Evidence map›Paper›PMID 29608575›Full record

ArticlePloS one2018

Ozanimod (RPC1063), a selective S1PR1 and S1PR5 modulator, reduces chronic inflammation and alleviates kidney pathology in murine systemic lupus erythematosus.

Kristen R Taylor Meadows, Marcos W Steinberg, Bryan Clemons, Matthew E Stokes, Gregory J Opiteck, Robert Peach, Fiona L Scott

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Sphingolipid signaling in kidney diseases.American journal of physiology. Renal physiology · 2025
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  11. Cenerimod, a selective S1PArthritis research & therapy · 2021
    Article
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  14. Article
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  16. Review
  17. Article
  18. Deletion ofFrontiers in immunology · 2020
    Article
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  20. Article
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

7 authors.

Kristen R Taylor MeadowsReceptos, a wholly owned subsidiary of Celgene Corporation, San Diego, California, United States of America.
Marcos W SteinbergReceptos, a wholly owned subsidiary of Celgene Corporation, San Diego, California, United States of America.
Bryan ClemonsReceptos, a wholly owned subsidiary of Celgene Corporation, San Diego, California, United States of America.
Matthew E StokesCelgene Corporation, Seattle, Washington, United States of America.
Gregory J OpiteckReceptos, a wholly owned subsidiary of Celgene Corporation, San Diego, California, United States of America.
Robert PeachReceptos, a wholly owned subsidiary of Celgene Corporation, San Diego, California, United States of America.
Fiona L ScottReceptos, a wholly owned subsidiary of Celgene Corporation, San Diego, California, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ozanimod (RPC1063) is a specific and potent small molecule modulator of the sphingosine 1-phosphate receptor 1 (S1PR1) and receptor 5 (S1PR5), which has shown therapeutic benefit in clinical trials of relapsing multiple sclerosis and ulcerative colitis. Ozanimod and its active metabolite, RP-101075, exhibit a similar specificity profile at the S1P receptor family in vitro and pharmacodynamic profile in vivo. The NZBWF1 mouse model was used in therapeutic dosing mode to assess the potential benefit of ozanimod and RP-101075 in an established animal model of systemic lupus erythematosus. Compared with vehicle-treated animals, ozanimod and RP-101075 reduced proteinuria over the duration of the study and serum blood urea nitrogen at termination. Additionally, ozanimod and RP-101075 reduced kidney disease in a dose-dependent manner, as measured by histological assessment of mesangial expansion, endo- and exo-capillary proliferation, interstitial infiltrates and fibrosis, glomerular deposits, and tubular atrophy. Further exploration into gene expression changes in the kidney demonstrate that RP-101075 also significantly reduced expression of fibrotic and immune-related genes in the kidneys. Of note, RP-101075 lowered the number of plasmacytoid dendritic cells, a major source of interferon alpha in lupus patients, and reduced all B and T cell subsets in the spleen. Given the efficacy demonstrated by ozanimod and its metabolite RP-101075 in the NZBWF1 preclinical animal model, ozanimod may warrant clinical evaluation as a potential treatment for systemic lupus erythematosus.

Indexed as

AnimalsDisease Models, AnimalDNAFemaleGene Expression RegulationImmunoglobulin GIndansInflammationKidneyKidney DiseasesKidney Function TestsLupus Erythematosus, SystemicMiceOxadiazolesReceptor, Interferon alpha-betaReceptors, LysosphingolipidDNAIfnar1 protein, mouseImmunoglobulin GIndansOxadiazolesozanimodReceptor, Interferon alpha-betaReceptors, LysosphingolipidS1pr1 protein, mouseSphingosine-1-Phosphate Receptors

Identifiers

PMID29608575
PMCPMC5880347
OpenAlexW2796268097

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.