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Last update 08 May 2025

GHRHR

Last update 08 May 2025

Basic Info

Synonyms

GHRH receptor, GHRHR, GRF receptor

+ [4]

Introduction

Receptor for GRF, coupled to G proteins which activate adenylyl cyclase. Stimulates somatotroph cell growth, growth hormone gene transcription and growth hormone secretion.

Drugs associated with GHRHR

MR-409

Target

GHRHR

Mechanism

GHRHR agonists

Active Org.

University of Turin [+2]

Originator Org.

University of Miami

Active Indication

Cardiomegaly [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

MIA-313

Target

GHRHR

Mechanism

GHRHR antagonists

Active Org.

Biscayne Pharmaceuticals, Inc. [+1]

Originator Org.

University of Miami

Active Indication

Acute Myeloid Leukemia [+1]

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NNC-26-0610

Target

GHRHR

Mechanism

GHRHR agonists

Active Org.-

Originator Org.

Novo Nordisk A/S

Active Indication-

Inactive Indication

Burns [+1]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with GHRHR

NCT01775358

/ CompletedPhase 1

A Randomized, Single-Blind, Placebo-Controlled, Single Ascending Dose Study to Evaluate the Safety and Tolerability of ALRN-5281 Administered by Subcutaneous Injection in Healthy Adult Volunteers

The primary objective of this study is to evaluate the safety and tolerability of a single dose of ALRN-5281 administered by subcutaneous injection to healthy adult volunteers.

Start Date01 Jan 2013

Sponsor / Collaborator-

EUCTR2005-003797-25-DE

/ Not yet recruitingNot Applicable

A Multicenter, Randomized, Placebo-controlled, Double-blind Phase 2 Study to Evaluate the Efficacy and Safety of CJC-1295 administered for 12 weeks in HIV-Infected Patients with HIV-associated Visceral Obesity

Start Date09 Dec 2005

Sponsor / Collaborator

ConjuChem, Inc.

NCT00267527

/ TerminatedPhase 2

A Multicenter, Randomized, Placebo-Controlled, Double-Blind, Phase 2 Study to Evaluate the Efficacy and Safety of CJC 1295 Administered for 12 Weeks in HIV Infected Patients With HIV Associated Visceral Obesity

This is a multicenter, randomized, placebo-controlled, double-blind, Phase 2 study. Patients will be treated for a total of 12 weeks. There will be a 6 week follow-up period after the treatment period ends. Patients will be randomly assigned to low dose CJC 1295, high dose CJC 1295 or placebo.
The objective is to assess and compare the efficacy, pharmacokinetics, safety, and tolerability of CJC 1295 in patients with human immunodeficiency virus (HIV) associated visceral obesity.

Start Date01 Dec 2005

Sponsor / Collaborator

ConjuChem LLC

100 Clinical Results associated with GHRHR

100 Translational Medicine associated with GHRHR

0 Patents (Medical) associated with GHRHR

616

Literatures (Medical) associated with GHRHR

01 Jan 2025·Digestive and Liver Disease

Integrated analysis of ncRNA in hepatocellular carcinoma with CTNNB1 mutations reveals miR-205-5p and miR-3940-3p Axes

Article

Author: Zhang, Guoqing ; Zhang, Haibin ; Lu, Siyu ; Zhang, Xiaolu ; Yu, Jingya

BACKGROUNDCatenin beta 1 (CTNNB1) mutations are one of the most common mutations involved in hepatocellular carcinoma (HCC) progression. However, the association between CTNNB1 mutations and HCC remains controversial.METHODSFive tumor samples with wild-type CTNNB1 and three tumor samples with CTNNB1 mutations were collected from patients with HCC for whole transcriptome sequencing. Selected ncRNAs and mRNAs were validated by qPCR in 48 HCC tumors. Selected ncRNA regulatory axes were verified in HCC cells by transfecting mimics and inhibitors of miRNA.RESULTSA network of differentially expressed (DE) lncRNA/circRNA-miRNA-mRNA was constructed to explore the effects of CTNNB1 mutations on ncRNA regulation. TXNRD1, CES1, MATN2, SERPINA5, lncRNA STAT4-210, hsa_circ_0007824, hsa_circ_0008234, hsa-miR-205-5p and hsa-miR-199a-5p were verified at the RNA expression level to validate the sequencing results. The down-up-down axes GLIS3-209/circ_0085440-miR-205-5p-GHRHR and WNK2-213-miR-3940-3p-LY6E were verified at the expression level, and proved to inhibit and promote cell proliferation, respectively.CONCLUSIONThis study demonstrated CTNNB1 mutations associated ncRNA regulatory axes playing different roles in HCC cell proliferation, providing novel insights into the controversial role of CTNNB1 in HCC.

30 Oct 2024·Endocrinology

Characterization and Regulation of the Neonatal Growth Hormone Surge

Article

Author: Gomes, Andre F ; Donato, Jose ; Campideli-Santana, Ana C ; Gusmao, Daniela O ; Rusew, Stephanie J R ; List, Edward O ; de Sousa, Maria E ; Szawka, Raphael E ; de Sousa, Ligia M M ; Kopchick, John J

AbstractHigh neonatal growth hormone (GH) secretion has been described in several species. However, the neuroendocrine mechanisms behind this surge remain unknown. Thus, the pattern of postnatal GH secretion was investigated in mice and rats. Blood GH levels were very high on postnatal day (P)1 and progressively decreased until near zero by P17 in C57BL/6 mice without sex differences. This pattern was similar to that observed in rats, except that female rats showed higher GH levels on P1 than males. In comparison, follicle-stimulating hormone exhibited higher secretion in females during the first 3 weeks of life. Hypothalamic Sst mRNA and somatostatin neuroendocrine terminals in the median eminence were higher in P20/P21 mice than in newborns. Knockout mice for GH-releasing hormone (GHRH) receptor showed no GH surge, whereas knockdown mice for the Sst gene displayed increased neonatal GH peak. Leptin deficiency caused only minor effects on early-life GH secretion. GH receptor ablation in neurons or the entire body did not affect neonatal GH secretion, but the subsequent reduction in blood GH levels was attenuated or prevented by these genetic manipulations, respectively. This phenotype was also observed in knockout mice for the insulin-like growth factor-1 (IGF-1) receptor in GHRH neurons. Moreover, glucose-induced hyperglycemia overstimulated GH secretion in neonatal mice. In conclusion, GH surge in the first days of life is not regulated by negative feedback loops. However, neonatal GH secretion requires GHRH receptor, and is modulated by somatostatin and blood glucose levels, suggesting that this surge is controlled by hypothalamic-pituitary communication.

01 Sep 2024·General and Comparative Endocrinology

Functional characterization of growth hormone releasing hormone and its receptor in amphioxus with implication for origin of hypothalamic-pituitary axis

Article

Author: Gao, Zhan ; Ji, Xiaohan ; Chen, Chaoyi ; Yi, Mengmeng ; Zhang, Shicui

Growth hormone-releasing hormone (GHRH) has been widely shown to stimulate growth hormone (GH) production via binding to GHRH receptor GHRHR in various species of vertebrates, but information regarding the functional roles of GHRH and GHRHR in the protochordate amphioxus remains rather scarce. We showed here that two mature peptides, BjGHRH-1 and BjGHRH-2, encoded by BjGHRH precursor, and a single BjGHRHR protein were identified in the amphioxus Branchiostoma. japonicum. Like the distribution profiles of vertebrate GHRHs and GHRHRs, both the genes Bjghrh and Bjghrhr were widely expressed in the different tissues of amphioxus, including in the cerebral vesicle, Hatschek's pit, neural tube, gill, hepatic caecum, notochord, testis and ovary. Moreover, both BjGHRH-1 and BjGHRH-2 interacted with BjGHRHR, and triggered the cAMP/PKA signal pathway in a dose-dependent manner. Importantly, BjGHRH-1 and BjGHRH-2 were both able to activate the expression of GH-like gene in the cells of Hatschek's pit. These indicate that a functional vertebrate-like GHRH-GHRHR axis had already emerged in amphioxus, which is a seminal innovation making physiological divergence including reproduction, growth, metabolism, stress and osmoregulation possible during the early evolution of vertebrates.

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