Mechanism of action SOLIRIS® (eculizumab) is indicated for the treatment of refractory generalised myasthenia gravis (gMG) in patients aged 6 years and above who are anti-acetylcholine receptor (AChR) antibody-positive.1 Please consult the Summary of Product Characteristics prior to prescribing.
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In anti-AChR antibody-positive gMG, complement activation leads to damage at the neuromuscular junction2,4
AChR, acetylcholine receptor; C1q, complement component 1q; C3, complement component 3; C5, complement component 5; C5a, complement component 5a; C5b-9, complement component 5b-9; gMG, generalised myasthenia gravis; MAC, membrane attack complex; NMJ, neuromuscular junction.
Healthcare professionals are asked to report any suspected adverse reactions. Please report any adverse reactions via your national reporting system. Adverse events should also be reported to Alexion pharmaceuticals by the following link: https://contactazmedical.astrazeneca.com/
SOLIRIS® (eculizumab) EU Summary of Product Characteristics. Available from: https://www.ema.europa.eu/en/documents/product-information/soliris-epar-product-information_en.pdf. Last accessed: February 2024. Melzer N, et al. Clinical features, pathogenesis, and treatment of myasthenia gravis: a supplement to the Guidelines of the German Neurological Society. J Neurol. 2016;263(8):1473–1494. Phillips WD, et al. Pathogenesis of myasthenia gravis: update on disease types, models, and mechanisms. F1000Res. 2016;5:1513. Conti-Fine, et al. Myasthenia gravis: past, present, and future. J Clin Invest. 2006; 116:2843–2854. Engel AG, et al. Immune complexes (IgG and C3) at the motor end-plate in myasthenia gravis: ultrastructural and light microscopic localization and electrophysiologic correlations. Mayo Clin Proc. 1977;52(5):267–280. Sahashi K, et al. Ultrastructural localization of the terminal and lytic ninth complement component (C9) at the motor end-plate in myasthenia gravis. J Neuropathol Exp Neurol. 1980;39(2):160–172. Rother PR, et al. Discovery and development of the complement inhibitor eculizumab for the treatment of paroxysmal nocturnal hemoglobinuria. Nat Biotechnol. 2007;25(11):1256–1264. Guptill JT, et al. Current treatment, emerging translational therapies, and new therapeutics targets for autoimmune myasthenia gravis. Neurotherapeutics. 2016;13(1):118–131. Vidarsson G, et al. IgG subclasses and allotypes: from structure to effector functions. Front Immunol. 2014;5:520. Huijbers MG, et al. Pathogenic immune mechanisms at the neuromuscular synapse: the role of specific antibody-binding epitopes in myasthenia gravis. J Intern Med. 2014;275(1):12–26. Howard JF, et al. Myasthenia gravis: the role of complement at the neuromuscular junction. Ann N Y Acad Sci. 2018;1412(1):113–128.