gnrh 2

GnRH antagonist 2 (formula I) is a potent GnRH receptor antagonist with valuable applications in endometriosis research [1].

GnRH-I acetate in release of biologically active Follicle-Stimulating Hormone (FSH) and Luteinizing Hormone (LH) in the blood.

Phoenixin-14 (PNX-14), an active endogenous isoform, induces an anxiolytic effect by activating the AHA GnRH system in mice and protects against ischemia/reperfusion-induced cytotoxicity in microglia [1] [2].

sGnRH-A, a salmon gonadotropin-releasing hormone (GnRH) analogue, promotes growth hormone secretion and serves as an ovulation inducer for artificial insemination [1] [2].

Acyline is a novel GnRH antagonist found in animal studies to be a potent suppressor of circulating gonadotropin and testosterone (T) levels. Acyline inhibits basal and GnRH-stimulated serum testosterone concentrations in male dogs. Acyline prevented ovulation, but did not affect ovarian follicular development or gestational corpora lutea in the domestic cat. A single dose of the potent gonadotropin-releasing hormone antagonist acyline suppresses gonadotropins and testosterone for 2 weeks in healthy young men.

NBI-42902 is a potent inhibitor of peptide radioligand binding to the human GnRH receptor (K(i) = 0.56 nm). Tritiated NBI-42902 binds with high affinity (K(d) = 0.19 nm) to a single class of binding sites and can be displaced by a range of peptide and nonpeptide GnRH receptor ligands. In vitro experiments demonstrate that NBI-42902 is a potent functional, competitive antagonist of GnRH stimulated IP accumulation, Ca(2+) flux, and ERK1/2 activation. It did not stimulate histamine release from rat peritoneal mast cells. Finally, it is effective in lowering serum LH in castrated male macaques after oral administration. Overall, these data provide a benchmark of pharmacological characteristics required for a nonpeptide GnRH antagonist to effectively suppress gonadotropins in humans and suggest that NBI-42902 may have clinical utility as an oral agent for suppression of the hypothalamic-pituitary-gonadal axis. (source: Endocrinology. 2007 Feb;148(2):857-67. Epub 2006 Nov 9.)

Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004). Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3 References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004).

sGnRH-A acetate, a salmon gonadotropin-releasing hormone (GnRH) analogue, stimulates growth hormone secretion and serves as an ovulation inducer for artificial insemination [1] [2].

Gonadotropin-Releasing Hormone-Associated Peptide (GAP) (25-53), Human, also known as hGAP-25-53, is a fragment of the human gonadotropin-releasing hormone-associated peptide that serves as an immunogen for producing antiseras such as MC-1, MC-2, and MC-3. This peptide is connected to the luteinizing hormone-releasing hormone (LH-RH) sequence through a 3 amino acid processing site [1].

Phoenixin-14 TFA (PNX-14) is a blood-brain barrier (BBB)-penetrable neuropeptide with anxiolytic, cardioprotective, and neuroprotective properties. It modulates pituitary gonadotrophin release by enhancing gonadotropin-releasing hormone (GnRH) receptor mRNA expression and promotes insulin secretion. Additionally, PNX-14 TFA protects against ischemia reperfusion (IR) injury in mice and combats oxidative stress by diminishing reactive oxygen species (ROS) and elevating glutathione (GSH) levels [1] [2] [3].