R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
TIM-3 (Cobolimab Biosimilar) Human mAb #43580
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Human IgG4 kappa |
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Description
TIM-3 (Cobolimab Biosimilar) Human mAb is a biosimilar antibody for Cobolimab. Cobolimab is a therapeutic human monoclonal antibody directed against human TIM-3, an immune checkpoint protein.
| Endotoxin | <0.1 EU/μg of antibody |
Product Usage Information
This product is intended for research use only (RUO). Optimal dilutions/concentrations should be determined by the end user.
Formulation
Supplied in 1X PBS, BSA and Azide Free.
Storage
Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.
Specificity / Sensitivity
TIM-3 (Cobolimab Biosimilar) Human mAb was confirmed to bind to its intended target protein TIM-3 using flow cytometry.
Species Reactivity:
Human
Source / Purification
TIM-3 (Cobolimab Biosimilar) Human mAb is produced at Cell Signaling Technology. Cobolimab is an antibody that is directed against the extacellular region of human TIM-3 protein.
Background
T cell Ig- and mucin-domain-containing molecules (TIMs) are a family of transmembrane proteins expressed by various immune cells. TIM-3 is an inhibitory molecule that is induced following T cell activation (1-3 ). TIM-3 is expressed by exhausted T cells in the settings of chronic infection and cancer (4,5), and tumor-infiltrating T cells that coexpress PD-1 and TIM-3 exhibit the most severe exhausted phenotype (5). Tumor-infiltrating dendritic cells (DCs) also express TIM-3. TIM-3 expression on DCs was found to suppress innate immunity by reducing the immunogenicity of nucleic acids released by dying tumor cells (6). Research studies show that heterodimerization of TIM-3 with CEACAM-1 is critical for the inhibitory function of TIM-3, and co-blockade of TIM-3 and CEACAM-1 enhanced anti-tumor responses in a mouse model of colorectal cancer (7). In addition, blockade of TIM-3 in mouse models of autoimmunity enhanced the severity of disease (1). Finally, binding of Galectin-9 to TIM-3 expressed by Th1 cells induces T cell death (8).
- Monney, L. et al. (2002) Nature 415, 536-41.
- Sánchez-Fueyo, A. et al. (2003) Nat Immunol 4, 1093-101.
- Sabatos, C.A. et al. (2003) Nat Immunol 4, 1102-10.
- Jones, R.B. et al. (2008) J Exp Med 205, 2763-79.
- Sakuishi, K. et al. (2010) J Exp Med 207, 2187-94.
- Chiba, S. et al. (2012) Nat Immunol 13, 832-42.
- Huang, Y.H. et al. (2015) Nature 517, 386-90.
- Zhu, C. et al. (2005) Nat Immunol 6, 1245-52.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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