Evidence map›Paper›PMID 27793992›Full record

ArticleThe Journal of biological chemistry2016

Identification of Iguratimod as an Inhibitor of Macrophage Migration Inhibitory Factor (MIF) with Steroid-sparing Potential.

Joshua Bloom, Christine Metz, Saisha Nalawade, Julian Casabar, Kai Fan Cheng, Mingzhu He, Barbara Sherry, Thomas Coleman, Thomas Forsthuber, Yousef Al-Abed

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
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

33 citing papers in PubMed, 73 citations in OpenAlex.

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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 at 5 institutions in 3 countries.

Joshua BloomFrom the Hofstra-Northwell School of Medicine, Hempstead, New York 11549, jbloom2@northwell.edu.
Christine MetzFrom the Hofstra-Northwell School of Medicine, Hempstead, New York 11549.
Saisha Nalawadethe Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249.
Julian Casabarthe Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249.
Kai Fan Chengthe Centers for Molecular Innovation.
Mingzhu Hethe Centers for Molecular Innovation.
Barbara SherryFrom the Hofstra-Northwell School of Medicine, Hempstead, New York 11549.
Thomas Colemanthe Office of Technology Transfer, The Feinstein Institute for Medical Research, Manhasset, New York 11030, and.
Thomas Forsthuberthe Department of Biology, University of Texas at San Antonio, San Antonio, Texas 78249.
Yousef Al-AbedFrom the Hofstra-Northwell School of Medicine, Hempstead, New York 11549, yalabed@northwell.edu.
The Centers · USThe University of Texas at San Antonio · USInstitute of Biomedical Science · GBInstitut thématique Immunologie, inflammation, infectiologie et microbiologie · FROffice of Technology Transfer · US

Funding

Developing Small MIF Inhibitors for Rheumatoid ArthritisR43AR062401 · NIAMS · BIOMEDICAL RESEARCH MODELS, INC. · PI COLEMAN, THOMAS R., GRANT, CHRISTIAN · 2012 to 2013
$452k
MIF inhibition as a novel treatment for autoimmune myocarditisR21AI110771 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI FORSTHUBER, THOMAS G. · 2014 to 2015
$404k
NIAID NIH HHS R21 AI110771NIAMS NIH HHS R43 AR062401
6 · The paper itself

Abstract

Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine that has been implicated in a broad range of inflammatory and oncologic diseases. MIF is unique among cytokines in terms of its release profile and inflammatory role, notably as an endogenous counter-regulator of the anti-inflammatory effects of glucocorticoids. In addition, it exhibits a catalytic tautomerase activity amenable to the design of high affinity small molecule inhibitors. Although several classes of these compounds have been identified, biologic characterization of these molecules remains a topic of active investigation. In this study, we used in vitro LPS-driven assays to characterize representative molecules from several classes of MIF inhibitors. We determined that MIF inhibitors exhibit distinct profiles of anti-inflammatory activity, especially with regard to TNFα. We further investigated a molecule with relatively low anti-inflammatory activity, compound T-614 (also known as the anti-rheumatic drug iguratimod), and found that, in addition to exhibiting selective MIF inhibition in vitro and in vivo, iguratimod also has additive effects with glucocorticoids. Furthermore, we found that iguratimod synergizes with glucocorticoids in attenuating experimental autoimmune encephalitis, a model of multiple sclerosis. Our work identifies iguratimod as a valuable new candidate for drug repurposing to MIF-relevant diseases, including multiple sclerosis.

Indexed as

AnimalsCell Line, TumorChromonesEncephalomyelitis, Autoimmune, ExperimentalGlucocorticoidsHumansIntramolecular OxidoreductasesLipopolysaccharidesMacrophage Migration-Inhibitory FactorsMaleMiceMice, Inbred BALB CMultiple SclerosisSulfonamidesTumor Necrosis Factor-alphaChromonesGlucocorticoidsiguratimodIntramolecular OxidoreductasesLipopolysaccharidesMacrophage Migration-Inhibitory FactorsMIF protein, humanSulfonamidesTumor Necrosis Factor-alphadrug discoverydrug screeningglucocorticoidiguratimodinflammationMIFsubstrate specificity

Identifiers

PMID27793992
PMCPMC5159510
OpenAlexW2540884398

What OpenQuestion holds

Textmetadata
Read underepoch 390

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 OpenQuestion graph.