Tadocizumab
Based on 1 Customer Validation
Tadocizumab (C4G1; YM-337) is a humanized monoclonal antibody tageting integrin αIIbβ3. Tadocizumab has antiplatelet and antithrombotic effects, and can be used for cardiovascular disease research.
For research use only. We do not sell to patients.
- Purity : 97%
- CAS No.: 339086-80-5
- Molecular Weight:47.619 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Fab-G1-kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
[1]|
GPIIb/IIIa |
In Vitro
Tadocizumab (YM-337) significantly inhibits ex vivo ADP-induced platelet aggregation, and completely inhibits arachidonic acid-induced platelet aggregation[1].
Tadocizumab (YM-337) inhibits human platelet adhesion to von Willebrand factor, fibrinogen, fibronectin and subendothelial matrix[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Tadocizumab (YM-337; C4G1) at a dose of 1 mg/kg intravenous injection followed by 6 μg/kg/min infusion for 60 min prevented occlusive thrombus formation in monkeys, in a photochemically-induced thrombosis model in squirrel monkeys[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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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Loaded Tadocizumab on ProA biosensor, can bind Integrin alpha 2B beta 3 Protein, Human (HEK293, His, HY-P77716) with an affinity constant of 1.268E-08 M as determined in BLI assay.
Chemical Information
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CAS No. 339086-80-5
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Appearance Liquid
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Molecular Weight 47.619 kDa
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Color Colorless to light yellow
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SMILES
[Tadocizumab]
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Synonyms
C4G1; YM-337
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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 (258 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
[1]. S Kaku, et al. Antiplatelet and antithrombotic effects of YM337, the Fab fragment of a humanized anti-GPIIb/IIIa monoclonal antibody in monkeys. Thromb Haemost. 1996 Apr;75(4):679-84. [Content Brief]
[2]. Ken-ichi Suzuki, et al. Comparative studies of a humanized anti-glycoprotein IIb/IIIa monoclonal antibody, YM337, and abciximab on in vitro antiplatelet effect and binding properties. Biol Pharm Bull. 2002 Aug;25(8):1006-12. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)