Buserelin
A GnRH agonist nonapeptide approved in Europe and Canada since the 1980s for prostate cancer, endometriosis, fibroids, IVF, and precocious puberty — but never FDA-approved in the US.
What is Buserelin?
Buserelin is a synthetic nonapeptide GnRH agonist (pyroGlu-His-Trp-Ser-Tyr-D-Ser(tBu)-Leu-Arg-Pro-NHEt) developed by Hoechst AG in the late 1970s under the code HOE-766. A D-serine(tert-butyl) substitution at position 6 and an ethylamide modification replacing Gly-NH2 at position 10 confer roughly 20-fold greater potency than native GnRH and substantial resistance to enzymatic degradation. Like other GnRH agonists, continuous administration produces an initial gonadotropin flare followed by pituitary receptor desensitization and downregulation, yielding medical castration levels of sex steroids. Buserelin has been approved across Europe, Canada, and many other markets since the mid-1980s for advanced prostate cancer, endometriosis, uterine fibroids, IVF controlled ovarian hyperstimulation, and central precocious puberty — but was never pursued for FDA approval in the United States, leaving it absent from the US market despite decades of clinical use elsewhere.
What Buserelin Is Investigated For
Buserelin is one of the original GnRH agonists — approved in Europe and Canada since the mid-1980s and in continuous clinical use across prostate cancer androgen deprivation therapy, endometriosis, uterine fibroids (preoperative), IVF controlled ovarian hyperstimulation, and central precocious puberty. The clinical efficacy evidence is strong across all of these indications: the EORTC GU Group Trial 30843, the Danish Buserelin Study Group trial, and decades of comparative data place buserelin's efficacy on essentially equivalent footing with leuprolide, goserelin, and triptorelin in the prostate cancer ADT setting, with similar class-level data in endometriosis (where dienogest has been shown non-inferior in head-to-head) and IVF pituitary suppression. The most important caveat is regulatory rather than scientific: buserelin was never pursued for FDA approval by its sponsor (Hoechst, later Sanofi-Aventis, now Sanofi), so it has never been marketed in the United States despite its international presence. US patients and clinicians are largely unfamiliar with it, and access in the US is essentially limited to compounding or importation. The second important caveat is route: the original intranasal formulation has well-documented low bioavailability (roughly 2.5–6% versus ~70% for SC injection), which is why higher daily nasal doses are required and why injection and depot formulations are preferred when reliability of suppression matters most. Class-level GnRH agonist concerns — testosterone flare in advanced prostate cancer, bone mineral density loss with extended use, cardiovascular considerations driving interest in GnRH antagonists in high-risk patients — apply to buserelin equally.
History & Discovery
Buserelin was among the very first GnRH agonists synthesized and developed for clinical use. Its discovery emerged directly from the foundational native GnRH (LHRH) characterization work of Andrew Schally and Roger Guillemin in the early 1970s — work that earned the 1977 Nobel Prize in Physiology or Medicine. Recognizing that continuous GnRH receptor stimulation paradoxically suppressed rather than stimulated the hypothalamic-pituitary-gonadal axis (via receptor desensitization and downregulation), pharmaceutical programs in Europe, the US, and Japan raced to develop D-amino-acid-substituted superagonists with enhanced potency and metabolic stability. Hoechst AG (Germany) synthesized buserelin under the internal code HOE-766 in the late 1970s. The nonapeptide design — replacing Gly-NH2 at position 10 with ethylamide and substituting D-serine(tert-butyl) at position 6 — produced a molecule with approximately 20-fold greater GnRH receptor affinity and sustained duration of action compared with native GnRH. Notably, buserelin's position-10 modification yields a nonapeptide rather than the decapeptide backbone retained by triptorelin, while sharing with leuprolide the ethylamide-at-position-10 and D-amino-acid-at-position-6 design pattern. Buserelin was launched in Europe in the mid-1980s as Suprefact (injection and nasal spray) for advanced prostate cancer and as Suprecur (nasal spray) for endometriosis, uterine fibroids, and IVF protocol use. Health Canada approval followed (Suprefact, Suprefact Depot), along with approvals across the UK, continental Europe, Australia, Japan, and most of Asia and Latin America. The 6.3 mg buserelin base depot implant (Suprefact Depot / Profact Depot) providing 2-month release via PLGA 75:25 polymer technology was added to the product family, with 9.45–9.9 mg 3-month formulations following. Critically, Hoechst and its successor companies (Hoechst Marion Roussel, Aventis, Sanofi-Aventis, Sanofi) never pursued US FDA approval for buserelin. The US market was instead dominated by leuprolide (FDA-approved 1985 as Lupron), goserelin (FDA-approved 1989 as Zoladex), histrelin, and eventually triptorelin (FDA-approved 2000 as Trelstar). The commercial decision not to pursue US approval — rather than any safety or efficacy concern — explains buserelin's curious status as a thoroughly established international drug that is simply absent from the US pharmacy shelf. In the EORTC GU Group Trial 30843 and the Danish Buserelin Study Group trial, buserelin was established as equivalent to surgical orchidectomy for metastatic prostate cancer, consolidating the GnRH agonist approach as the preferred form of medical castration. The dienogest-versus-intranasal-buserelin Japanese phase 3 trial (2008) later demonstrated that oral dienogest is non-inferior to buserelin for endometriosis pain, a finding that has shaped international endometriosis practice in markets where both drugs are available.
How It Works
Buserelin is a long-acting synthetic version of the brain's reproductive hormone GnRH. A single dose briefly stimulates the pituitary to release LH and FSH, but when given continuously — daily injections, nasal spray, or a 2-month depot implant — it overwhelms and shuts down the GnRH receptor. This stops LH and FSH production, which in turn stops testosterone and estrogen production. The effect is reversible after stopping.
Buserelin (pyroGlu-His-Trp-Ser-Tyr-D-Ser(tBu)-Leu-Arg-Pro-NHEt) is a nonapeptide GnRH superagonist. The D-Ser(tert-butyl) substitution at position 6 increases receptor binding affinity and confers resistance to proteolytic cleavage, while the ethylamide substitution replacing Gly-NH2 at position 10 further stabilizes the peptide and enhances receptor affinity. Binding potency at the GnRH receptor (GnRHR) is approximately 20-fold greater than native GnRH, and the prolonged duration of action is partly attributable to sustained receptor occupancy. Acute administration activates Gq/11-coupled GnRHR signaling in pituitary gonadotropes, triggering LH and FSH release (the clinically observed 'flare'). Sustained exposure — via repeated daily injection, continuous nasal administration, or slow-release depot implant — causes GnRHR internalization, uncoupling from phospholipase C signaling, and transcriptional downregulation of receptor expression. The net result is castrate-level testosterone (<50 ng/dL, or by contemporary standards <20 ng/dL) in men and postmenopausal-range estradiol in women, typically achieved within 2–4 weeks of continuous therapy. Recovery of pituitary responsiveness and gonadal function after discontinuation is gradual and typically complete in younger patients but may be incomplete in older men after prolonged ADT. The 6.3 mg buserelin base implant (Suprefact Depot / Profact Depot) uses a PLGA 75:25 biodegradable polymer matrix providing an initial release peak on day 1 followed by an 8-week plateau and a terminal release half-life of 20–30 days during polymer biodegradation, supporting the 2-month dosing interval.
Evidence Snapshot
Human Clinical Evidence
Extensive. Approved across Europe, Canada, and many international markets since the mid-1980s. Supported by the EORTC GU Group Trial 30843 in prostate cancer, the Danish Buserelin Study Group phase III trial, multiple endometriosis RCTs (including the dienogest head-to-head), multi-centre precocious puberty trials, and widespread IVF pituitary suppression protocol use.
Animal / Preclinical
Comprehensive. GnRH receptor desensitization, PLGA implant pharmacokinetics, and HPG-axis suppression are thoroughly characterized.
Mechanistic Rationale
Very strong. GnRH receptor pharmacology and D-amino acid substitution structure-activity relationships are well-established across the agonist class.
Research Gaps & Open Questions
What the current literature has not yet settled about Buserelin:
- 01Head-to-head buserelin vs. leuprolide, goserelin, or triptorelin comparative outcomes — most class-level data treat the agonists as interchangeable, but adequately powered head-to-head comparisons for prostate cancer outcomes are limited; subtle differences in testosterone suppression onset, cardiovascular safety, and quality-of-life endpoints might exist.
- 02GnRH agonist vs. GnRH antagonist comparative cardiovascular outcomes in buserelin-treated populations — the PRONOUNCE (degarelix vs. leuprolide) and HERO (relugolix vs. leuprolide) trials used leuprolide as comparator; dedicated buserelin data in this question is limited, and extrapolation from leuprolide is reasonable but imperfect.
- 03Optimal route and formulation selection — buserelin has unusually rich formulation diversity (SC injection, intranasal spray, 2-month implant, 3-month implant), but comparative effectiveness and patient-preference data across these routes is limited and largely historical.
- 04Intranasal absorption variability — low bioavailability (2.5–6%) with substantial inter-patient variability is a known limitation, but rigorous studies of clinical impact and absorption-enhancement strategies (cyclodextrin formulations, mucoadhesive vehicles) have not translated into widespread practice changes.
- 05Role of buserelin in contemporary ovarian suppression for premenopausal hormone-receptor-positive breast cancer — international guidelines generally recommend goserelin or triptorelin; buserelin data in this indication is older and less developed.
- 06Long-term outcomes of central precocious puberty treatment with buserelin specifically — long-term adult height, bone density, fertility, and metabolic outcome data exist but are mostly from registry or observational cohorts rather than dedicated long-term RCT follow-up.
Forms & Administration
Three formulations: (1) subcutaneous injection 1 mg/mL solution (Suprefact injection), typically 500 mcg TID during the first week then 200 mcg daily for prostate cancer; (2) intranasal spray 100 mcg/spray (Suprefact, Suprecur nasal) typically 150–400 mcg per nostril administered multiple times daily; (3) subcutaneous depot implant 6.3 mg buserelin base (Suprefact Depot, Profact Depot) providing 2-month sustained release, or 9.45–9.9 mg implant for 3-month release. All injectable or implanted peptides should only be administered under the guidance of a qualified healthcare provider. Never self-administer without clinician oversight.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
Advanced prostate cancer (Suprefact SC injection): 500 mcg subcutaneously three times daily (every 8 hours) for the first 7 days, then 200 mcg subcutaneously once daily for maintenance. Depot formulation (Suprefact Depot, Profact Depot): 6.3 mg buserelin base implant subcutaneously every 2 months, or 9.45–9.9 mg implant every 3 months. Intranasal formulation (Suprefact nasal, Suprecur): typically 400 mcg 3 times daily (one 100 mcg spray into each nostril, three times daily, totaling 1.2 mg/day) for prostate cancer after the initial 7-day injection phase; 150 mcg three times daily in each nostril (900 mcg/day total) for endometriosis; 100 mcg four times daily for most central precocious puberty protocols. IVF controlled ovarian hyperstimulation protocol use: 500–600 mcg daily SC (short or long protocol) or 150 mcg 4–6 times daily intranasally, started in the mid-luteal phase of the preceding cycle for the long protocol.
Frequency
SC injection dosing is TID initially then QD for maintenance. Intranasal dosing is typically 3–6 times daily reflecting the short intranasal half-life and low bioavailability. Depot implant dosing is every 2 months (6.3 mg) or every 3 months (9.45–9.9 mg). No dosing interval of once daily is adequate for the nasal spray — the multi-daily schedule is intrinsic to that route.
Timing Considerations
No specific timing requirements: can be administered at any time of day, with or without food, and is not tied to exercise timing. Consistency matters more than the specific clock — dose at roughly the same time each day (or same day each week, for weekly protocols) to keep exposure steady.
Cycle Length
Prostate cancer ADT is typically chronic indefinite for metastatic disease, time-limited (6 months to several years) as adjuvant to definitive radiation in localized high-risk disease, or intermittent in selected biochemical-recurrence patients. Endometriosis treatment is labeled for up to 6 months in most markets, with longer durations possible when hormonal add-back is used. Uterine fibroid treatment is typically up to 3 months preoperatively. Central precocious puberty treatment continues until appropriate physiologic age for puberty. IVF protocols run from mid-luteal suppression through the stimulation cycle — typically 3–6 weeks per cycle.
Protocol Notes
The initial gonadotropin flare and consequent testosterone or estrogen surge during the first 1–2 weeks is the clinically critical pharmacology to manage. In advanced prostate cancer with high tumor burden, bone metastases, or impending spinal cord compression, anti-androgen pre-loading is standard — cyproterone acetate is the traditional European practice, while bicalutamide or flutamide are more common elsewhere. The EORTC 30843 trial demonstrated that extended cyproterone combination does not improve survival over standard ADT, so the anti-androgen cover is specifically for flare management, not long-term combination. The intranasal formulation's low bioavailability (roughly 2.5–6% versus ~70% for SC injection) is the main reason multi-daily dosing is required, and it is also why SC injection and depot implant formulations are generally preferred when reliable, consistent suppression is the clinical priority (advanced prostate cancer, established endometriosis, IVF protocol suppression). Nasal mucosal conditions — rhinitis, upper respiratory infection, rhinorrhea — can substantially disrupt absorption and should prompt temporary switch to injection if suppression is questioned. Breakthrough bleeding in women on intranasal buserelin for endometriosis or fibroids is a common indicator of suboptimal absorption. The 6.3 mg buserelin base PLGA implant provides an initial release peak on day 1 followed by an 8-week plateau and polymer biodegradation with a 20–30 day terminal release half-life, supporting the 2-month dosing interval. The implant is inserted subcutaneously (typically in the abdominal wall) and generally does not require removal — the PLGA polymer biodegrades in situ. Bone mineral density loss with extended ADT is class-level and warrants the same proactive management as with leuprolide or triptorelin: baseline DXA, calcium and vitamin D, weight-bearing exercise, and consideration of bisphosphonate or denosumab in patients on extended therapy. For endometriosis and fibroid management, hormonal add-back (norethindrone acetate or low-dose estrogen plus progestin) extends the tolerable treatment duration and mitigates vasomotor and bone-loss burden.
Buserelin is approved across Europe, Canada, and many international markets for prostate cancer, endometriosis, uterine fibroids, IVF protocols, and central precocious puberty. It was never FDA-approved in the United States — US access is essentially through importation or compounding and is not standard. Any use should be under the supervision of a clinician familiar with GnRH agonist therapy and the relevant indication.
Timeline of Effects
Onset
After first SC injection or depot implant, an initial LH/FSH and consequent testosterone or estrogen 'flare' occurs over the first 7–14 days. Pituitary desensitization develops over the next 2–4 weeks. Castrate-level testosterone in men with advanced prostate cancer is typically achieved by week 3–4. For intranasal dosing, the onset is somewhat slower due to the lower and more variable bioavailability. PSA decline in advanced prostate cancer, pain reduction in endometriosis, and uterine/fibroid volume reduction typically become measurable within 4–8 weeks.
Peak Effect
Maximal hormonal suppression is sustained throughout the depot interval with appropriate redosing. Fibroid and uterine volume reduction typically continues through the first 2–3 months of continuous therapy — one prospective series documented leiomyoma volume reduction of ~54% versus ~42% whole-uterus reduction during buserelin treatment. PSA nadir in advanced prostate cancer is typically reached by months 3–6 and is prognostic of long-term outcome. BMD loss begins within the first months of continuous therapy and progresses without intervention.
After Discontinuation
Pituitary recovery and gonadal function return after discontinuation is gradual — testosterone recovery to baseline typically takes 2–6 months in younger men and can be slower or incomplete after extended ADT in older men. In premenopausal women treated for endometriosis or fibroids, menstrual cycles typically resume within 1–4 months after stopping. A well-documented pattern in uterine fibroid management is rapid regrowth after buserelin discontinuation — the preoperative shrinkage window is the clinical value, not durable disease modification. In central precocious puberty, normal pubertal progression resumes within months of discontinuation, allowing physiologically appropriate development.
Common Questions
Who Buserelin Is NOT For
- •Pregnancy — buserelin can cause fetal harm; effective non-hormonal contraception is required for women of reproductive potential during therapy and for a period after discontinuation.
- •Breastfeeding — not recommended.
- •Known hypersensitivity to buserelin or to GnRH or GnRH analogs (cross-reactivity across the class is possible).
- •Undiagnosed abnormal vaginal bleeding — should be evaluated before initiating gynecologic-indication therapy.
- •Severe spinal cord compression or urinary tract obstruction in advanced prostate cancer — the testosterone flare can acutely worsen these conditions. Anti-androgen pre-loading (cyproterone acetate, bicalutamide, flutamide) is mandatory; in some cases a GnRH antagonist (degarelix) is preferred to avoid the flare entirely.
- •Pre-existing severe osteoporosis without bone-protective co-therapy — relative contraindication for extended use; bone protection should accompany extended GnRH agonist therapy in at-risk patients.
- •Significant pre-existing cardiovascular disease — relative contraindication; class-level ADT cardiovascular signal warrants consideration of GnRH antagonist as an alternative in high-risk patients.
- •Significant nasal mucosal disease or recurrent rhinitis — relative contraindication for the intranasal formulation due to unreliable absorption; switch to SC injection or depot implant is appropriate.
- •Pediatric use outside central precocious puberty — not established for other pediatric indications.
Drug & Supplement Interactions
Buserelin's drug-interaction profile closely mirrors the class. Peptide proteolytic clearance does not engage CYP-mediated metabolism, so classical pharmacokinetic drug-drug interactions are minimal. The clinically important interactions are pharmacodynamic. Anti-androgens (cyproterone acetate, bicalutamide, flutamide, nilutamide, enzalutamide): co-administration during the testosterone flare is standard practice. In European prostate cancer practice, cyproterone acetate is the traditional partner; elsewhere, bicalutamide or flutamide are more common. The EORTC 30843 trial established that extended combination does not improve survival, so the anti-androgen cover is specifically for flare management rather than long-term combination therapy. Agents affecting nasal mucosal function (topical decongestants, intranasal corticosteroids, other intranasal medications): can alter buserelin absorption from the nasal formulation and theoretically reduce effective dose. Separate administration timing is commonly advised, and persistent nasal symptoms warrant consideration of switching to SC injection. QT-prolonging medications: GnRH agonists can prolong QT interval, and combination with other QT-prolonging agents (Class IA and III antiarrhythmics, certain antiemetics, fluoroquinolones, methadone) warrants ECG monitoring and electrolyte management in at-risk patients. Diabetic medications: long-term ADT alters insulin sensitivity and increases diabetes risk; patients on insulin or oral antihyperglycemics may need dose adjustment over months of therapy. Antihypertensives and lipid-lowering agents: ADT affects cardiovascular physiology and lipid profiles over time; medication adjustments may be needed over the course of extended therapy. Warfarin: minimal documented direct interaction, but overall metabolic shifts during ADT can affect anticoagulation control; continued INR monitoring is appropriate. Hormonal contraceptives: should not be relied upon for contraception during buserelin therapy for gynecologic indications — non-hormonal contraception is recommended. As with any chronic specialty therapy, patients should disclose all prescription, OTC, and supplement use to their prescriber.
Safety Profile
Common Side Effects
Cautions
- • Initial testosterone or estrogen flare can worsen symptoms in advanced prostate cancer or endometriosis
- • Long-term use causes bone mineral density loss
- • Cardiovascular considerations with extended androgen deprivation
- • Not for use in pregnancy
- • Intranasal formulation has low bioavailability (2.5–6%) requiring higher daily doses
- • Not FDA-approved in the US — access outside approved international markets is limited
What We Don't Know
Well-characterized safety profile with over 40 years of clinical use across Europe, Canada, and other markets. The class-level long-term cardiovascular and metabolic effects of ADT are monitored the same way as with leuprolide or triptorelin.
Legal Status
United States
Buserelin is NOT FDA-approved in the United States and has never been marketed in the US. Hoechst AG and its successor companies (Hoechst Marion Roussel, Aventis, Sanofi-Aventis, Sanofi) never pursued FDA approval — a commercial decision made in the context of leuprolide (Lupron) dominating the US GnRH agonist market from 1985 onward. US clinicians and patients seeking buserelin access typically do so through importation, compounding pharmacy, or clinical trial pathways, none of which constitute standard-of-care access. US practice uses leuprolide, goserelin, triptorelin, histrelin, or the newer GnRH antagonists (degarelix, relugolix) for the indications for which buserelin is used internationally.
International
Approved across Europe, Canada, Australia, Japan, and most international markets since the mid-1980s. Marketed as Suprefact (injection and nasal spray), Suprefact Depot / Profact Depot (2-month and 3-month implant), Suprecur (nasal spray for endometriosis / IVF), and under other brand names regionally. Health Canada, MHRA (UK), EMA national-authority approvals, and TGA (Australia) all cover the major indications: advanced prostate cancer, endometriosis, uterine fibroids (preoperative), central precocious puberty, and IVF controlled ovarian hyperstimulation protocols.
Sports & Competition
Buserelin and other GnRH agonists are prohibited on the WADA Prohibited List under S4 (Hormone and Metabolic Modulators) for male athletes in and out of competition. The classification captures non-therapeutic use in 'post-cycle therapy' contexts following anabolic-androgenic steroid administration, where GnRH agonists are sometimes used in bodybuilding culture in attempts to restart endogenous testosterone production — a use that lacks controlled-trial support and carries risk of unintended prolonged HPG-axis suppression. Therapeutic use for prostate cancer or other approved indications under appropriate Therapeutic Use Exemption is permitted.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
Buserelin is not FDA-approved because it's unsafe or ineffective.
Reality
Buserelin's absence from the US market is a commercial decision, not a safety or efficacy issue. Hoechst AG and its successor companies never pursued FDA approval — leuprolide (Lupron, FDA-approved 1985) and goserelin (Zoladex, FDA-approved 1989) already dominated the US GnRH agonist market. Buserelin has been approved and in continuous clinical use across Europe, Canada, Australia, Japan, and most international markets since the mid-1980s, with an efficacy and safety profile essentially equivalent to the US-approved GnRH agonists.
Myth
Buserelin nasal spray is a convenient substitute for injection — same effect, easier to use.
Reality
Intranasal buserelin bioavailability is roughly 2.5–6% versus about 70% for SC injection, which is why the nasal formulation requires multi-daily dosing (3–6 times per day) and higher total daily doses, and why suppression reliability is more variable than with injection. Rhinitis, upper respiratory infection, or nasal mucosal conditions can substantially disrupt absorption. For the strictest suppression requirements — advanced prostate cancer, established endometriosis, IVF protocol pituitary down-regulation — SC injection or depot implant is typically preferred.
Myth
The testosterone flare from buserelin means the drug is working incorrectly.
Reality
The flare is the expected pharmacology of every GnRH agonist. Initial receptor stimulation produces transient LH/FSH and gonadal hormone elevation before desensitization develops over 2–4 weeks. In advanced prostate cancer with high tumor burden, anti-androgen pre-loading (cyproterone acetate, bicalutamide, flutamide) is standard practice specifically to blunt flare-related symptom worsening. The EORTC 30843 trial examined whether extended cyproterone combination improved survival and found it did not — so the anti-androgen cover is for the flare window, not continuous combination.
Myth
All GnRH agonists (buserelin, leuprolide, goserelin, triptorelin) are the same drug in different boxes.
Reality
They share the class mechanism and have essentially equivalent clinical efficacy within the approved indications, but they differ in peptide structure (buserelin is a nonapeptide with D-Ser(tBu)6; leuprolide has D-Leu6; triptorelin has D-Trp6 on the native decapeptide), formulation options (buserelin uniquely pioneered the intranasal route; leuprolide and triptorelin are depot-dominant), depot pharmacokinetics and dosing intervals, and regional regulatory approval scope. Selection is typically driven by formulation availability, depot interval, payer access, and clinician familiarity rather than meaningful efficacy differences.
Myth
Buserelin-induced fibroid shrinkage is durable — the fibroids don't come back.
Reality
Buserelin effectively shrinks uterine fibroids during continuous therapy — roughly 40–55% volume reduction over 2–3 months — but rapid regrowth after discontinuation is the documented rule, not the exception. The clinical value of preoperative buserelin is creating a window of smaller fibroids and restored hemoglobin for surgical planning (particularly enabling less invasive approaches like hysteroscopic resection or vaginal hysterectomy), not achieving durable disease modification without surgery.
Published Research
35 studiesGonadotropin-releasing hormone agonists in prostate cancer: A comparative review of efficacy and safety
Are all gonadotrophin-releasing hormone agonists equivalent for the treatment of prostate cancer? A systematic review
Dienogest is as effective as intranasal buserelin acetate for the relief of pain symptoms associated with endometriosis—a randomized, double-blind, multicenter, controlled trial
Phase 3 Japanese RCT (271 patients) demonstrating that oral dienogest 2 mg/day is non-inferior to intranasal buserelin 900 mcg/day for endometriosis pain symptoms over 24 weeks, with less bone mineral density loss — a practice-changing head-to-head that has shaped endometriosis management decisions internationally.
GnRH agonist (buserelin) or hCG for ovulation induction in GnRH antagonist IVF/ICSI cycles: a prospective randomized study
In vitro and in vivo correlation of buserelin release from biodegradable implants using statistical moment analysis
A prospective randomized study comparing endocrinological and clinical effects of two types of GnRH agonists in cases of uterine leiomyomas or endometriosis
A comparison of three gonadotrophin-releasing hormone analogues in an in-vitro fertilization programme: a prospective randomized study
Maximum androgen blockade using LHRH agonist buserelin in combination with short-term (two weeks) or long-term (continuous) cyproterone acetate is not superior to standard androgen deprivation in the treatment of advanced prostate cancer. Final analysis of EORTC GU Group Trial 30843
Final analysis of the landmark EORTC 30843 three-arm phase 3 trial (orchidectomy vs. buserelin + 2-week cyproterone vs. buserelin + continuous cyproterone) — established that buserelin is equivalent to surgical castration and that extended maximum androgen blockade does not improve survival.
The effect of Buserelin versus conventional antiandrogenic treatment in patients with T2-4NXM1 prostatic cancer. A prospective, randomized multicentre phase III trial. The 'Danish Buserelin Study Group'
Danish multicenter phase III RCT comparing buserelin against conventional antiandrogen therapy in metastatic prostate cancer — established buserelin's efficacy parity with standard hormonal approaches and contributed to the consolidation of GnRH agonist ADT as first-line medical castration.
Intranasal nafarelin versus buserelin (short protocol) for controlled ovarian hyperstimulation before in vitro fertilization: a prospective clinical trial
Buserelin acetate in the treatment of pelvic pain associated with minimal and mild endometriosis: a controlled study
Short-term versus long-term addition of cyproterone acetate to buserelin therapy in comparison with orchidectomy in the treatment of metastatic prostate cancer. European Organization for Research and Treatment of Cancer—Genitourinary Group
Subcutaneous goserelin versus intranasal buserelin for pituitary down-regulation in patients undergoing IVF: a randomized comparative study
Differential reduction in the volume of leiomyoma and uterus during buserelin treatment
Final height in girls with central precocious puberty: comparison of two different luteinizing hormone-releasing hormone agonist treatments
Treatment with a luteinising-hormone-releasing-hormone analogue (buserelin) in premenopausal patients with metastatic breast cancer
A comparison of diethylstilbestrol or orchiectomy with buserelin and with methotrexate plus diethylstilbestrol or orchiectomy in newly diagnosed patients with clinical stage D2 cancer of the prostate
Efficacy of buserelin in advanced prostate cancer and comparison with historical controls
Treatment of central precocious puberty with an intranasal analogue of GnRH (Buserelin)
Buserelin treatment of advanced prostatic carcinoma. Long-term follow-up of antitumor responses and improved quality of life
Pharmacokinetic characteristics of the gonadotropin-releasing hormone analog D-Ser(TBU)-6EA-10luteinizing hormone-releasing hormone (buserelin) after subcutaneous and intranasal administration in children with central precocious puberty
The prolonged action of the LHRH agonist buserelin (HOE 766) may be due to prolonged binding to the LHRH receptor
Treatment of central precocious puberty with an LHRH agonist (Buserelin): effect on growth and bone maturation after three years of treatment
LH-RH agonist (buserelin): treatment of endometriosis. Clinical, laparoscopic, endocrine and metabolic evaluation
Pharmacokinetics and endocrine effects of the LHRH analogue buserelin after subcutaneous implantation of a slow release preparation in prostatic cancer patients
Foundational PK/PD study of the subcutaneous buserelin depot implant (now marketed as Suprefact Depot / Profact Depot) demonstrating sustained testosterone suppression across the dosing interval — the pharmacokinetic basis for the 2-month and 3-month implant formulations in current international use.
Ovarian suppression induced with Buserelin or danazol in the management of endometriosis: a randomized, comparative study
Orchidectomy versus Buserelin in combination with cyproterone acetate, for 2 weeks or continuously, in the treatment of metastatic prostatic cancer. Preliminary results of EORTC-trial 30843
Controlled ovarian hyperstimulation for in vitro fertilization using buserelin and gonadotropin in patients with previous failed cycles
Clinical predictors for buserelin acetate treatment of uterine fibroids: a prospective study of 40 women
Use of buserelin in an IVF programme for pituitary-ovarian suppression prior to ovarian stimulation with exogenous gonadotrophins
Luteinizing hormone-releasing hormone analogue (Buserelin) treatment for central precocious puberty: a multi-centre trial
Multi-centre open trial establishing intranasal buserelin as first-line treatment for central precocious puberty — demonstrated reduction of LH/FSH response to prepubertal levels, slowing of height velocity and bone age, and regression or arrest of secondary sexual development.
Buserelin. A review of its pharmacodynamic and pharmacokinetic properties, and clinical profile
The canonical ADIS Drugs journal review (Brogden, Buckley, and Ward, 1990) establishing buserelin's pharmacology, dosing, and clinical profile across prostate cancer, endometriosis, precocious puberty, and IVF — the most-cited comprehensive buserelin reference.
Intranasal buserelin versus surgery in the treatment of uterine leiomyomata: long-term follow-up
RCT of 42 women with symptomatic uterine myomas randomized to 6 months of intranasal buserelin 1200 mcg/day or immediate surgery — documented the ~40% uterine volume reduction during treatment but also the rapid myoma regrowth after discontinuation, establishing buserelin's role as preoperative rather than definitive fibroid therapy.
Effect of chemotherapy with or without buserelin on serum hormone levels in premenopausal women with breast cancer
Buserelin acetate versus expectant management in the treatment of infertility associated with minimal or mild endometriosis: a randomized clinical trial
Quick Facts
- Class
- GnRH Agonist
- Evidence
- Strong
- Safety
- Well-Studied
- Updated
- Apr 2026
- Citations
- 35PubMed
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Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.