Cetrorelix Acetate Injection

The drug competitively binds to GnRH receptors on pituitary cell membranes, completely blocking the binding of endogenous GnRH to its receptors, thereby directly inhibiting the secretion of LH and follicle-stimulating hormone (FSH) without an initial stimulatory effect. Unlike GnRH agonists, it does not undergo a "stimulation-then-suppression" phase; hormonal inhibition is achieved immediately after administration, preventing abnormal follicular development caused by transient elevations in LH levels.

Its inhibitory effect is clearly dose-dependent: daily administration of 0.25 mg maintains stable suppression for 24 hours, while a single 3 mg dose sustains suppression for at least 4 days, with approximately 70% inhibition of LH still observed on day 4. Following discontinuation, pituitary function recovers rapidly, and endogenous LH and FSH secretion return to normal without impairing subsequent follicular development or spontaneous ovulation. This profile of "rapid suppression, steady regulation, and reversible recovery" aligns perfectly with the need for precise hormonal control in assisted reproduction, providing a solid pharmacological basis for its core clinical applications.

Controlled ovarian stimulation is a central step in assisted reproductive techniques such as IVF-ET and ICSI. Its purpose is to stimulate the ovaries with exogenous gonadotropins (e.g., FSH, hMG) to promote synchronous maturation of multiple follicles, yielding sufficient high-quality oocytes for subsequent fertilization, embryo culture, and transfer.

However, during gonadotropin stimulation, accelerated follicular development often leads to a premature LH surge – an early rise in LH levels that triggers premature ovulation of immature oocytes, resulting in failed oocyte retrieval, reduced oocyte quality, and severely compromised ART success.A primary indication of cetrorelix acetate injection is the precise suppression of premature LH surges to prevent premature ovulation.

By maintaining consistent inhibition of pituitary LH secretion, it allows follicles to continue developing under gonadotropin support until optimal maturity (typically 18–20 mm in diameter).

In clinical practice, timing of cetrorelix administration is guided by follicular monitoring (ultrasound assessment of follicle size and number combined with hormonal measurements), ensuring synchronized follicular maturation.Human chorionic gonadotropin (hCG) is then administered at the optimal window to trigger ovulation and improve oocyte retrieval rates.

Clinical data show that use of cetrorelix during COS reduces the incidence of premature LH surges to below 5%, significantly lowering the risk of retrieval failure and increasing the proportion of high-quality oocytes by 12%–18% compared with untreated controls. It also improves outcomes in patients with unstable ovarian response or a history of premature LH surges, reducing cycle cancellations due to ovulatory disorders.

Embryo implantation is critical to successful assisted reproduction, and endometrial receptivity – the ability of the endometrium to support implantation – is the determining factor. Endometrial development must be precisely synchronized with embryonic development under the balanced regulation of estrogen and progesterone.

During COS, high-dose exogenous gonadotropins frequently cause excessive estrogen levels and premature progesterone elevation, disrupting synchrony between endometrial and embryonic development, reducing endometrial receptivity, and lowering implantation and clinical pregnancy rates.

It improves endometrial receptivity by fine-tuning hormonal levels, creating a more favorable environment for implantation. By inhibiting LH secretion, it reduces premature progesterone synthesis and release, delaying endometrial luteinization and aligning endometrial morphology, structure, and molecular markers (e.g., integrins, homeobox genes, leukemia inhibitory factor) with embryonic development. A stable hormonal milieu also reduces abnormal endometrial hyperplasia and vascular dysregulation, promoting normal glandular and stromal development and achieving an optimal implantation thickness of 8–12 mm.

Multicenter clinical studies show that cetrorelix-based antagonist protocols significantly improve endometrial receptivity compared with traditional GnRH agonist regimens, increasing implantation rates by 10%–15% and achieving clinical pregnancy rates above 55%. Benefits are particularly notable in patients with repeated implantation failure or poor endometrial receptivity. Cetrorelix acetate injection has no direct endometrial toxicity, and endometrial function recovers rapidly after cessation, supporting normal progression of subsequent pregnancies and confirming its safety and efficacy in ART.