Erlizumab
Based on 1 Customer Validation
Erlizumab (rhuMAb) is a monoclonal antibody against the Integrin b2/ITGB2/CD18 subunit of the Mac-1 receptor. Erlizumab can reduce reperfusion injury in myocardial infarction.
For research use only. We do not sell to patients.
- Purity : 98.49%
- CAS No.: 211323-03-4
- Molecular Weight:49.293 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Isotype
Fab-G1-kappa
Species Reactivity
Human
IC50 & Target
Integrin b2/ITGB2/CD18
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Fab-G1-kappa
Application
ELISA, FACS, Functional assay
Verified Bioactivity
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Immobilized Integrin alpha X beta 2 Protein, Human (HEK293, His, HY-P73863) can bind Erlizumab. The EC50 for this effect is 832.3 ng/mL.
Chemical Information
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CAS No. 211323-03-4
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Appearance Liquid
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Molecular Weight 49.293 kDa
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Color Colorless to light yellow
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SMILES
[Erlizumab]
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Synonyms
rhuMAb
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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.
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 (255 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)
Erlizumab Related Classifications
HY-P99946 Related Classifications
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