Triptorelin

Also known as: Trelstar, Decapeptyl

**Mechanism of Action** Triptorelin is a synthetic decapeptide analog of gonadotropin-releasing hormone (GnRH) with enhanced receptor affinity and prolonged half-life. Upon initial administration, it stimulates pituitary GnRH receptors, causing a transient surge in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) — the "flare effect." With continuous exposure, receptor downregulation and desensitization occur, leading to profound suppression of LH and FSH secretion. This reduces gonadal steroidogenesis, achieving castrate levels of testosterone in males and estradiol in females within 2–4 weeks. **Key Research Findings** Approved for advanced prostate cancer, triptorelin (e.g., Trelstar, Decapeptyl) demonstrates equivalent efficacy to surgical castration and other GnRH agonists in reducing testosterone to <50 ng/dL. In endometriosis, it alleviates pain and lesion size by inducing a hypoestrogenic state, though hypoestrogenic side effects (hot flashes, bone density loss) limit long-term use. Studies also support its utility in central precocious puberty and assisted reproduction (e.g., controlled ovarian hyperstimulation). Comparative trials show triptorelin’s 1-month, 3-month, and 6-month depot formulations provide sustained suppression with predictable pharmacokinetics. **Clinical Relevance** Triptorelin is a cornerstone of androgen deprivation therapy for hormone-sensitive prostate cancer and a second-line option for endometriosis when surgery or other hormonal therapies are contraindicated. Its depot formulations improve compliance, and the initial flare is managed with concurrent antiandrogens in prostate cancer to prevent tumor exacerbation. Monitoring of serum testosterone/estradiol and bone density is recommended during prolonged use. For research purposes only — not medical advice.

Key data

Research & studies

Frequently asked questions

Related peptides