospective study in Research and Reports in Urology by Trinh, Hung, and colleagues treated 19 azoospermic men with hypogonadotropic hypogonadism using hCG (mean 5,579 IU every 3 days) combined with clomiphene 25 mg daily for 12 months. Testosterone increased approximately 25-fold, from 0.76 to 19.6 nmol/L (p < 0.001), and 9 of 19 men (47.4%) achieved sperm return — including 100% (3/3) of those with partial hypogonadotropic hypogonadism and 37.5% (6/16) of those with total hypogonadotropic hypogonadism — with no serious adverse events. A 2018 systematic review in the Arab Journal of Urology by El Meliegy, Motawi, and El Salam reviewed 56 studies (screening 91 manuscripts spanning 1978–2017) and confirmed that combined hCG plus hMG therapy achieves spermatogenesis in up to 90% of hypogonadotropic hypogonadal men (with sperm appearance typically within 3–6 months), while low-dose hCG at 500 IU every other day maintains semen parameters in men on concurrent TRT — supporting hCG as a fertility-preserving strategy in men on androgen therapy. In adolescent males with hypogonadotropic hypogonadism, a 2020 retrospective review in Global Pediatric Health by Agarwal and Tu compared hCG (n = 4, doses of 500–1,500 IU two to three times weekly) with testosterone replacement (n = 48) over a mean of approximately 14 months and found that hCG produced significantly greater testicular growth — mean testicular volume of 8.3 mL vs. 3.4 mL with testosterone (p < 0.001) — while achieving comparable testosterone levels (503.5 vs. 385.9 ng/dL, p = 0.45). The very small hCG group limits the strength of this finding, but the testicular volume difference is clinically relevant when fertility potential is a treatment goal.

Side Effects and What to Expect

hCG is a biologic medication administered by injection. Side effects vary meaningfully between the male (hypogonadism/TRT adjunct) and female (fertility/IVF) contexts; the dose, frequency, and duration differ substantially between indications.

Common side effects:

• Injection site reactions — pain, redness, or swelling at the injection site; typically mild and transient
• Headache; reported at various frequencies across clinical studies, usually mild
• Mood changes or irritability; more commonly reported at higher doses used in fertility protocols
• Breast tenderness or gynecomastia in men; in early preclinical research, in vitro rat Leydig cell studies demonstrated that hCG acutely stimulates aromatization of testosterone to estradiol; more common at higher doses or in individuals with elevated baseline aromatase activity
• Testicular discomfort or swelling in men; reflects increased Leydig cell activity; typically resolves with dose adjustment

Less common but reported:

• Ovarian hyperstimulation syndrome (OHSS) in women — ranges from mild bloating and discomfort to severe fluid shifts and hemoconcentration in rare cases; risk is higher in women with polycystic ovarian morphology and in high-stimulation IVF protocols; managed by provider monitoring of follicle counts and estradiol levels
• Erythrocytosis (elevated hematocrit) in men, though at lower rates than seen with TRT; hematocrit monitoring is standard practice during any androgen-stimulating therapy
• Fluid retention; more common at higher doses
• Precocious puberty if administered to prepubertal males; not applicable in adult use contexts

Provider monitoring during hCG use includes testosterone levels, estradiol (to assess aromatization), hematocrit, and — in women undergoing fertility treatment — follicular ultrasound and serum estradiol to guide timing and reduce OHSS risk.

Who Is hCG Typically Prescribed For?

Men on TRT or With Hypogonadotropic Hypogonadism

Providers typically consider hCG for men on testosterone replacement who wish to preserve fertility, maintain testicular volume, or maintain the capacity for endogenous testosterone production. It is particularly well-suited to men with secondary hypogonadism (hypogonadotropic hypogonadism), where the problem lies at the pituitary or hypothalamic level rather than the testes: in this setting, hCG bypasses the absent LH signal directly. hCG monotherapy is an alternative for men who are symptomatic but prefer to avoid the HPG axis suppression associated with exogenous testosterone. A licensed provider evaluates LH, FSH, and testosterone levels as part of this assessment.

Women Undergoing Fertility Treatment or Ovulation Induction

hCG is a standard component of IVF protocols as the ovulation trigger shot, and it is used for ovulation induction in women with anovulatory infertility following ovarian stimulation. Providers administer it at a precisely timed interval before oocyte retrieval or natural conception attempt. Dual trigger protocols combining hCG with a GnRH agonist are used for women with diminished ovarian reserve based on RCT evidence showing improved live birth rates. Eligibility and dosing are individualized based on follicle count, estradiol levels, and prior stimulation response.

Who Should Not Take hCG

hCG is not indicated for weight loss. The FDA requires all approved hCG prescription labeling to include the following statement: there is no substantial evidence that hCG 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. This has been a mandatory labeling requirement since 1975.

A licensed provider will evaluate individual risk factors before prescribing. The following are generally considered contraindications:

• Precocious puberty — hCG stimulates gonadal hormone production and is contraindicated in prepubertal individuals in whom premature androgen or estrogen exposure could advance bone age and compromise adult height
• Androgen-sensitive tumors (including prostate cancer and certain testicular tumors) — hCG stimulates testosterone production, which can promote growth of androgen-sensitive malignancies
• Primary ovarian failure or premature ovarian insufficiency (in women) — the ovaries cannot respond to LH/hCG stimulation when follicular reserve is absent or severely depleted
• Uncontrolled thyroid or adrenal dysfunction — conditions that affect the hormonal environment may complicate hCG response and require stabilization before use
• Known hypersensitivity to hCG or any component of the formulation
• Pregnancy (in fertility-unrelated contexts) — although hCG is naturally produced in pregnancy, therapeutic administration is not indicated and may interfere with clinical monitoring of hCG levels used to assess fetal viability

This is not an exhaustive list. A licensed provider will evaluate individual contraindications, current medications, and hormonal baseline before prescribing.

What to Test Before Starting hCG

The biomarker baseline before hCG use differs meaningfully between the male and female contexts. Both require establishing hormonal status; the specific markers differ by indication.

• Total testosterone (men): Establishes the pre-treatment androgen status. Total testosterone is the primary diagnostic marker for hypogonadism and the reference point for assessing hCG response. Providers typically obtain morning values (when testosterone peaks) and confirm with a second measurement before initiating therapy.
• Free testosterone (men): Because testosterone is largely bound to SHBG and albumin, free testosterone reflects the biologically active fraction. In men with borderline total testosterone but high SHBG, free testosterone may be disproportionately low and is more clinically meaningful for symptom correlation.
• LH and FSH: LH and FSH levels distinguish primary hypogonadism (high LH/FSH, testicular failure) from secondary hypogonadism (low or normal LH/FSH, hypothalamic or pituitary dysfunction). hCG is appropriate for secondary hypogonadism; elevated LH/FSH with low testosterone indicates primary testicular failure where hCG would not restore production. In women, FSH and LH levels contextualize ovarian reserve and cycle phase.
• Estradiol: Estradiol baseline is relevant in both sexes. In men, elevated pre-treatment estradiol may predict greater aromatization during hCG therapy and may warrant aromatase inhibitor co-prescription. In women, estradiol is used throughout fertility treatment to monitor follicular development and guide trigger timing.
• SHBG: Sex hormone binding globulin modulates free testosterone availability. Low SHBG may indicate insulin resistance and is associated with metabolic patterns that affect hormonal therapy response. It is a standard component of a comprehensive hormonal workup.
• Hematocrit and CBC: Hematocrit baseline is required before any androgen-stimulating therapy in men. Elevated hematocrit at baseline represents a contraindication or dose-modification consideration. A complete blood count provides the full picture of red cell mass and rules out baseline polycythemia.
• PSA (men over 40): Prostate-specific antigen is assessed before any testosterone-stimulating therapy in men over 40. PSA elevation at baseline warrants urological evaluation before initiating any androgen therapy including hCG.
• AMH (women): Anti-Müllerian hormone is the primary marker of ovarian reserve and helps providers individualize stimulation protocols in fertility contexts. AMH levels guide the expected response to ovarian stimulation and help predict OHSS risk. AMH testing is standard before any assisted reproductive technology protocol.
• Progesterone (women): Progesterone at baseline confirms cycle phase and luteal function. After hCG trigger, progesterone rise confirms ovulation has occurred and is tracked to evaluate luteal phase support requirements.
• Complete metabolic panel: Covers liver and kidney function markers relevant to any prescription medication. Hepatic and renal function baselines are standard before initiating therapy with any biologic or hormone product.

What Your Bloodwork May Show While on hCG

Providers typically monitor testosterone levels (expected to increase with hCG) and estradiol (which may increase as testosterone is aromatized) during treatment in men. Hematocrit is tracked to identify erythrocytosis, though the effect is generally less pronounced than with direct testosterone administration. For men using hCG alongside TRT, semen analysis may be the most relevant functional endpoint if fertility preservation is the goal. In women undergoing fertility treatment, estradiol and follicular ultrasound guide timing from stimulation through the trigger shot; progesterone is monitored post-trigger to confirm ovulation. hCG levels themselves are not typically used to monitor treatment response — they are more relevant as a diagnostic marker in early pregnancy monitoring.

That principle — establishing a biomarker baseline before any intervention, then using follow-up data to evaluate response — is central to Superpower's approach to preventive health. Hormonal therapy decisions should start with knowing where your markers stand, not where they might be heading.

Is Compounded hCG Legal?

This is one of the most clinically important questions for patients who have previously obtained compounded hCG. The short answer: compounded hCG has been legally unavailable in the United States since March 2020.

Under the Biologics Price Competition and Innovation Act (BPCIA), hCG was reclassified as a biologic. This reclassification took effect on March 23, 2020. Under the applicable regulatory framework, biologics are not eligible for the compounding exemptions under Section 503A or 503B of the Federal Food, Drug, and Cosmetic Act. As a result, compounded hCG — which had been widely available before reclassification — became legally impermissible. FDA-approved brand-name products (Pregnyl, Novarel, and Ovidrel) remain the only legally available forms of hCG for human use in the United States. Superpower facilitates access to brand-name hCG only through its licensed provider network. Any source offering compounded hCG in the United States is operating outside current regulatory requirements.

Frequently Asked Questions

Is compounded hCG still available?

No. Compounded hCG has been legally unavailable in the United States since March 2020, when hCG was reclassified as a biologic under the BPCIA. Biologics cannot be compounded under the standard pharmacy compounding frameworks (503A or 503B). Only FDA-approved brand-name products — Pregnyl, Novarel, and Ovidrel — may be legally prescribed and dispensed. Any source offering compounded hCG is operating outside current FDA regulations.

Can hCG be used alongside TRT?

Yes, this is one of the most common clinical uses of hCG. When exogenous testosterone suppresses the HPG axis, intratesticular testosterone falls — taking spermatogenesis with it. Low-dose hCG co-administered with TRT maintains LH receptor stimulation in the testes, preserving intratesticular testosterone and, with it, the potential for spermatogenesis. A 2010 dose-ranging RCT in JCEM by Roth and colleagues (N = 37 healthy men with induced gonadotropin deficiency) found that subcutaneous hCG at 0–125 IU every other day for 10 days produced dose-dependent increases in intratesticular testosterone — from 77 nmol/L at 0 IU to 923 nmol/L at 125 IU (p < 0.001) — during testosterone suppression. A provider determines whether co-administration is appropriate and at what dose.

What is the difference between hCG and FSH?

hCG mimics LH and primarily acts on Leydig cells in men (stimulating testosterone production) and triggers ovulation in women. FSH (follicle-stimulating hormone) acts on Sertoli cells in men to support spermatogenesis and on granulosa cells in women to stimulate follicular development. In clinical fertility practice, exogenous FSH is used to grow follicles; hCG is then used as the trigger to release them. In men, both LH (via hCG) and FSH are often required together to initiate spermatogenesis in cases of hypogonadotropic hypogonadism where both gonadotropins are deficient.

Does hCG affect fertility?

In men, hCG supports rather than suppresses fertility by maintaining the intratesticular testosterone required for spermatogenesis. This is the opposite of what exogenous testosterone does. For men on TRT who want to father children, hCG co-administration is the standard fertility-preserving strategy. In women, hCG is used in fertility treatment specifically to trigger ovulation; it is a fertility intervention, not a contraceptive. Ovulation does not occur without either the natural LH surge or an exogenous hCG trigger.

How long does it take for hCG to work for testosterone?

In men using hCG for testosterone support, measurable increases in serum testosterone may take several weeks to months, with timing varying by individual and baseline hormonal status. Full assessment of response generally requires 6-8 weeks of consistent dosing. For spermatogenesis effects, the timeline is longer: sperm production is a roughly 72-day process, and meaningful changes in semen parameters may take 3-6 months to appear. A semen analysis at 3 and 6 months is the appropriate endpoint for evaluating fertility outcomes.

Who should not take hCG?

hCG is contraindicated in individuals with precocious puberty, androgen-sensitive tumors (including prostate and certain testicular cancers), primary ovarian failure in women, and known hypersensitivity to the formulation. In men with elevated PSA at baseline, urological evaluation is required before any androgen-stimulating therapy. A licensed provider evaluates these factors as part of standard pre-prescribing assessment.

Does insurance cover hCG?

Coverage depends on the indication and individual plan. When prescribed for fertility treatment in women, hCG trigger shots are often covered under fertility benefits where they exist, though coverage varies significantly by state and employer plan. When prescribed for male hypogonadism, coverage depends on whether the diagnosis meets the plan's criteria. Brand-name biologics (Pregnyl, Novarel, Ovidrel) are more expensive than the compounded hCG that was previously available, and cost is a material consideration. A provider can advise on the most appropriate product and whether prior authorization applies.

What blood tests should I get before starting hCG?

For men, the core panel includes total testosterone, free testosterone, LH, FSH, estradiol, SHBG, PSA (if over 40), and hematocrit. These markers establish whether hypogonadism is primary or secondary and identify safety considerations before therapy. For women in fertility contexts, AMH, FSH, estradiol, and progesterone are the core markers. A comprehensive hormonal workup through a licensed provider is the appropriate starting point for either indication.

IMPORTANT SAFETY INFORMATION

hCG is an FDA-approved prescription biologic indicated for ovulation induction, assisted reproductive technology, and hypogonadotropic hypogonadism in males. Compounded hCG has been legally unavailable in the United States since March 2020 following biologic reclassification. Only FDA-approved branded products (Pregnyl, Novarel, Ovidrel) are available. Superpower connects patients with licensed providers and pharmacies; Superpower does not prescribe or dispense medications.

hCG is not indicated for weight loss. The FDA requires all approved hCG prescription labeling to state that there is no substantial evidence that hCG 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.

Warnings: ovarian hyperstimulation syndrome (OHSS) in women; multi-fetal pregnancy risk; fluid retention; erythrocytosis.

Common side effects: injection site reactions, headache, mood changes, gynecomastia, testicular discomfort.