{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T16:19:21Z","timestamp":1791389961080,"version":"4.3.3"},"reference-count":37,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T00:00:00Z","timestamp":1763510400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T00:00:00Z","timestamp":1763510400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ann Clin Transl Neurol"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To 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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this prospective, exploratory real\u2010world study CH50 and AH50, eculizumab and ravulizumab blood levels were assessed in patients with acetylcholine\u2010receptor\u2010antibody (AChR\u2010ab) positive gMG. Patients were either pretreated with eculizumab or C5\u2010inhibitor na\u00efve. Samples were collected before the next infusion (end\u2010of\u2010dose). Laboratory data were correlated with patient\u2010reported subjective duration of the ravulizumab effect.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Overall, 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%\u20132%] versus 5% [3%\u20139%]; Cohen's\n                      <jats:italic>d<\/jats:italic>\n                      2.2 [95% CI 1.5\u20132.8]). Patients who discontinued ravulizumab due to insufficient effects (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200919; 33%) had higher median AH50 levels than those who continued (7% [4%\u201313%] versus 5% [3%\u20138%]; Cohen's\n                      <jats:italic>d<\/jats:italic>\n                      \u22120.9 [95% CI \u22121.3 to \u22120.4]). In 81% (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200946) of patients, the therapeutic effect of ravulizumab diminished before the subsequent infusion after the standard 8\u2010week interval. Higher AH50 levels were correlated with earlier symptom recurrence.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Our 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.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/acn3.70251","type":"journal-article","created":{"date-parts":[[2025,11,20]],"date-time":"2025-11-20T04:59:12Z","timestamp":1763614752000},"page":"688-699","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Inhibition of Classical and Alternative Complement Pathway by Ravulizumab and Eculizumab"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5746-068X","authenticated-orcid":false,"given":"Lea","family":"Gerischer","sequence":"first","affiliation":[{"name":"Department of Neurology With Experimental Neurology and Integrated Myasthenia Center Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin, Corporate Member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4t Zu Berlin  Berlin Germany"},{"name":"Neuroscience Clinical Research Center 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