Triptorelin Acetate (57773-63-4)

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Product Detail

Mechanism:

Triptorelin is a synthetic decapeptide agonist analogue of naturally occurring luteinizing hormone-releasing hormone (LHRH). LHRH is also known as gonadotropin releasing hormone (GnRH). Triptorelin acts as a potent inhibitor of gonadotropin secretion when given continuously and in therapeutic doses. Following the first administration, there is a transient surge in circulating levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol. Chronic and continuous administration, usually 2 to 4 weeks after initiation of therapy, desensitizes pituitary LHRH receptors and inhibits LH and FSH secretion and consequently marked reduction of testicular and ovarian steroidogenesis is observed. In men, a reduction of serum testosterone concentration to a level typically seen in surgically castrated men is obtained. As a result, tissues and functions that depend on these hormones for maintenance become quiescent. These effects are usually reversible after cessation of therapy.

Storage conditions: Store between 2- 8o C protected from light

Packaging: glass vials

CAS Number: 57773-63-4

Formula: C66H86N18O15    

Molecular Weight: 1310.5 g/mol

Method of Analysis: In house

Application:

Prostate cancer or breast cancer, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction (IVF)
Triptorelin is a gonadotropin releasing hormone agonist (GnRH agonist). By causing constant stimulation of the pituitary, it decreases pituitary secretion of gonadotropins luteinizing hormone (LH) and follicle stimulating hormone (FSH). Like other GnRH agonists, triptorelin may be used in the treatment of hormone-responsive cancers such as prostate cancer or breast cancer, precocious puberty, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction. During the treatment of prostate cancer it does cause a surge of testosterone (an initial uplevel of testosterone levels). In contrast gonadotropin releasing hormone Receptor antagonists does not cause a surge, but a sudden shut-down of testosterone level.