Triptorelin
Triptorelin is a synthetic decapeptide analog of gonadotropin-releasing hormone (GnRH) that functions as a potent agonist, initially stimulating the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) before causing receptor downregulation and subsequent suppression of gonadotropin secretion, thereby reducing testosterone levels in men and estrogen levels in women.[1][2] Primarily indicated for the palliative treatment of advanced prostate cancer through androgen deprivation therapy, it achieves castrate levels of testosterone, slowing cancer progression and alleviating symptoms such as bone pain.[3][4] Triptorelin is also approved for treating central precocious puberty in children by delaying puberty onset and reducing associated growth accelerations.[5] Administered via intramuscular depot injections (e.g., as Trelstar or Decapeptyl) at intervals of 1, 3, or 6 months, it demonstrates sustained efficacy in maintaining hormone suppression, though initial flare-ups may require anti-androgen co-therapy to mitigate transient tumor stimulation.[6][7] Common adverse effects include hot flashes, fatigue, and injection-site reactions, reflecting its impact on sex hormone pathways.[1]Pharmacology
Mechanism of action
Triptorelin is a synthetic decapeptide analogue of gonadotropin-releasing hormone (GnRH), functioning as a high-affinity agonist at GnRH receptors in the anterior pituitary gland.[2] [8] Upon initial administration, triptorelin binds to these receptors and stimulates the release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from gonadotroph cells, mimicking the pulsatile action of endogenous GnRH and thereby inducing a transient surge in circulating gonadotropins.[9] This acute phase elevates gonadal steroidogenesis, increasing testosterone levels in males and estrogen levels in females within hours to days, depending on the dose and formulation.[1] [10] With continuous or repeated dosing, triptorelin causes receptor desensitization through mechanisms including downregulation of GnRH receptor expression, internalization of receptor-ligand complexes, and uncoupling of signal transduction pathways.[9] [11] These processes lead to a marked suppression of LH and FSH secretion, typically achieving castrate levels of testosterone (below 50 ng/dL) in men after 2-4 weeks of therapy.[1] In women, estradiol levels are similarly reduced to postmenopausal ranges.[1] The net effect is profound inhibition of gonadal function, rendering triptorelin a potent suppressor of sex steroid production, which underpins its therapeutic applications in hormone-dependent conditions.[12] This biphasic response—initial flare followed by downregulation—is characteristic of GnRH agonists and distinguishes them from antagonists, which lack the stimulatory phase.[11]Pharmacokinetics
Triptorelin exhibits a three-compartment pharmacokinetic profile following intravenous (IV) administration, characterized by rapid initial distribution and slower elimination phases. After a single IV bolus of 0.5 mg, the drug is completely absorbed, with distribution half-lives of approximately 6 minutes and 45 minutes, followed by an elimination half-life of about 3 hours.[4] Total clearance in healthy male volunteers is approximately 211.9 mL/min.[4] For intramuscular (IM) depot formulations, such as triptorelin pamoate, absorption is sustained, with peak serum levels typically reached on days 2 to 4 post-injection.[13] After the initial release phase, serum concentrations stabilize at mean levels of about 0.06 ng/mL for roughly 12 weeks following a single IM dose of triptorelin pamoate 3.75 mg.[7] The volume of distribution remains consistent with IV data, reflecting distribution into extracellular fluids.[14] Metabolism of triptorelin in humans is not fully characterized but does not involve cytochrome P450 enzymes, and no specific metabolites have been identified; the peptide is likely degraded enzymatically in tissues or plasma.[2] Excretion occurs via both hepatic and renal routes, with the drug cleared completely through these pathways.[2] In patients with moderate to severe renal or hepatic impairment, the area under the curve (AUC) for triptorelin increases by approximately twofold compared to healthy subjects, though distribution half-lives remain unchanged; dose adjustments may be necessary in such populations.[15] The elimination half-life is generally 3 to 5 hours across formulations, unaffected by age or sex in adults.[16]Clinical uses
Prostate cancer
Triptorelin pamoate, marketed as Trelstar, is approved by the U.S. Food and Drug Administration for the palliative treatment of advanced prostate cancer in adult men.[17] As a gonadotropin-releasing hormone (GnRH) agonist, it forms the basis of androgen deprivation therapy (ADT) by suppressing gonadal testosterone production to castrate levels (typically below 50 ng/dL or 1.7 nmol/L), thereby inhibiting the growth of androgen-dependent prostate tumors.[7] Initial administration may cause a transient testosterone surge (flare), which can exacerbate symptoms in some patients; anti-androgens such as bicalutamide are often co-administered prophylactically for the first few weeks to mitigate this risk.[17] Available formulations include intramuscular injections of 3.75 mg (monthly), 11.25 mg (every 3 months), and 22.5 mg (every 6 months), allowing flexibility based on patient needs and monitoring requirements.[18] Clinical studies demonstrate that these sustained-release formulations achieve rapid and sustained testosterone suppression in over 95% of patients, with nadir levels often below 20 ng/dL, correlating with reductions in prostate-specific antigen (PSA) levels and tumor progression delay.[19] For instance, in phase III trials involving over 1,000 patients with advanced disease, triptorelin maintained castrate testosterone levels for the full dosing interval in 97-99% of cases, comparable to other GnRH agonists like leuprolide.[20] Triptorelin is particularly suited for long-term ADT in locally advanced or metastatic hormone-sensitive prostate cancer, where it is often combined with radiation therapy or used as monotherapy when surgery is not feasible.[7] Pooled analyses from nine phase III studies (n=1,511) showed that deeper testosterone suppression (nadir <20 ng/dL) was associated with improved clinical outcomes, including longer time to PSA progression and reduced risk of skeletal events, independent of baseline prognostic factors.[21] In real-world settings, it has also alleviated lower urinary tract symptoms (LUTS) in men with moderate-to-severe bother from prostate cancer-related obstruction, with significant improvements in International Prostate Symptom Scores observed within 3-6 months.[22] Ongoing research explores triptorelin in neoadjuvant settings before prostatectomy or as part of intermittent ADT to potentially reduce cumulative toxicity while preserving efficacy, though definitive superiority over continuous therapy remains unproven.[23] Patient selection emphasizes monitoring for breakthrough testosterone rises, which occur in <5% of cases and may necessitate dosage adjustments or switching agents.[24] Overall, triptorelin's efficacy profile supports its role as a standard ADT option, with evidence from randomized controlled trials confirming non-inferiority to historical standards in delaying disease progression.[25]Precocious puberty
Triptorelin, a gonadotropin-releasing hormone (GnRH) agonist, is approved for treating central precocious puberty (CPP) in pediatric patients aged 2 years and older, where it suppresses premature activation of the hypothalamic-pituitary-gonadal axis to halt pubertal progression.[26] The U.S. Food and Drug Administration approved the 6-month prolonged-release formulation (Triptodur, 22.5 mg) in June 2017 as the first GnRH agonist dosed every 6 months for this indication, based on pharmacokinetic and pharmacodynamic data demonstrating sustained suppression of luteinizing hormone (LH) and follicle-stimulating hormone (FSH).[27][28] Clinical trials have confirmed triptorelin's efficacy in suppressing gonadal hormones, reducing bone age advancement, and improving predicted adult height in children with CPP. In a phase 3 open-label trial of the 6-month formulation in Chinese children, triptorelin suppressed stimulated LH levels below 4 IU/L in over 90% of patients after 6 months, with consistent results up to 12 months, mirroring prior global data.[29] A long-term study of the 3-month depot in girls showed sustained inhibition of sex steroids, slowed skeletal maturation (bone age advance reduced to 0.4 years per chronological year), and height gains aligning with target heights after 2–5 years of treatment.[30] Comparative analyses indicate no significant efficacy differences versus leuprolide, another GnRH agonist, in suppressing pubertal progression or advancing final height.[31] Standard dosing involves a single 22.5 mg intramuscular injection every 6 months for children weighing at least 22 kg, with monitoring of LH, FSH, estradiol (in girls), testosterone (in boys), and bone age to assess response and guide discontinuation upon pubertal age attainment.[32] Long-term outcomes from retrospective and follow-up studies demonstrate improved final adult heights (e.g., gains of 5–7 cm over pretreatment predictions in treated cohorts) without adverse effects on fertility or reproductive function in adulthood.[33][34] Safety profiles align with GnRH agonist class effects, including injection-site reactions and transient initial hormone flares, but trials report no serious treatment-related adverse events beyond these, with effective suppression maintained over years.[35][31] Discontinuation typically restores normal pubertal progression without rebound acceleration.[30]Gynecological conditions
Triptorelin, a gonadotropin-releasing hormone (GnRH) agonist, is utilized in gynecological practice primarily for conditions driven by estrogen-dependent tissue proliferation, such as endometriosis, uterine fibroids (leiomyomas), and adenomyosis. By inducing a hypoestrogenic state through pituitary desensitization, it reduces lesion size, alleviates symptoms like dysmenorrhea, dyspareunia, chronic pelvic pain, and heavy menstrual bleeding, and may facilitate subsequent surgical or conservative management. Treatment durations typically range from 3 to 6 months, often with add-back hormone therapy to mitigate menopausal-like side effects, though long-term use is limited by bone density concerns.[36][37] In endometriosis, particularly deep infiltrating forms, triptorelin monotherapy or adjunctive therapy post-conservative surgery yields sustained symptom relief. A multicenter prospective study of up to 24 weeks of triptorelin following surgery for deep infiltrating endometriosis reported significant improvements in pain scores and low recurrence rates over 24 months of follow-up, with over 90% of patients experiencing reduced dysmenorrhea and dyspareunia. A randomized placebo-controlled trial confirmed triptorelin's superiority in reducing endometriosis-associated pain, with treated patients showing lower revised American Fertility Society scores for adhesions and implants compared to placebo. Comparative assessments of formulations, such as 3-month pamoate versus 1-month acetate, demonstrated noninferior estradiol suppression and symptom control in over 98% of cases.[38][39][40] For uterine fibroids, triptorelin serves as preoperative therapy to shrink tumors and decrease bleeding risk, enabling less invasive procedures. In a clinical trial involving monthly 3.75 mg injections for 3 months before hysterectomy, women achieved significant fibroid volume reduction (up to 40-50% in some cohorts) and uterine size decrease, correlating with improved surgical outcomes. Randomized comparisons with aromatase inhibitors like letrozole showed triptorelin's comparable efficacy in myoma volume reduction over 12 weeks, though with greater hypoestrogenic effects. Guidelines recommend its use for symptom control prior to myomectomy or hysterectomy, particularly in cases of heavy bleeding or anemia.[41][42][36] Adenomyosis responds favorably to triptorelin, with multicenter observational data indicating rapid symptom amelioration. A study of 3.75 mg monthly injections for 3-6 months in 120 patients reported marked reductions in heavy menstrual bleeding (from baseline scores >7 to <3 on visual analog scales) and pelvic pain, alongside improved uterine morphology on imaging and enhanced fertility outcomes in reproductive-age subsets, with 70% achieving pregnancy post-treatment. Adverse events were primarily vasomotor and manageable, supporting its role in both symptomatic relief and fertility preservation strategies. No serious treatment-related complications were noted across cohorts.[43][44]Other indications
Triptorelin is approved in the European Union for adjuvant treatment of hormone receptor-positive early-stage breast cancer in premenopausal women, typically in combination with tamoxifen or an aromatase inhibitor to suppress ovarian function and reduce estrogen levels.[45] In the United States, while not explicitly FDA-approved for this indication, it is used off-label for similar purposes in premenopausal patients with advanced or hormone-sensitive breast cancer, often alongside endocrine therapies like fulvestrant and palbociclib.[46] Clinical trials have demonstrated that GnRH agonists like triptorelin improve disease-free survival in this population by inducing chemical ovarian ablation, with data from randomized studies showing hazard ratios for recurrence of approximately 0.72 when added to tamoxifen.[45] In assisted reproductive technologies, triptorelin serves as an adjunct for pituitary downregulation during controlled ovarian stimulation in IVF cycles, particularly in long protocols to prevent premature luteinizing hormone surges.[47] Reduced doses, such as 0.1 mg, have been evaluated for flare-up protocols or luteal phase support, with studies indicating comparable implantation rates to higher doses or alternative GnRH agonists like leuprolide, though without significant improvements in overall pregnancy outcomes.[47][48] It is also employed as a trigger for final oocyte maturation in GnRH antagonist cycles, leveraging the initial gonadotropin flare effect, with meta-analyses reporting live birth rates of 25-30% in such regimens.[49] Off-label use of triptorelin as a puberty suppressant in adolescents with gender dysphoria has increased, particularly in protocols aiming to delay secondary sex characteristics, but this application lacks specific regulatory approval and relies on extrapolation from precocious puberty data.[50] Systematic reviews highlight limited long-term evidence for safety and efficacy in this context, with concerns over bone density loss, potential impacts on fertility, and unresolved questions about persistence of gender dysphoria, as fewer than 20% of treated youth in some cohorts desist post-suppression.[51][52] Peer-reviewed analyses emphasize that such use is experimental, with calls for randomized controlled trials amid reports of adverse events like mood alterations and sterile abscesses.[53][54]Safety profile
Common adverse effects
The most common adverse effects of triptorelin arise from its action as a gonadotropin-releasing hormone (GnRH) agonist, which initially stimulates followed by sustained suppression of gonadal steroid production, resulting in hypoestrogenic or hypogonadal states. These effects vary by indication and patient population but frequently include vasomotor symptoms such as hot flushes, reported in 58% to 73% of adult males receiving intramuscular depot formulations for prostate cancer across clinical trials involving 3.75 mg, 11.25 mg, or 22.5 mg doses.[17] Skeletal pain occurs in 12% to 13% of such patients, often linked to underlying disease progression or testosterone fluctuations.[17] In adult males, additional frequent effects encompass erectile dysfunction (7% to 10%), headache (5% to 7%), decreased libido, and lower extremity edema or pain (5% to 6%), with incidences derived from controlled studies where events ≥5% were tabulated.[17] Local injection site reactions, including pain, are reported across formulations due to intramuscular or subcutaneous administration.[17] For central precocious puberty in pediatric patients, injection site reactions predominate, with pain in 45%, redness in 14%, and swelling or pruritus in 2% to 3%; headache affects 14%, while hot flushes occur in about 5%.[55] Vaginal bleeding is noted in 8% of females in this group.[55] In gynecological applications such as endometriosis, menopausal-like symptoms including hot flushes and night sweats are commonly observed, aligning with hypoestrogenic effects seen in trials where such vasomotor disturbances affected a majority of treated women.[38] Overall, these effects are generally reversible upon discontinuation, though monitoring is advised due to potential exacerbation of underlying conditions during initial testosterone or estrogen surges.[17]Serious risks and long-term effects
Triptorelin administration can precipitate a transient surge in gonadotropins and sex hormones due to its agonistic action on GnRH receptors, potentially exacerbating symptoms in hormone-sensitive conditions such as advanced prostate cancer through tumor flare syndrome, which manifests as intensified bone pain, spinal cord compression, or ureteral obstruction in approximately 5-10% of cases during initial treatment.[7] This risk necessitates concurrent anti-androgen therapy or careful monitoring in high-risk patients.[7] Cardiovascular events represent a significant serious risk, with GnRH agonists like triptorelin linked to elevated incidences of myocardial infarction, stroke, and sudden cardiac death, particularly in men undergoing androgen deprivation therapy for prostate cancer; observational data indicate a 20% higher risk of incident coronary heart disease compared to non-users, attributed to hypogonadism-induced metabolic shifts including dyslipidemia and insulin resistance.[56] [57] This association persists across multiple cohort studies, though causality remains debated due to confounding factors like underlying comorbidities.[58] Prolonged triptorelin-induced hypogonadism substantially impairs bone mineral density, elevating fracture risk by up to 20-30% in long-term users, as estrogen and testosterone suppression disrupts osteoblast activity and calcium homeostasis; this effect is dose- and duration-dependent, with annual bone loss rates of 2-5% observed in adults on androgen deprivation therapy.[9] [58] In pediatric patients treated for central precocious puberty, bone density accrual diminishes during therapy (Z-scores dropping by 0.5-1.0 SD), but typically normalizes within 1-2 years post-discontinuation, though peak bone mass attainment may be subtly affected if treatment extends beyond 3-4 years.[59] [60] Long-term fertility outcomes following triptorelin use in children with precocious puberty show puberty resumption in over 95% of cases after cessation, with preserved ovarian function and successful pregnancies reported in cohort studies tracking patients into adulthood; however, subtle delays in menarche or reduced ovarian reserve cannot be ruled out without larger prospective data.[61] Metabolic derangements, including weight gain and hyperglycemia, may persist post-treatment in some adolescents, potentially compounding cardiovascular vulnerability into adulthood.[62] Rare but serious hypersensitivity reactions, including anaphylaxis, have been documented via pharmacovigilance databases, underscoring the need for immediate medical intervention.[12]Administration and dosing
Standard regimens
Triptorelin is administered exclusively via intramuscular injection into the buttock, using depot formulations that provide sustained release over weeks to months. The lyophilized powder must be reconstituted with sterile water for injection immediately prior to administration, and the suspension injected promptly to avoid settling. Dosage strengths are not interchangeable or additive; the chosen formulation determines the interval between doses. Therapy duration varies by indication, typically continuing until disease progression, symptom resolution, or as limited by safety concerns like bone density loss. For advanced prostate cancer, standard initial therapy often begins with the 3.75 mg dose every 4 weeks to assess tolerance and monitor for tumor flare, though longer-acting formulations may be used from the outset based on physician judgment. Recommended regimens include 3.75 mg every 4 weeks, 11.25 mg every 12 weeks, or 22.5 mg every 24 weeks, with serum testosterone and prostate-specific antigen levels monitored to confirm castrate levels (typically achieved by day 29) and therapeutic efficacy.[63][32] In central precocious puberty for children aged 2 years and older, the approved regimen is 22.5 mg every 24 weeks, with efficacy assessed via luteinizing hormone suppression, sex steroid levels, height velocity, and bone age progression 1-2 months post-initiation and periodically thereafter.[55] Treatment is discontinued at the age of anticipated natural puberty onset. For gynecological conditions like endometriosis or uterine fibroids—primarily approved outside the United States—a typical regimen involves 3.75 mg every 4 weeks for 3-6 months to achieve hypoestrogenic suppression, often combined with progestin add-back therapy to reduce adverse effects such as vasomotor symptoms and bone loss.[36][41]| Indication | Formulation Dose | Frequency | Key Monitoring |
|---|---|---|---|
| Advanced prostate cancer | 3.75 mg | Every 4 weeks | Testosterone, PSA levels |
| Advanced prostate cancer | 11.25 mg | Every 12 weeks | Testosterone, PSA levels |
| Advanced prostate cancer | 22.5 mg | Every 24 weeks | Testosterone, PSA levels |
| Central precocious puberty | 22.5 mg | Every 24 weeks | LH, sex steroids, growth |
| Endometriosis/fibroids* | 3.75 mg | Every 4 weeks | Symptom relief, bone density |
Formulation-specific considerations
Triptorelin is formulated primarily as pamoate (embonate) salt for sustained-release depot injections, with acetate salt used in some immediate-release contexts, though depots predominate clinically to achieve prolonged gonadotropin suppression.[7][2] Depot formulations incorporate triptorelin pamoate into biodegradable microspheres, enabling intramuscular release over 1, 3, or 6 months via doses of 3.75 mg, 11.25 mg, or 22.5 mg, respectively, which reduces injection frequency and improves adherence compared to daily subcutaneous acetate regimens.[15][64] Pharmacokinetics vary by duration: all depots exhibit an initial burst release peaking within hours post-injection, potentially inducing a transient testosterone surge (flare) before sustained suppression, but longer-acting versions maintain castrate levels (<50 ng/dL) for the full interval with minimal fluctuations, as evidenced by plasma profiles showing rapid C_max followed by pseudo-steady state decline.[65][24] Shorter 1-month formulations may require more frequent dosing, increasing procedural burden and site reaction risk, while 6-month options demand precise timing to avoid gaps in suppression, particularly in precocious puberty where consistent gonadal inhibition is critical.[66][67] Administration requires reconstitution with provided diluent, intramuscular injection into gluteal or deltoid muscle using specific needles to avoid clogging from microspheres, with recent data supporting subcutaneous feasibility for 3-month pamoate without efficacy loss, potentially easing delivery in pediatric or outpatient settings.[68][40] Formulation choice should account for patient factors like body mass (higher BMI may alter absorption in subcutaneous routes) and indication duration, with bioequivalence confirmed across brands for hormonal endpoints but monitoring recommended for inter-patient variability in release.[69][70]History and development
Discovery and early research
Triptorelin, a synthetic decapeptide analog of gonadotropin-releasing hormone (GnRH) featuring a D-tryptophan substitution at the sixth position in place of glycine, was first synthesized in the mid-1970s. This structural modification enhanced its potency, duration of action, and resistance to enzymatic degradation compared to native GnRH, which consists of 10 amino acids and was structurally elucidated by Andrew V. Schally and colleagues in 1971. The synthesis was conducted in Schally's laboratory at Tulane University, where Schally, a pioneer in hypothalamic hormone research, co-invented the compound as part of efforts to develop superagonists for therapeutic applications.[71][72][73] Initial evaluations, detailed in a 1977 U.S. patent, demonstrated triptorelin's superior luteinizing hormone (LH)- and follicle-stimulating hormone (FSH)-releasing activity in animal models at dosages as low as 0.1-1 μg/kg, outperforming native GnRH by factors of 10-50 in stimulating pituitary gonadotropin secretion. These preclinical studies, primarily in rodents, confirmed its rapid onset of action following subcutaneous or intravenous administration, with peak LH release occurring within 15-30 minutes. Schally's team highlighted its potential for treating hypogonadism and infertility through short-term stimulation, while noting the risk of tachyphylaxis—receptor desensitization—with repeated dosing.[71][74] Further early research in the late 1970s explored triptorelin's inhibitory effects upon chronic administration, revealing downregulation of GnRH receptors in the pituitary, which suppressed endogenous gonadotropin and gonadal steroid production. In ovariectomized rat models, it restored LH levels to precastration baselines without affecting basal secretion in intact animals, underscoring its agonist specificity. These findings, building on Schally's foundational work recognized by the 1977 Nobel Prize in Physiology or Medicine, established triptorelin's dual-phase mechanism: initial hyperstimulation followed by sustained suppression, paving the way for applications in endocrine disorders and hormone-dependent cancers.[75][76]Regulatory approvals and milestones
Triptorelin was first approved for medical use in France in 1986 under the brand name Decapeptyl for indications including prostate cancer and gynecological disorders. By the early 1990s, it had received marketing authorizations in multiple European countries, with national approvals expanding to over 60 nations by 2006.[77] In the European Union, triptorelin has primarily been authorized through national procedures rather than centralized EMA approval for initial indications, reflecting its early development and decentralized regulatory pathway.[78] In the United States, the Food and Drug Administration (FDA) granted initial approval to triptorelin pamoate (Trelstar) 3.75 mg on June 15, 2000, for the palliative treatment of advanced prostate cancer.[79] This was followed by approval of the 11.25 mg three-month formulation (Trelstar LA) in 2001.[80] The six-month 22.5 mg formulation for prostate cancer received FDA approval on March 15, 2010, providing a longer-duration option supported by phase III efficacy and safety data.[81] Key pediatric milestones include European approval of the six-month 22.5 mg formulation (Decapeptyl and Pamorelin) for central precocious puberty on January 9, 2017, in 22 countries via decentralized procedure.[82] The FDA approved Triptodur (triptorelin) 22.5 mg for the same indication on June 29, 2017, based on a pivotal phase III trial demonstrating suppression of luteinizing hormone levels.[83][28] Earlier, the six-month formulation for prostate cancer completed Europe's decentralized procedure in October 2009, enabling broader commercialization.[84]Society, regulation, and market
Brand names and availability
Triptorelin is marketed under multiple brand names worldwide, with formulations varying by region and indication. In the United States, it is available as Trelstar (triptorelin pamoate) for palliative treatment of advanced prostate cancer, approved by the FDA on June 15, 2000, and manufactured by Verity Pharmaceuticals.[80] Another U.S. brand, Triptodur, is indicated for central precocious puberty in pediatric patients.[3] Internationally, Decapeptyl (triptorelin pamoate or acetate) is a primary brand produced by Ipsen, used for prostate cancer, endometriosis, uterine fibroids, and precocious puberty.[4] Other notable brands include Pamorelin by Debiopharm, with Swissmedic approval for subcutaneous administration of 3.75 mg and 11.25 mg formulations for prostate cancer as of May 16, 2025.[85] Diphereline and Gonapeptyl are additional brands available in select markets for similar indications.[86]| Brand Name | Manufacturer | Key Indications and Notes |
|---|---|---|
| Trelstar | Verity Pharmaceuticals | Advanced prostate cancer (U.S.)[87] |
| Triptodur | Various | Central precocious puberty (U.S.)[3] |
| Decapeptyl | Ipsen | Prostate cancer, endometriosis, precocious puberty (global, excluding U.S.)[4] |
| Pamorelin | Debiopharm | Prostate cancer, including subcutaneous option (Europe/Switzerland)[85] |