Evidence map›Paper›PMID 24740824›Full record

ReviewDrugs2014

Teriflunomide and its mechanism of action in multiple sclerosis.

Amit Bar-Or, Andrew Pachner, Francoise Menguy-Vacheron, Johanne Kaplan, Heinz Wiendl

Registry-linked trialAbstract readReview
In one paragraph

Review in Drugs, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03464448 (Mechanistic Studies of Teriflunomide in Relapsing Remitting Multiple Sclerosis), which is not on this map. Cited by 173 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed, 1 pooled it
–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.

NCT03464448 completednot on this mapstarted 2018, after this paper: background citation

Mechanistic Studies of Teriflunomide in Relapsing Remitting Multiple Sclerosis: Regulatory B Lymphocytes as Central Mediators of the Therapeutic Effects of Teriflunomide in MS

TypeobservationalSponsorUniversity of MichiganRan2018 to 2021Enrolled30ConditionsRelapsing Remitting Multiple SclerosisArmsTeriflunomide
3 · Its place in the literature

Who cites it

173 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  4. Trial
  5. Review
  6. Article
  7. Immune reconstitution and tolerance-inducing therapies as promising therapeutic approaches in multiple sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  8. Article
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  11. Article
  12. Review
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  19. CDH1 Orchestrates Anabolic Events to Promote Cell Cycle Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  20. Article

113 more citing papers are in PubMed but not listed here.

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

5 authors.

Amit Bar-OrDepartment of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Canada.
Andrew Pachner
Francoise Menguy-Vacheron
Johanne Kaplan
Heinz Wiendl

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment of multiple sclerosis (MS) is challenging: disease-modifying treatments (DMTs) must both limit unwanted immune responses associated with disease initiation and propagation (as T and B lymphocytes are critical cellular mediators in the pathophysiology of relapsing MS), and also have minimal adverse impact on normal protective immune responses. In this review, we summarize key preclinical and clinical data relating to the proposed mechanism of action of the recently approved DMT teriflunomide in MS. Teriflunomide selectively and reversibly inhibits dihydro-orotate dehydrogenase, a key mitochondrial enzyme in the de novo pyrimidine synthesis pathway, leading to a reduction in proliferation of activated T and B lymphocytes without causing cell death. Results from animal experiments modelling the immune activation implicated in MS demonstrate reductions in disease symptoms with teriflunomide treatment, accompanied by reduced central nervous system lymphocyte infiltration, reduced axonal loss, and preserved neurological functioning. In agreement with the results obtained in these model systems, phase 3 clinical trials of teriflunomide in patients with MS have consistently shown that teriflunomide provides a therapeutic benefit, and importantly, does not cause clinical immune suppression. Taken together, these data demonstrate how teriflunomide acts as a selective immune therapy for patients with MS.

Indexed as

AnimalsB-LymphocytesCell ProliferationCrotonatesDihydroorotate DehydrogenaseEnzyme InhibitorsHumansHydroxybutyratesImmunologic FactorsMultiple SclerosisNitrilesOxidoreductases Acting on CH-CH Group DonorsT-LymphocytesToluidinesCrotonatesDihydroorotate DehydrogenaseEnzyme InhibitorsHydroxybutyratesImmunologic FactorsNitrilesOxidoreductases Acting on CH-CH Group DonorsteriflunomideToluidines

Identifiers

PMID24740824
PMCPMC4003395

What OpenQuestion holds

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Registered trials

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.