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TIGIT/VSTM3/VSIG9

Alpha Lifetech can provide TIGIT/VSTM3/VSIG9 corresponding products, help each customer's research and development.

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Introduction To TIGIT/VSTM3/VSIG9

Drug targets a biomolecule that can directly bind to drugs and then react. Generally, the target refers to a protein related to the cause of disease. The focus of the target began with focusing on tumors and then began to spread to various fields. Introduction to TIGIT/VSTM3/VSIG9  is a common target in medicine.
TIGIT, also known as WUCAM, Vstm 3, and VSIG 9, is a co-inhibitory receptor belonging to the immunoglobulin superfamily. TIGIT is composed of the extracellular immunoglobulin variable region (IgV) domain, the type 1 transmembrane domain, containing the immunoreceptor tyrosine inhibitory motif (ITIM), and the intracellular domain of the Ig tail tyrosine-like motif (ITT). TIGIT is a negative regulator of the immune response that is expressed on activated conventional α β T cells, and also on memory T cells, regulatory T cells, follicular helper cells, and natural killer T cells. In addition to T cells, TIGIT is also expressed in NK cells.
The ligands of TIGIT include CD112 and the poliovirus receptor (PVR), in which PVR is the high-affinity homologous receptor for TIGIT, also known as CD155 / Necl-5 / Tage 4. In addition, TIGIT also competes with ligands for CD226 (DNAM-1) and CD96 (TACTILE), compared with the highest affinity for CD155.

Function of Target TIGIT/VSTM3/VSIG9

TIGIT has multiple immunosuppressive effects on the cancer immune cycle, including inhibition of natural killer cell effector functions, inhibition of dendritic cell maturation, promotion of macrophage polarization into M2 phenotype, and differentiation of T cells into regulatory T cells. TIGIT Interacts with CD155 expressed on antigen-presenting cells or tumor cells and downregulates T cell and natural killer (NK) cell functions. TIGIT has emerged as a key inhibitor of the antitumor response and can hinder multiple steps of the cancer immune cycle. Preclinical studies have shown that TIGIT blockers can prevent various solid cancers and hematological cancers. The TIGIT pathway regulates T cell-mediated and natural killer cell-mediated tumor recognition in vitro and in vivo.

Gene Pathway of Target TIGIT/VSTM3/VSIG9

Dual PD-1 / TIGIT blockade is effective in increasing tumor antigen-specific CD8 T cell expansion and function in vitro and promotes tumor rejection in murine tumor models. TIGIT is associated with PD-1 expression and can synergize with PD-1 / PD-L1 blockade to enhance tumor rejection. Genetic and/or pharmacological modulation of the CD155 / TIGIT axis is sufficient to promote immune evasion by PDAC expressing native neoantigens. Activation of the TIGIT pathway could regulate B cell differentiation through the SPI-B-PAX 5-XBP 1 pathway, thereby reducing autoantibodies.
TIGIT
Fig 1: TIGIT Gene Pathway. (Reference source:  Cai L, Li Y, Tan J, Xu L, Li Y. Targeting LAG-3, TIM-3, and TIGIT for cancer immunotherapy. J Hematol Oncol. 2023 Sep 5;16(1):101. )

Alpha Lifetech Can Provide

Currently, various immune drugs targeting TIGIT/VSTM3/VSIG9 targets are in the updating iteration, and taking the disease alone or in combination with other products has become a new approach with remarkable achievements. The TIGIT/VSTM3/VSIG9 targets have shown important research value and application prospects in both biology and drug research and development. With further research and detection technology advances, TIGIT/VSTM3/VSIG9 target products are also essential in medical research. Alpha Lifetech can provide TIGIT/VSTM3/VSIG9 corresponding products and help each customer's research and development. In addition, Alpha Lifetech also provides advanced expression systems and purification services to accelerate antibody research and development. Our synthesized antibody expression undergoes rigorous quality validation, including sequencing validation and functional expression analysis, to ensure high fidelity and performance. In addition, Alpha Lifetech provides customized solutions for recombinant proteins, such as codon optimization, promoter selection, and vector design, supplemented by downstream applications such as protein expression analysis to meet specific experimental needs.

Reference 

[1] Harjunpää H, Guillerey C. TIGIT as an emerging immune checkpoint. Clin Exp Immunol. 2020 May;200(2):108-119.   
[2] Chauvin JM, Zarour HM. TIGIT in cancer immunotherapy. J Immunother Cancer. 2020 Sep;8(2):e000957.     
[3] Cai L, Li Y, Tan J, Xu L, Li Y. Targeting LAG-3, TIM-3, and TIGIT for cancer immunotherapy. J Hematol Oncol. 2023 Sep 5;16(1):101. 

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