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a clear glass vial with a grey cap, labeled "Triptorelin Acetate 10 mg, Batch No.003, 23-06-2025." The vial contains a white lyophilized powder, standing upright against a soft beige background, commonly used in pharmaceutical or peptide product packaging
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Triptorelin Acetate 10mg vial

Triptorelin Acetate 10mg vial

€75,00 EUR
Inkl. Steuern.

                                    NOT FOR HUMAN CONSUMPTION

Triptorelin is a long-acting gonadotropin-releasing hormone (GnRH/LHRH) agonist. After an initial LH/FSH “flare”, continued receptor stimulation on pituitary gonadotrophs causes desensitization/internalization and suppression of gonadotropins, leading to medical castration (↓ testosterone/estradiol). It is widely approved for advanced prostate cancer, central precocious puberty (CPP), and (ex-US) endometriosis, uterine fibroids, and assisted reproductiondown-regulation. Depot IM/SC formulations (e.g., 1-, 3-, 6-month) provide sustained exposure.

Additional Benefits of Triptorelin Now Under Investigation

Benefit Key take-aways
1 Optimized prostate-cancer control in combinations As the ADT backbone, triptorelin pairs with androgen-receptor pathway inhibitors(abiraterone, apalutamide, enzalutamide, darolutamide) in mHSPC/mCRPC to improve survival versus ADT alone. <br/><em>European Urology; Lancet Oncology</em>
2 Intermittent ADT strategies Intermittent triptorelin-based ADT can maintain disease control with better quality of life in selected patients; ongoing work refines PSA-based cycling criteria. <br/><em>NEJM; Journal of Clinical Oncology</em>
3 Cardiometabolic risk management Programs evaluate baselining CV risk, exercise/nutrition, and statin/SGLT2/GLP-1RA co-therapy to mitigate ADT-related dysmetabolism while on triptorelin. <br/><em>Circulation; JACC: CardioOncology</em>
4 Ovarian function suppression (OFS) in HR+ breast cancer In premenopausal ER+ disease, triptorelin-based OFS plus tamoxifen or aromatase inhibitor improves disease-free survival versus endocrine therapy alone. <br/><em>NEJM; Journal of Clinical Oncology</em>
5 Fertility preservation during chemotherapy Temporary ovarian suppression with triptorelin during cytotoxic therapy reduces premature ovarian insufficiency and may increase post-treatment pregnancy rates. <br/><em>JAMA; Annals of Oncology</em>
6 Endometriosis & adenomyosis control 3–6 months of depot therapy reduces pelvic pain and lesion activity; add-back therapy helps bone and vasomotor tolerability during prolonged courses. <br/><em>Human Reproduction Update; BJOG</em>
7 Uterine fibroids (pre-op or bridging) Pre-operative triptorelin shrinks fibroids and improves anaemia, easing surgical approaches or bridging to definitive therapy. <br/><em>Fertility and Sterility; Obstetrics & Gynecology</em>
8 IVF/ART down-regulation Long-protocol down-regulation with triptorelin prevents premature LH surge and can standardize follicular recruitment; antagonist protocols now compete—comparative trials continue. <br/><em>Reproductive BioMedicine Online; Human Reproduction</em>
9 CPP convenience & adherence 6-month depot schedules sustain T/E2 suppression with fewer injections and robust bone-age/height-velocity control. <br/><em>Pediatrics; Journal of Clinical Endocrinology & Metabolism</em>

2. Molecular Mechanism of Action

2.1 Receptor Pharmacodynamics

Triptorelin binds GnRH (GNRHR) GPCR on pituitary gonadotrophs → Gαq/11–PLCβ–IP₃/DAG–Ca²⁺/PKC → acute LH/FSH release (“flare,” days 1–7). Continuous exposure triggers receptor desensitization/internalization, suppressing LH/FSH and downstream testicular/ovarian steroidogenesis.

2.2 Down-stream Biology

Pathway Functional outcome Context
IP₃/Ca²⁺/PKC→ERK Acute LH/FSH secretion Pituitary
↓ GnRH signalling (chronic) ↓ LHB/FSHB transcription, gonadotropin suppression Pituitary
↓ LH→Leydig / ↓ FSH→Sertoli ↓ Testosterone; impaired spermatogenesis Testis
↓ LH/FSH→Ovary ↓ Estradiol/progesterone; anovulation Ovary

3. Pharmacokinetics

  • Formulations: Microsphere depots (e.g., 3.75 mg q4wk; 11.25 mg q12wk; 22.5 mg q24wk) and pediatric 24-week depot for CPP.

  • Absorption: Initial burst → sustained zero-order-like release from PLGA matrix.

  • Onset: Steroid “flare” within first week; castrate T typically by 2–4 weeks.

  • Half-life: Parent peptide t½ is short (hours) but effective duration reflects depot kinetics (1–6 months).

  • Clearance: Peptidase degradation; renal/hepatic peptide catabolism; no CYP interactions.

4. Pre-clinical and Translational Evidence

4.1 Prostate Cancer (ADT backbone)

Triptorelin achieves durable castration with PSA responses comparable to other agonists; combinations with AR pathway inhibitors significantly prolong rPFS/OS versus ADT alone.

4.2 Breast Cancer (premenopausal, HR+)

In SOFT/TEXT-style regimens, OFS with triptorelin plus tamoxifen or an aromatase inhibitor improves invasive disease-free survival, particularly in higher-risk patients.

4.3 CPP

Depot triptorelin suppresses pubertal progression, normalizes growth velocity, and improves predicted adult height, with convenient 6-month dosing options.

4.4 Endometriosis/Fibroids/ART

In endometriosis and fibroid protocols, triptorelin reduces estrogen-driven activity, facilitating symptom control and surgery. In IVF, long down-regulation prevents premature LH surge; antagonist regimens provide alternative flexibility.

5. Emerging Clinical Interests

Field Rationale Current status
ADT + cardiometabolic co-management Reduce CV events during long-term ADT Prospective cardio-oncology programs
Intermittent ADT QoL vs continuous ADT in mHSPC/biochemical relapse Ongoing refinement, patient-selected
OFS personalization Tailor duration/intensity in HR+ breast cancer Risk-adapted strategies under study
Non-binary/trans care GnRH analogs for puberty suppression/adult OFS Practice varies by region; triptorelin used ex-US

6. Safety and Tolerability

  • Common: Hot flashes, decreased libido, erectile/sexual dysfunction, mood change, headache, injection-site reactions.

  • Metabolic/Bone: Weight gain, insulin resistance, dyslipidemia, bone-mineral density loss (consider DXA and bisphosphonate/denosumab in long-term ADT/OFS).

  • On-treatment flare (men): Transient tumor-flare may cause bone pain, urinary obstruction, spinal cord compression—use antiandrogen lead-in/overlap in metastatic settings.

  • Women: Vasomotor symptoms, amenorrhea, initial ovarian cysts possible; use add-back therapy for longer courses.

  • Pediatrics: Initial pubertal signs may transiently appear; monitor height velocity and bone age.

  • Rare: Pituitary apoplexy shortly after first dose in patients with undiagnosed adenomas; immediate evaluation if severe headache/visual change.

Comparative safety matrix

Concern Triptorelin (GnRH agonist) GnRH antagonists (degarelix, relugolix) Orchiectomy / Oophorectomy
On-treatment flare Yes (mitigate with antiandrogen) No No
Time to castration 2–4 weeks 1–2 weeks (faster) Immediate
CV risk signal Class concern Some studies suggest lower CV events Baseline surgical risks
Convenience Monthly–6-monthly depot Monthly depot or daily oral One-time procedure
Reversibility Yes (after depot wanes) Yes No

7. Regulatory Landscape

  • Approved: Prostate cancer (ADT) and CPP (varies by region/formulation).

  • Common ex-US uses: Endometriosis, uterine fibroids, ART down-regulation.

  • Monitoring: For ADT/OFS, monitor T/E2 levels, metabolic panel, BMD, and disease markers (e.g., PSA).

  • Contraindications: Pregnancy, breastfeeding, hypersensitivity to GnRH analogs; caution in severe osteoporosisand unstable metastases (flare risk).

8. Future Directions

  • Depot innovation: Longer-acting and smaller-volume depots; SC auto-injectors.

  • Precision ADT/OFS: Risk-adapted durations, biomarker-guided restart/stop rules (PSA kinetics, ultrasensitive E2).

  • Cardio-oncology pathways: Integrated CV risk mitigation embedded in ADT protocols.

  • Combination trials: Triplet regimens (ADT + ARSI + RT/chemo) and de-escalation after deep responses.

  • Pediatric CPP: Long-term neurocognitive and bone outcomes with extended 6-month dosing.

Selected References

  • European Urology; Lancet Oncology — ADT backbones and AR-targeted combinations in mHSPC/mCRPC.

  • New England Journal of Medicine; Journal of Clinical Oncology — Intermittent vs continuous ADT; OFS in premenopausal HR+ breast cancer.

  • JAMA; Annals of Oncology — Ovarian suppression during chemotherapy and fertility preservation.

  • Human Reproduction Update; BJOG — Endometriosis/adenomyosis management with GnRH agonists and add-back therapy.

  • Fertility and Sterility; Obstetrics & Gynecology — Uterine fibroid pre-operative shrinkage and ART down-regulation protocols.

  • Pediatrics; JCEM — CPP efficacy, growth and bone-age outcomes with long-interval depots.

  • Circulation; JACC: CardioOncology — Cardiometabolic risk and mitigation during ADT