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Last update 08 May 2025

RYK

Last update 08 May 2025

Basic Info

Synonyms

D3S3195, JTK5, JTK5A

+ [6]

Introduction

May be a coreceptor along with FZD8 of Wnt proteins, such as WNT1, WNT3, WNT3A and WNT5A. Involved in neuron differentiation, axon guidance, corpus callosum establishment and neurite outgrowth. In response to WNT3 stimulation, receptor C-terminal cleavage occurs in its transmembrane region and allows the C-terminal intracellular product to translocate from the cytoplasm to the nucleus where it plays a crucial role in neuronal development.

Drugs associated with RYK

SLV-404

Target

RYK x Top I

Mechanism

RYK antagonists [+1]

Active Org.

Solve Therapeutics, Inc.

[+1]

Originator Org.

University of Turin [+1]

Active Indication

Richter's syndrome

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

US20240093194

Patent Mining

Target

RYK

Mechanism-

Active Org.

Qufu Normal University

Originator Org.

Qufu Normal University

Active Indication

Breast Cancer

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with RYK

100 Translational Medicine associated with RYK

0 Patents (Medical) associated with RYK

852

Literatures (Medical) associated with RYK

01 Dec 2025·Molecular Biology Reports

Antisense oligonucleotides as a targeted therapeutic approach in model of acute myeloid leukemia

Article

Author: Vaňková, Lenka ; Pitule, Pavel ; Bufka, Jiří ; Moravec, Jiří ; Hošek, Petr ; Macečková, Diana

BACKGROUNDThe genetic and epigenetic alterations observed in acute myeloid leukemia (AML) contribute to its heterogeneity, influencing disease progression response to therapy, and patient outcomes. The use of antisense oligonucleotides (ASOs) technology allows for the design of oligonucleotide inhibitors based on gene sequence information alone, enabling precise targeting of key molecular pathways or specific genes implicated in AML.METHODS AND RESULTSMidostaurin, a FLT3 specific inhibitor and ASOs targeting particular genes, exons, or mutations was conducted using AML models. This ASOs treatment was designed to bind to exon 7 of the MBNL1 (muscleblind-like) gene. Another target was the FLT3 gene, focusing on two aspects: (a) FLT3-ITD (internal tandem duplication), to inhibit the expression of this aberrant gene form, and (b) the FLT3 in general. Treated and untreated cells were analyzed using quantitative PCR (qPCR), dot blot, and Raman spectroscopy. This study contrasts midostaurin with ASOs that inhibit FLT3 protein production or its isoforms via mRNA degradation. A trend of increased FLT3 expression was observed in midostaurin-treated cells, while ASO-treated cells showed decreased expression, though these changes were not statistically significant.CONCLUSIONSIn AML, exon 7 of MBNL1 is involved in several cellular processes and in this study, exon 7 of MBNL1 was targeted for method optimization, with the highest block of the exon 7 gene variant observed 48 h post-transfection. Midostaurin, a multitargeted kinase inhibitor, acts against the receptor tyrosine kinase FLT3, a critical molecule in AML pathogenesis. While midostaurin blocks FLT3 signaling pathways, it paradoxically increases FLT3 expression.

01 Jun 2025·Molecular and Cellular Neuroscience

Interrogating mediators of single-cell transcriptional changes in the acute damaged cerebral cortex: Insights into endothelial-astrocyte interactions

Article

Author: Theus, Michelle H ; Soliman, Eman ; de Jager, Caroline

Traumatic brain injury (TBI) induces complex cellular and molecular changes, challenging recovery and therapeutic development. Although molecular pathways have been implicated in TBI pathology, the cellular specificity of these mechanisms remains underexplored. Here, we investigate the role of endothelial cell (EC) EphA4, a receptor tyrosine kinase receptor involved in axonal guidance, in modulating cell-specific transcriptomic changes within the damaged cerebral cortex. Utilizing single-cell RNA sequencing (scRNA-seq) in an experimental TBI model, we mapped transcriptional changes across various cell types, with a focus on astrocytes and ECs. Our analysis reveals that EC-specific knockout (KO) of EphA4 triggers significant alterations in astrocyte gene expression and shifts predominate subclusters. We identified six distinct astrocyte clusters (C0-C5) in the damaged cortex including as C0-Mobp/Plp1+; C1-Slc1a3/Clu+; C2-Hbb-bs/Hba-a1/Ndrg2+; C3-GFAP/Lcn2+; C4-Gli3/Mertk+, and C5-Cox8a+. We validate a new Sox9+ cluster expressing Mertk and Gas, which mediates efferocytosis to facilitate apoptotic cell clearance and anti-inflammatory responses. Transcriptomic and CellChat analyses of EC-KO cells highlights upregulation of neuroprotective pathways, including increased amyloid precursor protein (APP) and Gas6. Key pathways predicted to be modulated in astrocytes from EC-KO mice include oxidative phosphorylation and FOXO signaling, mitochondrial dysfunction and ephrin B signaling. Concurrently, metabolic and signaling pathways in endothelial cells-such as ceramide and sphingosine phosphate metabolism and NGF-stimulated transcription-indicate an adaptive response to a metabolically demanding post-injury hypoxic environment. These findings elucidate potential interplay between astrocytic and endothelial responses as well as transcriptional networks underlying cortical tissue damage.

01 May 2025·Biochemical and Biophysical Research Communications

Synthesis, molecular docking, and antiproliferative activity studies of bromine bearing Schiff bases

Article

Author: Kokbudak, Zülbiye ; Akkoc, Senem ; Turkmenoglu, Burçin ; Karatas, Halis

Bromine-bearing compounds are found in a variety of natural products and synthetic drugs and exhibit a variety of biological activities. They often display particular properties such as enhanced stability, improved lipophilicity, and larger molecular interactions, making them valuable in drug design and development. In this study, three bromine-bearing Schiff bases were synthesized, characterized, and tested in lung (A549) and colon (DLD-1) cancer cell lines for 72 h incubation time. The results demonstrated that compounds had antiproliferative activity in screened cell lines. The compounds were also tested on a healthy embryonic kidney cell line (HEK-293T) to evaluate their toxic effects on non-cancerous cells. In vitro results of compounds interacting with the most suitable target were confirmed by in silico approaches. All bromine-containing compounds were interacted with the receptor tyrosine kinase FLT3 target via molecular docking. From the interaction results of the 6JQR crystal structure with 2-Br, the docking score value was calculated as -8.178 kcal/mol, and this value was determined to be better than the docking score (-7.269 kcal/mol) value of gilteritinib. Pharmacokinetics, toxicity properties and Lipinski violations of the compounds were estimated by ADMET and were calculated to be in the range of recommended values. Molecules demonstrated limited efficacy against A549 cells line, however; they exhibited relatively greater effectiveness against DLD-1 cell line. Notably, the IC₅₀ value of 2-Br was comparable to that of cisplatin. All molecules exhibited minimal toxicity.

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