ReviewCells2019
Mechanism of Siponimod: Anti-Inflammatory and Neuroprotective Mode of Action.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled 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.
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
54 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Immunomodulators and immunosuppressants for relapsing-remitting multiple sclerosis: a network meta-analysis.The Cochrane database of systematic reviews · 2024Pooled it
- Intracerebral Hemorrhage Induces Monocyte TNF Signaling in Patients That Is Suppressed by BAF312.Annals of clinical and translational neurology · 2026Article
- Structural Characterization, Toxicity Assessment and Molecular Modeling of Forced Degradation Products of Siponimod.International journal of molecular sciences · 2026Article
- Rethinking MS Therapeutics: From Disease Pathogenesis Mechanisms to AI-Driven Drug Discovery.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Review
- Intracerebral hemorrhage induces monocyte TNF signaling that is suppressed by Siponimod (BAF312): a single-cell transcriptomics study in patients.medRxiv : the preprint server for health sciences · 2026Article
- Chronic Neuroplasticity Changes Following Neurotropic Viral Infection: Mechanisms and Implications.Cellular and molecular neurobiology · 2025Review
- Altered Lipid Metabolism in CNS Demyelination and Remyelination Are Key Elements Driving Progressive MS.International journal of molecular sciences · 2025Review
- TNFR2 Agonism: Basic Science and Promising Treatment for Multiple Sclerosis and Related Diseases.International journal of molecular sciences · 2025Review
- Current landscape of innovative drug development and regulatory support in China.Signal transduction and targeted therapy · 2025Review
- Article
- Siponimod supports remyelination in the non-supportive environment.Scientific reports · 2025Article
- Impact of Siponimod on Clinical and Radiological Parameters of Secondary Progressive Multiple Sclerosis: A Real-World Prospective Study.Journal of clinical neurology (Seoul, Korea) · 2024Article
- Siponimod treatment response shows partial BDNF dependency in multiple sclerosis models.Scientific reports · 2024Article
- Siponimod Attenuates Neuronal Cell Death Triggered by Neuroinflammation via NFκB and Mitochondrial Pathways.International journal of molecular sciences · 2024Article
- CNS cell-derived exosome signatures as blood-based biomarkers of neurodegenerative diseases.Frontiers in neuroscience · 2024Review
- Investigating the Mitoprotective Effects of S1P Receptor Modulators Ex Vivo Using a Novel Semi-Automated Live Imaging Set-Up.International journal of molecular sciences · 2023Article
- Anti-inflammatory Effects of Siponimod in a Mouse Model of Excitotoxicity-Induced Retinal Injury.Molecular neurobiology · 2023Article
- Imidazole-based sphingosine-1-phosphate transporter Spns2 inhibitors.Bioorganic & medicinal chemistry letters · 2023Article
- Article
- Central Versus Peripheral Drug Exposure Ratio, a Key Differentiator for Siponimod Over Fingolimod?Neurology and therapy · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a neuroinflammatory disorder of the central nervous system (CNS), and represents one of the main causes of disability in young adults. On the histopathological level, the disease is characterized by inflammatory demyelination and diffuse neurodegeneration. Although on the surface the development of new inflammatory CNS lesions in MS may appear consistent with a primary recruitment of peripheral immune cells, questions have been raised as to whether lymphocyte and/or monocyte invasion into the brain are really at the root of inflammatory lesion development. In this review article, we discuss a less appreciated inflammation-neurodegeneration interplay, that is: Neurodegeneration can trigger the formation of new, focal inflammatory lesions. We summarize old and recent findings suggesting that new inflammatory lesions develop at sites of focal or diffuse degenerative processes within the CNS. Such a concept is discussed in the context of the EXPAND trial, showing that siponimod exerts anti-inflammatory and neuroprotective activities in secondary progressive MS patients. The verification or rejection of such a concept is vital for the development of new therapeutic strategies for progressive MS.
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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.