Ralzapastotug
Based on 1 Customer Validation
Ralzapastotug (AB-308) is an anti-TIGIT (T cell immunoreceptor with Ig and ITIM domains) IgG1 monoclonal antibody.
For research use only. We do not sell to patients.
- Purity : 98.67%
- CAS No.: 2581724-89-0
- Molecular Weight:145.329 kDa
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
IC50 & Target
TIGIT
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 IgG1 kappa
Application
ELISA, FACS, Functional assay
Verified Bioactivity
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Immobilized TIGIT Protein, Human (HEK293, Fc, HY-P7414) can bind Ralzapastotug. The EC50 for this effect is 47.07 ng/mL. -
Flow cytometric analysis of 1X106 FaDu cells with Ralzapastotug (HY-P990030, red). Cells were fixed with 4% paraformaldehyde. Then stained with the primary antibody at 1/200 dilution for an hour at 4℃. AF 488-conjugated AffiniPure Goat Anti-Human IgG H&L (HY-P83776) was used as the secondary antibody at 1/1,000 dilution for 30 minutes at 4℃. Human IgG1 kappa (HY-P99001, blue) was used as the isotype control, cells without incubation with primary antibody were used as the unlabeled control (black).
Chemical Information
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CAS No. 2581724-89-0
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Appearance Liquid
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Molecular Weight 145.329 kDa
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Color Colorless to light yellow
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SMILES
[Ralzapastotug]
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Synonyms
AB-308
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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 Cancer Immunology
Cancer immunology studies how the immune system recognizes, suppresses, edits, or fails to eliminate malignant cells through tumor antigen release, antigen presentation, T-cell priming, immune trafficking, tumor-cell killing, and feedback inhibition in the tumor microenvironment. The cancer-immunity cycle links tumor antigenicity, dendritic-cell priming, CD8+ T-cell infiltration, cytotoxic function, and immune-checkpoint regulation to tumor rejection or immune escape. Immune-checkpoint pathways such as PD-1/PD-L1 and CTLA-4 suppress antitumor T-cell activity and can be therapeutically blocked, but many tumors remain resistant because of poor antigen presentation, weak T-cell infiltration, suppressive myeloid cells, regulatory T cells, and tumor-intrinsic immune-exclusion programs. Unresolved questions include which immune-cell states predict response, how tumor-intrinsic pathways exclude immune cells, how myeloid suppression limits checkpoint blockade, and which combination strategies
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)