Evidence map›Paper›PMID 42177676›Full record

ArticleCellular and molecular neurobiology2026

S3I-201, a STAT3 Inhibitor, Inhibits Proinflammatory Mediator Signalling in CD19 and CD45R/B220 Cells in a Mouse Model of Multiple Sclerosis.

Abdulaziz M S Alsaad, Ahmed Nadeem, Sabry M Attia, Mushtaq A Ansari, Saleh A Bakheet, Majed Ali Algonaiah, Haneen A Al-Mazroua, Hatun A Alomar, Wedad S Sarawi, Mohammed M Almutairi and 6 more

Abstract read
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In one paragraph

Article in Cellular and molecular neurobiology, 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

16 authors.

Abdulaziz M S AlsaadDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Ahmed NadeemDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Sabry M AttiaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Mushtaq A AnsariDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Saleh A BakheetDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Majed Ali AlgonaiahDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Haneen A Al-MazrouaDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Hatun A AlomarDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Wedad S SarawiDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Mohammed M AlmutairiDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Abdullah A AldossariDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Quaiser SaquibDepartment of Zoology, College of Science, King Saud University, Riyadh, 11451, Saudi Arabia.
Norah K AlgarzaeDepartment of Physiology, College of Medicine, King Saud University, Riyadh, 11451, Saudi Arabia.
Mohamed A MahmoudDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Marwa H HusseinDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia.
Sheikh F AhmadDepartment of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, 11451, Kingdom of Saudi Arabia. fashaikh@ksu.edu.sa.

Funding

King Saud University The work was supported by the Researchers Supporting Project Number (ORF-2026-709), King Saud University.
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic illness characterised by progressive central nervous system (CNS) degeneration. The efficacy of most current MS medicines is limited, and significant adverse effects remain a concern. STAT3 inhibitors show potential for treating several immunological diseases. The current study demonstrates that S3I-201, a well-established STAT3 inhibitor, effectively treats PLP

Indexed as

Antigens, CD19Encephalomyelitis, Autoimmune, ExperimentalInflammation MediatorsLeukocyte Common AntigensMultiple SclerosisSignal TransductionSTAT3 Transcription FactorAnimalsDisease Models, AnimalFemaleMiceAntigens, CD19CD19 antigen, mouseInflammation MediatorsLeukocyte Common AntigensPtprc protein, mouseStat3 protein, mouseSTAT3 Transcription FactorCD19/CD45R/B220 B cellsExperimental autoimmune encephalomyelitisMultiple sclerosisProinflammatory mediatorsS3I-201STAT3 inhibitor

Identifiers

PMID42177676
PMCPMC13376081

What OpenQuestion holds

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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.