LAG3 Monoclonal Antibody [17B4], ATTO 488 Conjugated
- Known as:
- LAG3 Monoclonal Antibody [17B4], ATTO 488 Conjugated
- Catalog number:
- a-0590-100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- LAG3 Monoclonal Antibody [17B4] ATTO 488 Conjugated
Related genes to: LAG3 Monoclonal Antibody [17B4], ATTO 488 Conjugated
- Gene:
- LAG3 NIH gene
- Name:
- lymphocyte activating 3
- Previous symbol:
- -
- Synonyms:
- CD223
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-03
- Date modifiied:
- 2016-10-05
Related products to: LAG3 Monoclonal Antibody [17B4], ATTO 488 Conjugated
Related articles to: LAG3 Monoclonal Antibody [17B4], ATTO 488 Conjugated
- The efficacy of chimeric antigen receptor T (CAR-T) cell therapy in solid tumors is limited by dense extracellular matrix deposition and an immunosuppressive tumor microenvironment. Tenascin-C (TNC), an extracellular matrix protein enriched in ovarian cancer stroma, may provide a stromal cue that restricts T-cell engagement while offering a complementary target to mesothelin (MSLN). This study evaluated whether combined targeting of MSLN and TNC could enhance CAR-T-cell function and remodel the ovarian cancer microenvironment. - Source: PubMed
Publication date: 2026/06/08
Wang XiaoqinZhang DuoyiWang TingtingLi XinZhang Jing - Anti-homocitrullinated protein/peptide antibodies are specific to rheumatoid arthritis (RA) and predictive of worse prognosis, suggesting a pathogenic role for autoreactivity to homocitrullinated peptides (HomoCitP). However, T-cell responses to HomoCitP remain largely unexplored. We investigated these responses in a humanized HLA-DR4-transgenic (DR4tg) mouse model of RA, which expresses the strongest genetic risk factor for this disease. - Source: PubMed
Publication date: 2026/06/08
Ulanova SofyaKaur JaspreetBuckley GabrielleHaeryfar S M MansourCameron LisaCairns EwaBarra Lillian - Immune checkpoint inhibitors (ICIs) have changed the treatment landscape of advanced gastric cancer (GC). However, acquired resistance remains common. For patients who initially benefit and later progress, immunotherapy rechallenge is biologically plausible but still investigational. - Source: PubMed
Publication date: 2026/05/20
Jiang Yu-CaiZheng Lin-LinFu Ming-GuiZheng Bi-Jin - LAG3 is a critical inhibitory receptor that is highly enriched on exhausted T cells within the tumor microenvironment (TME), where it acts as a key driver of T-cell exhaustion-an archetypal barrier to robust antitumor immunity. In a colon cancer model, LAG3CD8 tumor-infiltrating lymphocytes (TILs) constitute the predominant type of tumor-specific T cells but exhibit defective IL2 signaling. To address whether exogenous IL2 replenishment unpins their dysfunction, we engineered LAG3-LaIL2 (low-affinity IL2), a fusion protein that selectively delivers IL2 to LAG3CD8 TILs. LAG3-LaIL2 expanded pre-exhausted tumor-specific CD8 T cells, reprogrammed their exhaustion trajectory toward an intermediate effector state, and prevented terminal exhaustion, leading to tumor regression and prolonged survival in mice. Mechanistically, LAG3-LaIL2 restored IL2R-JAK3-STAT5 signaling by upregulating the high-affinity IL2 receptor subunit CD122, thereby restoring TIL functionality. Furthermore, LAG3-LaIL2 amplified tumor-specific effector and memory T cells in draining lymph nodes, enabling systemic antitumor immunity against distal tumors and preventing tumor recurrence. Collectively, our findings identify LAG3-LaIL2 as a precision immunotherapy that specifically targets exhausted TILs while restricting IL2 exposure to nontarget cells, thereby enhancing both the efficacy and safety of this approach. This approach provides a translatable strategy to overcome T-cell exhaustion in solid tumors and represents a promising avenue to improve clinical outcomes in cancer patients. - Source: PubMed
Publication date: 2026/06/02
Yu XiaohongLiao HuipingLv JiaoyunSun YuZhang RuiqiChen YiweiLin YifanLiu LuluLi ShijieTang HuiJia PanpanShao BinYang ZaopengFu Yang-XinRen Zhenhua - Colorectal cancer (CRC) is the third most frequently diagnosed malignancy and the second leading cause of cancer-related mortality worldwide, underscoring the need for the development of more effective and durable therapeutic strategies. A key mechanism of tumor immune evasion involves activation of immune checkpoint pathways through the upregulation of inhibitory ligand expression within the tumor microenvironment, leading to lymphocyte exhaustion and impaired antitumor immunity. Consequently, immune checkpoints have emerged as important targets for immunotherapeutic intervention, with significant advances over the past decade. Nevertheless, despite demonstrated clinical benefits in selected patient subpopulations, the overall therapeutic efficacy of immune checkpoint inhibitors remains limited, particularly in the context of CRC. In this review, we provide a comprehensive overview of currently approved immune checkpoint-based immunotherapies for cancer treatment, with a specific focus on CRC, as well as ongoing clinical trials and evolving trends in this area. Furthermore, we discuss emerging targets and novel therapeutic strategies, with particular emphasis on innovative small-molecule inhibitors as potential alternatives to monoclonal antibody-based approaches. Finally, we outline future perspectives and potential directions for advancing immune checkpoint-targeted therapies in CRC. - Source: PubMed
Publication date: 2026/05/21
Nakielska KatarzynaPlewka JacekLenart Marzena