Cetrorelix

Cetrotide, cetrorelix acetate, SB-75

Sexual health, hormones & signalling

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Note on this profile. Cetrorelix is an approved prescription medicine used in fertility clinics, not a research-only compound. This page explains the published science. Use outside a supervised IVF cycle, which is occasionally discussed online as a way to "switch off" sex hormones, has no evidence base and carries the risks discussed below.

Summary

Class: Synthetic GnRH (LHRH) antagonist decapeptide with five unnatural D-amino acids (third-generation antagonist)
Mechanism: Competitively blocks pituitary GnRH receptors, so LH and FSH fall within hours, with no initial flare and rapid reversal when stopped
Routes studied: Subcutaneous injection (approved); IM depot and oral formulations in discontinued development programmes
Dose range reported: Approved (controlled ovarian stimulation): 0.25 mg SC once daily from stimulation day 5–6 (or when lead follicle ~14 mm) until the day of trigger; or a single 3 mg dose on day 7 covering ≥4 days (EU; US 3 mg product discontinued). Research in BPH/endometriosis/fibroids: 3–10 mg SC weekly or depot 30–60 mg. Community use: anecdotal
Half-life: ~5 h after a single 0.25 mg dose; ~20 h after repeated 0.25 mg doses; ~63 h after 3 mg (label values)
Storage: 0.25 mg kit: refrigerate 2–8 °C in the carton; unopened kits may be kept at room temperature for up to 3 months per current label †. Use immediately after reconstitution
Regulatory status: Approved medicine (EU 1999, US 2000, UK, AU, ZA and others)

Doses are as reported in studies or by the community — never recommendations.

1What it is

Cetrorelix is a GnRH antagonist: where such as leuprolide work by exhausting the pituitary over weeks, cetrorelix simply blocks the receptor and the effect begins within hours. It was developed by Andrew Schally's group (as SB-75) and brought to market by ASTA Medica/Æterna Zentaris and Merck Serono. Its approved job is narrow: to stop a woman's own LH surge from releasing eggs prematurely during IVF stimulation. It was also studied for benign prostatic hyperplasia, endometriosis, fibroids and some cancers, but those programmes stalled, and newer oral non-peptide antagonists (elagolix, relugolix — not peptides) now fill those niches.

2How it's thought to work

Occupies the pituitary GnRH receptor without activating it. LH falls within about 4–8 hours; FSH falls less.

No flare, so no need for the two-week lead-in that protocols require, and ovarian stimulation can start with the natural cycle.

Because suppression is dose-dependent and reversible, the ovary's own hormones recover within days of the last dose, which is why antagonist cycles have shorter stimulation and lower OHSS risk.

A GnRH agonist trigger (e.g. triptorelin 0.2 mg) still works in an antagonist cycle, because the agonist displaces the antagonist and briefly activates the receptor.

The pituitary GnRH receptor occupied but not activated. LH falls within hours, with no flare, which is why antagonist IVF cycles need no two-week lead-in.Schematic — not to scale

3What the research shows

Prevention of premature LH surge in IVF

Daily 0.25 mg prevented premature LH surges in >95% of cycles with pregnancy rates comparable to buserelin long protocols and shorter stimulation (Albano 2000, Hum Reprod). A single 3 mg dose performed similarly against triptorelin (Olivennes 2000, Fertil Steril). The Cochrane review of 73 found no evidence of a difference in live birth between antagonist and protocols and a substantially lower OHSS rate with antagonists (Al-Inany 2016, Cochrane). [1][2][3]

Endometriosis and uterine fibroids

Intermittent 3 mg weekly for eight weeks reduced endometriosis stage and pain in small open studies (Küpker 2002, Reprod Biomed Online); a slow-release formulation shrank fibroids before surgery (Felberbaum 1998, Hum Reprod). Never progressed to approval. [4][5]

Graded A (unsuccessful)

Benign prostatic hyperplasia

A phase 2 trial of cetrorelix pamoate depot improved symptom scores versus placebo (Debruyne 2008, BJU Int), but phase 3 trials in 2009 failed to confirm benefit and development stopped. [6]

Prostate and ovarian cancer

Early studies in advanced prostate cancer showed rapid testosterone suppression without flare (Gonzalez-Barcena 1994, Prostate); a phase 2 in platinum-resistant ovarian cancer reported modest activity (Verschraegen 2003, Gynecol Oncol). Superseded by degarelix in prostate cancer. [7]

Non-medical "hormone switch-off"

Occasionally discussed online for suppressing oestrogen or testosterone without flare. No studies. Suppression at 0.25 mg/day is partial and short-lived; anything more is uncharted in this context.

4Reported side effects and interactions

Literature-reported

Common (literature). injection-site reactions (redness, itching, swelling, bruising — the most frequent, usually mild and transient), nausea, headache. Ovarian hyperstimulation syndrome occurs in antagonist cycles but less often than with ; it is a consequence of the gonadotrophins, not cetrorelix itself.

Serious / warnings. hypersensitivity reactions including a reported severe anaphylactoid reaction after seven months of use in a non-IVF indication; contraindicated in pregnancy and breastfeeding, in severe renal impairment, and with known hypersensitivity to GnRH analogues or mannitol. Congenital anomaly rates in cetrorelix cycles are in line with other assisted-reproduction populations.

Community-reported

essentially none beyond IVF patients' accounts of injection-site reactions.

Theoretical. oestrogen or testosterone suppression over weeks would bring the same bone, mood and metabolic effects as agonists, just without the flare.

Interactions. no formal interaction studies; metabolised by peptidases, not CYP enzymes, so pharmacokinetic interactions are unlikely. Pharmacodynamically it blocks gonadorelin, kisspeptin and GnRH agonist effects (except the agonist-trigger phenomenon described above).

Markers researchers commonly monitor

These follow IVF monitoring, since that is the only evidence-based context: For any non-IVF use, no markers are established.

Marker	Why it's watched
LH	the purpose of the drug is to keep LH low until trigger; a rise >10 IU/L suggests breakthrough.
Oestradiol	tracks follicular development and OHSS risk; antagonist cycles show a small dip after starting cetrorelix.
Progesterone (late follicular)	premature rise predicts poorer fresh-transfer outcomes.
Transvaginal ultrasound follicle count and size	timing of the first cetrorelix dose is driven by follicle size, not a calendar day.
Pregnancy test and OHSS symptoms	post-cycle.
Serum sodium, haematocrit, creatinine	only if OHSS develops.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Supplied as a kit: a vial of 0.25 mg powder plus a pre-filled syringe of 1 mL water for injection. The solvent is injected into the vial, swirled gently (not shaken) until clear, drawn back and injected subcutaneously into the lower abdomen. The dose is fixed, so no calculation is needed and the calculator is not applicable.

Open in calculator, pre-loaded →

6Commonly studied alongside

Ganirelix (the other approved antagonist; interchangeable in practice), recombinant FSH and HMG (stimulation), HCG or triptorelin/leuprolide (trigger), progesterone luteal support. Kisspeptin-54 (this batch) has been tested as a trigger in antagonist cycles.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	FDA-approved (Cetrotide 0.25 mg) for inhibition of premature LH surges in controlled ovarian stimulation; 3 mg presentation discontinued
European Union	EMA-authorised (Cetrotide 0.25 mg; 3 mg in some markets)
United Kingdom	MHRA-licensed; prescription-only
Australia	TGA-approved; S4
South Africa	SAHPRA-registered; prescription-only
Sport	Not specifically listed by WADA as of review date; GnRH antagonists lower rather than raise sex hormones †

8Open questions

Long-acting or oral peptide antagonists never reached the market; the field moved to non-peptide molecules.
Whether antagonist protocols give equal cumulative live-birth rates across all patient groups (poor responders remain debated).
No data on repeated or chronic use outside fertility treatment.

9References

1Albano C et al. (2000). Ovarian stimulation with HMG: results of a prospective randomized phase III European study comparing the luteinizing hormone-releasing hormone (LHRH)-antagonist cetrorelix and the LHRH-agonist buserelin. Hum Reprod. PubMed · DOI
2Olivennes F et al. (2000). Prospective, randomized, controlled study of in vitro fertilization-embryo transfer with a single dose of a luteinizing hormone-releasing hormone (LH-RH) antagonist (cetrorelix) or a depot formula of an LH-RH agonist (triptorelin). Fertil Steril. PubMed · DOI
3Al-Inany HG et al. (2016). Gonadotrophin-releasing hormone antagonists for assisted reproductive technology. Cochrane Database Syst Rev. PubMed · DOI
4Felberbaum RE et al. (1998). Treatment of uterine fibroids with a slow-release formulation of the gonadotrophin releasing hormone antagonist cetrorelix. Hum Reprod. PubMed · DOI
5Küpker W et al. (2002). Use of GnRH antagonists in the treatment of endometriosis. Reprod Biomed Online. PubMed · DOI
6Debruyne F et al. (2008). Sustained-release cetrorelix pamoate in benign prostatic hyperplasia: a phase II randomized, placebo-controlled trial. BJU Int. PubMed
7Verschraegen CF et al. (2003). Phase II study of cetrorelix, a luteinizing hormone-releasing hormone antagonist, in patients with platinum-resistant ovarian cancer. Gynecol Oncol. PubMed · DOI
8Cetrotide prescribing information / SmPC (current). PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

26 Oct 2026Profile published — awaiting medical review

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