Evidence map›Paper›PMID 38802492›Full record

ArticleScientific reports2024

Ebselen analogues delay disease onset and its course in fALS by on-target SOD-1 engagement.

Seiji Watanabe, Kangsa Amporndanai, Raheela Awais, Caroline Latham, Muhammad Awais, Paul M O'Neill, Koji Yamanaka, S Samar Hasnain

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. Nose-to-brain delivery of a SOD1-stabilizing small molecule ameliorates pathology in an ALS mouse model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Article
  4. Article
  5. Structural insights into the role of reduced cysteine residues in SOD1 amyloid filament formation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Seiji Watanabe *Department of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Furo-Cho, Chikusa-Ku, Nagoya, 464-8601, Japan.
Kangsa Amporndanai *Molecular Biophysics Group, Department of Biochemistry and System Biology, Institute of System, M0polecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, L69 7ZB, UK.
Raheela Awais *School of Life Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, L69 7ZB, UK.
Caroline LathamSchool of Life Sciences, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, L69 7ZB, UK.
Muhammad AwaisDepartment of Molecular and Clinical Cancer Medicine, Institute of System, Molecular and Integrative Biology, University of Liverpool, Liverpool, L69 3GE, UK.
Paul M O'NeillDepartment of Chemistry, Faculty of Science and Engineering, University of Liverpool, Liverpool, L69 7ZD, UK. P.M.Oneill01@liverpool.ac.uk.
Koji YamanakaDepartment of Neuroscience and Pathobiology, Research Institute of Environmental Medicine, Nagoya University, Furo-Cho, Chikusa-Ku, Nagoya, 464-8601, Japan. koji.yamanaka@riem.nagoya-u.ac.jp.
S Samar HasnainMolecular Biophysics Group, Department of Biochemistry and System Biology, Institute of System, M0polecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, L69 7ZB, UK. S.S.Hasnain@liverpool.ac.uk.

Funding

ALS Association WA1198
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) selectively affects motor neurons. SOD1 is the first causative gene to be identified for ALS and accounts for at least 20% of the familial (fALS) and up to 4% of sporadic (sALS) cases globally with some geographical variability. The destabilisation of the SOD1 dimer is a key driving force in fALS and sALS. Protein aggregation resulting from the destabilised SOD1 is arrested by the clinical drug ebselen and its analogues (MR6-8-2 and MR6-26-2) by redeeming the stability of the SOD1 dimer. The in vitro target engagement of these compounds is demonstrated using the bimolecular fluorescence complementation assay with protein-ligand binding directly visualised by co-crystallography in G93A SOD1. MR6-26-2 offers neuroprotection slowing disease onset of SOD1

Indexed as

Amyotrophic Lateral SclerosisAzolesIsoindolesOrganoselenium CompoundsSuperoxide Dismutase-1AnimalsDisease Models, AnimalHumansMiceMice, TransgenicNeuroprotective AgentsAzolesebselenIsoindolesNeuroprotective AgentsOrganoselenium CompoundsSOD1 protein, humanSuperoxide Dismutase-1Amyotrophic lateral sclerosisDrug developmentEbselenMotor neuron diseaseRiluzoleSuperoxide dismutaseTarget engagement

Identifiers

PMID38802492
PMCPMC11130262

What Socratic holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.