Lifitegrast-d6
Lifitegrast-d6 (SAR 1118-d6) is deuterium labeled Lifitegrast. Lifitegrast (SAR 1118) is a potent integrin antagonist. Lifitegrast blocks the binding of intercellular adhesion molecule 1 (ICAM-1) to lymphocyte function-associated antigen 1 (LFA-1), interrupting the T cell-mediated inflammatory cycle. Lifitegrast inhibits Jurkat T cell attachment to ICAM-1 with an IC50 of 2.98 nM. Lifitegrast can be used for researching dry eye disease.
For research use only. We do not sell to patients.
- CAS No.: 2249814-79-5
- Formula: C29H18D6Cl2N2O7S
- Molecular Weight:621.52
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
Application
1. This compound can be used as a tracer
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.
Chemical Information
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CAS No. 2249814-79-5
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Unlabeled CAS 1025967-78-5
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Molecular Weight 621.52
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Formula C29H18D6Cl2N2O7S
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SMILES
ClC1=C2C(CN(CC2)C(C3=CC=C(C=CO4)C4=C3)=O)=CC(Cl)=C1C(N[C@H](C(O)=O)C([2H])([2H])C5=C([2H])C(S(C)(=O)=O)=C([2H])C([2H])=C5[2H])=O
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Synonyms
SAR 1118-d6; SHP-606-d6
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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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
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)