Best-Selling Active Acetate - Ganirelix Acetate Peptide API – Gentolex

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Best-Selling Active Acetate - Ganirelix Acetate Peptide API – Gentolex Detail:

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Name	Ganirelix Acetate
CAS number	123246-29-7
Molecular formula	C80H113ClN18O13
Molecular weight	1570.34

Synonyms

Ac-DNal-DCpa-DPal-Ser-Tyr-DHar(Et2)-Leu-Har(Et2)-Pro-DAla -NH2;Ganirelixum;ganirelix Acetate; GANIRELIX; Ganirelix Acetate USP/EP/

Description

Ganirelix is a synthetic decapeptide compound, and its acetate salt, Ganirelix acetate is a gonadotropin-releasing hormone (GnRH) receptor antagonist. The amino acid sequence is: Ac-D-2Nal-D-4Cpa-D-3Pal-Ser-Tyr-D-HomoArg(9,10-Et2)-Leu-L-HomoArg(9,10-Et2)-Pro-D- Ala-NH2. Mainly clinically, it is used in women undergoing assisted reproductive technology controlled ovarian stimulation programs to prevent premature luteinizing hormone peaks and to treat fertility disorders due to this cause. The drug has the characteristics of less adverse reactions, high pregnancy rate and short treatment period, and has obvious advantages compared with similar drugs in clinical practice.

Pharmacological Action

The pulsatile release of gonadotropin-releasing hormone (GnRH) stimulates the synthesis and secretion of LH and FSH. The frequency of LH pulses in the mid and late follicular phases is approximately 1 per hour. These pulses are reflected in transient rises in serum LH. During mid-menstrual period, the massive release of GnRH causes a surge of LH. The midmenstrual LH surge can trigger several physiological responses, including: ovulation, oocyte meiotic resumption, and corpus luteum formation. The formation of the corpus luteum causes serum progesterone levels to rise, while estradiol levels fall. Ganirelix acetate is a GnRH antagonist that competitively blocks GnRH receptors on pituitary gonadotrophs and subsequent transduction pathways. It produces a rapid, reversible inhibition of gonadotropin secretion. The inhibitory effect of ganirelix acetate on pituitary LH secretion was stronger than that on FSH. Ganirelix acetate failed to induce the first release of endogenous gonadotropins, consistent with antagonism. Complete recovery of pituitary LH and FSH levels occurred within 48 hours after ganirelix acetate was discontinued.

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