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Triptorelin

Also known as Trelstar, Decapeptyl, Triptodur, D-Trp6-LHRH, triptorelin pamoate, triptorelin acetate

Long-acting GnRH agonist: an initial hormone flare followed by sustained suppression of testosterone or oestradiol.

clinically proven Hormonal & sexual approved drug

At a glance

Category
Hormonal & sexual
Status
approved drug
Route
intramuscular or subcutaneous depot injection depending on formulation
Half-life
after intravenous dosing the peptide shows phases of roughly 6 minutes, 45 minutes and 3 hours; the depot formulation releases drug over 1 to 6 months
Onset
hormone flare over the first 1-2 weeks; castrate testosterone levels typically by week 3-4
Molecular weight
1699.9 g/mol as the pamoate salt (peptide C64H82N18O13 combined with pamoic acid)
Sequence
pGlu-His-Trp-Ser-Tyr-D-Trp-Leu-Arg-Pro-Gly-NH2 (native GnRH with D-tryptophan substituted at position 6)

Approved in the US as Trelstar for advanced prostate cancer 1 and as Triptodur for central precocious puberty. In Europe, Decapeptyl and equivalents are additionally licensed for endometriosis, uterine fibroids, female infertility as part of assisted reproduction, and hormone-receptor-positive breast cancer in premenopausal women. Supplied as depot microgranules or microspheres, not as a research powder.

Doping status: Prohibited in males (WADA S2.2.1, GnRH agonist analogues)

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

Triptorelin is a decapeptide analogue of gonadotropin-releasing hormone in which glycine at position 6 is replaced by D-tryptophan. That single substitution does two things: it makes the molecule resistant to the peptidases that clear native GnRH within minutes, and it increases GnRH receptor affinity. The result is a molecule that occupies the receptor for far longer than the natural hormone.

This is where GnRH agonists diverge from what people intuitively expect. Native GnRH is released in pulses roughly every 60-120 minutes, and the pituitary gonadotroph is built to respond to that pulsatility. A long-acting agonist replaces the pulse with continuous occupancy. In the first days this is straightforward agonism — LH, FSH, testosterone and oestradiol all rise sharply. This is the flare. Testosterone in men can transiently rise well above baseline in the first 1-2 weeks. Then the gonadotroph downregulates: GnRH receptors are internalised and the cell becomes desensitised. From roughly week 2-4 onward, LH and FSH fall and gonadal steroid production drops to castrate or postmenopausal levels.

The clinically important consequence is that a GnRH agonist temporarily makes a hormone-driven disease worse before it makes it better. In advanced prostate cancer that transient testosterone surge can worsen bone pain, cause urinary obstruction or, if there are vertebral metastases, precipitate spinal cord compression. Standard practice is to cover the first weeks with an antiandrogen such as bicalutamide, or to use a GnRH antagonist instead when the flare is unacceptable.

Compare the mechanism with the two other GnRH-active classes in this reference. Gonadorelin is native GnRH and, given in pulses, stimulates the axis rather than suppressing it. Cetrorelix and ganirelix are competitive antagonists: they block the receptor from the first injection and produce immediate suppression with no flare at all. Triptorelin, leuprolide and nafarelin all sit in the agonist camp — flare first, suppression later.

What the research shows

The evidence base is that of a mainstream oncology and endocrinology drug: multiple registrational trials, decades of use, and inclusion in prostate cancer and precocious puberty guidelines. Suppression of testosterone to castrate levels is a reproducible, objectively measured endpoint, and triptorelin achieves it in the large majority of treated men.

Research in humans

Registrational studies for the 3.75 mg, 11.25 mg and 22.5 mg depot formulations demonstrated testosterone suppression below 50 ng/dL maintained across the dosing interval in around 95% of patients 1. Triptodur, the 6-month paediatric formulation, showed suppression of LH to prepubertal levels in children with central precocious puberty. European licensure for endometriosis and for premenopausal breast cancer rests on separate controlled trials. In assisted reproduction, agonist protocols have been compared directly against antagonist protocols in a large body of randomised trials summarised by Cochrane 2.

Animal and lab research

Rodent and canine studies established the downregulation phenomenon and confirmed that continuous exposure suppresses while pulsatile exposure stimulates. Triptorelin is also used veterinarily. These data underpin the mechanism but are not the basis of human licensure.

Caveats. The evidence concerns disease outcomes and hormone endpoints, not off-label or lifestyle applications. Long-term consequences of profound sex-steroid deprivation — bone loss, metabolic and cardiovascular effects — are well documented but hard to attribute cleanly in populations who are often older and have competing illness. Head-to-head data between individual GnRH agonists are sparse; they are largely treated as interchangeable at the class level.

What it is used for

  • Advanced prostate cancer (androgen deprivation therapy) 1
  • Central precocious puberty in children
  • Endometriosis and uterine fibroids (European labelling)
  • Premenopausal hormone-receptor-positive breast cancer, for ovarian suppression (European labelling)
  • Pituitary downregulation in long-protocol IVF, and as an alternative ovulation trigger in antagonist protocols
  • Ovarian protection during chemotherapy, and as part of gender-affirming care to suppress endogenous sex steroids

Dosing

Dose
3.75 mg, 11.25 mg or 22.5 mg depot (Trelstar); 22.5 mg 6-month depot (Triptodur, paediatric)
Frequency
3.75 mg every 4 weeks, 11.25 mg every 12 weeks, 22.5 mg every 24 weeks
Route
intramuscular injection into either buttock (Trelstar); intramuscular (Triptodur). Some European formulations are subcutaneous
Duration
Prostate cancer: usually indefinite. Endometriosis: limited to 6 months per course because of bone loss. Precocious puberty: until the appropriate age for puberty to resume
  • This is a clinician-administered depot product. There is no meaningful self-administration protocol and no credible reason to reconstitute it outside a clinical setting.
  • Trelstar is reconstituted with the supplied sterile water only — no other diluent — and must be injected within 2 minutes, because the microgranules settle out of suspension quickly 1.
  • During the first 1-2 weeks of therapy in prostate cancer, an antiandrogen is commonly co-prescribed to blunt the clinical consequences of the testosterone flare.
  • Testosterone should be measured to confirm castrate levels rather than assumed; a minority of men do not suppress adequately.
  • In assisted reproduction, short-acting daily triptorelin (typically 0.1 mg subcutaneously) is used rather than the depot, and dosing is directed by the fertility unit.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Trelstar depot (advanced prostate cancer)

approved product information

Source: TRELSTAR (triptorelin pamoate) prescribing information, DailyMed

3.75 mg strengthone intramuscular injection into either buttock every 4 weeks
11.25 mg strengthone intramuscular injection every 12 weeks
22.5 mg strengthone intramuscular injection every 24 weeks

The three strengths are alternatives, not a sequence: one is chosen and repeated. Triptorelin is an agonist, so the first injection raises testosterone for roughly a week before suppression follows, and an antiandrogen is commonly co-prescribed over the first 1-2 weeks where that flare would be clinically dangerous. Clinician-administered: the suspension settles within about two minutes of reconstitution.

'Triptorelin PCT' one-shot in steroid users (user-reported)

user protocol — not validated

Source: The pattern repeated across anabolic-steroid forums, tracing to a single small proof-of-concept study; not an approved use

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Reported single doseroughly 100 mcg of short-acting triptorelin subcutaneously, given once at the end of a steroid cycle
Reported rangeabout 100-200 mcg; a one-off rather than a course

This is the same molecule used for the opposite purpose. The label uses long-acting depot triptorelin to suppress the gonadal axis for months in prostate cancer and precocious puberty. Steroid users instead take a single small dose of the short-acting form to exploit the initial flare — the transient surge in LH, FSH and testosterone that precedes suppression — as a post-cycle 'kick-start' to restart their own testosterone after a cycle. The idea traces to one small proof-of-concept study and has circulated as a 'one-shot PCT' ever since. The contradiction is built into the pharmacology and is the main warning attached to it: give too much, or mistime it, and continuous rather than pulsatile receptor occupancy produces exactly the suppression the user was trying to escape. There is no controlled evidence that a single dose reliably restarts the axis, reports of it backfiring are common, and grey-market short-acting triptorelin is of unverified identity and purity.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
3.75 mg, 11.25 mg, 22.5 mg
Solvent
Sterile water for injection, supplied with the kit. No other diluent is acceptable — bacteriostatic water is not used for this product
Storage
Store the unreconstituted kit at controlled room temperature. Reconstituted suspension must be administered within 2 minutes.

Worked example

The Trelstar single-dose kit contains the lyophilised microgranules and a prefilled syringe of sterile water; the entire reconstituted volume is one dose. There is no per-unit dose calculation to perform.

The 2-minute window is not a formality — the microgranules sediment, and delay results in an underdosed injection and a partially blocked needle. This is a depot suspension, not a solution.

This is not reconstituted from a powder — it is supplied as a ready-made solution, or as a kit that mixes to a single fixed dose. The vial-and-solvent arithmetic used elsewhere on this site does not apply.

Safety

Side effects

  • Hot flushes and sweating, the most common effect; reported in roughly 58-73% of men on Trelstar depending on formulation 1
  • Tumour flare in the first weeks: the initial testosterone surge can worsen prostate cancer symptoms and cause spinal cord compression and urinary tract obstruction 1
  • Loss of bone mineral density with prolonged use, progressing to osteoporosis and fracture risk over years of androgen or oestrogen deprivation
  • Erectile dysfunction or impotence, reported in about 7-10% 1, with loss of libido and testicular atrophy in men
  • Amenorrhoea, vaginal dryness and menopausal symptoms in women
  • Injection site pain, erythema and inflammation
  • Hyperglycaemia, new-onset diabetes and hyperlipidaemia, for which the label advises periodic monitoring 1
  • Increased risk of myocardial infarction, sudden cardiac death and stroke in men receiving androgen deprivation 1
  • QT/QTc interval prolongation with androgen deprivation therapy 1
  • Depression and mood disturbance
  • Headache (about 5-7%), fatigue, and skeletal pain (about 12-13%) 1
  • Rare hypersensitivity including angioedema and anaphylactic shock
  • Rare pituitary apoplexy, typically within hours to days of the first dose in patients with an undiagnosed pituitary adenoma

Do not use if

  • Hypersensitivity to triptorelin, other GnRH analogues or any excipient 1
  • Pregnancy and breastfeeding
  • Not for use in women planning conception outside a supervised fertility protocol
  • Caution in men with vertebral metastases or urinary tract obstruction, where the flare can cause spinal cord compression or obstruction 1 — antagonist therapy may be preferable
  • Caution with pre-existing osteoporosis or major risk factors for it
  • Caution with congenital long QT syndrome, electrolyte disturbance or concomitant QT-prolonging drugs
  • History of depression warrants monitoring rather than absolute avoidance

Interactions

Formal drug interaction studies are limited. The clinically relevant interactions are pharmacodynamic. Concomitant QT-prolonging drugs — class IA and III antiarrhythmics, methadone, moxifloxacin, some antipsychotics — add to the QT risk of androgen deprivation. Drugs that raise prolactin or dopamine antagonists can affect the gonadotropin response. Combining a GnRH agonist with a GnRH antagonist is pharmacologically self-defeating. Hormonal contraceptives and exogenous sex steroids confound both the intended effect and any monitoring. In diabetics, glucose-lowering therapy may need adjustment because androgen deprivation worsens insulin resistance.

Sources