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tim 3 ligands  (Galectin Therapeutics)

 
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    Structured Review

    Galectin Therapeutics tim 3 ligands
    Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, <t>TIM-3,</t> LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.
    Tim 3 Ligands, supplied by Galectin Therapeutics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/tim+3/pmc12964005-330-0-2?v=Galectin+Therapeutics
    Average 86 stars, based on 1 article reviews
    tim 3 ligands - by Bioz Stars, 2026-06
    86/100 stars

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    1) Product Images from "Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy"

    Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy

    Journal: Pharmaceutical Science Advances

    doi: 10.1016/j.pscia.2026.100109

    Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.
    Figure Legend Snippet: Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.

    Techniques Used: Cell Function Assay, Expressing, Derivative Assay

    Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.
    Figure Legend Snippet: Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.

    Techniques Used: Activity Assay, Transplantation Assay, Gene Knockout, Modification



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    Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.

    Journal: Pharmaceutical Science Advances

    Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy

    doi: 10.1016/j.pscia.2026.100109

    Figure Lengend Snippet: Factors influencing the exhausted state of NK cells. The exhaustion of NK cells in the TME is regulated by multiple factors which results in NK cell function impairment due to: the downregulated expression of NK cell-activating receptors (e.g., NKG2D, DNAM-1, NKp30), the reduced secretion of effector cytokines (such as IFN-γ), and the upregulated expression of immunosuppressive molecules (e.g., PD-1, NKG2A, TIGIT, CD96, TIM-3, LAG-3). Additionally, transforming growth factor-β (TGF-β) secreted by tumor cells, cancer-associated fibroblasts (CAFs), and extracellular vesicles (EVs); hypoxic microenvironment; indoleamine 2,3-dioxygenase (IDO); prostaglandin E2 (PGE2); and immunosuppressive cells including macrophages, regulatory T cells (Treg), and myeloid-derived suppressor cells (MDSC) are involved in regulating NK cell exhaustion through multiple pathways.

    Article Snippet: TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity.

    Techniques: Cell Function Assay, Expressing, Derivative Assay

    Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.

    Journal: Pharmaceutical Science Advances

    Article Title: Mechanisms of tumor cell evasion from NK cell-mediated killing and advances in NK cell-based cancer immunotherapy

    doi: 10.1016/j.pscia.2026.100109

    Figure Lengend Snippet: Strategies for enhancing NK cell anti-tumor activity. The anti-tumor efficacy of NK cells can be improved through multiple approaches: Adoptive NK cell infusions, including autologous NK cells (combined with HAIC), allogeneic NK cells (with high potential), and infusions with or without allogeneic transplantation; NK cell checkpoint inhibitors targeting molecules such as PD-1/PD-L1, KIRs (KIR2DL1/2/3/5), NKG2A/CD94, TIM-3, and LAG-3; Advanced applications of CAR-NK cells, including IL-15-secreting CAR-NK cell therapy targeting mesothelin, TIPE2 gene-knockout CAR-NK therapy, and application of modified CCCR-NK92; Administration of stimulatory cytokines like IL-2, IL-15, IL-18, and IL-21; Bi or trispecific killer engagers, including Bispecific antibody: LB1410 (anti-PD-1/TIM-3) and trispecific nanobody: PDL1/PD-1/NKG2A.

    Article Snippet: TIM-3 ligands-including Galectin-9, PS, HMGB1, and CEACAM-1-play crucial roles in regulating NK activity.

    Techniques: Activity Assay, Transplantation Assay, Gene Knockout, Modification