luteinizing hormone receptor

Seganserin, a non-selective 5-hydroxytryptamine 2-HT receptor antagonist, reversed the inhibitory effects of fluoxetine and quipazine on luteinizing hormone-induced hyperphagia, depression and nociception, and reversed the antidepressant and analgesic effects induced by fluoxetine and quipazine.

16a,17a-Epoxy-4-Pregnen-3,20-Dione is a synthetic progestin, a metabolite of the luteinizing hormone hormone, which acts by binding to the luteinizing hormone receptor. It has been used to study the effects of progesterone on reproductive organs, the effects of the hormone on cell growth and development, and the effects of the hormone on the immune system.

AC-262536 is a selective androgen receptor (SAR) modulator. It has partial agonist activity with respect to testosterone and suppresses luteinizing hormone.

BAY-298 is an orally active and selective luteinizing hormone receptor (LH-R) antagonist with IC50s of 96 nM, 23 nM, and 78 nM for hLH (human LH), rLH (rat LH), and cLH (cynomolgus monkey LH), respectively. It is the first nanomolar hLH-R antagonist that reduces sex hormone levels in vivo [1].

BAY-899 is an orally active and selective antagonist of the luteinizing hormone receptor (LH-R), with IC50 values of 185 nM for human LH (hLH) and 46 nM for rat LH (rLH). In vivo studies have shown that BAY-899 effectively reduces sex hormone levels[1].

Cyproterone acetate (Cyproterone 17-O-acetate) binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. Cyproterone acetate is the acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.Cyproterone binds the androgen receptor (AR), thereby preventing androgen-induced receptor activation in target tissues and inhibiting the growth of testosterone-sensitive tumor cells. Cyproterone Acetate is the acetate salt of a synthetic steroidal antiandrogen with weak progestational and antineoplastic activities. This agent also exerts progestational agonist properties at the level of the pituitary that reduce luteinizing hormone (LH), resulting in reductions in testicular androgen secretion and serum testosterone levels. Treatment with cyproterone alone results in incomplete suppression of serum testosterone levels.

ADX61623 is an effective negative allosteric modulator (NAM) of the follicle-stimulating hormone receptor (FSHR). It also exhibits activity on the luteinizing hormone receptor (LH-R) but is inactive on the thyroid-stimulating hormone (TSH) receptor. ADX61623 can be utilized in research on estrogen-dependent diseases.

Clomifene is a selective estrogen receptor modulator (SERM), it has both estrogenic and anti-estrogenic activities. This agent causes the release of the pituitary gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH), leading to ov

Sufugolix (TAK-013) is a potent and orally available luteinizing hormone-releasing hormone (LHRH) receptor antagonist.

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).

Relugolix (RVT-601) is an orally available, non-peptide gonadotropin-releasing hormone (GnRH or luteinizing hormone-releasing hormone (LHRH)) antagonist, with potential antineoplastic activity. Relugolix competitively binds to and blocks the GnRH receptor in the anterior pituitary gland, which both prevents GnRH binding to the GnRH receptor and inhibits the secretion and release of both luteinizing hormone (LH) and follicle stimulating hormone (FSH). In males, the inhibition of LH secretion prevents the release of testosterone from Leydig cells in the testes. Since testosterone is required to sustain prostate growth, reducing testosterone levels may inhibit hormone-dependent prostate cancer cell proliferation.

Cridanimod can increase progesterone receptor (PR) expression, with potential antineoplastic adjuvant activity. Cridanimod is able to induce the expression of PR in endometrial cancer. In combination with a progestin, cancer cells could be eradicated thro

LUF5771 is a highly potent allosteric inhibitor of recombinant luteinizing hormone (recLH) and Org 43553. It exhibits partial activation of the LH receptor with low efficacy [1].

(R)-BAY-899 is an R-isomer of BAY-899. BAY-899 is a selective, orally active luteinizing hormone receptor (LH-R) antagonist that acts on hLH (human LH) (IC50: 185 nM) and rLH (rat LH) (IC50: 46 nM).

Org 43553 is an orally active, low molecular weight (LMW) luteinizing hormone receptor (LH-R) agonist that activates human LH receptors (EC50: 3.7 nM) and FSH receptors (EC50: 110 nM). Org 43553 can be used for endocrine studies.

Abarelix acetate is a synthetic third generation gonadotropin-releasing hormone receptor (GnRHR) antagonist. It increases histamine release from rat peritoneal mast cells in vitro and from a human skin model ex vivo. In vivo, abarelix decreases plasma luteinizing hormone (LH) levels six hours post-treatment in castrated rats, with levels returning to baseline within 24 hours.3 Abarelix (2 mg kg) also transiently decreases plasma testosterone levels in intact rats, with levels returning to baseline within seven days post-treatment. Formulations containing abarelix have previously been used in the treatment of advanced prostate cancer.

Ozarelix is a fourth generation GnRH antagonist, induces apoptosis in hormone refractory androgen receptor negative prostate cancer cells modulating expression and activity of death receptors. Mechanistically, LHRH antagonists exert rapid inhibition of luteinizing hormone and follicle stimulating hormone with an accompanying rapid decrease in sex hormones and would therefore be expected to be effective in a variety of hormonally dependent disease states including ovarian cancer, prostate cancer, BPH, infertility, uterine myoma and endometriosis. BPH is a non-cancerous enlargement of the prostate that is caused by testosterone. Unlike LHRH agonists, ozarelix has the potential to reduce testosterone just enough to reduce both prostate size and symptoms without the severe side effects associated with a reduction in testosterone.

Dicetrorelix pamoate is a synthetic decapeptide with gonadotropin-releasing hormone (GnRH) antagonistic activity. GnRH induces the production and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the gonadotrophic cells of the anterior pituitary. Due to a positive estradiol (E2) feedback at midcycle, GnRH liberation is enhanced resulting in an LH-surge. This LH-surge induces the ovulation of the dominant follicle, resumption of oocyte meiosis and subsequently luteinization as indicated by rising progesterone levels. Cetrorelix competes with natural GnRH for binding to membrane receptors on pituitary cells and thus controls the release of LH and FSH in a dose-dependent manner. Cetrorelix binds to the gonadotropin releasing hormone receptor and acts as a potent inhibitor of gonadotropin secretion. It competes with natural GnRH for binding to membrane receptors on pituitary cells and thus controls the release of LH and FSH in a dose-dependent manner......

BAY 1214784, a potent, selective, and orally active spiroindoline derivative compound, serves as an antagonist of the human gonadotropin-releasing hormone receptor (hGnRH-R). It notably reduces plasma luteinizing hormone levels by up to 49%, demonstrating low pharmacokinetic variability and good tolerability. This compound shows promise for research into uterine fibroids.

[D-Lys6]-LH-RH, a Luteinizing-hormone-releasing hormone (LHRH) analogue, serves as a GnRH receptor agonist [1].

[D-Glp1,D-Phe2,D-Trp3,6]-LH-RH, a luteinizing hormone-releasing hormone (LHRH) analogue, acts as a gonadotropin-releasing hormone (GnRH) receptor antagonist [1].

[D-Ala6]-LH-RH, a Luteinizing-hormone-releasing hormone (LHRH) analogue, functions as a gonadotropin-releasing hormone (GnRH) receptor agonist [1].

NK3R-IN-1 (compound 16x), an orally active imidazolepiperazine derivative, functions as a Neurokinin Receptor NK3R inhibitor and has been demonstrated to reduce blood luteinizing hormone concentrations in an ovariectomy (OVX) model [1].

Kisspeptin-10, a neuropeptide present in the brains, ovaries, and testes of zebrafish, plays a critical role in gonadal development and steroid expression. At a concentration of 10 ng/ml, it enhances the mRNA levels for the luteinizing hormone (Lh) receptor and both progestin receptor a (Pra) and Prb in zebrafish ovarian follicles. In female goldfish, doses of 0.1 and 1 µg/g of Kisspeptin-10 elevate serum levels of luteinizing hormone, with no similar effect observed in male goldfish.