Last update 01 Nov 2024

GAL3

Last update 01 Nov 2024

Basic Info

Synonyms

3型甘丙肽受体, GAL3-R, galanin receptor 3

+ [4]

Introduction

Receptor for the hormone galanin (PubMed:25691535). Receptor for the hormone spexin-1 (PubMed:24517231).

Drugs associated with GAL3

GAL3 receptor antagonist(Pfizer)

Target

GAL3

Mechanism

GAL3 antagonists

Active Org.

Pfizer Global Manufacturing

Originator Org.

Pfizer Inc.

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2024073511

Patent Mining

Target

GAL3

Mechanism-

Active Org.

TrueBinding, Inc.Startup

Originator Org.

TrueBinding, Inc.Startup

Active Indication

Nutritional and Metabolic Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2023180533

Patent Mining

Target

GAL3

Mechanism-

Active Org.

Les Laboratoires Servier SAS

Originator Org.

Les Laboratoires Servier SAS

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with GAL3

NCT01413932 / CompletedPhase 1/2

A Two-part Study: Part 1 is a Multiple-dose (7-day), Open-label Evaluation of the Safety, Tolerability, and Pharmacokinetics of HT-2157 in Healthy Subjects. Part 2 is a Randomized, Double-blind, Placebo-controlled, Multiple (21-day) Ascending-dose Evaluation of the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of HT-2157 in Patients With Major Depressive Disorder

This is a two part study. The objective of Part 1 is to evaluate the safety, tolerability, and pharmacokinetics of HT-2157 in healthy normal volunteers
Part 2 is a randomized, double-blind, placebo-controlled, multiple (21-day) ascending-dose evaluation of the safety, tolerability, pharmacokinetics, and pharmacodynamics of HT-2157 in patients with major depressive disorder

Start Date01 Jul 2011

Sponsor / Collaborator

Dart NeuroScience LLC

100 Clinical Results associated with GAL3

100 Translational Medicine associated with GAL3

0 Patents (Medical) associated with GAL3

1,713

Literatures (Medical) associated with GAL3

01 Jan 2025·American Journal of Ophthalmology

Nonredundant Role of Leishmanolysin-Like (Lmln) Zinc-Metallopeptidase in Retinal Homeostasis

Article

Author: Zegeye, Yeshumenesh ; Ludwig, Sara ; Shrestha, Sangita ; Ufret-Vincenty, Rafael L. ; Moresco, Eva Marie Y. ; Yuksel, Seher ; Ulker-Yilmazer, Gizem ; He, Yu-Guang ; Kirman, Dogan Can ; Beutler, Bruce ; Moresco, Eva Marie Y ; Ufret-Vincenty, Rafael L ; Aredo, Bogale ; Turpin, Emily

PURPOSETo determine if Lmln, a Zinc-metallopeptidase, is important for retinal homeostasis.DESIGNBasic research in mouse models of retinal degeneration.METHODSCombining an unbiased N-ethyl-N-nitrosourea mutagenesis pipeline in mice with optical coherence tomography (OCT) screening and automated meiotic mapping, we identified an allele (nemeth) that seemed to be associated with outer nuclear layer (ONL) thinning. Since nemeth was predicted to lead to a nonsense mutation of the Lmln gene, we targeted Lmln using CRISPR/Cas-9 technology and characterized the impact on retinal anatomy and function.RESULTSOCT imaging demonstrated an outer retinal degeneration in Lmln^-/- mice (P = 7.3 × 10^-9 for ONL at 2 m) that progressed over the first 6 months of life and then stabilized. Light microscopy showed loss of ONL nuclei (P ranged between .00033 and .0097 for posterior measurements), and a TUNEL assay revealed a small but significant increase in apoptosis (P = .034). Lmln^-/- mice accumulated fundus spots (P = .0030 by 2 m of age) and activated subretinal microglia (P ranged from .0007 to 8 × 10^-13 for Gal3⁺ cells). Scotopic electroretinography demonstrated a decrease in retinal function in Lmln^-/- mice both at 6 m (only a-wave, P < .01 for all stimuli) and at 10 m of age (P < .01 for both a-wave and b-wave with all stimuli).CONCLUSIONSOur work revealed a previously unknown essential role for Lmln in maintaining retinal anatomy and function. Further studies using this new model will be aimed at determining the cellular expression of Lmln and its mechanisms of action within the retina.

01 Dec 2024·Carbohydrate Polymers

Oligosaccharides from Stellaria dichotoma L. var. lanceolate bind to galectin-3 and ameliorate effects of colitis

Article

Author: Mayo, Kevin H ; Cui, Liangnan ; He, Zhen ; Wu, Jing ; Sun, Lin ; Zhao, Zihan ; Mayo, Kevin H. ; Su, Jiyong ; Zhou, Yifa ; Xu, Xuejiao ; Wang, Xiang

Even though Stellaria dichotoma L. var. lanceolate (S. dichotoma) is a well-known medicinal plant in the family Caryophyllaceae, its oligosaccharides remain unexplored in terms of their potential as bioactive agents. Here, we isolated a mixture of oligosaccharides from S. dichotoma (Yield: 12 % w/w), that are primarily non-classical raffinose family oligosaccharides (RFOs). Nine major oligosaccharides were purified and identified from the mixture, including sucrose, raffinose, 1-planteose, lychnose, stellariose, along with four new non-classical RFOs. Two of the four new oligosaccharides are linear hexose pentamers with α-galactosyl extensions on their lychnose moieties, and the other two are branched hexose hexamers with α-galactosyl extensions on their stellariose groups. Their interactions with galectin-3 (Gal-3) revealed significant binding, with the terminal galactose providing enhanced affinity for the lectin. Notably, Gal-3 residues Arg144, His158, Asn160, Arg162, Asn174, Trp181, Glu184 and Arg186 coordinate with the lychnose. In vivo studies using the dextran sulfate sodium (DSS) mouse model for colitis demonstrated the ability of these carbohydrates in mitigating ulcerative colitis (UC). Overall, our study has provided structural information and potential applications of S. dichotoma oligosaccharides, also offers new approaches for the development of medicinal oligosaccharides.

01 Dec 2024·Cellular and Molecular Life Sciences

NPRL2 promotes TRIM16-mediated ubiquitination degradation of Galectin-3 to prevent CD8+T lymphocyte cuproptosis in glioma

Article

Author: Yue, Jianhe ; Luo, Xu ; Wang, Feng ; Chen, Jin ; Cheng, Yuan ; Zhang, Hao ; Sun, Maoyuan ; Zhang, Maoxin ; Wu, Yuanyuan ; Huang, Ning

BACKGROUNDOur previous study found that tumor suppressor nitrogen permease regulator like-2(NPRL2) is frequently downregulated in glioma, leading to malignant growth. However, NPRL2-mediated crosstalk between tumor cells and immune cells remains unclear.METHODSThe regulatory effects of NPRL2 on tripartite motif-containing protein 16(TRIM16) dependent ubiquitination degradation of Galectin-3(Gal-3) were explored. The effects of Gal-3 on copper uptake, immunocompetence and cuproptosis were investigated in CD8⁺T lymphocytes(CD8⁺T cells). The ability of NPRL2 to protect CD8⁺T cells from Gal-3 damage was evaluated. Furthermore, the correlations among NPRL2, TRIM16, Gal-3 and CD8⁺T cell accumulation were analyzed in glioma clinical specimens.RESULTSNPRL2 increased the TRIM16 expression via inactivation of ERK1/2, which in turn promoted the ubiquitination-mediated degradation of Gal-3 and diminished Gal-3 release from glioma cells. Moreover, Gal-3 accelerated copper uptake and triggered cuproptosis in CD8⁺T cells, whereas NPRL2 increased CD8⁺T cell recruitment and prevented impairment of CD8⁺T cells by Gal-3. Clinical samples revealed that NPRL2 expression was positively associated with TRIM16 expression and negatively correlated with Gal-3, but Gal-3 expression was negatively associated with CD8⁺T cell accumulation.CONCLUSIONGlioma-derived NPRL2/TRIM16/Gal-3 axis participates in the regulation of CD8⁺T cell cuproptosis, which provides a promising strategy to rescue the immune activity of CD8⁺T cells and reverse immunosuppression in glioma.

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