Gonadorelin (GnRH)

Gonadorelin (GnRH) at a Glance

Gonadorelin is synthetic GnRH, a decapeptide identical to the hormone the hypothalamus releases in pulses to drive LH and FSH from the pituitary. That pulsatility is the whole mechanism: delivered in pulses it stimulates the reproductive axis, while delivered continuously it shuts it down — the basis of an entire class of hormone-suppressing drugs. It was approved for pituitary function testing and for inducing ovulation, and those products have largely been discontinued; it is now used mainly in compounded fertility and testosterone-support protocols.

History & Development

Gonadorelin is the body’s own GnRH, synthesised. It was approved twice, for two quite different jobs, and both products have since been discontinued - which is why a molecule with a genuine regulatory history now has no approved form at all.

First described	Not established in the sources consulted for this section
Discovered / synthesised by	Not established in the sources consulted for this section
Institution	Not established in the sources consulted for this section
Origin	Synthetic decapeptide identical to endogenous gonadotropin-releasing hormone (GnRH / LHRH)
Key patent	Not established in the sources consulted for this section
Assignee	Not established in the sources consulted for this section
Development status	Formerly approved - marketed as Factrel (diagnostic) and Lutrepulse (pulsatile fertility therapy); both discontinued

Discovery

GnRH sits at the top of the reproductive hormone cascade. The hypothalamus releases it in pulses, the pituitary answers with LH and FSH, and the gonads answer those with testosterone or estrogen. Gonadorelin is that decapeptide made synthetically - not an analogue, but the identical molecule.

The pulsatility is the whole pharmacology, and it cuts both ways. Delivered in pulses, GnRH drives the axis. Delivered continuously, it shuts the axis down, because the pituitary receptors desensitise - which is the basis of the long-acting GnRH agonists used to suppress sex hormones in prostate cancer and endometriosis. Same molecule, opposite outcome, decided entirely by timing.

Development & ownership

Gonadorelin reached the market in two forms. Factrel was the diagnostic product: a single intravenous bolus of roughly 100 µg provokes an LH and FSH rise, and the shape of that response distinguishes pituitary from hypothalamic causes of reproductive failure. Lutrepulse was the therapeutic one - a pump delivering micro-doses at roughly 90-minute intervals to reproduce natural pulsatility and induce ovulation in hypothalamic amenorrhoea.

Lutrepulse worked, and it was displaced anyway. Injectable gonadotropins achieve ovulation induction without requiring a patient to wear an infusion pump for weeks, and the diagnostic test was superseded by better assays. Both products were discontinued for practical and commercial reasons rather than safety ones.

How it reached the market

There is now no approved gonadorelin product. It reaches people through compounding pharmacies, prescribed mainly in men’s-health clinics on the theory that pulsatile GnRH maintains testicular function during testosterone therapy - a use that is mechanistically coherent and was never the indication either approved product carried.

What It's Used For

Gonadorelin is synthetic gonadotropin-releasing hormone — a decapeptide (pyroGlu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH₂, ~1,182 Da) with a sequence identical to the hormone the hypothalamus itself uses to drive the pituitary. It is not a gray-market research chemical and never was: it held two genuine US new drug approvals — Factrel (gonadorelin hydrochloride, NDA 018123, now held by Hikma, 0.1/0.2/0.5 mg base per vial) for pituitary-gonadal stimulation testing, and Lutrepulse Kit (gonadorelin acetate, NDA 019687, Ferring, 0.8 and 3.2 mg per vial) for pump-delivered pulsatile ovulation induction. Both are listed in Drugs@FDA with marketing status Discontinued. So the evidence here is real human clinical data, but it is old, mostly cohort- and case-series-grade rather than modern RCT, and it belongs to two narrow jobs — a diagnostic test and a pump-delivered fertility therapy — neither of which is what gonadorelin is mostly sold for today.

One fact governs this entire page, and it is a genuine safety issue rather than a curiosity. GnRH-receptor signaling is pattern-dependent, not dose-dependent in the ordinary sense. Delivered in brief pulses roughly every 90 minutes — the hypothalamus’s own rhythm — gonadorelin stimulates the axis, raising LH and FSH and driving the gonads. Delivered continuously, or at sustained high exposure, the identical molecule at the identical receptor does the opposite: the pituitary gonadotroph desensitizes and downregulates, and LH/FSH output collapses. That inversion is not a theoretical edge case — it is the exact mechanism by which the long-acting GnRH agonists leuprolide, goserelin, triptorelin and nafarelin achieve medical castration in prostate cancer, endometriosis and central precocious puberty. Same receptor, opposite clinical outcome, decided entirely by administration pattern. A badly-timed self-administered protocol can therefore suppress the very axis it was intended to support.

That inversion also makes the literature treacherous. A ClinicalTrials.gov search for “gonadorelin” returns overwhelmingly leuprolide, goserelin and triptorelin androgen-deprivation and ovarian-suppression trials — studies of suppression, not stimulation. Where evidence is cited, it is evidence generated with native GnRH/gonadorelin delivered pulsatilely, and where a source pools broader “LHRH” preparations that distinction is called out in the toggle rather than glossed. Route and pattern are load-bearing throughout: gonadorelin has negligible oral bioavailability, must be injected, and clears within minutes ^{11,12Reference 11Handelsman DJ · 1986ReviewPharmacokinetics of gonadotropin-releasing hormone and its analogs — review (PK)View study →Reference 12Cissewski K et al. · 1987Metabolism of GnRH in man: influence of estrogens — human (PK / metabolic clearance, n=9 men, 7 women)View study →}.

Evidence by IndicationStrength of support · Beta

Support is an experimental score I’m building — a composite weighted by study type (human > animal > in vitro > review) and study volume. It’s a beta: a fast way to rank strength of evidence at a glance, not a validated metric. Each application links down to its write-up.

Two readings of this table need care. The cryptorchidism 30% is not absence of evidence — that indication was tested at RCT level, found to work modestly, and then deliberately discontinued in favor of surgery ^{10Reference 10Thorsson AV et al. · 2007ReviewEfficacy and safety of hormonal treatment of cryptorchidism: current state of the art — reviewView study →}. And the TRT-adjunct row carries no bar on purpose: it is the most common current use of gonadorelin and it has no controlled data at all, so scoring it — even low — would misrepresent vendor and clinic practice as a weak evidence base rather than an absent one.

01GnRH stimulation testing (diagnostic)Promising72%Human; a former FDA-approved indication (Factrel); large pediatric validation series. A diagnostic, not a therapy — and the product is discontinued.

02Pulsatile ovulation induction in hypothalamic amenorrheaPromising70%Human; a former FDA-approved indication (Lutrepulse); consistent ~70–100% cumulative pregnancy over 6 cycles + a completed Phase 3 (n=39). Largely observational; requires a pump.

03Pulsatile puberty induction & spermatogenesis in CHHPromising60%Human cohorts (n=45, n=54, n=21) showing testicular growth and spermatogenesis. All retrospective, single-center, no RCT.

04Cryptorchidism (undescended testis)Shaky30%RCT meta-analysis — a real but small effect (~20%), pooled across “LHRH” preparations rather than gonadorelin specifically. Abandoned, not merely untested.

05TRT adjunct / testicular preservationShaky0%Mechanism, analogy to hCG, and clinic/community practice. Zero controlled trials. Not evidence, so not given a score.

Mechanisms

The pulsatile-versus-continuous inversion is the single most important entry in this table. It is the reason two drug classes with directly opposite clinical purposes act at the same receptor, and it is the reason dosing pattern — not dose — is the safety-critical variable for anyone using this compound outside a supervised protocol.

Pharmacokinetics

Gonadorelin has negligible oral bioavailability — a decapeptide is digested rather than absorbed, so any oral product is pharmacologically inert regardless of its label. It must be given parenterally: intravenously or subcutaneously for pulsatile pump therapy, intravenously as a bolus for the diagnostic test; intranasal delivery was used historically in the cryptorchidism work ^{9Reference 9Pyörälä S et al. · 1995Meta-analysisA review and meta-analysis of hormonal treatment of cryptorchidism — human (meta-analysis, 33 studies, 3,282 boys)View study →}.

Its defining property is an extremely short half-life, on the order of minutes — commonly cited as 2–10 minutes, reflecting rapid enzymatic cleavage. The canonical pharmacokinetic review of GnRH and its analogues is the reference point here ^{11Reference 11Handelsman DJ · 1986ReviewPharmacokinetics of gonadotropin-releasing hormone and its analogs — review (PK)View study →}, and what has been measured directly in humans is metabolic clearance rate rather than a clean elimination half-life: continuous infusion studies put GnRH clearance at roughly 455 mL/min in men and ~1,769 mL/min in women (the latter varying cyclically), with estrogen status modulating it ^{12Reference 12Cissewski K et al. · 1987Metabolism of GnRH in man: influence of estrogens — human (PK / metabolic clearance, n=9 men, 7 women)View study →}. A single definitive human elimination half-life figure is not established in the accessible literature, and the widely-quoted “2–10 minutes” should be read as a well-supported approximation rather than a measured constant.

That brevity is the load-bearing PK fact, and it cuts both ways. It is what makes pulsatile delivery necessary — each pulse must clear before the next for the rhythm to register as a rhythm — and what makes it possible, since a pump can shape an exposure profile that a syringe cannot. It is equally why an every-few-days bolus schedule is a poor pharmacological match for the pump protocols that generated the evidence here. The approved products were supplied as lyophilized powder requiring reconstitution for pump loading; stability once reconstituted is limited, and stability parameters for compounded and gray-market material are not independently documented.

Clinical & regulatory status

Gonadorelin is a prescription drug that has essentially exited the US market. Per Drugs@FDA, two human products hold US new drug applications and both are listed with marketing status “Discontinued”: Factrel (gonadorelin hydrochloride, NDA 018123, Hikma; EQ 0.1, 0.2 and 0.5 mg base per vial, injectable) for pituitary-gonadal stimulation testing, and Lutrepulse Kit (gonadorelin acetate, NDA 019687, Ferring; 0.8 and 3.2 mg per vial, injectable) for pulsatile ovulation induction.

A precise distinction is worth drawing here, because it differs from the neighboring case of sermorelin. Sermorelin’s approvals were formally withdrawn by FDA in 2009, and FDA later published a determination that this was not for reasons of safety or effectiveness. For gonadorelin, a search of the Federal Register returns no withdrawal-of-approval notice and no safety-or-effectiveness determination for either NDA — the only Federal Register entries mentioning “Factrel” concern the veterinary product and horse-racing anti-doping rules. So the accurate statement is that these are approved applications that are no longer marketed, not applications whose approval has been revoked, and no published FDA finding characterizes why marketing stopped. This page will not infer a reason that no primary source states.

One identity trap follows from that veterinary listing: “Factrel” today is most visibly a cattle product (gonadorelin injection, Zoetis, regulated as an animal drug under 21 CFR 522.1077). A search on the brand name will surface veterinary labeling, which is not the human NDA 018123 product and carries different formulation and quality expectations.

Registered-trial activity is sparse and easy to misread. A ClinicalTrials.gov search for “gonadorelin” returns mostly leuprolide, goserelin and triptorelin trials — long-acting GnRH agonists used for androgen deprivation and ovarian suppression, which are pharmacologically opposite in effect. Filtering to genuine pulsatile-gonadorelin studies leaves the completed Phase 3 NCT01976728 (n=39, results posted) and the completed Phase 2 NCT00796289 (Lutrepatch iontophoretic patch, n=350, completed 2010 with no results posted). There are no registered controlled trials of gonadorelin as a TRT or testicular-preservation adjunct.

Last checked: July 2026.

Sourcing, Route & Legal Status

Regulatory status. Gonadorelin is a genuine prescription pharmaceutical — not a research chemical, and not a dietary supplement. It held two US approvals (Factrel, NDA 018123; Lutrepulse Kit, NDA 019687), both now listed as Discontinued in Drugs@FDA, meaning there is no currently marketed FDA-approved human gonadorelin product in the United States. It remains registered in some other jurisdictions. The limits of that credential deserve stating plainly, because the marketing leans on it: the approvals covered a diagnostic pituitary test and pump-delivered pulsatile fertility therapy. They did not cover testosterone-replacement support, testicular preservation, libido, or any anti-aging use, and an approval never transfers from the indication and population it was granted for. Gonadorelin is not a scheduled or controlled substance.

How it’s supplied and administered. Lyophilized powder requiring reconstitution, given by injection — subcutaneous or intravenous. Clinical fertility use is delivered by a programmable pulsatile infusion pump at roughly 90-minute intervals; the diagnostic use was a single intravenous bolus. Oral routes do not work at all. The pump is not a convenience: it is the delivery mechanism under which the fertility evidence was generated, and the minutes-long half-life means the pattern it produces cannot be approximated by injections spaced days apart.

Sourcing reality (this is a safety issue, not a footnote). Because the approved products have left the US market, virtually all gonadorelin reaching consumers now comes through compounding pharmacies or unregulated research-chemical vendors. Compounded preparations are not FDA-approved products — they are not reviewed for safety, efficacy or manufacturing quality the way an approved drug is, and FDA has been actively scrutinizing the bulk-substance pathway that peptide compounding depends on, so availability is not stable. Gray-market powder has no oversight at all: uncertain identity and peptide content, mislabeling, under- or over-concentration, bacterial endotoxin, and no sterility guarantee. Self-reconstitution and self-injection add technique and contamination risk on top, and a peptide this labile degrades readily if mishandled or stored improperly. A vendor’s own certificate of analysis is not independent verification and can be falsified. None of the human efficacy data here were generated with compounded or gray-market material. This page does not recommend or link vendors.

Safety

Gonadorelin’s direct toxicity is low — it is a molecule the body already makes, given in micrograms. The hazard is pharmacological rather than toxicological: the same receptor stimulates under pulsatile dosing and shuts down under continuous dosing, so a mis-timed protocol can achieve the exact opposite of what was intended.

Safety at a Glance

✅ Low / no toxicityDrug interactions

• The dosing pattern decides the direction. Continuous or overly frequent exposure suppresses the axis — the same mechanism used to produce chemical castration.
• Initiation can cause a gonadotropin flare. In hormone-sensitive conditions that is the main starting consideration, and why it is a supervised event.
• Every positive result came from a pump. Nothing establishes that ad-hoc injection schedules reproduce 90-minute pulses.
• Sex-steroid drugs confound it. Concurrent testosterone or estrogen blunts the response and invalidates the diagnostic test.
• Long-term pump therapy has real adverse effects. Gynecomastia in 8 of 45 men and subcutaneous induration in 6.
• No marketed US product. Supply is compounded or gray-market, adding identity, purity and endotoxin risk on an injected route.

Full Safety & Interactions Detail

Overall posture. Direct toxicity is low, and that is the least interesting thing about gonadorelin’s safety. It is a molecule the body already makes, given in microgram amounts, and the approved uses were either a single diagnostic dose or short cyclic therapy under supervision. Reported adverse effects in clinical use are mostly mild — injection-site reactions, headache, nausea, abdominal discomfort, and rare hypersensitivity. The largest modern cohort gives concrete figures: among 45 CHH men on long-term pump therapy, gynecomastia occurred in 8 and subcutaneous induration in 6, alongside allergic reactions ^{2Reference 2Niu YH et al. · 2024ObservationalEffect and safety of pulsatile GnRH therapy for male congenital hypogonadotropic hypogonadism — human (retrospective cohort, n=45 men)View study →}. With pump therapy, catheter and infusion-site infection and mechanical failure are practical concerns.

The dominant hazard is pharmacological, not toxicological — and it is specific. Because the GnRH receptor stimulates under pulsatile exposure and desensitizes under continuous or sustained exposure, the direction of gonadorelin’s effect is determined by the administration pattern rather than by the molecule or the dose. This is not a theoretical concern: continuous GnRH-agonist exposure is precisely how leuprolide, goserelin, triptorelin and nafarelin produce chemical castration. The practical consequence for anyone self-administering is blunt — a mis-timed or overly frequent protocol can suppress the hypothalamic-pituitary-gonadal axis rather than support it, achieving the opposite of the intended effect. Every positive finding here was produced by pump-delivered pulses at roughly 90-minute intervals. Nothing establishes that ad-hoc injection schedules reproduce that, and the pharmacology gives specific reason to doubt it.

The flare. Initiation can produce a transient rise in gonadotropins and sex steroids before any suppression develops. In hormone-sensitive conditions this is the main consideration on starting, and it is why initiation of GnRH-receptor agonists in that setting is a supervised event.

Interactions. No comprehensive modern interaction assessment exists for off-label protocols. Recognized in the prescribing literature: drugs that alter pituitary function or sex-hormone levels — other GnRH analogues, androgens and estrogens, and dopaminergic or antipsychotic agents affecting prolactin — can blunt or confound the response, and the diagnostic test is invalidated by concurrent sex-steroid therapy. Concurrent exogenous testosterone is the norm in the off-label TRT setting and is itself axis-suppressing, so the interaction that matters most in practice is also the least studied.

Who should avoid it. Anyone with a hormone-sensitive malignancy or condition in which a gonadotropin flare would be harmful; anyone pregnant, breastfeeding or trying to conceive outside a supervised fertility protocol; children outside a diagnosed and supervised indication; and anyone unwilling to accept a non-approved compounded or gray-market product of unverified composition on an injected route. Because gonadorelin’s effect direction depends on delivery pattern, self-administration without monitoring of LH, FSH and testosterone means there is no way to know which direction the axis is actually moving.

Scope disclosure (honesty, not a claim):

• Human data? Yes — decades of it, from two formerly approved indications. But it is concentrated in diagnostic testing and pump-delivered fertility therapy, is largely cohort- and case-series-grade, and includes one completed Phase 2 (n=350) whose results were never posted. There is no human data of any kind for the TRT-adjunct use that now dominates real-world consumption.
• Interactions assessed? Partially — sex-steroid and pituitary-acting drug classes are recognized in the prescribing literature. No modern interaction screen covers off-label protocols, including the near-universal combination with exogenous testosterone.
• Pregnancy/lactation assessed? Not for chronic use; see the verdict above.
• Long-term safety established? No. Approved use was a single diagnostic dose or cyclic fertility therapy. The longest human follow-up here is CHH pump therapy to about two years ^{2,3Reference 2Niu YH et al. · 2024ObservationalEffect and safety of pulsatile GnRH therapy for male congenital hypogonadotropic hypogonadism — human (retrospective cohort, n=45 men)View study →Reference 3Jiang H et al. · 2025ObservationalTherapeutic effects of a pulsatile GnRH pump on adult male patients with congenital hypogonadotropic hypogonadism (CHH): a retrospective study — human (retrospective cohort, n=54 men)View study →}. Indefinite off-label injection has not been studied, and absence of reports is not evidence of safety.
• Does the former approval make current use safe? No — and this is the specific misreading to guard against. Two narrow indications, delivered by pump or in a clinic, with products that are no longer marketed, say nothing about ongoing self-administered use for a different purpose entirely.

Never imply safety from silence. Where gonadorelin has not been studied — the TRT-adjunct use, long-term dosing, interactions with exogenous testosterone, and compounded or gray-market product quality — the correct statement is “not assessed,” not “safe.”

Pregnancy & Lactation

• Caution in pregnancy? Not established in lactation

Used to achieve pregnancy, not continued through it. In pulsatile ovulation induction the goal is conception, and gonadorelin is not required to sustain an established pregnancy; any use in pregnancy should be specialist-directed only. Lactation data are not established. Off-label use during pregnancy or breastfeeding is not assessed and not advised.

Dosage

There is no consumer or oral dose for gonadorelin, and none is recommended here. Every figure below is a clinical or approved-era dose reported as data, not a protocol — and each is inseparable from the delivery method that produced it.

The diagnostic dose was a single intravenous bolus of about 100 µg in adults, with LH and FSH sampled afterward; a single sample at 40 minutes is sufficient for diagnosis ^{8Reference 8Kandemir N et al. · 2011GnRH stimulation test in precocious puberty: single sample is adequate for diagnosis and dose adjustment — human (diagnostic study, 584 tests)View study →}. For pulsatile ovulation induction, the studied regimens are 5 µg per pulse intravenously or 15 µg per pulse subcutaneously every ~90 minutes by pump ^{6Reference 6Christou F et al. · 2017The induction of ovulation by pulsatile administration of GnRH: an appropriate method in hypothalamic amenorrhea — human (clinical series, n=12 women, 33 cycles)View study →}, with the Ferring Phase 3 testing fixed subcutaneous doses of 10, 15 and 20 µg per pulse (NCT01976728). For pulsatile therapy in congenital hypogonadotropic hypogonadism, cohorts used 7–15 µg per pulse every 90 minutes by microinfusion pump, continued over months to years ^{2,3Reference 2Niu YH et al. · 2024ObservationalEffect and safety of pulsatile GnRH therapy for male congenital hypogonadotropic hypogonadism — human (retrospective cohort, n=45 men)View study →Reference 3Jiang H et al. · 2025ObservationalTherapeutic effects of a pulsatile GnRH pump on adult male patients with congenital hypogonadotropic hypogonadism (CHH): a retrospective study — human (retrospective cohort, n=54 men)View study →}.

The pattern in every one of those figures is the point: a dose only means something paired with a pulse interval and a pump. A microgram figure lifted out of a 90-minute pulsatile protocol and delivered as a bolus twice a week is not the same intervention, and given the receptor’s pulsatile-versus-continuous inversion it may not even act in the same direction. Off-label TRT-adjunct doses are not listed here, because there is nothing to source them from except clinic and vendor practice, and this site does not launder those into dose figures. Oral products cannot deliver intact peptide whatever the label claims.

References

1. Young J, et al. (2019). Clinical management of congenital hypogonadotropic hypogonadism — review. Endocrine Reviews. https://pubmed.ncbi.nlm.nih.gov/30698671/
2. Niu YH, et al. (2024). Effect and safety of pulsatile GnRH therapy for male congenital hypogonadotropic hypogonadism — human (retrospective cohort, n=45 men). Zhonghua Nan Ke Xue (National Journal of Andrology). https://pubmed.ncbi.nlm.nih.gov/39210488/
3. Jiang H, et al. (2025). Therapeutic effects of a pulsatile GnRH pump on adult male patients with congenital hypogonadotropic hypogonadism (CHH): a retrospective study — human (retrospective cohort, n=54 men). Translational Andrology and Urology. https://pubmed.ncbi.nlm.nih.gov/40800099/
4. Delemarre-Van de Waal HA. (1993). Pulsatile GnRH treatment in boys and girls with idiopathic hypogonadotrophic hypogonadism — human (clinical study, n=21 males plus 5 adolescents). Human Reproduction. https://pubmed.ncbi.nlm.nih.gov/8276956/
5. Gronier H, et al. (2014). Ovulation induction by pulsatile GnRH therapy in 2014: literature review and synthesis of current practice — review. Gynécologie Obstétrique & Fertilité. https://pubmed.ncbi.nlm.nih.gov/25245838/
6. Christou F, et al. (2017). The induction of ovulation by pulsatile administration of GnRH: an appropriate method in hypothalamic amenorrhea — human (clinical series, n=12 women, 33 cycles). Gynecological Endocrinology. https://pubmed.ncbi.nlm.nih.gov/28277105/
7. Koca SB, et al. (2024). Diagnostic utility of the average peak LH levels measured during GnRH stimulation test — human (diagnostic accuracy, n=76 girls). Journal of Pediatric Endocrinology and Metabolism. https://pubmed.ncbi.nlm.nih.gov/39163851/
8. Kandemir N, et al. (2011). GnRH stimulation test in precocious puberty: single sample is adequate for diagnosis and dose adjustment — human (diagnostic study, 584 tests). Journal of Clinical Research in Pediatric Endocrinology. https://pubmed.ncbi.nlm.nih.gov/21448328/
9. Pyörälä S, et al. (1995). A review and meta-analysis of hormonal treatment of cryptorchidism — human (meta-analysis, 33 studies, 3,282 boys). Journal of Clinical Endocrinology & Metabolism. https://pubmed.ncbi.nlm.nih.gov/7673426/
10. Thorsson AV, et al. (2007). Efficacy and safety of hormonal treatment of cryptorchidism: current state of the art — review. Acta Paediatrica. https://pubmed.ncbi.nlm.nih.gov/17462056/
11. Handelsman DJ, Swerdloff RS. (1986). Pharmacokinetics of gonadotropin-releasing hormone and its analogs — review (PK). Endocrine Reviews. https://pubmed.ncbi.nlm.nih.gov/3007081/
12. Cissewski K, et al. (1987). Metabolism of GnRH in man: influence of estrogens — human (PK / metabolic clearance, n=9 men, 7 women). Hormone Research. https://pubmed.ncbi.nlm.nih.gov/3108133/
13. Kacimi L, Prévot V. (2025). GnRH and cognition — review. Endocrinology. https://pubmed.ncbi.nlm.nih.gov/39996304/

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