Render Target: STATIC
Render Timestamp: 2024-12-20T11:52:48.282Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-04-24 20:37:11.212
Product last modified at: 2024-06-07T08:00:16.183Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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