ReviewDrug design, development and therapy2014
Molecular pharmacodynamics of new oral drugs used in the treatment of multiple sclerosis.
Review in Drug design, development and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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.
Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Targeting of kinases to treat neurodegenerative diseases.Pharmacological reviews · 2026Review
- Inhibition of Sphingosine-1-Phosphate Receptor 2 (S1PBiomolecules & therapeutics · 2025Article
- Identification of novel antiviral host factors by functional gene expression analysis using in vitro HBV infection assay systems.PloS one · 2025Article
- Alopecia associated with dimethyl fumarate treatment for multiple sclerosis.Wiener medizinische Wochenschrift (1946) · 2023Article
- New and Old Horizons for an Ancient Drug: Pharmacokinetics, Pharmacodynamics, and Clinical Perspectives of Dimethyl Fumarate.Pharmaceutics · 2022Review
- Thyroid Disorders in Patients Treated with Dimethyl Fumarate for Multiple Sclerosis: A Retrospective Observational Study.Antioxidants (Basel, Switzerland) · 2022Article
- Sphingosine-1-Phosphate Signaling in Ischemic Stroke: From Bench to Bedside and Beyond.Frontiers in cellular neuroscience · 2021Review
- Nitrated fatty acids: from diet to disease.Current opinion in physiology · 2019Article
- Acute exacerbation of Hashimoto's thyroiditis in a patient treated with dimethyl fumarate for multiple sclerosis: A case report.Medicine · 2019Article
- Experimental Autoimmune Encephalomyelitis (EAE)-Induced Elevated Expression of the E1 Isoform of Methyl CpG Binding Protein 2 (MeCP2E1): Implications in Multiple Sclerosis (MS)-Induced Neurological Disability and Associated Myelin Damage.International journal of molecular sciences · 2017Article
- Nogo-A Antibodies for Progressive Multiple Sclerosis.CNS drugs · 2017Review
- Sphingosine 1-phosphate receptor modulation suppresses pathogenic astrocyte activation and chronic progressive CNS inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- From Leflunomide to Teriflunomide: Drug Development and Immunosuppressive Oral Drugs in the Treatment of Multiple Sclerosis.Current neuropharmacology · 2017Review
- [Monitoring of blood parameters under course-modified MS therapy : Substance-specific relevance and current recommendations for action].Der Nervenarzt · 2016Review
- Antidepressant activity of fingolimod in mice.Pharmacology research & perspectives · 2015Article
- Inflammation, Iron, Energy Failure, and Oxidative Stress in the Pathogenesis of Multiple Sclerosis.Oxidative medicine and cellular longevity · 2015Review
- Visual detection of glial cell line-derived neurotrophic factor based on a molecular translator and isothermal strand-displacement polymerization reaction.Drug design, development and therapy · 2015Article
- Varicella-zoster virus infections in patients treated with fingolimod: risk assessment and consensus recommendations for management.JAMA neurology · 2015Article
- Effectiveness and safety of dimethyl fumarate in progressive multiple sclerosis.Multiple sclerosis journal - experimental, translational and clinicalArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
New oral drugs have considerably enriched the therapeutic armamentarium for the treatment of multiple sclerosis. This review focuses on the molecular pharmacodynamics of fingolimod, dimethyl fumarate (BG-12), laquinimod, and teriflunomide. We specifically comment on the action of these drugs at three levels: 1) the regulation of the immune system; 2) the permeability of the blood-brain barrier; and 3) the central nervous system. Fingolimod phosphate (the active metabolite of fingolimod) has a unique mechanism of action and represents the first ligand of G-protein-coupled receptors (sphingosine-1-phosphate receptors) active in the treatment of multiple sclerosis. Dimethyl fumarate activates the nuclear factor (erythroid-derived 2)-related factor 2 pathway of cell defense as a result of an initial depletion of reduced glutathione. We discuss how this mechanism lies on the border between cell protection and toxicity. Laquinimod has multiple (but less defined) mechanisms of action, which make the drug slightly more effective on disability progression than on annualized relapse rate in clinical studies. Teriflunomide acts as a specific inhibitor of the de novo pyrimidine biosynthesis. We also discuss new unexpected mechanisms of these drugs, such as the induction of brain-derived neurotrophic factor by fingolimod and the possibility that laquinimod and teriflunomide regulate the kynurenine pathway of tryptophan metabolism.
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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.