Rovelizumab
Based on 1 publication(s) in Google Scholar
Rovelizumab is a humanized monoclonal leukointegrin antibody. Rovelizumab is a monoclonal antibody directed against the CD11/CD18 cell adhesion proteins. Rovelizumab can be used for research of multiple sclerosis (MS), hemorrhagic shock, myocardial infarction (MI) and stroke.
For research use only. We do not sell to patients.
- Purity : 97.23%
- CAS No.: 339086-79-2
- Molecular Weight:145.98 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Rovelizumab
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Biological Activity
Description
Isotype
Human IgG4 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
ITGAL & ITGB2
In Vitro
Rovelizumab binds CD18 and has activity against CD18-integrin complexes including the CD11b-CD18 heterodimer[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Human IgG4 kappa
Application
ELISA, FACS, Functional assay
Chemical Information
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CAS No. 339086-79-2
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Appearance Liquid
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Molecular Weight 145.98 kDa
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Color Colorless to light yellow
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SMILES
[Rovelizumab]
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Synonyms
Hu23F2G
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Shipping
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
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Cell Commun Signal
β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury. [Abstract]2025 Feb 8;23(1):70. PMID: 39923080
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
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Data Sheet (257 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)