Peptide Schedule
Triptorelin10 residuesQHWSYGLRPGEach bubble = one amino acid. Size = residue mass. Color = chemical class.Triptorelin
Benefits
About Triptorelin
Triptorelin is a synthetic decapeptide analog of gonadotropin-releasing hormone (GnRH), with a D-tryptophan substitution at position 6 that makes it resistant to enzymatic degradation. It is FDA-approved under the brand name Trelstar for the palliative treatment of advanced prostate cancer, and also used clinically for endometriosis, uterine fibroids, central precocious puberty, and gender-affirming hormone therapy. The defining feature of triptorelin is its dose-dependent paradox. A single low dose (100mcg SC/IM) produces an acute flare — a rapid surge in LH and FSH from the pituitary — which stimulates the testes to produce testosterone. This is the basis of its off-label use in post-cycle therapy (PCT) after anabolic steroid cycles. A landmark case report by Pirola et al. (2010) documented a bodybuilder with 13 years of steroid-induced hypogonadism whose testosterone normalized within one month after a single 100mcg triptorelin injection. In contrast, continuous or depot administration (3.75mg monthly, 11.25mg quarterly, or 22.5mg semi-annually) causes sustained GnRH receptor stimulation. After an initial 1-2 week flare, the pituitary GnRHR receptors internalize and downregulate, shutting off LH/FSH production entirely. Testosterone drops to castrate levels — which is the therapeutic goal in prostate cancer. The same molecule that restarts hormone production at 100mcg will permanently suppress it at milligram doses. This is why triptorelin must never be dosed repeatedly in a PCT context.
Who Should Consider Triptorelin
- Men in post-cycle therapy after anabolic steroid use
- Men with prolonged hypogonadotropic hypogonadism from exogenous androgens
- Clinicians managing steroid-induced HPTA suppression
- Prostate cancer patients (at depot doses — different use case)
How Triptorelin Works
Triptorelin binds to GnRH receptors (GnRHR) on gonadotroph cells in the anterior pituitary with ~100x greater affinity than native GnRH, thanks to its D-Trp6 substitution that resists enzymatic cleavage by endopeptidases. On binding, it triggers the same Gq/11-phospholipase C-calcium signaling cascade as endogenous GnRH, causing LH and FSH exocytosis. The paradox is timing-dependent. A single acute exposure (as in a 100mcg PCT dose) produces the "flare effect" — a burst of LH and FSH release — because the pituitary gonadotrophs respond normally to an isolated GnRH signal. There is no sustained receptor occupancy, so no downregulation occurs. LH acts on testicular Leydig cells to produce testosterone, and FSH drives Sertoli cell-mediated spermatogenesis. Continuous exposure (depot formulations) changes the picture entirely. Persistent receptor activation causes GnRHR internalization via beta-arrestin-mediated endocytosis, uncoupling of the Gq signaling pathway, and eventual receptor degradation. The pituitary becomes refractory to GnRH stimulation. LH and FSH secretion ceases, testosterone falls to castrate levels (<50 ng/dL), and this suppression persists for the duration of the depot formulation (1-6 months). This is the intended therapeutic mechanism for prostate cancer, endometriosis, and precocious puberty.
What to Expect
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.
Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 100mcg | Single dose |
| Moderate | 100mcg | Single dose |
| Aggressive | 100mcg | Single dose |
Note: IMPORTANT: In PCT context, triptorelin is used as a ONE-TIME 100mcg injection — not repeated dosing. A single low dose triggers an acute LH/FSH surge that can restart testosterone production. Do NOT repeat the dose. Repeated or high-dose administration causes the opposite effect: pituitary downregulation and chemical castration. This is the same compound sold as Trelstar for prostate cancer, but at 37,500x the PCT dose.
How to Inject Triptorelin
Reconstitute the 0.1mg (100mcg) vial with 1mL bacteriostatic water. For PCT: inject the entire vial as a single subcutaneous or intramuscular injection. Abdominal SC or deltoid IM are both acceptable. Do NOT split the dose across multiple days. Do NOT repeat the injection. Get baseline bloodwork (LH, FSH, total testosterone, free testosterone, estradiol) before the injection and recheck at 2 weeks and 4 weeks post-injection to confirm HPTA recovery. If testosterone has not normalized by 6 weeks, consult an endocrinologist.
Cycling Protocol
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.
Pharmacokinetics
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.
Side Effects
At PCT doses (100mcg single shot): transient hot flush, headache, nausea, and injection site pain. An initial testosterone flare may cause temporary acne or mood changes. The primary risk is overdosing — exceeding 100mcg or repeating the injection can cause paradoxical pituitary downregulation, leading to prolonged LH/FSH suppression and chemical castration. At depot/clinical doses (mg range): hot flashes, erectile dysfunction, decreased libido, bone density loss, mood disturbances, injection site reactions, and tumor flare in prostate cancer patients during the first 1-2 weeks.
Contraindications
- Hormone-sensitive cancers (unless under oncologist supervision at depot doses)
- Pregnancy — causes fetal harm (Category X)
- Primary hypogonadism — pituitary stimulation will not help if testes cannot respond
- Known hypersensitivity to GnRH analogs or any component of the formulation
- Do not use if already on GnRH agonist/antagonist therapy
Drug Interactions
- Androgens — concurrent exogenous testosterone negates the purpose of PCT stimulation
- GnRH antagonists (degarelix, cetrorelix) — directly block the receptor triptorelin needs to activate
- Dopamine agonists (cabergoline, bromocriptine) — may blunt gonadotropin response
- Hyperprolactinemia-inducing drugs — elevated prolactin suppresses GnRH signaling
Storage & Stability
Molecular Profile
Related Peptides
References
- Anabolic steroids purchased on the Internet as a cause of prolonged hypogonadotropic hypogonadismPubMed 20416868
- Pharmacokinetics of triptorelin after intravenous bolus administration in healthy males and in males with renal or hepatic insufficiencyPubMed 9354307
- Pharmacokinetics and pharmacodynamics of triptorelinPubMed 16302716
- Trelstar (triptorelin pamoate) FDA Prescribing InformationFDA Label
- Dose-finding study of triptorelin acetate for prevention of a premature LH surge in IVFPubMed 11056128