Alemtuzumab: the advantages and challenges of a novel therapy in MS.

Til Menge, Olaf Stüve, Bernd C. Kieseier, Hans Peter Hartung

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Our understanding of the pathogenesis of multiple sclerosis has increased considerably, leading to the development of novel therapeutic approaches and compounds. Several agents have undergone clinical testing and have recently received market authorization or are being evaluated for approval. Alemtuzumab is a humanized monoclonal antibody that rapidly depletes CD52+ cells of the lymphoid lineage from peripheral blood, but spares lymphoid precursor cells. Clinical efficacy and safety data from clinical phase II and III trials-all using interferon-β-1a as active comparator-are summarized and placed in perspective. This review further analyzes the differential reconstitution of T and B cells as a potential mode of action and the pathogenic link to treatment-emergent secondary autoimmune conditions. Given recent positive opinions by regulatory agencies, this new drug will be positioned for the treatment of active relapsing-remitting multiple sclerosis and enlarge our therapeutic armamentarium.

Original languageEnglish (US)
Pages (from-to)87-97
Number of pages11
JournalNeurology
Volume83
Issue number1
DOIs
StatePublished - 2014

Fingerprint

Antibodies, Monoclonal, Humanized
Relapsing-Remitting Multiple Sclerosis
Phase III Clinical Trials
Phase II Clinical Trials
Cell Lineage
Interferons
Action Potentials
Multiple Sclerosis
B-Lymphocytes
Lymphocytes
T-Lymphocytes
Safety
Therapeutics
Pharmaceutical Preparations
alemtuzumab
Cells
Therapy
Testing
Precursor
Blood

ASJC Scopus subject areas

  • Clinical Neurology
  • Arts and Humanities (miscellaneous)

Cite this

Alemtuzumab : the advantages and challenges of a novel therapy in MS. / Menge, Til; Stüve, Olaf; Kieseier, Bernd C.; Hartung, Hans Peter.

In: Neurology, Vol. 83, No. 1, 2014, p. 87-97.

Research output: Contribution to journalArticle

Menge, Til ; Stüve, Olaf ; Kieseier, Bernd C. ; Hartung, Hans Peter. / Alemtuzumab : the advantages and challenges of a novel therapy in MS. In: Neurology. 2014 ; Vol. 83, No. 1. pp. 87-97.
@article{c678d3b816db41b78d9bb1119ba31664,
title = "Alemtuzumab: the advantages and challenges of a novel therapy in MS.",
abstract = "Our understanding of the pathogenesis of multiple sclerosis has increased considerably, leading to the development of novel therapeutic approaches and compounds. Several agents have undergone clinical testing and have recently received market authorization or are being evaluated for approval. Alemtuzumab is a humanized monoclonal antibody that rapidly depletes CD52+ cells of the lymphoid lineage from peripheral blood, but spares lymphoid precursor cells. Clinical efficacy and safety data from clinical phase II and III trials-all using interferon-β-1a as active comparator-are summarized and placed in perspective. This review further analyzes the differential reconstitution of T and B cells as a potential mode of action and the pathogenic link to treatment-emergent secondary autoimmune conditions. Given recent positive opinions by regulatory agencies, this new drug will be positioned for the treatment of active relapsing-remitting multiple sclerosis and enlarge our therapeutic armamentarium.",
author = "Til Menge and Olaf St{\"u}ve and Kieseier, {Bernd C.} and Hartung, {Hans Peter}",
year = "2014",
doi = "10.1212/WNL.0000000000000540",
language = "English (US)",
volume = "83",
pages = "87--97",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Alemtuzumab

T2 - the advantages and challenges of a novel therapy in MS.

AU - Menge, Til

AU - Stüve, Olaf

AU - Kieseier, Bernd C.

AU - Hartung, Hans Peter

PY - 2014

Y1 - 2014

N2 - Our understanding of the pathogenesis of multiple sclerosis has increased considerably, leading to the development of novel therapeutic approaches and compounds. Several agents have undergone clinical testing and have recently received market authorization or are being evaluated for approval. Alemtuzumab is a humanized monoclonal antibody that rapidly depletes CD52+ cells of the lymphoid lineage from peripheral blood, but spares lymphoid precursor cells. Clinical efficacy and safety data from clinical phase II and III trials-all using interferon-β-1a as active comparator-are summarized and placed in perspective. This review further analyzes the differential reconstitution of T and B cells as a potential mode of action and the pathogenic link to treatment-emergent secondary autoimmune conditions. Given recent positive opinions by regulatory agencies, this new drug will be positioned for the treatment of active relapsing-remitting multiple sclerosis and enlarge our therapeutic armamentarium.

AB - Our understanding of the pathogenesis of multiple sclerosis has increased considerably, leading to the development of novel therapeutic approaches and compounds. Several agents have undergone clinical testing and have recently received market authorization or are being evaluated for approval. Alemtuzumab is a humanized monoclonal antibody that rapidly depletes CD52+ cells of the lymphoid lineage from peripheral blood, but spares lymphoid precursor cells. Clinical efficacy and safety data from clinical phase II and III trials-all using interferon-β-1a as active comparator-are summarized and placed in perspective. This review further analyzes the differential reconstitution of T and B cells as a potential mode of action and the pathogenic link to treatment-emergent secondary autoimmune conditions. Given recent positive opinions by regulatory agencies, this new drug will be positioned for the treatment of active relapsing-remitting multiple sclerosis and enlarge our therapeutic armamentarium.

UR - http://www.scopus.com/inward/record.url?scp=84904020925&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84904020925&partnerID=8YFLogxK

U2 - 10.1212/WNL.0000000000000540

DO - 10.1212/WNL.0000000000000540

M3 - Article

C2 - 24920854

AN - SCOPUS:84904020925

VL - 83

SP - 87

EP - 97

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 1

ER -