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Last update 08 May 2025

GluK5 x GRIK

Last update 08 May 2025

Basic Info

Related Targets

GluK5GRIK

Drugs associated with GluK5 x GRIK

LY-466195

Target

GRIK x GluK5

Mechanism

GluK5 antagonists [+1]

Active Org.

Eli Lilly & Co. [+1]

Originator Org.

Eli Lilly & Co.

Active Indication

Migraine Disorders

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

LBG20304

Target

GluK5

Mechanism

GluK5 agonists

Active Org.

University of Copenhagen

Originator Org.

University of Copenhagen

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NS3763

Target

GluK5

Mechanism

GluK5 antagonists

Active Org.-

Originator Org.

Neurosearch

Active Indication-

Inactive Indication

Epilepsy [+2]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GluK5 x GRIK

100 Translational Medicine associated with GluK5 x GRIK

0 Patents (Medical) associated with GluK5 x GRIK

262

Literatures (Medical) associated with GluK5 x GRIK

01 Apr 2025·Current Opinion in Neurology

State-of-the-art gene therapy in epilepsy

Review

Author: Walker, Matthew C

Purpose of reviewGene therapy in epilepsy has undergone a rapid expansion in recent years. This has largely been driven by both advances in our understanding of epilepsy genetics and mechanisms, and also significant advances in gene therapy tools, in particular safe and effective viral vectors. Epilepsy remains an ideal target disease for gene therapy and this review highlights recent developments in this area.Recent findingsThere have been continued advances in the development of antisense oligonucleotide therapies to knock down genes in the treatment of monogenic epilepsies with some now entering clinical trial. However, the greatest recent advances have been in vector gene therapy, which offers a more permanent solution by delivering therapeutic genes directly to the brain as a one-off therapy. In particular, there has been a growth in methods that target focal epilepsy. Such promising approaches close to or in clinical trial include expressing NPY and its Y2 receptor, knocking-down GluK5, a kainate receptor subunit, and the over-expression of Kv1.1, an endogenous potassium channel.In the future, it is likely that we will take advantage of approaches of regulating more precisely network excitability by using methods such as optogenetics, designer receptors exclusively activated by designer drugs (DREADDs), ‘inhibitory’ glutamate receptors activated by excessive glutamate spill-over, and activity-dependent promoters, which target gene expression to the ‘hyperactive’ neurons.SummaryGene therapies offer a novel approach to the treatment of not just genetic epilepsies but any form of epilepsy and may in the future offer an alternative to drug and surgical therapies, allowing more precise, permanent and targeted treatment with fewer adverse effects.

01 Mar 2025·Brain and Behavior

Transcriptomic Dysregulation in Animal Models of Attention‐Deficit Hyperactivity Disorder and Nicotine Dependence Suggests Shared Neural Mechanisms

Article

Author: Van Horn, Sarah ; Toufexis, Donna J ; Driscoll, Heather

ABSTRACTIntroductionAttention‐deficit‐hyperactivity disorder (ADHD) is highly heritable and increases the likelihood of nicotine dependence (ND). The self‐medication hypothesis of nicotine use in ADHD proposes that ADHD patients seek nicotine for its ability to improve their symptoms, and they have less success quitting, possibly due to the worsening of ADHD symptoms in withdrawal.MethodsThe present analysis compared transcriptomic data from the brains of rodent models of ADHD and those of ND, with a focus on striatal gene expression. Differential expression analysis, pathway enrichment analysis, and gene‐network mapping identified signaling networks and candidate genes that may contribute to the high co‐occurrence between ADHD and ND.ResultsWe identified novel differentially expressed genes (PRKAG2, MAPK1), and genes with known associations to either ADHD or ND (ANK3, CALD1, CHRNA4, CHRNA7, CMTM8, DLG4, DUSP6, GNG3, GNG11, GRIK5, GRINA2, GRM5, ICAM2, KCNJ6, PRKAB1, SNAP25, SYNPO, SYT1, VAMP2). In addition, synaptic transmission (hsa04728, R‐HAS‐112315, R‐HSA‐442755) and MAPK signaling pathways (hsa04010, hsa04014, hsa04015, R‐HSA‐5673001, R‐HSA‐5684996) were enriched in both ADHD and ND.ConclusionThe signaling pathways implicated by this analysis mediate neurological mechanisms known to contribute to ND. The association of analogous differently expressed genes and common signaling pathways suggests an important causal relationship between ND and ADHD that may be clinically important.

01 Jan 2025·Proteins: Structure, Function, and Bioinformatics

Partial agonism in heteromeric GLUK2/GLUK5 kainate receptor

Article

Author: Berka, Vladimir ; Paudyal, Nabina ; Carrillo, Elisa ; Das, Anindita ; Jayaraman, Vasanthi

AbstractKainate receptors are a subtype of ionotropic glutamate receptors that form transmembrane channels upon binding glutamate. Here, we have investigated the mechanism of partial agonism in heteromeric GluK2/K5 receptors, where the GluK2 and GluK5 subunits have distinct agonist binding profiles. Using single‐molecule Förster resonance energy transfer, we found that at the bi‐lobed agonist‐binding domain, the partial agonist AMPA‐bound receptor occupied intermediate cleft closure conformational states at the GluK2 cleft, compared to the more open cleft conformations in apo form and more closed cleft conformations in the full agonist glutamate‐bound form. In contrast, there is no significant difference in cleft closure states at the GluK5 agonist‐binding domain between the partial agonist AMPA‐ and full agonist glutamate‐bound states. Additionally, unlike the glutamate‐bound state, the dimer interface at the agonist‐binding domain is not decoupled in the AMPA‐bound state. Our findings suggest that partial agonism observed with AMPA binding is mediated primarily due to differences in the GluK2 subunit, highlighting the distinct contributions of the subunits towards activation.

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