Xeligekimab
Based on 1 Customer Validation
Xeligekimab (GR 1501) is an anti-human interleukin 17A (IL-17A) humanized monoclonal antibody. Xeligekimab inhibits the pro-inflammatory cascade. Xeligekimab can be used for the research of inflammatory disease, such as radiographic axial spondyloarthritis.
For research use only. We do not sell to patients.
- Purity : 95.00%
- CAS No.: 2382921-73-3
- Molecular Weight:145.66 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Human IgG4 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
[1]|
IL-17A |
In Vitro
Xeligekimab binds to and inhibits the activity of interleukin-17A and improves signs and symptoms of active radiographic axial spondyloarthritis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| 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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Human IgG4 kappa
Application
ELISA, FACS, Functional assay
Chemical Information
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CAS No. 2382921-73-3
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Appearance Liquid
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Molecular Weight 145.66 kDa
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Color Colorless to light yellow
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SMILES
[Xeligekimab]
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Synonyms
GR 1501
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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 Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
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Data Sheet (256 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)