Last update 01 Nov 2024

LINGO-1

Last update 01 Nov 2024

Basic Info

Synonyms

FLJ14594, LERN1, leucine rich repeat and Ig domain containing 1

+ [7]

Introduction

Functional component of the Nogo receptor signaling complex (RTN4R/NGFR) in RhoA activation responsible for some inhibition of axonal regeneration by myelin-associated factors (PubMed:14966521, PubMed:15694321). Is also an important negative regulator of oligodentrocyte differentiation and axonal myelination (PubMed:15895088). Acts in conjunction with RTN4 and RTN4R in regulating neuronal precursor cell motility during cortical development (By similarity).

Drugs associated with LINGO-1

Anti-LINGO-1 antibody(Biogen)

Target

LINGO-1

Mechanism

LINGO-1 inhibitors

Active Org.

Biogen, Inc.

Originator Org.

Biogen, Inc.

Active Indication

Demyelinating Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

CN116549632

Patent Mining

Target

LINGO-1

Mechanism-

Active Org.

Academy of Military Medical Sciences

Originator Org.

Academy of Military Medical Sciences

Active Indication

Neurologic Manifestations

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Opicinumab

Target

LINGO-1

Mechanism

LINGO-1 inhibitors [+1]

Active Org.-

Originator Org.

Biogen, Inc. [+1]

Active Indication-

Inactive Indication

Multiple sclerosis relapse [+2]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with LINGO-1

NCT03222973 / TerminatedPhase 2

A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study With Optional Open-Label Extension in Subjects With Relapsing Multiple Sclerosis to Evaluate the Efficacy and Safety of BIIB033 as an Add-On Therapy to Anti-Inflammatory Disease-Modifying Therapies

The primary objective of Part 1 of this study is to evaluate the effects of BIIB033 versus placebo on disability improvement over 72 weeks. The primary objective of Part 2 of this study is to evaluate the long-term safety profile of BIIB033 as an add-on therapy in participants with MS.
The secondary objective of Part 1 is to evaluate the effects of BIIB033 versus placebo on additional measures of disability improvement. The secondary objective of Part 2 is to investigate long-term efficacy (disability improvement) and additional safety measures of BIIB033 as an add-on therapy in participants with MS.

Start Date15 Nov 2017

Sponsor / Collaborator

Biogen, Inc.

NCT02833142 / CompletedPhase 1

A Randomized, Blinded, Parallel-Group, Phase 1 Study of Pharmacokinetics, Safety and Tolerability of Single Intravenous Doses of BIIB033 (Opicinumab ) Produced by 2 Manufacturing Processes, in Healthy Volunteers

The primary objective of the study is to characterize the pharmacokinetics (PK) of BIIB033-B and to compare the PK profile with that of BIIB033-A in healthy volunteers. Secondary objectives are: To assess the safety and tolerability of BIIB033-A and BIIB033-B; To assess the secondary PK parameters of BIIB033-A and BIIB033-B; To assess the immunogenicity of BIIB033-A and BIIB033-B.

Start Date01 Jul 2016

Sponsor / Collaborator

Biogen, Inc.

NCT02657915 / CompletedPhase 2

A Multicenter, Follow-Up Study to Assess Long-Term Electrophysiologic and Clinical Outcomes in Subjects Previously Enrolled in Study 215ON201

The primary objective of the study is to assess full-field visual evoked potential (FF-VEP) latency in subjects who were enrolled in Study NCT01721161 2 years (+ up to 12 months) after the last study visit. The secondary objective is to assess clinical progression and severity of central nervous system (CNS) demyelinating disease in subjects who were enrolled in Study NCT01721161 2 years (+ up to 12 months) after the last study visit. Intervention was administered in the previous study. The participants, investigator and outcome assessors remain blinded in this follow-up study.

Start Date10 Mar 2016

Sponsor / Collaborator

Biogen, Inc.

100 Clinical Results associated with LINGO-1

100 Translational Medicine associated with LINGO-1

0 Patents (Medical) associated with LINGO-1

274

Literatures (Medical) associated with LINGO-1

01 Dec 2024·Clinical Proteomics

Identification of brain-enriched proteins in CSF as biomarkers of relapsing remitting multiple sclerosis

Article

Author: Stengelin, Martin ; Atkinson, Hunter J ; Pittock, Sean ; Saadeh, Ruba ; Knyazhanskaya, Evdokiya ; Willrich, Maria Alice V ; Freedman, Mark S ; Wurtz, Lincoln I ; Prassas, Ioannis ; Scarisbrick, Isobel A ; Thebault, Simon ; Diamandis, Eleftherios P ; Gupta, Ruchi ; Sohaei, Dorsa ; Grill, Diane

AbstractBackgroundMultiple sclerosis (MS) is a clinically and biologically heterogenous disease with currently unpredictable progression and relapse. After the development and success of neurofilament as a cerebrospinal fluid (CSF) biomarker, there is reinvigorated interest in identifying other markers of or contributors to disease. The objective of this study is to probe the predictive potential of a panel of brain-enriched proteins on MS disease progression and subtype.MethodsThis study includes 40 individuals with MS and 14 headache controls. The MS cohort consists of 20 relapsing remitting (RR) and 20 primary progressive (PP) patients. The CSF of all individuals was analyzed for 63 brain enriched proteins using a method of liquid-chromatography tandem mass spectrometry. Wilcoxon rank sum test, Kruskal-Wallis one-way ANOVA, logistic regression, and Pearson correlation were used to refine the list of candidates by comparing relative protein concentrations as well as relation to known imaging and molecular biomarkers.ResultsWe report 30 proteins with some relevance to disease, clinical subtype, or severity. Strikingly, we observed widespread protein depletion in the disease CSF as compared to control. We identified numerous markers of relapsing disease, including KLK6 (kallikrein 6, OR = 0.367, p < 0.05), which may be driven by active disease as defined by MRI enhancing lesions. Other oligodendrocyte-enriched proteins also appeared at reduced levels in relapsing disease, namely CNDP1 (carnosine dipeptidase 1), LINGO1 (leucine rich repeat and Immunoglobin-like domain-containing protein 1), MAG (myelin associated glycoprotein), and MOG (myelin oligodendrocyte glycoprotein). Finally, we identified three proteins—CNDP1, APLP1 (amyloid beta precursor like protein 1), and OLFM1 (olfactomedin 1)—that were statistically different in relapsing vs. progressive disease raising the potential for use as an early biomarker to discriminate clinical subtype.ConclusionsWe illustrate the utility of targeted mass spectrometry in generating potential targets for future biomarker studies and highlight reductions in brain-enriched proteins as markers of the relapsing remitting disease stage.

01 Nov 2024·Naunyn-Schmiedeberg's Archives of Pharmacology

Therapeutic potential of Bergenin in the management of neurological-based diseases and disorders

Review

Author: Rezaiezadeh, Hojjat ; Tavakoli, Marziye Ranjbar ; Banazadeh, Mohammad ; Kohlmeier, Kristi A ; Shabani, Mohammad ; Sabokro, Mohammad ; Langarizadeh, Mohammad Amin

Originally sourced from plants, Bergenin has been used as a medicinal compound in traditional medicine for centuries, and anecdotal reports suggest a wide range of therapeutic uses. Naturally-occurring and lab-synthesized Bergenin, as well as some of its related compounds, have been shown in in vivo and in vitro studies to alter activity of several enzymes and proteins critical in cellular functioning, including reelin, GSK-3β, Lingo-1, Ten-4, GP-43, Aβ 1-42, P-tau, SOD1,2, GPx, Glx1, NQO1, HO1, PPAR-ɣ, BDNF, VEGF, and STAT6. Additionally, Bergenin alters levels of several cytokines, such as IL-6, IL-1β, TNF-α, and TGF-β. Behavioral and cellular effects of Bergenin have been shown to involve PI3K/Akt, NF-κB, PKC, Nrf2, and Sirt1/FOXO3a pathways. These pathways, enzymes, and proteins have been shown to be important in normal neurological functioning, and/or dysfunctions in these pathways and proteins have been shown to be important in several neuro-based disorders or diseases, which suggests that Bergenin could be therapeutic in management of neuropsychiatric conditions or neurological disorders. In preclinical studies, Bergenin has been shown to be useful for the management of Alzheimer's disease, Parkinson's disease, anxiety, depression, addiction, epilepsy, insomnia, stroke, and potentially, state control. Our review aims to summarize current evidence supporting the conclusion that Bergenin could play a role in treating various neuro-based disorders and that future studies should be conducted to evaluate the mechanisms by which Bergenin could exert its therapeutic effects.

30 Aug 2024·Current Neurovascular Research

Targeting Oligodendrocyte Dynamics and Remyelination: Emerging Therapies and Personalized Approaches in Multiple Sclerosis Management

Article

Author: Narula, Acharan S. ; Gupta, Ghanshyam Das ; Khan, Zuber ; Mehan, Sidharth ; Tiwari, Aarti ; Sharma, Tarun

Abstract:Multiple sclerosis [MS] is a progressive autoimmune condition that primarily affects young people and is characterized by demyelination and neurodegeneration of the central nervous system [CNS]. This in-depth review explores the complex involvement of oligodendrocytes, the primary myelin- producing cells in the CNS, in the pathophysiology of MS. It discusses the biochemical processes and signalling pathways required for oligodendrocytes to function and remain alive, as well as how they might fail and cause demyelination to occur. We investigate developing therapeutic options that target remyelination, a fundamental component of MS treatment. Remyelination approaches promote the survival and differentiation of oligodendrocyte precursor cells [OPCs], restoring myelin sheaths. This improves nerve fibre function and may prevent MS from worsening. We examine crucial parameters influencing remyelination success, such as OPC density, ageing, and signalling pathway regulation [e.g., Retinoid X receptor, LINGO-1, Notch]. The review also examines existing neuroprotective and antiinflammatory medications being studied to see if they can assist oligodendrocytes in surviving and reducing the severity of MS symptoms. The review focuses on medicines that target the myelin metabolism in oligodendrocytes. Altering oligodendrocyte metabolism has been linked to reversing demyelination and improving MS patient outcomes through various mechanisms. We also explore potential breakthroughs, including innovative antisense technologies, deep brain stimulation, and the impact of gut health and exercise on MS development. The article discusses the possibility of personalized medicine in MS therapy, emphasizing the importance of specific medicines based on individual molecular profiles. The study emphasizes the need for reliable biomarkers and improved imaging tools for monitoring disease progression and therapy response. Finally, this review focuses on the importance of oligodendrocytes in MS and the potential for remyelination therapy. It also underlines the importance of continued research to develop more effective treatment regimens, taking into account the complexities of MS pathology and the different factors that influence disease progression and treatment.

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LINGO-1

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