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Last update 08 May 2025

RXRG

Last update 08 May 2025

Basic Info

Synonyms

NR2B3, Nuclear receptor subfamily 2 group B member 3, Retinoic acid receptor RXR-gamma

+ [6]

Introduction

Receptor for retinoic acid. Retinoic acid receptors bind as heterodimers to their target response elements in response to their ligands, all-trans or 9-cis retinoic acid, and regulate gene expression in various biological processes. The RAR/RXR heterodimers bind to the retinoic acid response elements (RARE) composed of tandem 5'-AGGTCA-3' sites known as DR1-DR5. The high affinity ligand for RXRs is 9-cis retinoic acid (By similarity).

Drugs associated with RXRG

Betamethasone dipropionate/Bexarotene

Target

GR x RXRA x RXRB x RXRG

Mechanism

GR agonists [+3]

Active Org.-

Originator Org.

Almirall SA

Active Indication-

Inactive Indication

Arthritis, Psoriatic [+3]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

6FWA-201

Target

RXRG

Mechanism

RXRG modulators

Active Org.-

Originator Org.

Teijin Pharma Ltd.

Active Indication-

Inactive Indication

Multiple Sclerosis

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

HG-1082

Target

RARγ x RXRG

Mechanism

RARγ modulators [+1]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Neoplasms [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with RXRG

NCT02955693

/ CompletedPhase 1

Randomized, Open-label, Single-center, Four-way Crossover, Single Dose Study to Investigate the Pharmacokinetics of LAS41008 120 mg Gastro-resistant Tablet and Fumaderm® 120 mg Gastro-resistant Tablet Under Fasting and Fed Conditions in Healthy Subjects

The purpose of this study is to determine how the organism affects MMF (metabolite of dimethyl fumarate [DMF]) after single oral dose administration of LAS41008 120 mg gastroresistant tablet and Fumaderm® 120 mg gastro-resistant tablet under fasting and fed conditions. The study also aims to assess the safety of the study treatments.

Start Date01 Sep 2016

Sponsor / Collaborator

Almirall SA

NCT02180464

/ CompletedPhase 2

A Phase IIa, 28-day Treatment, Multi-center, Randomized, Comparator-controlled, Observer-blind Trial With Intra-individual Left/Right Comparison to Investigate the Anti-psoriatic Efficacy and the Safety of an LAS41004 Formulation in Comparison to an Active Reference in Patients With Mild to Moderate Plaque Psoriasis

Proof-of concept study to competitively investigate antipsoriatic efficacy and safety of a LAS41004 formulation vs active control No formal study hypothesis, but descriptive evaluation (PoC).

Start Date01 Jun 2014

Sponsor / Collaborator

Almirall SA

NCT02111499

/ CompletedPhase 1/2

A Randomized, Controlled, Observer-blind Psoriasis Plaque Test to Investigate the Anti-psoriatic Efficacy, Tolerability and Safety (Skin Atrophy) of LAS41004 Formulations in Patients With Mild to Moderate Plaque Psoriasis

Clinical investigation of anti-psoriatic efficacy and atrophy

Start Date01 Mar 2014

Sponsor / Collaborator

Almirall SA

[+1]

100 Clinical Results associated with RXRG

100 Translational Medicine associated with RXRG

0 Patents (Medical) associated with RXRG

320

Literatures (Medical) associated with RXRG

02 Jan 2025·Nutritional Neuroscience

The symptomatology of Attention-Deficit/Hyperactivity Disorder and the genetic control of vitamin D levels

Article

Author: Bau, Claiton Henrique Dotto ; Dresch, Fabiane ; Rovaris, Diego Luiz ; Shansis, Flávio Milman ; Grevet, Eugenio Horacio ; da Silva, Caroline ; das Neves, Fernando Godoy Pereira ; Bandeira, Cibele Edom ; Genro, Júlia Pasqualini ; da Silva, Bruna Santos ; Contini, Verônica ; Dias-Soares, Monique

OBJECTIVESVitamin D deficiency has been associated with psychiatric disorders and behavioral phenotypes such as Attention-Deficit/Hyperactivity Disorder (ADHD). Considering that vitamin D levels are polygenic, we aim to evaluate the overall effects of its genetic architecture on symptoms of inattention, hyperactivity, and impulsivity and on the serum levels of vitamin D in two independent samples of adults, as well as the specific effects of five relevant polymorphisms in vitamin D-related genes.METHODSWe evaluated 870 subjects from an ADHD sample (407 cases and 463 controls) and 319 subjects from an academic community (nutrigenetic sample). Vitamin D serum levels were obtained through Elisa test and genetic data by TaqMan™ allelic discrimination and Infinium PsychArray-24 BeadChip genotyping. Polygenic Scores (PGS) were calculated on PRSice2 based on the latest GWAS for Vitamin D and statistical analyses were conducted at Plink and SPSS software.RESULTSVitamin D PGSs were associated with inattention in the ADHD sample and with hyperactivity when inattention symptoms were included as covariates. In the nutrigenetic sample, CYP2R1 rs10741657 and DHCR7 rs12785878 were nominally associated with impulsivity and hyperactivity, respectively, and both with vitamin D levels. In the clinical sample, RXRG rs2134095 was associated with impulsivity.DISCUSSIONOur findings suggest a shared genetic architecture between vitamin D levels and ADHD symptoms, as evidenced by the associations observed with PGS and specific genes related to vitamin D levels. Interestingly, differential effects for vitamin D PGS were found in inattention and hyperactivity, which should be considered in further studies involving ADHD.

01 Jan 2025·Experimental Neurology

Theta-burst transcranial magnetic stimulation attenuates chronic ischemic demyelination and vascular cognitive impairment in mice

Article

Author: Zhang, Xiaohao ; Zhu, Wusheng ; Yuan, Kang ; Wang, Di ; Li, Yunzi ; Huang, Zhenqian ; Xie, Yi ; Lv, Qiushi ; Zhao, Ying ; Wu, Min ; Xu, Gelin ; Wang, Xinyi ; Zha, Mingming ; Wang, Jia

Vascular cognitive impairment and dementia (VCID) is mainly caused by chronic cerebral hypoperfusion and subsequent white matter lesions. Noninvasive transcranial magnetic stimulation has been utilized in treating various neurological disorders. However, the function of theta-burst transcranial magnetic stimulation on VCID remains to be defined. We utilized 4-week bilateral carotid artery stenosis model of male mice to mimic VCID. Intermittent theta-burst stimulation (iTBS) or consecutive theta-burst stimulation (cTBS) was administered for 14 consecutive days. Through luxol fast blue staining, electron microscopy and immunofluorescence, we found that iTBS, not cTBS, significantly improved demyelination, axonal damage and β-amyloid deposition, without affecting cerebral blood flow in VCID mice. At cellular levels, iTBS rescued the loss of mature oligodendrocytes, promoted precursor cell differentiation, and inhibited pro-inflammatory activation of astrocytes and microglia. Notably, iTBS attenuated cognitive deterioration in both short-term retention and long-term spatial memory of VCID mice as indicated by serial neurobehavioral tests. To explore the molecular involvement of iTBS, mRNA sequencing was carried out. By real-time PCR and combined RNA fluorescence in situ hybridization with immunofluorescence, iTBS was confirmed to increase Rxrg expression specifically in mature oligodendrocytes. Collectively, iTBS could ameliorate vascular cognitive dysfunction, probably via mitigating white matter lesions and neuroinflammation in the corpus callosum. Rxrg signaling in mature oligodendrocytes, which was increased by iTBS, might be a potential target for VCID treatment.

01 Jan 2025·Molecular Psychiatry

Evidence for thyroid hormone regulation of amygdala-dependent fear-relevant memory and plasticity

Article

Author: Chen, Michelle X ; Ressler, Kerry J ; Klengel, Claudia ; Zaleski, Cole E ; Hollenberg, Anthony N ; Ponomareva, Olga Y ; Maddox, Stephanie A ; Vella, Kristen R

The amygdala is an established site for fear memory formation, and clinical studies suggest involvement of hormone signaling cascades in development of trauma-related disorders. While an association of thyroid hormone (TH) status and mood disorders is established, the related brain-based mechanisms and the role of TH in anxiety disorders are unknown. Here we examine the role that TH receptor (TR, a nuclear transcriptional repressor when unbound and a transcriptional activator when bound to TH) may have in mediating the initial formation of fear memories in the amygdala. We identified mRNA levels of TR and other TH pathway regulatory genes, including thyrotropin-releasing hormone (Trh), transthyretin (Ttr), thyrotropin-releasing hormone receptor (Trhr), type 2 iodothyronine deiodinase (Dio2), mediator complex subunit 12 (Med12/Trap230) and retinoid X receptor gamma (Rxrg) to be altered in the amygdala following Pavlovian fear conditioning. Using TH agonist and antagonist infusion into the amygdala, we demonstrated that this pathway is both necessary and sufficient for fear memory consolidation. Inhibition of TH signaling with the TR antagonist 1-850 decreased fear memory consolidation; while activation of TR with T3 (triiodothyronine) resulted in increased memory formation. Using a systemic hypothyroid mouse model, we found that intra-amygdala infusions of T3 were sufficient to rescue deficits in fear memory. Finally, we demonstrated that T3 was sufficient to activate TR-specific gene pathways in the amygdala. These findings on the role of activity-dependent TR modulation support a model in which local TH is a critical regulator of fear memory-related plasticity in the amygdala.

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