rovelizumab

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rovelizumab

GtoPdb Ligand ID: 9598

Synonyms: Hu23F2G | LeukArrest

Comment: Rovelizumab (Hu23F2G) is a humanized IgG4 bispecific monoclonal antibody targeting integrin alpha L subunit (ITGAL, CD11A) and integrin beta 2 subunit (ITGB2, CD18) [5], which are components of the leukocyte adhesion integrin LFA-1. Rovelizumab was developed by Icos Corporation (later acquired by Eli Lilly) for potential use in multiple sclerosis, myocardial infarction and ischemic stroke.
Annotated peptide sequences for this antibody are available from its IMGT/mAb-DB record.

No information available.

No information available.

Summary of Clinical Use
Rovelizumab reached Phase 3 clinical trial for ischemic stroke, Phase 2 for myocardial infarction and Phase 2 for multiple sclerosis. However, there are no trials currently listed on ClinicalTrials.org (June 2017).

Summary of Clinical Use

Rovelizumab reached Phase 3 clinical trial for ischemic stroke, Phase 2 for myocardial infarction and Phase 2 for multiple sclerosis. However, there are no trials currently listed on ClinicalTrials.org (June 2017).

Mechanism Of Action and Pharmacodynamic Effects
LFA-1 (a CD11/CD18 integrin) on leukocytes binds to the endothelial transmembrane glycoprotein ICAM-1 and this interaction facilitates leukocyte transmigration into tissues [4]. Regulation of leukocyte CD11/CD18 integrins is relevant in biological and clinical settings [3]. Antibodies which inhibit the LFA-1/ICAM-1 interaction reduce leukocyte extrasavation to sites of inflammation or tissue damage, and thereby reduce activated leukocyte-mediated inflammation, including that noted to exacerbate ischemic damage following stroke and cardiac infarction.

Mechanism Of Action and Pharmacodynamic Effects

LFA-1 (a CD11/CD18 integrin) on leukocytes binds to the endothelial transmembrane glycoprotein ICAM-1 and this interaction facilitates leukocyte transmigration into tissues [4]. Regulation of leukocyte CD11/CD18 integrins is relevant in biological and clinical settings [3]. Antibodies which inhibit the LFA-1/ICAM-1 interaction reduce leukocyte extrasavation to sites of inflammation or tissue damage, and thereby reduce activated leukocyte-mediated inflammation, including that noted to exacerbate ischemic damage following stroke and cardiac infarction.