Cetrorelix Acetate (SB-75 acetate) is a potent gonadotropin-releasing hormone (GnRH) receptor antagonist with an IC50 of 1.21 nM.
CAT No: HB00121
CAS No:130143-01-0
Synonyms/Alias:130143-01-0;Cetrorelix diacetate;Cetrotide acetate;Cetrotide;W9Y8L7GP4C;Cetrorelix (diacetate);SB-075 ACETATE;Cetrorelix acetate [MI];Cetrorelix acetate [JAN];UNII-W9Y8L7GP4C;Cetrorelix acetate [USAN];Cetrorelix acetate [VANDF];Cetrorelix acetate [MART.];Cetrorelix acetate [WHO-DD];D-Alaninamide, N-acetyl-3-(2-naphthalenyl)-D-alanyl-4-chloro-D-phenylalanyl-3-(3-pyridinyl)-D-alanyl-L-seryl-L-tyrosyl-N5-(aminocarbonyl)-D-ornithyl-L-leucyl-L-arginyl-L-prolyl-, diacetate (salt);Cetrorelix acetate (MART.);D-Alaninamide, N-acetyl-3-(2-naphthalenyl)-D-alanyl-4-chloro-D-phenylalanyl-3-(3-pyridinyl)-D-alanyl-L-seryl-L-tyrosyl-N(sup 5)-(aminocarbonyl)-D-ornithyl-L-leucyl-L-argyinyl-L-prolyl-, acetate (salt);N-Acetyl-3-(2-naphthyl)-D-alanyl-p-chloro-D-phenylalanyl-3-(3-pyridyl)-D-alanyl-L-seryl-L-tyrosyl-N(sup 5)-carbamoyl-D-ornithyl-L-leucyl-L-arginyl-L-prolyl-D-alaninamide acetate (salt);SB 075 acetate;NS 75a;Cetrorelixdiacetate;SB-075 diacetate;N-acetyl-3-(naphthalen-2-yl)-D-alanyl-4-chloro-D-phenylalanyl-3-(pyridin-3-yl)-D-alanyl-L-seryl-L-tyrosyl-N(5)-carbamoyl-D-ornithyl-L-leucyl-L-arginyl-L-prolyl-D-alaninamide acetate;SCHEMBL6149471;D 20761;HY-P0009B;EX-A3856;AKOS037748846;Cetrorelix acetate [USAN:JAN:WHO-DD];BS-15110;CS-0134655;D-Alaninamide, N-acetyl-3-(2-naphthalenyl)-D-alanyl-4-chloro-D-phenylalanyl-3-(3-pyridinyl)-D-alanyl-L-seryl-L-tyrosyl-N5-(aminocarbonyl)-D-ornithyl-L-leucyl-L-arginyl-L-prolyl-, acetate (salt);D81833;Q27895653;N-Acetyl-3-(2-naphthyl)-D-alanyl-p-chloro-D-phenylalanyl-3-(3-pyridyl)-D-alanyl-L-seryl-L-tyrosyl-N5-carbamoyl-D-ornithyl-L-leucyl-L-arginyl-L-prolyl-D-alanin-amide acetate;
Cetrorelix, a synthetic decapeptide and potent gonadotropin-releasing hormone (GnRH) antagonist, is widely recognized for its ability to regulate the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) through competitive inhibition of endogenous GnRH at pituitary receptors. This peptide compound is characterized by its rapid onset of action and reversible suppression of gonadotropin release, making it a valuable tool in both basic and applied research settings. Owing to its distinct mechanism of action, cetrorelix has become an indispensable reagent in studies aiming to modulate reproductive hormone cascades, dissect endocrine pathways, and explore the physiological regulation of the hypothalamic-pituitary-gonadal (HPG) axis. Its high specificity and predictable pharmacodynamic profile also support its application in experimental protocols that require precise temporal control over pituitary hormone release.
Reproductive Endocrinology Research: In the realm of reproductive biology, cetrorelix is employed to investigate the intricate feedback mechanisms governing gonadotropin secretion. By selectively blocking GnRH receptors, researchers can delineate the downstream effects of LH and FSH suppression on ovarian and testicular function. This approach facilitates the study of folliculogenesis, spermatogenesis, and steroidogenesis under controlled hormonal conditions, enabling a deeper understanding of reproductive physiology and the identification of novel regulatory factors involved in fertility and gametogenesis.
Assisted Reproductive Technology (ART) Model Systems: The GnRH antagonist properties of cetrorelix are harnessed in laboratory models simulating ART protocols, such as in vitro fertilization (IVF) and controlled ovarian stimulation. Through precise inhibition of premature LH surges, it allows for the synchronization of follicular development and oocyte maturation in animal models. This utility is crucial for optimizing experimental designs that aim to improve oocyte yield, quality, and developmental competence, as well as for testing new interventions targeting ovarian response dynamics.
Endocrine Feedback Loop Analysis: Cetrorelix serves as a strategic tool for dissecting the complex feedback loops within the endocrine system, particularly those involving the HPG axis. By transiently suppressing endogenous GnRH activity, investigators can measure compensatory hormonal responses, map receptor sensitivity, and evaluate the impact of exogenous hormone administration. Such studies are instrumental in elucidating the adaptability of endocrine circuits and the pathophysiology of hormone-related disorders in preclinical models.
Cancer Research: The suppression of gonadotropin release by cetrorelix is leveraged in oncology research, especially in the context of hormone-sensitive tumors. In vitro and in vivo studies utilize this peptide to modulate the hormonal environment, thereby assessing the growth, proliferation, and signaling pathways of gonadotropin-dependent cancer cells. These investigations contribute to the identification of potential therapeutic targets and the development of new strategies for limiting tumor progression through endocrine manipulation.
Comparative Physiology and Species-Specific Studies: The application of cetrorelix extends to comparative endocrinology, where it is used to explore species-specific differences in GnRH receptor structure, function, and regulatory mechanisms. By applying this antagonist in diverse animal models, researchers can uncover evolutionary adaptations in reproductive hormone control and inform translational research efforts aimed at improving reproductive management in veterinary and agricultural contexts.
Neuroendocrine Regulation Studies: In addition to its established roles, cetrorelix is increasingly utilized in neuroendocrine research to probe the central regulation of reproductive hormones and their influence on behavior, metabolism, and stress responses. By modulating GnRH signaling in experimental systems, scientists can investigate the integration of neural and endocrine cues that govern reproductive timing, sexual differentiation, and adaptive responses to environmental changes. This multifaceted application underscores the peptide's value in advancing our understanding of neuroendocrine physiology and its broader implications for health and disease.
4. Autoinhibition and phosphorylation-induced activation of phospholipase C-γ isozymes
5. The spatiotemporal control of signalling and trafficking of the GLP-1R
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