Alemtuzumab Therapy in Multiple Sclerosis Management

Alemtuzumab is a humanised monoclonal antibody directed against the CD52 antigen on mature lymphocytes. In relapsing-remitting multiple sclerosis (RRMS), it is delivered as two annual intravenous courses, inducing profound lymphocyte depletion followed by phased immune repopulation. Clinical programmes have demonstrated durable reductions in relapse frequency, slowed disability progression and sustained radiological stabilisation without continuous dosing. Mechanistically, alemtuzumab not only eradicates autoreactive T and B cells but also promotes restoration of a more tolerogenic repertoire, marked by expanded regulatory subsets and diminished proinflammatory signatures. Its unique dosing schedule and long-term efficacy distinguish it within the therapeutic armamentarium for highly active RRMS. However, treatment carries risks of secondary autoimmunity—particularly thyroid disorders—and opportunistic infections, necessitating rigorous surveillance. Advances in understanding patterns of immune reconstitution and identification of predictive biomarkers are refining patient selection and risk‐management strategies, underscoring the global significance and practical application of alemtuzumab in precision neurology.

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Alemtuzumab Therapy in Multiple Sclerosis Management publication trend

The graph below shows the total number of articles in alemtuzumab therapy in multiple sclerosis management across all publications each year (not limited to Nature Index journals).

Technical terms

Alemtuzumab: A humanised monoclonal antibody targeting CD52 on lymphocytes, used to treat relapsing-remitting multiple sclerosis.

CD52: A glycoprotein expressed on the surface of mature T and B lymphocytes; the antigenic target of alemtuzumab.

Relapsing-remitting multiple sclerosis (RRMS): A form of MS characterised by discrete neurological relapses followed by periods of partial or complete recovery.

Immune reconstitution: The phased restoration and rebalancing of immune cell populations following depletion by therapy.

Regulatory T/B cells: Lymphocyte subsets that suppress aberrant immune activity and maintain self-tolerance.

Secondary autoimmunity: The onset of new autoimmune conditions—most often thyroid disorders—triggered by immune system alterations after treatment.

References

1. Immune reconstitution following alemtuzumab therapy is characterized by exhausted T cells, increased regulatory control of proinflammatory T cells and reduced B cell control. Frontiers in Immunology (2023).
2. A new computational workflow to guide personalized drug therapy. Journal of Biomedical Informatics (2023).
3. Repopulation of T, B, and NK cells following alemtuzumab treatment in relapsing-remitting multiple sclerosis. Journal of Neuroinflammation (2020).
4. Alemtuzumab in Multiple Sclerosis: Mechanism of Action and Beyond. International Journal of Molecular Sciences (2015).
5. Alemtuzumab in the long-term treatment of relapsing-remitting multiple sclerosis: an update on the clinical trial evidence and data from the real world. Therapeutic Advances in Neurological Disorders (2017).
6. Long-term efficacy and safety of alemtuzumab in patients with RRMS: 12-year follow-up of CAMMS223. Journal of Neurology (2020).
7. Alemtuzumab-Induced Thyroid Dysfunction Exhibits Distinctive Clinical and Immunological Features. The Journal of Clinical Endocrinology & Metabolism (2018).
8. Listeria Meningitis Complicating Alemtuzumab Treatment in Multiple Sclerosis—Report of Two Cases. International Journal of Molecular Sciences (2015).
9. Restoration of regulatory B cell deficiency following alemtuzumab therapy in patients with relapsing multiple sclerosis. Journal of Neuroinflammation (2018).