Triptorelin: what it is, what it does to testosterone and what the trials show

Triptorelin belongs to the family of GnRH agonists, alongside leuprorelin (leuprolide), goserelin, buserelin and nafarelin. All are variations on the ten-amino-acid hormone gonadorelin, redesigned to bind the pituitary GnRH receptor more strongly and resist breakdown. In triptorelin the change is a single substitution, D-tryptophan for glycine at position 6, which the Trelstar label reports gives it roughly 13-fold higher LH-releasing and 21-fold higher FSH-releasing activity than the native hormone in animal studies ^[1].

The clinical products are depot formulations: triptorelin pamoate or acetate embedded in biodegradable microgranules that release the peptide over weeks. Decapeptyl SR is available in the UK as 3 mg (one month), 11.25 mg (three months) and 22.5 mg (six months) intramuscular injections ^{[2] [3]}; Trelstar in the US comes in the same three strengths ^[1]; and Triptodur is a 22.5 mg six-monthly injection for children with central precocious puberty ^[4]. An immediate-release 0.1 mg daily form is used in fertility clinics to prevent premature ovulation.

Research vendors sell the triptorelin peptide, usually as triptorelin acetate, as a freeze-dried powder, typically 100 microgram or 2 mg vials, and it is marketed in bodybuilding forums as a one-off injection to restart testosterone after anabolic steroids. That material is not a licensed medicine, and the use is not one any trial has examined. Related compounds on this site include HCG, HMG and kisspeptin-10, all of which act on the same axis in different places. Our guide to what research peptides are explains the research label.

The pituitary only responds to GnRH when the signal comes in pulses. A 1978 primate experiment showed that continuous GnRH exposure fails to sustain LH and FSH release and desensitises the gland ^[5]. A depot GnRH agonist exploits this. The Trelstar label describes what happens: after the first injection there is a transient surge in LH, FSH, testosterone and oestradiol, and then, after two to four weeks of continuous exposure, a sustained fall in LH and FSH and a marked reduction in testicular steroid production, bringing testosterone down to the level seen in surgically castrated men ^[1].

The initial surge is called the flare. In prostate cancer it can temporarily worsen the disease, and the label warns of bone pain, neuropathy, blood in the urine, urinary obstruction and spinal cord compression during the first weeks of treatment ^[1]; the UK SmPC advises considering an anti-androgen during the initial phase ^[2]. In children with precocious puberty, Triptodur’s label warns that signs of puberty, including vaginal bleeding, may increase during the first two to four weeks because gonadotropins and sex steroids rise above baseline before they fall ^[4]. The flare is a side effect of the medicine, not a treatment in itself.

Once suppression is established, the effect is medical castration for as long as the depot lasts. In men, testosterone falls below 50 ng/dL within about four weeks ^[1]; in women, oestrogen falls to postmenopausal levels, which is what shrinks endometriosis deposits and fibroids. That is the triptorelin testosterone curve: a flare, then a shutdown. When the drug is stopped the axis recovers over weeks to months, more slowly after long treatment.

Triptorelin was compared head to head with leuprorelin in 284 men with advanced prostate cancer, randomised to triptorelin 3.75 mg or leuprolide 7.5 mg into muscle every 28 days for nine injections. At day 29, fewer men on triptorelin had reached castrate testosterone (91.2% against 99.3%), but by day 57 the two were equivalent (97.7% against 97.1%), and the cumulative castration maintenance rate between days 29 and 253 was 96.2% for triptorelin and 91.2% for leuprolide. Nine-month survival was higher with triptorelin (97.0% against 90.5%), a secondary finding the authors did not over-interpret. Both drugs were well tolerated ^[6].

The Trelstar label’s clinical studies section reports that in the majority of patients testosterone rose above baseline and then declined to castrate levels within four weeks ^[1]. The UK licence covers locally advanced and metastatic prostate cancer, as an alternative to surgical castration, and as adjuvant or neoadjuvant treatment with radiotherapy or radical prostatectomy in high-risk disease ^{[2] [3]}.

In premenopausal women with early breast cancer, triptorelin has been tested as a way to protect the ovaries during chemotherapy. The PROMISE-GIM6 trial randomised 281 women at 16 Italian sites to chemotherapy alone or with monthly triptorelin. Twelve months after the last chemotherapy cycle, 25.9% of the chemotherapy-alone group had early menopause against 8.9% with triptorelin, an absolute difference of 17 percentage points ^[7]. Long-term follow-up (median 7.3 years) found a five-year cumulative incidence of menstrual resumption of 72.6% with triptorelin against 64.0% without; eight pregnancies against three, a difference that was not statistically significant; and no significant difference in disease-free survival, although the study was not powered for that outcome ^[8]. The UK SmPC also licenses triptorelin as adjuvant treatment, with tamoxifen or an aromatase inhibitor, for endocrine-responsive early breast cancer in women at high risk of recurrence who remain premenopausal after chemotherapy ^[2].

For endometriosis and uterine fibroids, the UK licence is for one 3 mg injection every 28 days, started in the first five days of the cycle, for a maximum of six months (and at least three months for fibroids before surgery); a further course beyond six months is not to be given because of bone loss ^[2]. In central precocious puberty, a 48-week phase 3 study of the six-monthly formulation in 44 children found 93.2% had prepubertal (suppressed) LH levels at month 6 and 97.7% at month 12, with no unexpected drug-related adverse events ^[9]. Triptodur is licensed in the US for children aged 2 and over with central precocious puberty ^[4], and Decapeptyl SR 22.5 mg carries the equivalent UK indication for onset before 8 years in girls and 10 in boys ^[3].

A small subcutaneous dose of triptorelin is also used as a diagnostic stimulation test in children, in place of scarce native GnRH. A 2025 study of 341 girls found that an LH peak above 7.14 IU/L three hours after triptorelin identified central precocious puberty with 94% sensitivity and 96% specificity ^[10]. The test works because a single dose of the agonist produces the stimulatory flare and nothing more.

The licensed indications are set out above and all involve prolonged suppression of the axis or a single diagnostic dose in children. Triptorelin is also used, in specialist services and under national guidelines, to suppress puberty in adolescents with gender dysphoria; that use is outside the licensed indications in most markets and is governed by clinical guidance that has changed in recent years, so we do not summarise it here.

Research-store use is different in kind. The claim, usually searched as triptorelin PCT, is that one 100 microgram injection of triptorelin after a course of anabolic steroids will restart natural testosterone production, using the flare as a jump-start. We searched for a trial of this and found none. The pharmacology argues against relying on it: the flare lasts days, the pituitary in a man coming off steroids is already suppressed by the steroids themselves, and the dose is the one used to test children’s pituitaries, not to treat anything. Repeated or larger doses risk the opposite effect, because sustained agonist exposure is exactly how the drug produces castration ^{[1] [5]}. The evidence for helping recovery after steroids, such as it is, involves HCG and selective oestrogen receptor modulators, and is reviewed on the HCG page.

Suppression is not immediate. In the prostate cancer trial, 91.2% of men had reached castrate testosterone by day 29 and 97.7% by day 57 ^[6], and the label gives about four weeks for testosterone to fall below 50 ng/dL after the initial rise ^[1]. Before that comes the flare, with hormone levels above baseline for the first two to four weeks ^{[1] [4]}. After a single 100 microgram immediate-release dose, the triptorelin itself is largely gone within a couple of days: the Decapeptyl SmPC reports a half-life of 7.6 hours in healthy volunteers and 11.7 hours in men with prostate cancer, after a three to four hour distribution phase ^[2].

Reported for information; not recommendations, and not transferable to vials of unknown content. In prostate cancer, Trelstar is given as a single intramuscular injection of 3.75 mg every 4 weeks, 11.25 mg every 12 weeks or 22.5 mg every 24 weeks; the label states the strengths are not additive because they release differently, so two 3.75 mg doses are not a 7.5 mg dose ^[1]. Decapeptyl SR in the UK uses the same three strengths at the same intervals, with the 3 mg monthly injection for endometriosis and fibroids ^{[2] [3]}. For central precocious puberty, Triptodur is 22.5 mg into muscle once every 24 weeks, with LH levels checked one to two months after starting ^[4].

In the breast cancer trial, triptorelin was given intramuscularly at least a week before chemotherapy and then every four weeks for the duration of chemotherapy ^[7]. The diagnostic test in children uses a single subcutaneous dose of the immediate-release form, with LH measured at 180 minutes ^[10]. The 100 microgram “PCT” dose circulating online is borrowed from that diagnostic use. The peptide calculator can convert a research triptorelin vial into micrograms per syringe unit; it cannot tell you what a dose will do to your own axis, and the literature does not either.

Every licensed long-acting product is an intramuscular depot of microgranules reconstituted with sterile water immediately before injection ^{[1] [2] [4]}; the Trelstar label specifies no other diluent. The immediate-release 0.1 mg form is a daily subcutaneous injection. Triptorelin is a decapeptide and is not absorbed by mouth. Research vendors sell the acetate as a freeze-dried powder, which is an immediate-release form: a research vial cannot reproduce the month-long release of a depot, whatever the label says.

Most side effects follow from the loss of sex hormones. The Trelstar label lists hot flushes, skeletal pain, impotence and headache as the most common reactions (5% or more) with the 3.75 mg strength, with leg oedema and leg pain added at the higher strengths ^[1]. The label also carries warnings on tumour flare, metabolic changes including raised glucose and cardiovascular risk with androgen deprivation, convulsions, severe cutaneous adverse reactions, QT interval prolongation, anaphylaxis and angioedema, and embryo-fetal toxicity ^[1]. The UK SmPC warns that GnRH agonists reduce bone mineral density, which is why courses for endometriosis and fibroids are capped at six months and why particular caution is needed in people with osteoporosis risk factors ^[2].

In children, Triptodur’s most common reactions (4.5% or more) were injection-site reactions, vaginal bleeding, hot flush, headache, cough and common infections; the label also warns of psychiatric events such as emotional lability and of idiopathic intracranial hypertension with GnRH agonists ^[4]. In the six-monthly formulation study, no unexpected drug-related adverse events were reported over 48 weeks ^[9]. In the breast cancer trials the drug was given alongside chemotherapy, so its own adverse effects were not separately reported in the abstracts ^{[7] [8]}.

For a man injecting research-grade triptorelin, the specific hazard is the one the label describes as pharmacology: an initial testosterone surge followed, if exposure is sustained, by suppression to castrate levels that can take months to reverse. That risk is dose- and formulation-dependent and cannot be assessed for a vial whose content and release profile are unknown. Unlicensed vials also carry the usual risks of unknown purity, contamination and absent batch release.

Triptorelin is a prescription-only medicine in the UK (Decapeptyl SR, Gonapeptyl), the US (Trelstar, Triptodur), the EU and other markets. It is not a controlled drug under the UK Misuse of Drugs Act, but supplying an unlicensed triptorelin product is an offence under medicines law, as set out on the UK legal status page. In the US, products sold as research chemicals for human use fall under the FDA’s rules on unapproved drugs, described on the US legal status page; the legal status overview covers Canada, Australia and Europe.

For athletes, triptorelin is named in section S2.2.1 of the WADA Prohibited List, testosterone-stimulating peptides in males, alongside gonadorelin, buserelin, goserelin, leuprorelin and nafarelin, and is prohibited at all times in men ^[11]. The paradox that a drug used to abolish testosterone is banned as a testosterone stimulant is explained by the flare: a single dose stimulates. A vial sold as a research chemical is not a licensed medicine and is not covered by the safety data on this page.

Trelstar is stored at 20 °C to 25 °C and must not be frozen ^[1]; Decapeptyl SR is kept below 25 °C in its carton and used immediately after reconstitution ^[2]. These are depot microgranules, and the instructions do not transfer to research powder. For a freeze-dried acetate the usual rules apply: cold, dry, protected from light, and refrigerated once reconstituted, as set out in our guides to storing peptides and bacteriostatic water.

PepFinder does not sell triptorelin. To compare research vendors, see triptorelin prices, with UK and US listings. A decapeptide is straightforward to verify: a certificate of analysis should show a mass close to 1311 g/mol for the free peptide and an HPLC purity figure, and our guide to reading a peptide COA explains what those mean. The third-party tested list shows which vendors publish independent results, and our guides to third-party peptide testing and spotting a fake peptide supplier cover the rest. Given what a mis-dosed GnRH agonist can do to the axis, identity and quantity are the two things worth checking.