Evidence map›Paper›PMID 42601022›Full record

ArticleCellular and molecular gastroenterology and hepatology2026

Suppressing α-1,6-Fucosyltransferase With a Novel Small Molecule Inhibitor Ameliorates Inflammation in Murine T-Cell-Mediated Colitis Models.

Akiko Asakura, Shinichiro Shinzaki, Yoshiyuki Manabe, Koki Hizume, Yuri Tsujii, Taku Tashiro, Takahiro Amano, Mizuki Tani, Yuriko Otake-Kasamoto, Takeo Yoshihara and 14 more

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In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 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

24 authors.

Akiko AsakuraDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Shinichiro ShinzakiDepartment of Gastroenterology, Hyogo Medical University School of Medicine, Hyogo, Japan.
Yoshiyuki ManabeDepartment of Chemistry, Graduate School of Science, The University of Osaka, Osaka, Japan; Department of Materials Engineering Science, Graduate School of Engineering Science, The University of Osaka, Osaka, Japan.
Koki HizumeDepartment of Chemistry, Graduate School of Science, The University of Osaka, Osaka, Japan.
Yuri TsujiiDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Taku TashiroDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Takahiro AmanoDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Mizuki TaniDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Yuriko Otake-KasamotoDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Takeo YoshiharaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Ryotaro UemaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Yoshiki TsujiiDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Hideki IijimaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan; Department of Gastroenterology, Osaka International Medical and Science Center, Osaka Keisatsu Hospital, Osaka, Japan.
Yoshihiro KamadaDepartment of Advanced Metabolic Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Daisuke OkuzakiNGS Core Facility, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Daisuke MotookaNGS Core Facility, Research Institute for Microbial Diseases, The University of Osaka, Osaka, Japan.
Tomohiko FukudaDivision of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Miyagi, Japan.
Takashi KudoLaboratory Animal Resource Center in Transborder Medical Research Center, and Department of Anatomy and Embryology, Institute of Medicine, University of Tsukuba, Ibaraki, Japan.
Satoru TakahashiLaboratory Animal Resource Center in Transborder Medical Research Center, and Department of Anatomy and Embryology, Institute of Medicine, University of Tsukuba, Ibaraki, Japan.
Jianguo GuDivision of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Miyagi, Japan.
Eiji MiyoshiDepartment of Molecular Biochemistry and Clinical Investigation, Graduate School of Medicine, The University of Osaka, Osaka, Japan.
Koichi FukaseDepartment of Chemistry, Graduate School of Science, The University of Osaka, Osaka, Japan; Institute for Radiation Sciences, The University of Osaka, Osaka, Japan.
Yoshito HayashiDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan. Electronic address: y.hayashi@gh.med.osaka-u.ac.jp.
Tetsuo TakeharaDepartment of Gastroenterology and Hepatology, Graduate School of Medicine, The University of Osaka, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsInflammatory bowel disease involves intractable intestinal inflammation often refractory to current pharmacotherapies. We investigated the therapeutic potential of a novel, orally available inhibitor targeting α-1,6-fucosyltransferase-the sole glycosyltransferase catalyzing core fucosylation of N-glycans in mammals-as an anti-inflammatory agent.

methodsα-1,6-Fucosyltransferase inhibitor efficacy was evaluated in 2 murine models: a trinitrobenzene sulfonic acid-induced colitis model and a naive CD4

resultsOral administration of the α-1,6-fucosyltransferase inhibitor effectively decreased T-cell core fucosylation and ameliorated trinitrobenzene sulfonic acid-induced colitis and colitis induced by adoptive T-cell transfer. These clinical effects were accompanied by decreased T helper 1 and 2 cytokine production from CD4

conclusionsα-1,6-Fucosyltransferase inhibition modulated T-cell core fucosylation and reduced inflammation in murine colitis models without apparent toxicity, indicating that targeting α-1,6-fucosyltransferase may offer a novel therapeutic approach for inflammatory bowel disease by disrupting proinflammatory T-cell responses.

Indexed as

Core FucosylationFUT8 InhibitorInflammatory Bowel DiseaseMurine Colitis

Identifiers

PMID42601022
PMCPMC13635695

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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.