Anti-HER2 monoclonal antibody that blocks HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized anti-HER2 monoclonal antibody (IgG1) that binds the extracellular domain of HER2 (ERBB2), inhibits HER2-driven signaling (PI3K/AKT/MAPK), promotes receptor internalization/degradation, and induces immune-mediated tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC) in HER2-overexpressing cancers.
Trastuzumab binds HER2 on target cells; its Fc engages Fcγ receptors on NK cells to trigger antibody‑dependent cellular cytotoxicity (ADCC), with some complement activation, leading to lysis/apoptosis of HER2+ cells.
Anti-HER2 monoclonal antibody that prevents HER2/HER3 dimerization and mediates ADCC.
Humanized anti-HER2 monoclonal antibody that binds the HER2 extracellular dimerization domain, preventing HER2/HER3 dimerization and downstream PI3K/AKT/MAPK signaling, leading to growth inhibition/apoptosis; also engages immune effector cells to mediate ADCC.
Pertuzumab binds HER2 and recruits FcγR-bearing immune cells (e.g., NK cells) to mediate ADCC, killing target cells; HER2 dimerization blockade can also promote apoptosis.
Ex vivo generated and expanded autologous cytotoxic T cells engineered by selection/expansion to recognize TAA peptides (NY-ESO-1, MAGEA4, PRAME, Survivin, SSX) presented on HLA class I, administered as adoptive cellular immunotherapy to eradicate residual lymphoma.
Autologous cytotoxic T lymphocytes are generated and expanded ex vivo for endogenous TCR specificity to tumor‑associated antigen peptides (NY-ESO-1, MAGEA4, PRAME, Survivin, SSX) presented on HLA class I. After infusion, these CTLs recognize HLA-restricted TAA on lymphoma cells and induce targeted killing via perforin/granzyme release and cytokine-mediated effector functions to eradicate residual disease.
Adoptively transferred TAA-specific CTLs recognize NY-ESO-1 peptide presented on HLA class I via their TCR and induce apoptosis of target cells through perforin/granzyme release (and Fas/FasL).
Ex vivo generated and expanded autologous cytotoxic T cells engineered by selection/expansion to recognize TAA peptides (NY-ESO-1, MAGEA4, PRAME, Survivin, SSX) presented on HLA class I, administered as adoptive cellular immunotherapy to eradicate residual lymphoma.
Autologous cytotoxic T lymphocytes are generated and expanded ex vivo for endogenous TCR specificity to tumor‑associated antigen peptides (NY-ESO-1, MAGEA4, PRAME, Survivin, SSX) presented on HLA class I. After infusion, these CTLs recognize HLA-restricted TAA on lymphoma cells and induce targeted killing via perforin/granzyme release and cytokine-mediated effector functions to eradicate residual disease.
Adoptively transferred TAA-specific CTLs recognize MAGE-A4–derived peptides on HLA class I via their TCRs and directly kill target cells by perforin/granzyme-mediated cytolysis (and Fas/FasL), with supportive cytokine effects.
Ex vivo generated and expanded autologous cytotoxic T cells engineered by selection/expansion to recognize TAA peptides (NY-ESO-1, MAGEA4, PRAME, Survivin, SSX) presented on HLA class I, administered as adoptive cellular immunotherapy to eradicate residual lymphoma.
Autologous cytotoxic T lymphocytes are generated and expanded ex vivo for endogenous TCR specificity to tumor‑associated antigen peptides (NY-ESO-1, MAGEA4, PRAME, Survivin, SSX) presented on HLA class I. After infusion, these CTLs recognize HLA-restricted TAA on lymphoma cells and induce targeted killing via perforin/granzyme release and cytokine-mediated effector functions to eradicate residual disease.
Infused autologous TAA-specific CTLs recognize PRAME-derived peptides presented on HLA class I via their TCR and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas/FasL).