Evidence map›Paper›PMID 32915379›Full record

ReviewBioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy2020

Monoclonal Antibody-Based Therapies for Myasthenia Gravis.

Sawsan Alabbad, Mohanad AlGaeed, Patricia Sikorski, Henry J Kaminski

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 4 pooled it
2.0field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 4 syntheses or guidelines pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Review
  7. Article
  8. Article
  9. Evaluation of nonmotor symptoms in myasthenia gravis patients.Turkish journal of medical sciences · 2025
    Article
  10. Myasthenia gravis: the future is here.The Journal of clinical investigation · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. CD40-CD40L in Neurological Disease.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Review
  18. Advances and challenges in the treatment of myasthenia gravis.Therapeutic advances in neurological disorders · 2021
    Review
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

4 authors at 1 institution in 1 country.

Sawsan AlabbadDepartment of Neurology, George Washington University, 2150 Pennsylvania Avenue NW, Washington, DC, 20008, USA.
Mohanad AlGaeedDepartment of Neurology, George Washington University, 2150 Pennsylvania Avenue NW, Washington, DC, 20008, USA.
Patricia SikorskiDepartment of Neurology, George Washington University, 2150 Pennsylvania Avenue NW, Washington, DC, 20008, USA.
Henry J KaminskiDepartment of Neurology, George Washington University, 2150 Pennsylvania Avenue NW, Washington, DC, 20008, USA. HKaminski@mfa.gwu.edu.ORCID http://orcid.org/0000-0002-8195-0141
George Washington University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myasthenia gravis (MG) is an autoimmune, neuromuscular disorder that produces disabling weakness through a compromise of neuromuscular transmission. The disease fulfills strict criteria of an antibody-mediated disease. Close to 90% of patients have antibodies directed towards the nicotinic acetylcholine receptor (AChR) on the post-synaptic surface of skeletal muscle and another 5% to the muscle-specific kinase, which is involved in concentrating the AChR to the muscle surface of the neuromuscular junction. Conventional treatments of intravenous immunoglobulin and plasma exchange reduce autoantibody levels to produce their therapeutic effect, while prednisone and immunosuppressives do so by moderating autoantibody production. None of these treatments were specifically developed for MG and have a range of adverse effects. The extensive advances in monoclonal antibody technology allowing specific modulation of biological pathways has led to a tremendous increase in the potential treatment options. For MG, monoclonal antibody therapeutics target the effector mechanism of complement inhibition and the reduction of antibody levels by FcRn inhibition. Antibodies directed against CD20 and signaling pathways, which support lymphocyte activity, have been used to reduce autoantibody production. Thus far, only eculizumab, an antibody against C5, has reached the clinic. We review the present status of monoclonal antibody-based treatments for MG that have entered human testing and offer the promise to transform treatment of MG.

Indexed as

Myasthenia GravisReceptors, NicotinicAutoantibodiesHumansNeuromuscular JunctionAutoantibodiesReceptors, Nicotinic

Identifiers

PMID32915379
PMCPMC7484611
OpenAlexW3086923654

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.