Evidence map›Paper›PMID 42134274›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026

Investigations of remibrutinib in models pertinent to multiple sclerosis.

Rajiv W Jain, Atefeh Rayatpour, Kathleen Hagen, Marlene T Morch, Gurleen Randhawa, Maryam Mobarakabadi, Xiangyu Zhang, Cenxiao Li, Maryam Nakhaei-Nejad, Fabrizio Giuliani and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 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

13 authors.

Rajiv W JainHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Atefeh RayatpourHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Kathleen HagenHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Marlene T MorchHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Gurleen RandhawaHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Maryam MobarakabadiHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Xiangyu ZhangHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Cenxiao LiHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada.
Maryam Nakhaei-NejadDivision of Neurology, Department of Medicine, University of Alberta, Canada.
Fabrizio GiulianiDivision of Neurology, Department of Medicine, University of Alberta, Canada.
Bruno CenniNovartis BioMedical Research, Basel, Switzerland.
Mengzhou XueDepartment of Cerebrovascular Diseases, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
V Wee YongHotchkiss Brain Institute and the Department of Clinical Neurosciences, University of Calgary, Canada. Electronic address: vyong@ucalgary.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhibitors of Bruton tyrosine kinase (BTK) are actively being pursued as potential disease-modifying therapies for multiple sclerosis (MS), as attested by several completed or ongoing Phase 3 clinical trials. Yet, key aspects of BTK inhibitors biology remain unclear. Here, we assessed the effects of remibrutinib, a BTK inhibitor in Phase 3 MS trials, in preclinical models of MS. Remibrutinib was evaluated in the myelin oligodendrocyte glycoprotein (MOG)35-55 model of experimental autoimmune encephalomyelitis (EAE) and in the lysolecithin model of demyelination. In culture, we assessed its ability to reduce tumor necrosis factor-α (TNF-α) elicited by immune complex-activation of primary human and mouse microglia, mouse macrophages, and human inducible pluripotent stem cell (iPS)-derived microglia. We also examined the impact of remibrutinib on T-bet

Indexed as

Agammaglobulinaemia Tyrosine KinaseEncephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisPyrimidinesTyrosine Kinase InhibitorsAnimalsCells, CulturedDisease Models, AnimalFemaleHumansMacrophagesMiceMice, Inbred C57BLMicrogliaMyelin-Oligodendrocyte GlycoproteinAgammaglobulinaemia Tyrosine KinaseMyelin-Oligodendrocyte GlycoproteinPyrimidinesremibrutinibTyrosine Kinase InhibitorsBTK inhibitorMultiple sclerosisRemibrutinibT-bet+ memory B cells

Identifiers

PMID42134274
PMCPMC13181286

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Registered trials

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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.