Evidence map›Paper›PMID 33178636›Full record

ReviewImmunoTargets and therapy2020

Emerging Role of Fractalkine in the Treatment of Rheumatic Diseases.

Yoshiya Tanaka, Kana Hoshino-Negishi, Yoshikazu Kuboi, Fumitoshi Tago, Nobuyuki Yasuda, Toshio Imai

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in ImmunoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02960438 (A Dose Response Study of E6011 in Subjects With Rheumatoid Arthritis Inadequately Responding to Methotrexate), which is not on this map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 21% 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.

NCT02960438 phase2completednot on this map

A Dose Response Study of E6011 in Subjects With Rheumatoid Arthritis Inadequately Responding to Methotrexate

TypeinterventionalSponsorEisai Co., Ltd.Ran2016 to 2019Enrolled273ConditionsRheumatoid ArthritisArmsE6011, Placebo
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Article
  7. Review
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  10. Observational
  11. Review
  12. Article
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  15. Review
  16. Article
  17. Article
  18. Fractalkine Signalling (CXJournal of clinical medicine · 2023
    Review
  19. Article
  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

6 authors at 3 institutions in 1 country.

Yoshiya TanakaFirst Department of Internal Medicine, University of Occupational and Environmental Health, Fukuoka, Japan.ORCID 0000-0002-0807-7139
Kana Hoshino-NegishiKAN Research Institute Inc, Hyogo, Japan.
Yoshikazu KuboiKAN Research Institute Inc, Hyogo, Japan.
Fumitoshi TagoEisai Co. Ltd., Tokyo, Japan.
Nobuyuki YasudaKAN Research Institute Inc, Hyogo, Japan.
Toshio ImaiKAN Research Institute Inc, Hyogo, Japan.ORCID 0000-0002-4022-1962
KAN Research Institute · JPEisai (Japan) · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disorder that affects joints and is characterized by synovial hyperplasia and bone erosion associated with neovascularization and infiltration of proinflammatory cells. The introduction of biological disease-modifying anti-rheumatic drugs has dramatically changed the treatment of RA over the last 20 years. However, fewer than 50% of RA patients enter remission, and 10-15% are treatment refractory. There is currently no cure for RA. Fractalkine (FKN, also known as CX3CL1) is a cell membrane-bound chemokine that can be induced on activated vascular endothelial cells. FKN has dual functions as a cell adhesion molecule and a chemoattractant. FKN binds specifically to the chemokine receptor CX3CR1, which is selectively expressed on subsets of immune cells such as patrolling monocytes and killer lymphocytes. The FKN-CX3CR1 axis is thought to play important roles in the initiation of the inflammatory cascade and can contribute to exacerbation of tissue injury in inflammatory diseases. Accordingly, studies in animal models have shown that inhibition of the FKN-CX3CR1 axis not only improves rheumatic diseases but also reduces associated complications, such as pulmonary fibrosis and cardiovascular disease. Recently, a humanized anti-FKN monoclonal antibody, E6011, showed promising efficacy with a dose-dependent clinical response and favorable safety profile in a Phase 2 clinical trial in patients with RA (NCT02960438). Taken together, the preclinical and clinical results suggest that E6011 may represent a new therapeutic approach for rheumatic diseases by suppressing a major contributor to inflammation and mitigating concomitant cardiovascular and fibrotic diseases. In this review, we describe the role of the FKN-CX3CR1 axis in rheumatic diseases and the therapeutic potential of anti-FKN monoclonal antibodies to fulfill unmet clinical needs.

Indexed as

CD16+ monocyteCX3CR1fractalkinehumanized anti-fractalkine monoclonal antibody (E6011)rheumatic diseases

Identifiers

PMID33178636
PMCPMC7649223
OpenAlexW3097432564

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.