Evidence map›Paper›PMID 41680254›Full record

ArticleScientific reports2026

Efficacy of mebendazole in the spontaneous NZBxNZWF1 animal model of systemic lupus erythematosus.

M L Eloranta, P Nygren, R Larsson, A Loskog, N Woodworth, M Hultqvist, Richard Svensson, Ylva Gravenfors, L Rönnblom, Mårten Fryknäs

Abstract read
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

M L ElorantaDepartment of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden.
P NygrenDepartment of Immunology, Genetics and Pathology, Uppsala University, SE-75185, Uppsala, Sweden.
R LarssonDepartment of Medical Sciences, Division of Cancer Pharmacology and Computational Medicine, Uppsala University, SE-75185, Uppsala, Sweden.
A LoskogDepartment of Immunology, Genetics and Pathology, Uppsala University, SE-75185, Uppsala, Sweden.
N WoodworthRedoxis AB, Medicon Village, Scheelevägen 2, SE-223 81, Lund, Sweden.
M HultqvistRedoxis AB, Medicon Village, Scheelevägen 2, SE-223 81, Lund, Sweden.
Richard SvenssonDepartment of Pharmacy, SciLifeLab Drug Discovery and Development, Uppsala University, SE-751 23, Uppsala, Sweden.
Ylva GravenforsScience for Life Laboratory, Drug Discovery & Development Platform, Department of Biochemistry and Biophysics, Stockholm University, SE-171 21, Solna, Sweden.
L RönnblomDepartment of Medical Sciences, Rheumatology, Uppsala University, Uppsala, Sweden.
Mårten FryknäsDepartment of Medical Sciences, Division of Cancer Pharmacology and Computational Medicine, Uppsala University, SE-75185, Uppsala, Sweden. marten.fryknas@medsci.uu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex etiology involving both innate and adaptive immune dysregulation. Among several perturbed signaling pathways, decreased ERK activity in CD4⁺ T-cells has been linked to DNA hypomethylation and aberrant gene expression in SLE. Mebendazole (MBZ), an anti-helminthic drug with a well-established safety profile, has shown immunomodulatory effects in preclinical studies, including activation of the MEK/ERK pathway and inhibition of MAPK14 (p38), a known driver of inflammation. To evaluate the therapeutic potential of MBZ in SLE, we tested its efficacy in NZBxNZWF1 mice, a spontaneous and well-characterized SLE model. MBZ treatment resulted in reduced proteinuria, lower anti-dsDNA antibody levels, and diminished glomerular IgG deposition, both in preventive and therapeutic settings. Exploratory in vitro data suggest that MBZ may also influence ERK signaling in B cells, while the mechanistic basis of these effects remains to be clarified. Our findings demonstrate robust phenotypic improvements and support further investigation of MBZ as a repositioned candidate for SLE.

Indexed as

Lupus Erythematosus, SystemicMebendazoleAnimalsAntibodies, AntinuclearB-LymphocytesDisease Models, AnimalFemaleImmunoglobulin GMAP Kinase Signaling SystemMiceProteinuriaAntibodies, AntinuclearImmunoglobulin GMebendazoleDrug repositioningMebendazoleSystemic lupus erythematosus

Identifiers

PMID41680254
PMCPMC12905218

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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 OpenQuestion graph.