Ask about this productRelated genes to: GHRHR Blocking Peptide
- Gene:
- GHRHR NIH gene
- Name:
- growth hormone releasing hormone receptor
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-22
- Date modifiied:
- 2016-10-05
Related products to: GHRHR Blocking Peptide
Related articles to: GHRHR Blocking Peptide
- Isolated growth hormone deficiency (IGHD) involves multiple genes, yet characterization of its mutational landscape and genotype-phenotype correlations remains limited. The aim of this study is to analyze a large cohort of patients with genetic IGHD and describe associated genotypes and phenotypes. - Source: PubMed
Publication date: 2026/04/29
Aouchiche KarineRomanet PaulineCharnay ThéoBarlier AnneRoche CatherineGrunenwald SolangeLe Collen LaurianePorques Bordes ValérieBarat PascalCastinetti FredericBrue ThierryReynaud RachelSaveanu Alexandru - Growth hormone-releasing hormone (GHRH) has shown therapeutic potential in the treatment of various diseases. However, the clinical translation of GHRH receptor (GHRH-R) agonists has been hampered by the short half-life and suboptimal activity. Herein, we report a series of hybrid GHRH analogs developed using sulfono-γ-AA peptide-based peptidomimetic optimization. These hybrid peptides exhibit significantly enhanced potency in activating GHRH-R and stimulating growth hormone release while demonstrating markedly improved serum stability ( > 24 h). Subcutaneous administration of selected peptides in mice with ischemic hindlimb enhanced blood perfusion and preservation of limb function. They also promoted endothelial regeneration and collateral vessel formation, enhancing vascular remodeling and tissue repair. In vitro, the peptides enhanced the angiogenic potential of endothelial cells, primarily through activation of the ERK signaling pathway. Our findings lay a strong foundation for the development of long-acting GHRH-R agonists with promising therapeutic potential for the treatment of vascular and regenerative disease. - Source: PubMed
Publication date: 2026/04/13
Shao HaodongWu YulingMao MengyuNiu XiaokeZhang ChiChen MengGuo ZhitaoLuo JiayanSu XingWang BoYu HongTeng Peng - Growth hormone (GH) insensitivity syndrome (GHIS) is a childhood growth disorder characterized by an inability to generate insulin-like growth factor-1 (IGF-1) in response to GH. Consequently, GH therapy is ineffective in patients with GHIS. Patients are often treated with recombinant IGF-1 instead, which requires twice-daily injections and is associated with adverse effects including hypoglycemia. In the current study, we evaluated CV1623-1, a cartilage-targeted antibody-like IGF-1 fusion protein as a potential new treatment for GHIS and for other disorders of linear growth involving IGF-1 deficiency. Using Ghrhr mice as a model for IGF-1 deficiency, we found that CV1623-1 stimulated the growth plate at a lower dose and decreased dose frequency compared with IGF-1. Alternate-day injections of CV1623-1 significantly increased body weight, tail length, and tibial bone length. In addition, CV1623-1, unlike IGF-1, did not induce hypoglycemia. Taken together, our findings indicate that CV1623-1 represents a promising new drug candidate for GHIS with improved efficacy, longer duration of action, and reduced hypoglycemia compared with the current treatment, recombinant IGF-1. Preclinical studies and clinical trials would be required to further validate the safety and efficacy of CV1623-1, paving the way for its potential clinical application as a new treatment for GHIS. - Source: PubMed
Publication date: 2026/03/24
Tailor KrishmaStowe TimothyHansdah KirtalCourtis JoannaRama-Krishnan ArunSisk Connorvan Ree Janinevan Deursen JanVentura BritO'Brien RobertBaron JeffreyLui Julian C - Glaucoma is a leading cause of irreversible blindness worldwide. One hallmark of glaucoma is the degeneration of retinal ganglion cells (RGCs). In this study, a dual role for growth hormone-releasing hormone receptor (GHRHR) modulation under glaucoma-relevant conditions and complementary injury paradigms involving the RGCs is identified. Using acute IOP elevation (retinal ischemia-reperfusion), chronic ocular hypertension (microbead-induced), and traumatic axonal injury (optic nerve crush) models, we show that GHRHR deficiency preserves RGC survival and uniquely restores visual functions-contrasting with GHRHR activation, which solely promotes cellular survival. Single-cell transcriptomic analysis uncovers RGC-specific alterations in genes associated with ferroptosis, lipid metabolism, oxidative stress, and mitochondrial dynamics. At the mechanistic level, GHRHR deficiency prevents the pathological downregulation of key anti-ferroptotic mediators GPX4 and FTH1 while suppressing pro-ferroptotic factors ACSL4 caused by glaucomatous neurodegeneration. This multifaceted regulation attenuated iron accumulation, lipid peroxidation, and reactive oxygen species (ROS) accumulation, effects that are diminished by the ferroptosis inducer RSL3. Notably, in mitochondria damaged primary RGCs, pharmacological GHRHR inhibition replicates these benefits, reducing lipid peroxidation and mitochondrial ROS to bolster RGC survival. Collectively, these findings establish GHRHR inhibition as a potent therapeutic strategy for glaucomatous neurodegeneration, synergistically rescuing both structural and functional integrity of the retina. - Source: PubMed
Publication date: 2026/03/18
Tong YanYam Ming HoZhang JiaxinDu LinZhou LinbinYip Yolanda Wong YingHo Bo ManBisnauthsing HemlataLi JiahuiKong IvanXu ShushuFu ChangzhenSo Karl K HVong Joaquim S LCen Ling-PingYang Ming-MingYousaf KhazeemaSham Mai HarChan Sun OnChan Poemen PPang Chi PuiTham Clement CHe Jing NaLi JianChu Wai Kit - - Source: PubMed
Publication date: 2026/03/18
Wang Ming-WeiHang KainiQiu YueChen XianyueChen YanyanHuang ShengtianCong ZhaotongZhou Qingtong