HAVCR2 (LBL-003 Biosimilar) Recombinant Monoclonal Antibody

Code: CSB-RA010145MB5HU

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100ug

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US$199

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Species Reactivity: Human

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Target Background

Product Details

Uniprot NO.

Q8TDQ0

Alternative Names

LBL003 research-grade biosimilar; LBL 003 research-grade biosimilar ;HAVCR2 antibody; TIM3 antibody; TIMD3 antibody; Hepatitis A virus cellular receptor 2 antibody; HAVcr-2 antibody; T-cell immunoglobulin and mucin domain-containing protein 3 antibody; TIMD-3 antibody; T-cell immunoglobulin mucin receptor 3 antibody; TIM-3 antibody; T-cell membrane protein 3 antibody; CD antigen CD366 antibody

Species Reactivity

Human

Immunogen

Recombinant Human HAVCR2 protein

Conjugate

Non-conjugated

Clonality

Monoclonal

Buffer

0.01M PBS，pH7.4

Storage

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

Notes

Validation Status
Application-specific performance (e.g., in flow cytometry, ELISA, IHC or other assay formats) has not yet been experimentally verified by CUSABIO. Users are advised to determine the optimal working conditions empirically in their own assay systems.
Guaranteed Quality
① Antibody purity > 95% tested by SDS-PAGE.
② Endotoxin level < 0.1EU/ug tested by LAL method.

Lead Time

3-4 weeks
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.

Concentration

It differs from different batches. Please contact us to confirm it.

Usage

It is a non-therapeutic biosimilar antibody, owning the same variable region from the corresponding approved therapeutic antibody. In conclusion, it is a research-grade biosimilar antibody and expressed in mammalian cell, which can be directly used as positive controls in drug discovery or used for rapid verification of the biological functions of target protein.

Datasheet & COA

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Description

This recombinant monoclonal antibody is developed as a research-grade biosimilar to LBL-003, targeting HAVCR2 (Hepatitis A Virus Cellular Receptor 2), also known as TIM-3 (T-cell Immunoglobulin and Mucin domain-containing protein 3). HAVCR2 functions as an immune checkpoint receptor expressed on various immune cells, including T cells, natural killer cells, and myeloid cells. Upon ligand binding, HAVCR2 negatively regulates immune responses by inducing T cell exhaustion and suppressing anti-tumor immunity. This checkpoint molecule plays a critical role in immune tolerance and has been implicated in multiple pathological conditions, including cancer immune evasion, chronic viral infections, and autoimmune disorders.

LBL-003 is a reference antibody designed to block HAVCR2 interactions with its ligands, thereby restoring immune cell function and enhancing anti-tumor responses. This biosimilar antibody serves as a valuable research tool for investigating HAVCR2-mediated immune regulation, exploring combination immunotherapy strategies, and studying T cell exhaustion mechanisms in oncology and infectious disease models. It enables researchers to evaluate checkpoint blockade approaches and understand the therapeutic potential of HAVCR2 inhibition across various disease contexts.

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Target Background

Function(From Uniprot)

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. Regulates macrophage activation. Inhibits T-helper type 1 lymphocyte (Th1)-mediated auto- and alloimmune responses and promotes immunological tolerance. 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. In contrast, shown to activate TCR-induced signaling in T-cells probably implicating ZAP70, LCP2, LCK and FYN. Expressed on Treg cells can inhibit Th17 cell responses. Receptor for LGALS9. 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. However, the function as receptor for LGALS9 has been challenged. Also reported to enhance CD8+ T-cell responses to an acute infection such as by Listeria monocytogenes. 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. Expressed on natural killer (NK) cells acts as a coreceptor to enhance IFN-gamma production in response to LGALS9. In contrast, shown to suppress NK cell-mediated cytotoxicity. Negatively regulates NK cell function in LPS-induced endotoxic shock.

Gene References into Functions

TIM-3 expression was predominantly localized to myeloid cells in both human and murine tumors PMID:29316433
TIM-3 and IL-37 may be used as potential biomarkers of active rheumatoid arthritis. PMID:30106887
High TIM3 expression is associated with gastric cancer. PMID:30106451
miR-498 can effectively suppress TIM-3 expression in the acute myeloid leukemia cell line PMID:30107988
These results indicate that TIM-3 may be involved in the pathogenesis of immune thrombocytopenia which subsequently can represent an opportunity for new therapeutic plan, moreover. This may have a prognostic value for disease severity. PMID:28974109
Within many tumors, PD-1/Tim-3 coexpressing CD8-T cells lose their ability to secrete cytokines and their intratumoral infiltration correlates with a bad prognosis. Tim-3 appeared as a potential biomarker of anti-PD-1 resistance. Combined blockade of PD-1 and Tim-3 axis demonstrated potent clinical efficacy in preclinical models and reinforced the rationale of using an anti-Tim-3 to override tumor resistance.[review] PMID:29547109
this study shows that TIM-3 expression identifies a distinctive PD-1(+) follicular helper T cell subset, with reduced interleukin 21 production and B cell help function in ovarian cancer patients PMID:29482158
TIM-3 high expression rate was an independent prognostic factor for extranodal NK/T cell lymphoma, nasal type PMID:28901003
sTim-3 is a promising biomarker for allograft dysfunction, but unable to differentiate allograft rejection from other causes of renal dysfunction in kidney transplantation recipients PMID:29310109
The expression of Tim-3 on CD14+ monocytes is involved in systemic inflammatory reaction after intracerebral hemorrhage. PMID:29310959
TIM-3 gene may play an important role as a genetic risk factor for the progression and prognosis of invasive breast cancer. PMID:29263040
Tim-3(+) NK cells had decreased capability of IFN-r secretion, while Tim-3(+) monocytes showed a M2-like phenotype. Importantly, Tim-3 level on both NK cells and monocytes positively correlated with the ratio of Ki-67(+) tumor cells. PMID:29174343
T-cell immunoglobulin mucin-3/galectin-9 (Tim-3/Gal-9) binding signaling can also engage other binding partners to induce distinct cellular responses [Review]. PMID:29027155
Polymorphism +4259A>C in exon 3 of the TIM-3 gene is associated with susceptibility to multiple sclerosis but polymorphism -1637C>T in the promoter region of TIM-1 is not. PMID:29141799
The interaction between Gal-9/TIM-3 pathway and follicular helper cells contributed to viral persistent in chronic hepatitis C virus infection. PMID:28772217
Exosomal total protein, Tim-3 and Galectin-9 were up-regulated in non-small cell lung cancer plasma. PMID:29452091
the monitoring of sTim3 in urine may be a novel and promising noninvasive approach for the detection of AR. Furthermore, measurement of sTim3 in urine may contribute to predict the response to antirejection therapy and a poor outcome following AR. PMID:28586044
the CD4(+)CD25(+)Foxp3(+) Treg cells from RA patients demonstrated a reduction of Tim3 and were less functional than Treg cells from healthy controls in a Tim3-related manner. PMID:28478516
our study highlights the role of TIM-3 as a potential prognostic marker and a promising therapeutic target in solid tumors. PMID:28423646
HAVCR2 regulates cytokines, chemokines, prostaglandins and cell adhesion molecules in the presence of viral infection, which suggests a potential for HAVCR2 activators as therapeutics for the management of preterm birth associated with viral infections. PMID:28466996
serum levels may be increased in patients with early phase diffuse cutaneous systemic sclerosis and associated with cardiac involvement and renal crisis PMID:27651303
Preoperative Tim3 expression on peripheral NK cells is correlated with differential staging in colorectal cancer, and may be useful as a serum biomarker. PMID:28440449
TIM-3 polymorphism is associated with response to therapy in hepatitis B virus-related hepatocellular carcinoma. PMID:27034168
BMI-1, TIM-3 and CLL-1 have roles in acute myeloid leukemia prognosis and therapy PMID:27506934
Quantification of TIM-3 and KIM-1 mRNA expressions, along with KIM-1 protein measurements in urine and blood could be employed as promising tools for noninvasive diagnosis of allograft dysfunction. PMID:28757398
Results show that human acute myeloid leukemia (AML) cells possess a secretory pathway which leads to the production and release of soluble Tim-3 and galectin-9. Both proteins prevent the activation of NK cells and impair their AML cell-killing activity. PMID:28750861
after 14 days of glucocorticoid therapy, clinical findings (serum bilirubin, skin GVHD) and plasma biomarkers (TIM3, ST2, sTNFR1) can predict failure of GVHD treatment and nonrelapse mortality. PMID:28478120
These findings suggested that rs10053538 in TIM-3 might increase susceptibility to and promote the progression of breast cancer in Chinese women PMID:27248321
Results indicate that T cell Ig and mucin domain 3 protein (TIM-3) polymorphisms (-1516G/T, -574G/T, and +4259T/G) were associated with the increased risk of cancer in Chinese Han population. PMID:27008699
In cultured MART1-specific CD8 T cells stimulated with peptide-loaded artificial antigen-presenting cells, anti-TIM-3 antibody treatment promotes generation of effector T cells, with acquisition of an activated phenotype, increased cytokine production, enhanced proliferation, and a transcription program associated with T cell differentiation. Anti-TIM-3 drives CD8 T cell differentiation through activation of mTORC1. PMID:29127145
Our results show that Tim-3 is a critical negative regulator of NLRP3 inflammasome and provides a potential target for intervention of diseases with uncontrolled inflammasome activation. PMID:28799242
soluble Tim-3 might play inhibitory roles in impaired Tim-3-mediated clearance of apoptotic cells in systemic lupus erythematosus. PMID:28754800
We found a novel mechanism through which Tim-3 could suppress antitumor immunity by utilizing the suppression of CD4(+) follicular helper cells (Tfh) function and provide new insight in the regulation of Tfh cells in breast cancer patients PMID:27156907
Tim3/Gal-9 alleviates the inflammation of TAO patients via suppressing Akt/NF-kappaB signaling pathway. PMID:28756232
this study shows that severe aplastic anemia untreated patients have lower TIM-3 expression on NK cells and CD56dim NK subsets compared with normal controls, and are correlated with the severity of pancytopenia of SAA PMID:28637584
We conclude that Tim-3 is a biomarker of dysfunctional plasmacytoid dendritic cells PMID:28264968
The present study defines the minimal TIM-3 promoter region and demonstrates its interaction with c-Jun during TIM-3 transcription in CD4(+) T cells. PMID:27243212
Our findings establish intratumoral Tim-3(+)PD1(+)CD8(+) T cells as critical mediators of an aggressive phenotype in RCC. PMID:27872087
Osteosarcoma patients with higher Tim-3 had relatively lower survival. Multivariate analyses for overall survival revealed that high serum soluble Tim-3 level was an independent prognostic factor for osteosarcoma PMID:28671022
urther analyses revealed that the levels of Tim-3 on CD4+ T cells and CD8+ T cells exhibited different expression patterns in terms of localization depending on pathological category of prostate cancer and metastasis. Immunohistochemical analysis revealed that positive staining of Tim-3 in prostate cancer but little or no staining of Tim-3 was observed in benign prostate hyperplasia epithelium. PMID:28681697
this review discusses the recent findings on Tim-3, the role it plays in regulating immune responses in different cell types and the rationale for targeting Tim-3 for effective cancer immunotherapy PMID:28258697
The -1516G > T, -574G > T and +4259T > G SNPs within TIM-3 gene might play an important role as a genetic risk factor in the pathogenesis of ET. PMID:27990849
this study shows that that Tim-3 expression defines a subpopulation of PD-1+ exhausted NY-ESO-1-specific CD8+ T cell and PD-1+Tim-3+ CD8+ T cells represented the largest subset of NY-ESO-1-specific CD8+ T cells in gastric cancer patients PMID:28110884
Increased TIM3+CD8+T cells with lower perforin and granzyme B expression and higher CD95 expression in MDS patients had been observed. These findings suggested that TIM3 might be related to CD8+T cells defect. PMID:27846431
our results suggested that PD-1 and TIM-3 blockade might be necessary in developing effective immunotherapeutic strategies in malignant Schwannoma, in which TIM-3 may play a more important role. PMID:28475007
these data suggest that the high Tim-3 expression in monocytes could be utilized by tumor-promoting Gal-9 expression on CD4(+) T cells PMID:28466780
In conclusion, Tim-3 on immune cells negatively regulates cell-mediated immunity against Plasmodium infection, and blocking Tim-3 signaling enhances sterile immunity and may play a protective role during malarial parasite infections. PMID:27638944
this study shows that the transcription factor T-bet controls Tim-3-mediated inhibition of monocyte/macrophage function during chronic hepatitis C virus infection PMID:27809352
this study shows that TIM-3 expressed on myeloid leukaemia cells may facilitate functional exhaustion in T helper cells PMID:27565576
this study shows that in osteosarcoma patients, Tim3 expression did not directly mediate immune suppression, but the interaction between Tim3+ T cells and monocytes, naive CD4+ T cells, and Gal9-expressing CD4+ CD25+ Tregs could resulting in progressive suppression of Th1 responses PMID:28103502

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Subcellular Location

Membrane; Single-pass type I membrane protein. Cell junction. Cell membrane.

Protein Families

Immunoglobulin superfamily, TIM family

Tissue Specificity

Expressed in T-helper type 1 (Th1) lymphocytes. Expressed on regulatory T (Treg) cells after TCR stimulation. Expressed in dendritic cells and natural killer (NK) cells. Expressed in epithelial tissues. Expression is increased on CD4+ and CD8+ T-cells in

Database Links

HGNC: 18437

UNIGENE: Hs.710500

KEGG: hsa:84868

STRING: 9606.ENSP00000312002

OMIM: 606652

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