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Triptorelin10 residuesQHWSYGLRPGEach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: Decapeptyl, Trelstar, Diphereline
One case report changed how the steroid community thinks about post-cycle therapy. Triptorelin (Trelstar, Decapeptyl) is a synthetic GnRH analog, FDA-approved for prostate cancer at milligram depot doses. At a single 100 mcg injection, it does the opposite: it triggers an acute LH and FSH surge that can restart natural testosterone production. Pirola et al. (2010)[1] documented full testosterone recovery in a bodybuilder after 13 years of steroid-induced hypogonadism. The catch is real, though. A 10x dosing error turns a pituitary reset into chemical castration. This peptide tolerates zero margin for reconstitution mistakes.
Triptorelin is a synthetic decapeptide analog of gonadotropin-releasing hormone with a D-tryptophan substitution at position 6 (CAS 57773-63-4). One case report defines its reputation in the peptide community: a 34-year-old bodybuilder, suppressed for over 13 years on anabolic steroids, had testosterone normalize within one month after a single 100 mcg injection (Pirola et al. 2010)[1]. That case is the entire published evidence base for triptorelin in post-cycle therapy. The modification makes it resistant to enzymatic degradation and roughly 100x greater affinity at the GnRH receptor than native GnRH. Under the brand name Trelstar, it carries FDA approval for advanced prostate cancer. Clinical uses also include endometriosis, uterine fibroids, central precocious puberty, and gender-affirming hormone therapy. The defining characteristic is a dose-dependent paradox. A single acute pulse of 100 mcg triggers a burst of LH and FSH from the pituitary, stimulating the testes to produce testosterone. Sustained depot exposure at 3,750 mcg monthly or higher causes the opposite: receptor internalization, LH/FSH shutdown, and castrate testosterone levels. The same molecule restarts or permanently suppresses hormone production depending entirely on dose and duration. PCT users in the AAS community (r/steroids, MESO-Rx, thinksteroids.com) have adopted the single-shot protocol broadly; dozens to low hundreds of dedicated threads document bloodwork-confirmed recoveries. The evidence is thin by clinical standards (n=1) but the mechanism is pharmacologically sound.
Triptorelin binds GnRH receptors on gonadotroph cells in the anterior pituitary with approximately 100-fold greater binding affinity than endogenous GnRH. The D-Trp6 substitution at position 6 blocks cleavage by endopeptidases, extending receptor occupancy. On binding, it activates the same Gq/11-phospholipase C-calcium signaling cascade that native GnRH uses, forcing exocytosis of stored LH and FSH. Timing determines everything. A single acute exposure (the 100 mcg PCT dose) produces the "flare effect." Pituitary gonadotrophs respond normally to an isolated GnRH signal. LH acts on testicular Leydig cells to produce testosterone; FSH drives Sertoli cell function and spermatogenesis. Because the peptide clears within hours (terminal half-life 2.8 to 7.6 hours per Muller et al.)[2], there is no sustained receptor occupancy and no downregulation. Continuous exposure from depot formulations changes the picture completely. Persistent receptor activation triggers beta-arrestin-mediated GnRH receptor internalization, uncoupling of the Gq signaling pathway, and eventual receptor degradation. The pituitary becomes refractory to any GnRH stimulation. LH and FSH secretion stops. Testosterone drops below 50 ng/dL, the clinical definition of castrate levels. This suppression persists for the duration of the depot (1 to 6 months) and is the intended mechanism for prostate cancer treatment.
Mechanism anchored to FDA depot pharmacodynamics (Trelstar label) and one case report: Pirola et al. 2010 [1], n=1. A single 100 mcg dose triggers an acute GnRH receptor pulse producing an LH/FSH flare without receptor desensitization. No PCT RCTs exist.
Pirola et al. 2010 (PMID 20416868), n=1 case report
Evidence base is a single case report (n=1), not an RCT. No FDA-approved 100 mcg vial in the US. 10x dosing error risks chemical castration.
Single-shot PCT protocol used by AAS community. Triptorelin 100 mcg triggers LH/FSH restart. Usually combined with SERM bridge (tamoxifen + clomiphene).
Both science and community converge on 100 mcg single-dose protocol and the same mechanism (acute GnRH receptor pulse → LH/FSH flare). Diverge on evidence quality: community extrapolates broadly from one case report; clinicians have no RCT data to endorse off-label PCT use. Both agree that repeated dosing is contraindicated.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Single dose |
| Moderate | 100mcg | Single dose |
| Aggressive | 100mcg | Single dose |
The reconstitution math matters more here than with any other peptide. Getting it wrong by 10x is the difference between PCT and chemical castration. Slow down and verify. For a 0.5 mg vial: add 5 mL bacteriostatic water. Each 1 mL drawn equals 100 mcg. That full 1 mL is your entire PCT dose. For a 1 mg vial: add 10 mL bacteriostatic water. Same result, 100 mcg per mL; draw exactly 1 mL. On a U-100 insulin syringe, that is 100 units (a full syringe). You'll want to triple-check the vial label before reconstituting. A 0.5 mg vial looks almost identical to a 1 mg vial from some research vendors. If you add only 1 mL of water to a 0.5 mg vial and draw the whole thing, you've just injected 500 mcg. That is 5x the target dose. Don't split the dose. Don't save any for later. Don't repeat it. If testosterone hasn't recovered by week 6, the answer is an endocrinologist, not a second shot. Request a third-party certificate of analysis from any research vendor. Pharmaceutical-grade Decapeptyl from an international pharmacy is preferable if you can source it.
Not cycled. PCT use is a ONE-TIME single injection of 100mcg. Do not repeat. If HPTA recovery is not achieved within 4-6 weeks, reassess with bloodwork before considering any additional intervention. Repeated dosing risks pituitary desensitization.
Triptorelin for PCT is a single-use HPTA reset, not a cycled protocol. One acute GnRH receptor pulse triggers the LH/FSH flare without causing receptor downregulation. Repeating the dose initiates the same receptor internalization mechanism used therapeutically in prostate cancer treatment (chemical castration). There is no on/off cycle: the injection IS the protocol. Recovery monitoring continues for 4–6 weeks post-injection.
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Expected: LH/FSH surge within 1–4 hours of injection; testosterone rising by week 2; normalization by week 4–6 in responders
Monitor: Baseline: LH, FSH, total T, free T, estradiol, SHBG. Recheck at weeks 2 and 4–6. If testosterone has not normalized by week 6, refer to endocrinologist.
Get baseline bloodwork before touching the vial: LH, FSH, total testosterone, free testosterone, estradiol. These values confirm you have hypogonadotropic hypogonadism (low LH/FSH) and that triptorelin is appropriate.
Wait at least 2 half-lives of the longest-acting ester you were running.
For a 0.5 mg vial: add 5 mL bacteriostatic water slowly along the glass wall. Swirl gently. For a 1 mg vial: add 10 mL bacteriostatic water. Both give you 100 mcg per mL.
That is your full 100 mcg PCT dose. Verify the math one more time before injecting.
Inject subcutaneously into the abdomen or upper thigh (27 to 31 gauge needle). Intramuscular into the deltoid is also acceptable. Both routes produce the same acute LH/FSH flare.
Do not save it for a second dose. There is no second dose.
Recheck bloodwork at week 2 (LH, FSH, total testosterone) and again at weeks 4 to 6. Testosterone should begin rising by week 2 and normalize by week 4 to 6 in responders.
If testosterone has not normalized by week 6, consult an endocrinologist. Do not re-inject triptorelin.
Same 100 mcg dose. SC absorption creates flip-flop kinetics (absorption rate-limited), extending effective half-life ~10x vs IV and sustaining receptor stimulation through the flare window.
Abdomen or upper thigh. 27–31 gauge insulin syringe. Draw entire volume for 100 mcg dose. Standard for community PCT use.
Same 100 mcg dose. Slightly faster absorption than SC; tmax ~1–3 hours per Trelstar FDA label.
Deltoid or ventrogluteal. Either SC or IM is considered equivalent for the acute PCT flare purpose. IM is the route specified in the Trelstar label for depot formulations.
Bridges the post-triptorelin gonadotropin refractory window. Estrogen receptor antagonist at pituitary maintains LH/FSH support while testes recover. Prevents testosterone relapse observed in some triptorelin-only users.
Tamoxifen 20 mg/day starting day 1 (same day as injection), continue 30–45 days
Additional SERM support for persistent gonadotropin suppression. Often co-administered with tamoxifen for dual-SERM coverage during the recovery window.
Clomiphene 25–50 mg/day days 1–30, concurrent with tamoxifen
Used as a less potent alternative for milder HPTA suppression before escalating to triptorelin, or as ongoing pulsatile GnRH support. Gonadorelin is generally used BEFORE or INSTEAD of triptorelin: triptorelin is the escalation when gonadorelin has been insufficient.
Most PCT protocols recommend HCG before triptorelin to prime Leydig cells for the LH surge. HCG stimulates testicular testosterone directly. Triptorelin is the escalation step when HCG has failed.
HCG 500–1,000 IU 3x/week for 2–3 weeks, then discontinue before injecting triptorelin
Concurrent exogenous testosterone directly suppresses HPG axis via negative feedback, negating the entire purpose of PCT. Triptorelin must be administered only after androgens have cleared.
Do not combineDirectly block the GnRH receptor that triptorelin must activate. Concurrent use renders triptorelin completely ineffective.
Do not combineMay blunt the gonadotropin response to triptorelin. Cabergoline is common in PCT for prolactin control: time administration to minimize overlap with the acute triptorelin flare window (first 24–48 hours).
Elevated prolactin suppresses GnRH signaling and reduces LH/FSH response to triptorelin. Normalize prolactin before injection.
Pricing updated 2026-04-09
The most dangerous risk with triptorelin is not a side effect. It is a dosing error. A single injection of 1 mg instead of 0.1 mg (a 10x miscalculation during reconstitution) can trigger the same pituitary receptor downregulation used therapeutically in prostate cancer. The result is prolonged chemical castration from what was supposed to be a PCT dose. This margin is not forgiving. At the correct 100 mcg PCT dose, published and community-reported side effects are generally mild and transient. Hot flushes occur in the hours following injection as the LH/FSH surge drives a rapid testosterone spike. Headache, nausea, and injection site pain are common (greater than 10% incidence based on Trelstar label extrapolation). Some users report temporary acne or mood volatility in the first 3 to 5 days, attributed to the initial testosterone flare. A less obvious risk is the gonadotropin refractory window. After the acute LH/FSH flare, gonadotropin levels can dip temporarily before stabilizing. Users who skip the SERM bridge (tamoxifen, clomiphene) sometimes report testosterone normalization followed by a relapse at weeks 2 to 4. This is not a direct side effect of triptorelin but a predictable pharmacodynamic consequence that the community figured out before any formal study documented it. Pituitary apoplexy is the rarest but most severe risk. Anyone with an undiagnosed pituitary adenoma faces the possibility of hemorrhage or infarction triggered by the acute LH/FSH surge. Symptoms include sudden severe headache, vision changes, nausea, and altered consciousness. This is a medical emergency. The Trelstar FDA label explicitly warns about this risk. A pituitary MRI before injection is the prudent screening step, though almost nobody in the community actually gets one. At depot/clinical doses (milligram range, not applicable to PCT): hot flashes, erectile dysfunction, decreased libido, bone density loss, mood disturbances, and tumor flare in prostate cancer patients during the first 1 to 2 weeks are expected and well-documented. Contraindications: hormone-sensitive cancers (unless under oncologist supervision), pregnancy (Category X, causes fetal harm), primary hypogonadism (pituitary stimulation cannot help if testes cannot respond), known hypersensitivity to GnRH analogs, and concurrent GnRH agonist or antagonist therapy. Stop and seek medical attention immediately if you experience sudden severe headache, vision problems, or altered consciousness after injection.
Verify Triptorelin dosing and safety with a second opinion
No FDA-approved 0.1 mg (100 mcg) triptorelin vial exists in the US. PCT users import international Decapeptyl (Ferring) or purchase from unregulated research peptide vendors and reconstitute larger vials (0.5 mg, 1 mg). A 10x dosing error, 1 mg instead of 0.1 mg, is easily made during reconstitution and can cause prolonged chemical castration even as a single injection.
| Test | When | Target |
|---|---|---|
| Total testosterone | Baseline (before injection); week 2; week 4–6 | 400–900 ng/dL (normal adult male) |
| LH and FSH | Baseline; week 2; week 4–6 | LH: 1.7–8.6 IU/L; FSH: 1.5–12.4 IU/L |
| Estradiol (E2) | Baseline; week 4–6 | 20–40 pg/mL (physiologic male) |
| Free testosterone | Baseline; week 4–6 | 9–30 ng/dL (age-dependent) |
| Prolactin | Baseline (especially if using dopaminergic drugs or antipsychotics) | <15 ng/mL (male reference) |
| Pituitary MRI (sella turcica) | Before injection: ideal but rarely performed in community PCT users | — |
Primary endpoint: confirms whether triptorelin successfully restarted Leydig cell steroidogenesis
Elevated LH/FSH at baseline = primary hypogonadism (triptorelin inappropriate). Low LH/FSH at baseline = hypogonadotropic (triptorelin correct target). Post-injection LH/FSH should flare then normalize.
Confirms testosterone is rising (E2 rises with T via aromatization). Excessive E2 elevation may require aromatase inhibitor management.
More sensitive than total T for borderline recovery cases; useful if SHBG is elevated
Hyperprolactinemia suppresses GnRH signaling and blunts triptorelin effectiveness. Normalize before injection.
Rules out undiagnosed pituitary adenoma. Acute LH/FSH surge from triptorelin can trigger pituitary apoplexy (hemorrhage/infarction) in adenoma patients: a medical emergency. Explicitly cited in the Trelstar FDA label.
Acute LH and FSH surge measurable on bloodwork. Triptorelin reaches peak plasma concentration within 1-3 hours.
LH and FSH remain elevated from the initial flare. Testes begin responding to gonadotropin stimulation.
Testosterone levels start rising as Leydig cells resume steroidogenesis. Early subjective improvements in energy and mood possible.
Full HPTA recovery expected if pituitary and testes are functional. Testosterone should be in normal range on labs. Libido and energy normalized.
Hours 1 to 4: Triptorelin reaches peak plasma concentration within 1 to 3 hours after injection (Trelstar FDA label). LH and FSH levels surge measurably on bloodwork within this window. Some users report a brief flush of energy or mild libido bump; most feel nothing acutely. Transient hot flush, headache, or nausea can occur. Days 1 to 7: LH and FSH remain raised from the initial flare. Leydig cells in the testes begin responding to gonadotropin stimulation and initiating steroidogenesis. Subjective changes are minimal during week 1. Users who skipped the SERM bridge sometimes notice a gonadotropin dip around days 5 to 7 as the refractory window opens. Mild transient acne is possible from the testosterone flare. Week 2: Testosterone levels start climbing as Leydig cells resume full steroidogenesis. Bloodwork at this point should show measurable improvement. Most responding users report better energy, improved mood, and early libido return. No change at week 2 doesn't mean failure; weeks 4 to 6 are the true endpoint. Weeks 4 to 6: The expected finish line. In pituitary- and gonad-competent individuals, full HPTA recovery should be confirmed on labs. Testosterone within normal range, LH and FSH normalized. The majority of successful community cases report bloodwork-confirmed testosterone normalization by this point. Users who ran the SERM bridge report more consistent recovery compared to standalone triptorelin protocols. No side effects expected if recovery is progressing normally.
Triptorelin reaches peak plasma concentration within 1–3 hours (IM, Trelstar label). Measurable LH and FSH surge on bloodwork within 1–4 hours of injection.
Some users report heightened energy or mild libido within hours, attributed to the testosterone flare effect. Most notice nothing acutely.
LH and FSH remain elevated. Testes begin responding to gonadotropin stimulation. Leydig cells initiate steroidogenesis.
Limited subjective change in week 1. Some report mild mood improvement. Users without SERM bridge may notice a gonadotropin dip around days 5–7 (refractory window).
Testosterone levels start climbing as Leydig cells resume steroidogenesis. Bloodwork at week 2 should show measurable improvement.
Most responding users report improved energy, mood, and early libido return. No change at week 2 is not definitive failure: week 4–6 is the true endpoint.
Full HPTA recovery in pituitary- and gonad-competent individuals. Testosterone within normal range. LH/FSH normalized.
Majority of successful cases report testosterone normalization confirmed by bloodwork. SERM bridge users report more consistent recovery vs standalone triptorelin.
Source: Muller et al. 1997 (PMID 9354307): terminal t½ 2.8h in healthy males, 6.6-7.7h in renal/hepatic impairment; SC bioavailability extends effective t½ ~10x vs IV per Lahlou 2005 (PMID 16302716)
Loading the interactive decay curve.
Triptorelin is FDA-approved in the United States under the brand name Trelstar (triptorelin pamoate) for palliative treatment of advanced prostate cancer. The approved formulations are depot injections at 3.75 mg (monthly), 11.25 mg (quarterly), and 22.5 mg (semi-annually), all requiring a prescription. No FDA-approved 100 mcg (0.1 mg) triptorelin product exists in the US. The Decapeptyl 0.1 mg daily subcutaneous formulation (Ferring Pharmaceuticals) is available in Europe and other international markets but has no US approval. PCT users in the US typically source triptorelin from international pharmacies (import legality varies by jurisdiction) or from unregulated research peptide vendors sold "for research purposes only." Triptorelin is a WADA-prohibited substance under the S2 class (peptide hormones, growth factors, and related substances). Athletes subject to anti-doping testing should be aware that detection windows may extend beyond the pharmacological half-life. This content is for educational and informational purposes only. It does not constitute medical advice. Consult a qualified healthcare provider before using any peptide.
Peptide Schedule Research TeamReviewed Apr 20265 Citations
