Evidence map›Paper›PMID 41261457›Full record

ArticleAnnals of clinical and translational neurology2026

Inhibition of Classical and Alternative Complement Pathway by Ravulizumab and Eculizumab.

Lea Gerischer, Frauke Stascheit, Maximilian Mönch, Paolo Doksani, Carla Dusemund, Meret Herdick, Philipp Mergenthaler, Maike Stein, Amani Suboh, Jutta Schröder-Braunstein and 5 more

Abstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
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  4. Observational
  5. Review
  6. Article
  7. CFDFrontiers in immunology · 2026
    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

15 authors.

Lea GerischerDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0001-5746-068X
Frauke StascheitDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0001-5306-7880
Maximilian MönchInstitute of Biometry and Clinical Epidemiology, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0009-0006-6267-5400
Paolo DoksaniDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0009-0009-5381-5995
Carla DusemundDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0001-6477-8901
Meret HerdickDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0003-0119-9499
Philipp MergenthalerDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0002-9753-6711
Maike SteinDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0009-0002-1514-8385
Amani SubohDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0009-0002-8128-9178
Jutta Schröder-BraunsteinLaboratory of Complement Diagnostics, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0002-4296-9026
Guido WabnitzLaboratory of Complement Diagnostics, Institute of Immunology, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0001-5101-9885
Jan D LünemannDepartment of Neurology, University Hospital Münster, Münster, Germany.ORCID 0000-0002-3007-708X
Sophie LehnererDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0001-9007-027X
Sarah HoffmannDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0001-9549-2594
Andreas MeiselDepartment of Neurology With Experimental Neurology and Integrated Myasthenia Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität Zu Berlin, Berlin, Germany.ORCID 0000-0001-7233-5342

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo explore the feasibility of classical (CH50) and alternative (AH50) complement pathway activity as potential biomarkers for treatment guidance and monitoring during therapy with ravulizumab in patients with generalized myasthenia gravis (gMG) and compare these to therapeutic drug monitoring under eculizumab.

methodsIn this prospective, exploratory real-world study CH50 and AH50, eculizumab and ravulizumab blood levels were assessed in patients with acetylcholine-receptor-antibody (AChR-ab) positive gMG. Patients were either pretreated with eculizumab or C5-inhibitor naïve. Samples were collected before the next infusion (end-of-dose). Laboratory data were correlated with patient-reported subjective duration of the ravulizumab effect.

resultsOverall, 61 patients were enrolled. At the end of their respective dosing interval, median AH50 levels were more strongly suppressed with eculizumab than with ravulizumab (1% [0%-2%] versus 5% [3%-9%]; Cohen's d 2.2 [95% CI 1.5-2.8]). Patients who discontinued ravulizumab due to insufficient effects (n = 19; 33%) had higher median AH50 levels than those who continued (7% [4%-13%] versus 5% [3%-8%]; Cohen's d -0.9 [95% CI -1.3 to -0.4]). In 81% (n = 46) of patients, the therapeutic effect of ravulizumab diminished before the subsequent infusion after the standard 8-week interval. Higher AH50 levels were correlated with earlier symptom recurrence.

interpretationOur results indicate potential differences in the ability of eculizumab and ravulizumab to suppress complement pathway activity through their respective dosing intervals. Additionally, higher AH50 levels might be a potential biomarker to predict poor therapy response and faster wearing off of ravulizumab's effect. However, these findings need to be validated in large multicenter studies.

Indexed as

Antibodies, Monoclonal, HumanizedComplement Inactivating AgentsComplement Pathway, AlternativeMyasthenia GravisAdultAgedDrug MonitoringFemaleHumansMaleMiddle AgedProspective StudiesAntibodies, Monoclonal, HumanizedComplement Inactivating Agentseculizumabravulizumabcomplement inhibitioncomplement pathwayeculizumabmyasthenia gravisravulizumab

Identifiers

PMID41261457
PMCPMC13071113

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Registered trials

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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.