Triptorelin
Triptorelin (Trelstar, Triptodur, Decapeptyl), GnRH receptor agonist
Written by Aaron CuhaReviewed Sep 2026
Also known as: Trelstar, Triptodur, Decapeptyl, D-Trp6-LHRH, triptorelin pamoate
A decapeptide GnRH agonist approved in the United States in 2000 for advanced prostate cancer and in 2017 for central precocious puberty. In a pooled analysis of 920 men, 91 to 93 percent held testosterone below 20 ng/dL from month 3 onward. It causes a testosterone flare in the first days of treatment, which is the clinical reason the antagonists exist.
Overview
Triptorelin is a synthetic ten-amino-acid analogue of gonadotrophin-releasing hormone, the hypothalamic signal that drives the pituitary to release luteinising hormone and follicle-stimulating hormone. It is an agonist, which sounds like it should raise sex hormones and briefly does, before shutting the axis down.
The FDA approved Trelstar under NDA 020715 on 15 June 2000, with further formulations under NDA 021288 in 2001 and NDA 022437 in 2010, for palliative treatment of advanced prostate cancer. Triptodur, a paediatric six-month formulation, was approved under NDA 208956 on 29 June 2017 for central precocious puberty in children aged two years and older. Outside the United States, under the Decapeptyl brand, it also carries approvals in endometriosis and other gynaecological indications.
The flare is the defining pharmacological property. Because the drug first stimulates the receptor before desensitising it, testosterone or oestrogen rises for several days at the start of treatment. In advanced prostate cancer that transient rise can worsen symptoms, which is why agonists are often given with an antiandrogen for the first weeks. The GnRH antagonists, degarelix and relugolix, exist specifically to avoid this.
The evidence base is unusual in shape. Testosterone suppression is very well documented, and the paediatric data on hormonal suppression are solid. What does not exist is a modern randomised head-to-head of triptorelin against leuprolide, goserelin or degarelix on survival or any clinical outcome. Most of the large randomised trials that feature triptorelin use it as the background androgen deprivation while testing radiotherapy timing or added chemotherapy, so they measure the added intervention, not the hormone drug.
Mechanism of action
Continuous rather than pulsatile occupancy of the GnRH receptor on pituitary gonadotrophs. Physiological GnRH arrives in pulses, and the receptor requires that rhythm to keep signalling. Sustained exposure from a depot formulation first stimulates the receptor, producing a surge of luteinising hormone and therefore of testosterone or oestradiol over the first days, then desensitises and downregulates it. Gonadotrophin output falls, and gonadal steroid production follows it down to castrate levels within roughly two to four weeks. The suppression is reversible on stopping, though recovery can be slow after prolonged use.
Human evidence
Large and consistent on hormone suppression, thin to absent on comparative clinical outcomes. Testosterone falls to castrate levels in around nine of ten men and stays there, and luteinising hormone is suppressed in over 93 percent of children with central precocious puberty. No randomised trial compares triptorelin with another GnRH drug on survival.
- Pooled analysis, 920 men: testosterone below 20 ng/dL in 92, 93, 90 and 91 percent at months 3, 6, 9 and 12.
- Central precocious puberty, 44 children, open-label and non-comparative: prepubertal stimulated luteinising hormone in 93.2 percent at month 6 and 97.7 percent at month 12.
- Large randomised trials including GETUG-AFU 17 and the docetaxel addition trial use triptorelin as background therapy in both arms, so they are not evidence about triptorelin.
- No modern randomised head-to-head against leuprolide, goserelin or degarelix on any clinical outcome has been published.
What this does not tell you: Everything above is a hormone measurement. Testosterone below 20 ng/dL is the licensing standard and the thing clinicians check, but it is a surrogate: it does not by itself tell you about survival, and the differences in suppression between available GnRH drugs are small enough that nobody has demonstrated a clinical consequence. The paediatric trial had 44 patients, no control group, and measured luteinising hormone rather than the outcome parents care about, which is adult height.
Reading the research record
Testosterone suppression is a surrogate endpoint. It is the thing these drugs were licensed on, and it is reliably achieved, but no randomised trial has shown that any one gonadotrophin-releasing hormone drug produces longer survival than another. The modern trials that include triptorelin or degarelix mostly use them as the background androgen deprivation while testing something else, such as when to give radiotherapy or whether to add chemotherapy. Those trials tell you about the added intervention. They do not rank the hormone drugs against each other.
One specific correction is worth recording, because it circulates. Papers on GnRH agonist trigger protocols in in vitro fertilisation are sometimes filed as triptorelin evidence. They are about the trigger protocol, they typically use a single dose in a fertility cycle, and several are retrospective. They are not evidence about triptorelin as a sustained androgen deprivation therapy and belong to a different literature entirely.
The evidence, charted
Fig. 1 · evidence composition
4of 4 citations (100%) are in people
Every citation cited here is Human work; no other study type is cited on this page. This count is of our own citation list and understates any literature larger than the sources we cite.
Fig. 2 · evidence over time
Evidence spans 4 distinct years, 2016 to 2020, counted from the citation list on this page. The newest citation on file is from 2020, more than five years ago; the published record may have gone quiet.
Fig. 3 · legal status at a glance
US
Approved
UK
Approved
AU
Approved
CA
Approved
Approved in all four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Fig. 4 · dose response
No human dose response curve exists
We draw this figure where the data supports it. For this compound in humans it does not, so the panel stays empty rather than borrowing an animal curve and implying it transfers.
Key studies & citations
- Human2017
Efficacy of Testosterone Suppression with Sustained-Release Triptorelin in Advanced Prostate Cancer
Pooled analysis of 920 men from nine prospective studies, with testosterone as the primary endpoint. The proportion reaching testosterone below 20 ng/dL was 79 percent at month 1, then 92, 93, 90 and 91 percent at months 3, 6, 9 and 12. This is a pooled analysis of prospective studies, not itself a randomised trial, despite how PubMed indexes it, and it should not be cited as one.
Advances in Therapy - Human2016
Efficacy and safety of triptorelin 6-month formulation in patients with central precocious puberty
International phase 3 study at 18 centres in the United States, Chile and Mexico, in 44 treatment-naive children, 39 girls and five boys. 41 of 44 (93.2 percent) had prepubertal stimulated luteinising hormone at or below 5 IU/L at month 6, rising to 97.7 percent at month 12. Note the design: non-comparative and open-label, with no control group, and the endpoint is hormone suppression rather than adult height.
Journal of Pediatric Endocrinology and Metabolism - Human2020
Adjuvant radiotherapy versus early salvage radiotherapy plus short-term androgen deprivation therapy in men with localised prostate cancer after radical prostatectomy (GETUG-AFU 17): a randomised, phase 3 trial
A randomised phase 3 trial in which triptorelin is the background androgen deprivation given to both arms while the randomisation tests immediate versus early salvage radiotherapy. Included here as the correction it represents: trials like this are frequently listed as triptorelin evidence, and they tell you about radiotherapy timing, not about the hormone drug.
The Lancet Oncology - Human2019
Effect of Adding Docetaxel to Androgen-Deprivation Therapy in Patients With High-Risk Prostate Cancer With Rising Prostate-Specific Antigen Levels After Primary Local Therapy: A Randomized Clinical Trial
The same pattern again. Androgen deprivation is the constant in both arms and docetaxel is the variable under test. A reader searching for randomised triptorelin trials will land on studies of this shape and should read the randomisation before reading the result.
JAMA Oncology
Frequently asked questions
What is triptorelin approved for?
In the United States, palliative treatment of advanced prostate cancer as Trelstar, and central precocious puberty in children aged two and older as Triptodur. In the United Kingdom and other markets the Decapeptyl licence also covers endometriosis and uterine fibroids. It is not approved anywhere for use in healthy adults.
What is the testosterone flare and does it matter?
Because triptorelin first stimulates the GnRH receptor before desensitising it, testosterone rises for several days at the start of treatment before falling. In men with advanced prostate cancer that transient rise can aggravate symptoms, which is why an antiandrogen is often given alongside the first weeks of treatment and why the antagonist class exists.
Is triptorelin better than leuprolide?
Nobody has shown that, and no modern randomised head-to-head on clinical outcomes has been published. Both reliably reach castrate testosterone. The choice between them in practice is about formulation, injection interval, route and cost, not about demonstrated superiority.
Is it used for fertility or bodybuilding?
GnRH agonists are used in fertility cycles as a trigger, which is a single dose in a controlled protocol and a completely different pharmacology from depot suppression. Use to restart the axis after anabolic steroid use is off-label, unstudied in that population, and pharmacologically backwards, since sustained exposure suppresses rather than stimulates.
How quickly does it work and how quickly does it reverse?
Castrate testosterone is typically reached within two to four weeks after the initial flare. Recovery after stopping is variable and can take months, longer after prolonged treatment, and in some men after extended androgen deprivation it is incomplete.