Products
Surzebiclimab Biosimilar Monoclonal Antibody (TIM-3) for Research
Pre-Made Surzebiclimab biosimilar, Whole mAb, Anti-HAVCR2/TIM3 Antibody: Anti-CD366/KIM-3/SPTCL/TIMD3/Tim-3/TIMD-3/HAVcr-2 therapeutic antibody is a biosimilar expressed by mammalian cell line as a benchmark reference therapeutic antibody for biological drug disovery items including cell culture, assay development, animal model development, PK/PD model development (Pharmacokinetics & Pharmacodynamic) and mechanism of action (MOA) research.
Order Information
| Catalog No. | Package | List Price(In USD) | Discount off | Discount Price |
|---|---|---|---|---|
| GMP-Bios-ab-536-1mg | 1mg | 3090 |
Size： 1mg | 10mg | 100mg
Product Details
| Products Name (INN Index) | Pre-Made Surzebiclimab biosimilar, Whole mAb, Anti-HAVCR2/TIM3 Antibody: Anti-CD366/KIM-3/SPTCL/TIMD3/Tim-3/TIMD-3/HAVcr-2 therapeutic antibody |
| INN Name | Surzebiclimab |
| Target | HAVCR2 |
| Format | Whole mAb |
| Derivation | |
| Species Reactivity | Human |
| CH1 Isotype | IgG1 |
| VD LC | Kappa |
| Highest_Clin_Trial (Jan '20) | Phase-I/II |
| Est. Status | Active |
| 100% SI Structure | None |
| 99% SI Structure | None |
| 95-98% SI Structure | None |
| Year Proposed | 2020 |
| Year Recommended | na |
| Companies | BeiGene |
| Conditions Approved | na |
| Conditions Active | Solid tumours |
| Conditions Discontinued | na |
| Development Tech | na |
About target - HAVCR2
1. Protein Hepatitis A virus cellular receptor 2
2. Gene HAVCR2
3. Organism Homo sapiens (Human)
Function
Cell surface receptor implicated in modulating innate and adaptive immune responses. Generally accepted to have an inhibiting function. Reports on stimulating functions suggest that the activity may be influenced by the cellular context and/or the respective ligand (PubMed:24825777).
Regulates macrophage activation (PubMed:11823861).
Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance (PubMed:14556005).
In CD8+ cells attenuates TCR-induced signaling, specifically by blocking NF-kappaB and NFAT promoter activities resulting in the loss of IL-2 secretion. The function may implicate its association with LCK proposed to impair phosphorylation of TCR subunits, and/or LGALS9-dependent recruitment of PTPRC to the immunological synapse (PubMed:24337741, PubMed:26492563).
In contrast, shown to activate TCR-induced signaling in T-cells probably implicating ZAP70, LCP2, LCK and FYN (By similarity).
Expressed on Treg cells can inhibit Th17 cell responses (PubMed:24838857).
Receptor for LGALS9 (PubMed:16286920, PubMed:24337741).
Binding to LGALS9 is believed to result in suppression of T-cell responses; the resulting apoptosis of antigen-specific cells may implicate HAVCR2 phosphorylation and disruption of its association with BAG6. Binding to LGALS9 is proposed to be involved in innate immune response to intracellular pathogens. Expressed on Th1 cells interacts with LGALS9 expressed on Mycobacterium tuberculosis-infected macrophages to stimulate antibactericidal activity including IL-1 beta secretion and to restrict intracellular bacterial growth (By similarity).
However, the function as receptor for LGALS9 has been challenged (PubMed:23555261).
Also reported to enhance CD8+ T-cell responses to an acute infection such as by Listeria monocytogenes (By similarity).
Receptor for phosphatidylserine (PtSer); PtSer-binding is calcium-dependent. May recognize PtSer on apoptotic cells leading to their phagocytosis. Mediates the engulfment of apoptotic cells by dendritic cells. Expressed on T-cells, promotes conjugation but not engulfment of apoptotic cells. Expressed on dendritic cells (DCs) positively regulates innate immune response and in synergy with Toll-like receptors promotes secretion of TNF-alpha. In tumor-imfiltrating DCs suppresses nucleic acid-mediated innate immune repsonse by interaction with HMGB1 and interfering with nucleic acid-sensing and trafficking of nucleid acids to endosomes (By similarity).
Expressed on natural killer (NK) cells acts as a coreceptor to enhance IFN-gamma production in response to LGALS9 (PubMed:22323453).
In contrast, shown to suppress NK cell-mediated cytotoxicity (PubMed:22383801).
Negatively regulates NK cell function in LPS-induced endotoxic shock (By similarity).
Caution
Experimental results based on the injection of HAVCR2/TIM-3 antibodies or use of HAVCR2/TIM-3-Fc fusion proteins can reflect changes in the activity of several cell types and pathways as HAVCR2/TIM-3 is expressed by multiple immune cell types.
