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Background: Complement activation may promote atherosclerosis. Yet, data on the to which extent complement, and more specifically the alternative complement pathway, is activated in patients with carotid atherosclerosis and related to adverse outcome in these patients, are scarce.

Methods And Results: We measured, by ELISA, plasma levels of factor D, properdin, C3bBbP (C3 convertase), and factor H in patients with advanced carotid atherosclerosis in a (n=324) and in a (n=206) cohort in relation to adverse outcome (mean follow-up 7.

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Invasive meningococcal diseases (IMD) caused by Neisseria meningitidis are generally rare. They affect mostly selected age categories and risk groups of patients (in terms of age, comorbidities, or applied therapy), and the immune system and its defects may play an important modifying role. Meningococcal infections could be the first and only clinical sign of unrecognised immunodeficiency.

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Article Synopsis
  • Tarperprumig (ALXN1820) is a bispecific antibody designed to treat conditions caused by dysregulated activity in the complement alternative pathway, usable via small volume injections either under the skin or intravenously.
  • It consists of two variable domains that target properdin and human serum albumin, showing a high binding affinity and forming a stable complex.
  • The antibody effectively inhibits key processes related to complement pathway activation and is currently undergoing clinical development for relevant disorders.
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Article Synopsis
  • * Deficiencies or abnormalities in complement proteins can lead to health issues like increased infection risk, autoimmune diseases, and thrombosis, depending on which protein is affected.
  • * Diagnosis is done through functional assays to assess overall complement activity and specific factors, while management includes vaccinations, antibiotics, and monitoring for autoimmune conditions.
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