IVF Medications Overview

Why Does IVF Need Four Different Medication Phases?

IVF relies on four sequential medication phases: pituitary suppression, ovarian stimulation, oocyte (egg) maturation triggering, and luteal phase support.^[1][3] Each one targets a specific point where the body's normal hormonal cycle would either fight the treatment or fail to support it.

• Suppression prevents the pituitary from releasing luteinizing hormone (LH) at the wrong time, which would trigger ovulation before the eggs can be retrieved.^[1][4]
• Stimulation uses gonadotropins to push the ovaries to mature multiple follicles in one cycle instead of the single follicle a natural cycle produces.^[1][7]
• Triggering delivers a precisely timed hormonal signal that completes egg maturation roughly 34 to 36 hours before retrieval.^[9][11]

Luteal phase support replaces the progesterone that the disrupted post-retrieval ovary can't reliably produce. Without it, progesterone levels may be insufficient for optimal endometrial receptivity and to sustain implantation.^[3][12]

Think of it as a controlled hijacking of the menstrual cycle - the brain's signals are silenced, the ovaries are pushed harder than they normally would be, ovulation is fired off at a clinic-chosen moment, and the luteal phase is rebuilt from outside the body.

→ Learn more: In Vitro Fertilization (IVF)

Suppression - GnRH Agonists or Antagonists?

Suppression medications work by either downregulating or blocking GnRH (gonadotropin-releasing hormone) receptors in the pituitary gland, which reduces LH and FSH (follicle stimulating hormone) secretion and prevents premature ovulation, allowing controlled ovarian stimulation.^[1][3] Two drug classes do this in opposite ways.

→ Learn more: Contraception

How Do GnRH Agonists Work?

A GnRH agonist binds the pituitary's GnRH receptor and over-stimulates it. The initial effect is a brief surge - the “flare” - of LH and FSH, followed by receptor desensitization that suppresses hormone release for the rest of the stimulation period.^[1] Common brands include leuprolide (Lupron, Lucrin), triptorelin (Decapeptyl), buserelin (Suprefact), and nafarelin (Synarel).^[1][25]

The standard “long” agonist protocol starts the agonist in the mid-luteal phase of the cycle before stimulation, runs roughly 10 to 14 days of suppression before gonadotropins begin, and continues the agonist throughout stimulation.^[1][4] It's long. It's effective.

How Do GnRH Antagonists Work?

A GnRH antagonist blocks the GnRH receptor directly and immediately - no flare, no desensitization period, no pre-treatment phase.^[1][6] Two approved drugs are used in IVF: cetrorelix (Cetrotide) and ganirelix (Orgalutran, Antagon), given once daily by subcutaneous injection from around day 5 or 6 of stimulation until trigger.^[6][18][19]

A 2025 study of more than 9,000 antagonist-cycle patients found that cetrorelix and ganirelix produced comparable live birth rates (47.2% vs 49.4%). Cetrorelix showed superior LH surge suppression and lower OHSS (ovarian hyperstimulation syndrome) incidence (0.4% vs 1.1%). Both drugs have relatively low absolute OHSS rates, so they remain clinically valid antagonists.^[6]

What Does the Evidence Show?

A 2024 systematic review and meta-analysis comparing antagonists with long-agonist protocols across IVF/ICSI (intracytoplasmic sperm injection) studies found that antagonist protocols significantly reduced OHSS rates and produced similar live birth rates. Clinical pregnancy rates, retrieved oocytes, and high-quality embryo counts were lower in the antagonist arm.^[4] In women with PMOS (polyendocrine metabolic ovarian syndrome – the 2026 term that replaced polycystic ovary syndrome [PCOS])28 specifically, a 2022 systematic review and meta-analysis concluded that antagonist protocols were a safer and more cost-effective alternative to the long agonist protocol without compromising clinical outcomes.^[17]

The picture isn't uniform, though. In a 983-couple retrospective study of severe male-factor infertility, the long agonist protocol produced higher live birth rates (41.0% vs. 31.3%) than the antagonist protocol, with corresponding gains in implantation and ongoing pregnancy rates.^[5] In poor ovarian responders, the 2024 meta-analysis reported that the main difference between protocols was fewer oocytes retrieved with the antagonist, with no significant differences in other clinical outcomes specifically in that subgroup.^[4]

The 2023/2024 ASRM (American Society for Reproductive Medicine) guideline on OHSS prevention recommends GnRH antagonist protocols when there is concern for OHSS, with strong evidence supporting that choice.^[2]

Key Insight:
The antagonist protocol is faster, simpler, uses less gonadotropin, and is associated with lower OHSS risk. For specific subgroups (severe male factor, poor responders), the long agonist may still produce better pregnancy outcomes.^[2][4][5]

### Comparison: GnRH Agonists vs. Antagonists

Source: Orvieto et al., Delphi consensus (2021)^[1]; ASRM OHSS Prevention Guideline (2023)^[2]; Liu et al., systematic review and meta-analysis (2024)^[4]; Lv et al., severe male factor cohort (2022)^[5]; Peng et al. (2025)^[6]; Kadoura et al., PCOS-focused systematic review and meta-analysis (2022)^[17]; EMA EPARs and emc SmPCs for Cetrotide, Orgalutran, and Decapeptyl^[18],^[19],^[25].

* Approximate durations and timing vary by protocol and clinic.

What Are the Side Effects of Suppression Drugs?

The two suppression classes have very different side-effect profiles.

GnRH agonist protocols are linked to a hypoestrogenic side-effect profile from the sustained drop in estradiol - hot flashes, headaches, vaginal dryness, mood changes, and sleep disturbance. There’s also an increased risk of ovarian cyst formation and a prolonged protocol duration relative to antagonist regimens.^[17]

GnRH antagonists have a notably milder profile. Because there's no extended estrogen suppression, hypoestrogenic symptoms may not develop, and the main reported adverse events are localized injection-site reactions.^[6]

IVF Stimulation Medications: Do You Need LH or Just FSH?

Stimulation drugs are gonadotropins - either FSH alone, or FSH combined with LH - drugs that stimulate the ovaries to mature multiple follicles instead of the single follicle a natural cycle produces.^[1][7]

→ Learn more: Intrauterine Insemination (IUI)

FSH-Only Preparations

Recombinant FSH (rFSH) is the most widely used stimulation drug. Brands include follitropin alfa (Gonal-f, Bemfola, Ovaleap), follitropin beta (Puregon, Follistim), and follitropin delta (Rekovelle), the last of which uses an algorithm-based individualized dose calculated from AMH (Anti Müllerian Hormone) and body weight.^[1][20][21] For the conventional preparations, follitropin alfa and follitropin beta, daily doses are usually 150 to 225 international units (IU), individualized to ovarian reserve, age, weight, and serum AMH.^[29] Follitropin delta is the exception: it is dosed in micrograms, not IU. It uses a fixed algorithm based on serum AMH and body weight (approximately 6 to 12 micrograms per day in a first cycle). These microgram doses are specific to Rekovelle and cannot be applied to other gonadotropins.^[21]

Corifollitropin alfa (Elonva) is a long-acting FSH analog with a half-life of around 70 hours (range 59–82 hours) - a single subcutaneous dose can replace the first seven days of daily FSH injections, with additional FSH added later if needed.^[1][22]

FSH Plus LH Preparations

Combined preparations add LH activity to FSH. Two routes dominate practice.

• Human menopausal gonadotropin (hMG) - Menopur, Meriofert - contains FSH plus LH activity from postmenopausal urine, with LH-receptor-mediated bioactivity primarily attributable to its hCG (human chorionic gonadotropin) component^[8][26]
• Recombinant FSH + recombinant LH - Pergoveris - provides a fixed 2:1 ratio of follitropin alfa and lutropin alfa7,23

What Does the Evidence Show?

For most women under 35 with normal ovarian reserve, FSH alone has proven to be sufficient to stimulate adequate follicular growth.^[1][7] For women aged 35 to 40 with a normal ovarian response (5 to 14 oocytes retrieved), a 2024 real-world analysis from the Deutsches IVF-Register reported that r-hFSH plus r-hLH was associated with higher live birth rates than r-hFSH alone (22.5% vs. 19.4%). However, the overall live birth difference across all women aged 35 to 40 was not statistically significant (20.3% vs. 18.0%).^[7]

A 2022 retrospective matched case-control study of GnRH antagonist cycles compared rLH and hMG supplementation on top of rFSH. r-hFSH plus r-hLH was associated with a higher cumulative live birth rate than r-hFSH plus hMG (64% vs. 53%), with comparable endometrial thickness, embryo development, and implantation rate but higher oocyte retrieval and more mature/fertilized oocytes. OHSS rates did not differ.^[8]

Important:
LH supplementation isn't routine. It's targeted - typically considered for advanced maternal age, hypogonadotropic hypogonadism (low levels of LH and FSH from the pituitary gland leading to reduced sex hormone production and impaired gonadal function), poor responders, or suboptimal response in a previous cycle.^[7][8]

What Are the Side Effects of Stimulation Drugs?

Gonadotropin stimulation commonly causes abdominal pain or distension, pelvic discomfort, breast tenderness, headache, nausea, fatigue, and injection-site reactions - reflecting the combined effects of multifollicular ovarian growth and daily subcutaneous injections.^[2]

The most serious complication is OHSS, which occurs at moderate-to-severe grade in approximately 1% to 5% of IVF cycles.^[2] Rare but documented serious events include thromboembolism, ovarian torsion, and severe allergic reactions.^[2]

Trigger Shots - hCG, Agonist, or Both?

The trigger shot is usually a single injection that finalizes egg maturation, given roughly 34 to 36 hours before oocyte retrieval.^[9][11] The exception is a dual or double trigger, which uses two injections - a GnRH agonist plus hCG given together (dual), or the agonist about 40 hours and hCG about 34 hours before retrieval (the sequential "double" trigger).^[9][10][30]

hCG Trigger

Human chorionic gonadotropin has a structure similar to LH and binds the LH receptor on granulosa cells, mimicking the natural LH surge.^[9] Brands include choriogonadotropin alfa (Ovidrel, Ovitrelle) and urinary preparations like Pregnyl.^[9][24]

hCG has a long half-life (around 55 hours), which sustains the corpus luteum effectively - but that same persistence is the main driver of OHSS in high responders.^[2][9]

GnRH Agonist Trigger

In antagonist cycles only, a single dose of a GnRH agonist (e.g. triptorelin or leuprolide) flares the pituitary to release endogenous LH and FSH, producing a more physiological surge that lasts only 24 to 36 hours.^[9]

The trade-off matters. The short surge significantly reduces severe OHSS, but the corpus luteum fails to support the early luteal phase, and fresh-transfer pregnancy rates drop unless rescue hCG or intensified luteal support is added.^[2][9]

Dual Trigger

Dual trigger combines a GnRH agonist with a low dose of hCG (typically 1,000 to 1,500 IU), aiming to keep the OHSS-protective benefit of the agonist surge while restoring enough luteal support for a successful fresh transfer.^[9][10]

A 2023 systematic review and meta-analysis of randomized trials found that dual trigger improved live birth and clinical pregnancy rates compared with hCG trigger alone in fresh IVF cycles, with no statistically significant increase in OHSS.^[10] A separate 2023 meta-analysis restricted to GnRH-antagonist cycles in normal and low responders reached a similar conclusion: dual triggering improved oocyte maturity and embryo grading in normal responders compared with hCG trigger alone.^[9]

Does Timing Matter?

It does. A 2025 retrospective cohort of 59,206 retrieval cycles found that the optimal trigger-to-retrieval interval differs by trigger type: hCG produced the highest oocyte yield with shorter intervals, while the GnRH agonist trigger produced more mature (MII) oocytes and blastocysts when the interval was longer than 36.5 hours.^[11]

Important:
For high responders or anyone with PMOS, ASRM 2023/2024 guidance recommends a GnRH antagonist suppression protocol paired with an agonist or dual trigger - the most effective combination for OHSS prevention currently supported by evidence.^[2]

What Are the Side Effects of Trigger Drugs?

The trigger injection itself is generally well tolerated; reported events include headache, injection-site reactions, and short-term abdominal discomfort.^[2][9] The dominant side-effect issue is what happens after.

hCG triggers sustain the corpus luteum because of hCG's long half-life, which is exactly why OHSS risk peaks in the days immediately after an hCG trigger in high responders. The hCG molecule itself drives the syndrome's pathophysiology.^[2][9]

GnRH agonist triggers produce a short-lived LH and FSH surge of around 24 to 36 hours and almost eliminate severe OHSS.^[2][9] The trade-off is a luteal-phase deficiency that lowers fresh-transfer pregnancy rates unless rescue luteal support is intensified.^[2][9]

A 2023 meta-analysis of randomized trials found that dual trigger did not significantly increase OHSS rates compared with hCG trigger alone, while improving live birth and clinical pregnancy outcomes.^[10] The dual-trigger side-effect spectrum mirrors hCG but with a more favorable safety margin for high-risk patients.^[9][10]

Luteal Support - Progesterone, Estrogen, or Both?

Luteal phase support replaces the progesterone that the post-IVF ovary can't produce reliably, keeping the endometrium receptive so an embryo can implant and an early pregnancy can be supported.^[3][12]

→ Learn more: Intracytoplasmic Sperm Injection (ICSI)

Why Is Luteal Support Needed?

Supraphysiological estradiol and progesterone from ovarian stimulation suppress pituitary LH through negative feedback, leaving the corpus luteum without the LH signal it needs to function normally.^[3] Egg retrieval physically disrupts the granulosa cells that produce progesterone, and any residual hCG from trigger further suppresses endogenous LH via a negative feedback mechanism.^[3][12] The net effect is a luteal phase that may be insufficient to support implantation and early pregnancy without exogenous hormonal support.^[3]

Progesterone Routes and Brands

Several routes are used clinically, each with different pharmacokinetics and side-effect profiles.

• Vaginal: micronized progesterone capsules (Utrogestan) or vaginal inserts (Endometrin, Lutinus) or gel (Crinone, Prochieve) - the most widely used route, with good local endometrial delivery and limited systemic absorption3,12,27
• Intramuscular: progesterone in oil, producing the highest serum progesterone levels but with painful injections and frequent site reactions12,14
• Subcutaneous: progesterone in aqueous solution (Prolutex), shown to be non-inferior to vaginal progesterone in luteal support trials12
• Oral: dydrogesterone (Duphaston) - a synthetic, orally bioavailable progestogen used in growing numbers of clinics13,15

What Does the Evidence Show?

A 2020 individual-participant data meta-analysis of nearly 2,000 women found that oral dydrogesterone (20–40 mg/day) was associated with significantly higher ongoing pregnancy and live birth rates compared with micronized vaginal progesterone (600 to 800 mg/day capsules or 90 mg gel) in fresh IVF cycles.^[15] A 2025 systematic review and meta-analysis extended this comparison to frozen-thawed embryo transfer cycles, reporting comparable pregnancy outcomes between oral dydrogesterone and vaginal progesterone.^[13]

For frozen embryo transfer specifically, a 2023 systematic review found that intramuscular progesterone was associated with higher ongoing pregnancy rates than vaginal progesterone in artificially prepared cycles - though the included trials were small and heterogeneous, so confidence remains moderate.^[14]

Does Adding Estrogen Help?

In artificial frozen embryo transfer cycles, oral estradiol valerate (typically 4 to 8 mg/day) or transdermal estrogen is used to prepare the endometrium before progesterone starts.^[12] In fresh cycles, adding estradiol on top of progesterone shows no consistent benefit in current evidence.^[12]

So what does this mean in practice? Pick the route you'll actually use consistently. Vaginal is the easiest. Oral dydrogesterone is becoming a credible alternative for fresh and frozen cycles. Intramuscular is reserved for situations where higher serum progesterone matters - typically frozen transfer in artificially prepared cycles.^[13][14][15]

What Are the Side Effects of Luteal Support?

Side effects depend heavily on route.

• Vaginal progesterone (Utrogestan, Crinone, Endometrin) - vaginal irritation, discharge, and occasional spotting are the most common complaints. Systemic effects are limited because of local absorption.^[3][12][27]
• Intramuscular progesterone - painful injection sites, local inflammation, and occasional sterile abscesses, reflecting the oil-based formulation.^[12][14]
• Subcutaneous progesterone (Prolutex) - injection-site reactions; otherwise non-inferior to micronized vaginal progesterone.^[12]
• Oral dydrogesterone (Duphaston) - generally well tolerated. Reported events include nausea, headache, and breast tenderness.^[13][15]

On the question of pregnancy safety, a 2024 systematic review and meta-analysis in Human Reproduction Open (Katalinic et al.) found no additional risk of congenital anomalies with first-trimester dydrogesterone use.^[16]

Estradiol preparations used in artificial frozen embryo transfer cycles (oral estradiol valerate, transdermal patches) may cause headache, nausea, and breast tenderness. They are generally well tolerated for short-term endometrial preparation.^[12]

Warning Signs - When to Call the Clinic?

Most IVF medication side effects are mild and resolve within days. A small subset - driven mostly by OHSS - are dangerous and need urgent attention.^[2]

Moderate-to-severe OHSS occurs in approximately 1% to 5% of IVF cycles, though the precise rate is difficult to define because a consensus definition is still lacking.^[2] OHSS symptoms include abdominal distension and discomfort, shortness of breath (dyspnea), ovarian enlargement, fluid accumulation in the abdomen (ascites), hemoconcentration (thickening of blood due to a decrease in plasma volume), hypercoagulability (increased tendency of the blood to clot) , and electrolyte imbalances.^[2]

Severe complications, though uncommon, are real: OHSS can be complicated by ovarian torsion or rupture, venous thromboembolism (a blood clot in a vein that can potentially travel to the lungs), acute respiratory distress, and acute kidney injury, which is why the warning signs below aren't optional to ignore.^[2]

Important:
Contact your clinic the same day if you develop rapid weight gain (more than 1 kg in 24 hours), severe abdominal pain or bloating, persistent vomiting, reduced urine output, shortness of breath, or calf or chest pain. These can signal moderate-to-severe OHSS, ovarian torsion, or thrombosis - all of which need urgent assessment.^[2]

The highest-risk patients are those with AMH above 3.4 ng/mL, antral follicle count above 24, PMOS, peak estradiol above 3,500 pg/mL, or 24 or more oocytes retrieved.^[2] If that profile applies, ASRM 2023/2024 recommends a GnRH antagonist suppression protocol with an agonist or dual trigger - currently the most effective evidence-backed prevention strategy.^[2]

So, What Should You Do Now?

Once the medication phases make sense, the next moves are practical.

Step 1: Confirm Your Protocol in Writing

Ask your clinic exactly which protocol they're using - long agonist, antagonist, mild stimulation, or progestin-primed - and why it suits your ovarian reserve and history.

Step 2: Map Out the Medication Schedule

Write down every drug, dose, timing, and route. The trigger time is the single most important moment in the cycle - mark it on a calendar precisely.

Step 3: Know Your OHSS Risk

Discuss your AMH, antral follicle count, and previous ovarian response. If any are in the high-risk range, discuss prevention strategies before stimulation starts.

Step 4: Set Up Symptom Monitoring

If you're at higher risk of OHSS - or your clinic tells you to - weigh yourself each morning during and after stimulation and watch for a rapid jump, and keep an eye on your urine output. Whatever your risk level, keep the red-flag symptoms listed above somewhere visible and call your clinic the same day if any of them appear.

Step 5: Identify Who to Call

Confirm the after-hours clinic number and clarify which symptoms warrant a call to the clinic versus a trip to emergency care.

Step 6: Compare Clinics If Unsure

Protocols, drug choices, and OHSS prevention strategies vary widely. If your current clinic's plan doesn't match recent guideline-backed approaches, get a second opinion.

→ Compare fertility clinics worldwide: MedicalNavigator.com/clinics/reproductive-medicine

Too Long, Didn't Read

• IVF uses four medication phases: suppression, stimulation, trigger, and luteal support.
• GnRH antagonists lower OHSS risk and are widely used for most patients, especially those with PMOS or high AMH.
• Long GnRH agonist protocols may still produce higher live birth rates in severe male-factor and selected other subgroups.
• Adding LH to FSH appears to help women aged 35–40 and selected poor responders, but not unselected normal responders.
• Dual trigger (GnRH agonist + low-dose hCG) improves pregnancy rates over hCG alone in fresh cycles while preserving OHSS protection.
• Contact your clinic urgently for weight gain over 1 kg per day, severe abdominal pain, shortness of breath, or reduced urination.

References

1. Orvieto R, Venetis CA, Fatemi HM, et al. Optimising Follicular Development, Pituitary Suppression, Triggering and Luteal Phase Support During Assisted Reproductive Technology: A Delphi Consensus. Front Endocrinol (Lausanne). 2021;12:675670. ↩
2. Practice Committee of the American Society for Reproductive Medicine. Prevention of moderate and severe ovarian hyperstimulation syndrome: a guideline. Fertil Steril. 2024;121(2):230-245. ↩
3. Garg A, Zielinska AP, Yeung AC, et al. Luteal phase support in assisted reproductive technology. Nat Rev Endocrinol. 2024;20(3):149-167. ↩
4. Liu C, Tian T, Lou Y, et al. Live birth rate of gonadotropin-releasing hormone antagonist versus luteal phase gonadotropin-releasing hormone agonist protocol in IVF/ICSI: a systematic review and meta-analysis. Expert Rev Mol Med. 2024. 26:e2. ↩
5. Lv M, Yu J, Chen P, et al. Ovarian stimulation in IVF couples with severe male factor infertility: GnRH antagonist versus long GnRH agonist. Front Endocrinol (Lausanne). 2022;13:1037220. ↩
6. Peng X, Lv X, Li P, et al. Comparison of pregnancy outcomes and safety between cetrorelix and ganirelix in IVF/ICSI antagonist protocols: a retrospective cohort study. Front Reprod Health. 2025;7:1492441. ↩
7. Bielfeld AP, Schwarze JE, Verpillat P, et al. Effectiveness of recombinant human FSH: recombinant human LH combination treatment versus recombinant human FSH alone for assisted reproductive technology in women aged 35-40 years. Reprod Biomed Online. 2024;48(6):103725. ↩
8. Chen MJ, Yi YC, Guu HF, et al. A retrospective, matched case-control study of recombinant LH versus hMG supplementation on FSH during controlled ovarian hyperstimulation in the GnRH-antagonist protocol. Front Endocrinol (Lausanne). 2022;13:931756. ↩
9. He FF, Hu W, Yong L, Li YM. Triggering of ovulation for GnRH-antagonist cycles in normal and low ovarian responders undergoing IVF/ICSI: A systematic review and meta-analysis of randomized trials. 00320-2/fulltext) Eur J Obstet Gynecol Reprod Biol. 2023;289:65-73. ↩
10. Hsia LH, Lee TH, Lin YH, et al. Dual trigger improves the pregnancy rate in fresh in vitro fertilization (IVF) cycles compared with the human chorionic gonadotropin (hCG) trigger: a systematic review and meta-analysis of randomized trials. J Assist Reprod Genet. 2023;40(9):2089-2101. ↩
11. Enatsu N, Furuhashi K, Otsuki J, et al. Optimal timing for triggering oocyte maturation during in vitro fertilization cycles varies between gonadotropin-releasing hormone agonist and human chorionic gonadotropin use. F\&S Reports. 2025;6(4). ↩
12. Greenbaum S, Athavale A, Hershko Klement A, Bentov Y. Luteal phase support in fresh and frozen embryo transfers. Front Reprod Health. 2022;4:919948. ↩
13. Stavridis K, Balafoutas D, Kalampokas T, et al. Oral Dydrogesterone Versus Vaginal Progesterone for Luteal Phase Support in Frozen-Thawed Embryo Transfer Cycles: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. J Clin Med. 2025;14(9):3238. ↩
14. Almohammadi A, Raveendran A, Black M, Maheshwari A. The optimal route of progesterone administration for luteal phase support in a frozen embryo transfer: a systematic review. Arch Gynecol Obstet. 2023;308(2):341-350. ↩
15. Griesinger G, Blockeel C, Kahler E, et al. Dydrogesterone as an oral alternative to vaginal progesterone for IVF luteal phase support: A systematic review and individual participant data meta-analysis. PLoS One. 2020;15(11):e0241044. ↩
16. Katalinic A, Noftz MR, Garcia-Velasco JA, Shulman LP, van den Anker JN, Strauss JF III. No additional risk of congenital anomalies after first-trimester dydrogesterone use: a systematic review and meta-analysis. Hum Reprod Open. 2024;2024(1):hoae004. ↩
17. Kadoura S, Alhalabi M, Nattouf AH. Conventional GnRH antagonist protocols versus long GnRH agonist protocol in IVF/ICSI cycles of polycystic ovary syndrome women: a systematic review and meta-analysis. Sci Rep. 2022;12(1):4456. ↩
18. European Medicines Agency. Cetrotide (cetrorelix): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
19. European Medicines Agency. Orgalutran (ganirelix): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
20. European Medicines Agency. Gonal-f (follitropin alfa): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
21. European Medicines Agency. Rekovelle (follitropin delta): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
22. European Medicines Agency. Elonva (corifollitropin alfa): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
23. European Medicines Agency. Pergoveris (follitropin alfa / lutropin alfa): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
24. European Medicines Agency. Ovitrelle (choriogonadotropin alfa): EPAR - Product Information. Accessed 2026. EMA, Amsterdam. ↩
25. Ipsen Ltd. Decapeptyl SR 3mg (triptorelin acetate): Summary of Product Characteristics. Electronic Medicines Compendium (emc). Accessed 2026. ↩
26. Ferring Pharmaceuticals Ltd. Menopur 75 IU (highly purified menotropin): Summary of Product Characteristics. Electronic Medicines Compendium (emc). Accessed 2026. ↩
27. Besins Healthcare (UK) Ltd. Utrogestan Vaginal 200 mg Capsules (micronized progesterone): Summary of Product Characteristics. Electronic Medicines Compendium (emc). Accessed 2026. ↩
28. Teede HJ, Bahri Khomami M, Morman R, et al. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. 00717-8) Lancet. Published online May 12, 2026. ↩