GLP1R Antibody
- Known as:
- GLP1R Antibody
- Catalog number:
- csb-pa009514la01hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- GLP1R Antibody
Related genes to: GLP1R Antibody
- Gene:
- GLP1R NIH gene
- Name:
- glucagon like peptide 1 receptor
- Previous symbol:
- -
- Synonyms:
- GLP-1R
- Chromosome:
- 6p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-11
- Date modifiied:
- 2017-02-07
Related products to: GLP1R Antibody
Related articles to: GLP1R Antibody
- Metabolic dysfunction-associated steatohepatitis (MASH), the progressive form of metabolic dysfunction-associated steatotic liver disease (MASLD), is a heterogeneous and systemic disease that confers risk not only for cirrhosis and hepatocellular carcinoma (HCC) but also for extrahepatic complications including cardiovascular disease and chronic kidney disease. Over the past decade, numerous late-stage clinical trials have advanced the therapeutic landscape of MASH, culminating in a pivotal inflection point with accelerated approval of the thyroid hormone receptor-β (THRβ) agonist resmetirom and the glucagon-like peptide-1 receptor (GLP-1R) agonist semaglutide, establishing pharmacological options for patients with non-cirrhotic MASH and fibrosis. Concurrently, growing evidence indicates that MASH comprises distinct, partially overlapping disease subsets, ranging from liver-centric phenotypes with accelerated fibrogenesis and liver-related outcomes to cardiometabolic phenotypes characterized by insulin resistance and increased cardiovascular risk. This suggests that optimal treatment efficacy will require stratified and potentially combinatorial approaches. In addition to lifestyle interventions, a cornerstone of MASLD management, pharmacotherapies targeting metabolic dysfunction (including PPAR agonists, FGF21 analogues or incretin-based and glucagon-based therapies), fibrogenesis, inflammation and/or the gut-liver axis are emerging. In this Review, we summarize the therapeutic landscape for MASH and discuss how recent advances in disease phenotyping and biomarkers may enable a transition towards personalized therapy. - Source: PubMed
Publication date: 2026/09/02
Gallage SuchiraGovaere OlivierAnstee Quentin MShulman Gerald ITacke FrankHeikenwalder Mathias - Pharmacological glucagon-like peptide-1 receptor (GLP-1R) activation reduces food intake and is an effective therapy for type 2 diabetes and obesity. The use of GLP-1 medicines has revealed pleiotropic beneficial effects beyond glucose and weight control, but little is known about the underlying basis of the pleiotropic effects. Here, treatment of 20-month-old female C57BL/6 mice with the GLP-1R agonist semaglutide for 3 months improved physiological function, attenuated hallmarks of ageing and modulated nutrient sensors and conserved genetic regulators of ageing. Continued treatment extended mouse lifespan. These effects parallel key features of calorie restriction, a dietary intervention that slows ageing, extends lifespan and alleviates a wide spectrum of ageing-associated diseases. In a longitudinal study in direct comparison to matched calorie restriction, semaglutide treatment preserved baseline function and recapitulated many functional benefits of calorie restriction by attenuating age-associated decline, while also producing improvements above baseline and more favourable trajectories than calorie restriction in exploratory drive, spatial memory and glucose control. Together, these findings demonstrate that GLP-1R activation initiated late in life slows ageing and extends lifespan in female mice, supporting its function as a calorie restriction mimetic and providing a mechanistic framework that may help to explain its broad beneficial effects while revealing effects beyond those attributable to reduced calorie intake. - Source: PubMed
Publication date: 2026/09/02
Feng YufanBarthez MarineWang YifeiChen YibingQiu HuixianWang Chih-LingHeydari KartooshDelcroix MelaineRasmussen Lene JuelBohr Vilhelm AChen Danica - GLP1 receptor agonists (GLP-1RAs) have transformed obesity treatment, but their impact on neuropsychiatric outcomes remains poorly understood. We conducted an observational study of 63,215 patients with preexisting neuropsychiatric conditions and evaluated 24 incident neuropsychiatric outcomes following treatment initiation. In propensity-matched analyses, semaglutide was associated with broadly lower neuropsychiatric event risk over two years compared with metformin, SGLT2 inhibitors, and DPP-4 inhibitors. Within the semaglutide-treated cohort, higher attained dose during the first two years after treatment initiation ("pre-landmark period") was associated with significantly lower incidence during the subsequent two years ("post-landmark period") of substance-related disorders (P < 0.001), mood disorders (P < 0.001), anxiety- and stress-related disorders (P < 0.001), central nervous system (CNS) atrophies (P < 0.001), neuromuscular disorders (P = 0.013), eating/sleep/behavioral disorders (P = 0.022), and personality/impulse-control disorders (P = 0.028). Consistent with prior clinical trials, the post-landmark incidence of dementia or CNS degenerative diseases was similar between the high-dose and low-dose semaglutide cohorts (P = 0.15). For most neuropsychiatric diagnoses, post-landmark incidence was strongly associated with the maximum attained dose. In contrast, incident cognitive symptoms and speech/language symptoms were more closely associated with weight loss (p < 0.001 and p < 0.003, respectively). Bulk and single-cell transcriptomic analyses identified low-level, regionally restricted GLP1R transcript signals in central and peripheral nervous system tissues, providing hypothesis-generating context for future experimental investigation. Together, these findings support an association between semaglutide exposure and multiple neuropsychiatric outcomes, and motivate prospective mechanistic and clinical studies. - Source: PubMed
Publication date: 2026/09/01
Murugadoss KarthikVenkatakrishnan A JSoundararajan Venky - - Source: PubMed
Pyburn Jaeden SZhao JuanWang LingSchank Madison BHill Addison CBanik PujaOrfield Holly KHensley Culton RMoorman Adam BWu YuezuHajipour Mohammad JNing ShunbinEl Gazzar MohamedMoorman Jonathan PYao Zhi Q - A major recent breakthrough in the treatment of type 2 diabetes has been the development of glucagon-like peptide-1 receptor agonists (GLP-1RAs). However, current translational frameworks struggle to predict the clinical outcomes of these drugs from preclinical data. Several challenges contribute to this struggle and are relevant to many drugs: GLP-1RAs act through multi-timescale mechanisms in which short-term effects propagate into long-term changes, no single preclinical system can capture all their effects in humans, and mechanistic extrapolation requires modelling numerous whole-body biological processes. To address this gap, we present a new extrapolation approach, M4 drug discovery, and retrospectively apply it to the GLP-1RA exenatide in a manner that is generalisable to other drugs. The method integrates: multi-level data (cellular to whole-body), multi-timescale data (minutes to months), multi-species data (e.g., rodents to humans), and mechanistic knowledge. In this study, we integrate human cell and animal data with drug-free human studies to successfully predict human pharmacokinetics (cost < χ², p=0.05; 64 < 97) and the outcomes of a 30-week clinical trial (36 < 45). We found that integrating information across the four M4 axes improved predictive performance and physiological relevance: multi-species data inform pharmacokinetics, human cell data provide human population- and donor-specific potency estimates, animal data reveal additional drug effects not observable in cell cultures, and the multi-timescale mathematical modelling enables short-term effects of exenatide and meals to inform long-term changes in insulin sensitivity. This work provides a new framework for translational drug development, supporting safer and more informed preclinical-to-clinical translation. - Source: PubMed
Publication date: 2026/08/30
Silfvergren OscarRigal SophieSchimek KatharinaSimonsson ChristianKanebratt Kajsa PForschler FelixYesildag BurcakMarx UweVilén LiisaGennemark PeterCedersund Gunnar