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 TAA-specific CTLs recognize Survivin peptide presented on HLA class I and directly kill target cells via TCR engagement, releasing perforin/granzymes (and ancillary Fas–FasL/cytokine-mediated 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 TCR-native CTLs recognize SSX-derived peptides on HLA class I and directly kill target cells via perforin/granzyme-mediated cytolysis (with cytokine-mediated effects).
Pertuzumab biosimilar; a humanized anti-HER2 monoclonal antibody that binds HER2 subdomain II to block ligand-dependent HER2 dimerization (especially HER2/HER3), suppress downstream PI3K/AKT and MAPK signaling, and promote ADCC.
Pertuzumab biosimilar; a humanized anti-HER2 monoclonal antibody that binds HER2 subdomain II to block ligand‑dependent HER2 dimerization (especially HER2/HER3), thereby suppressing downstream PI3K/AKT and MAPK signaling and eliciting antibody-dependent cellular cytotoxicity (ADCC).
Anti-HER2 IgG1 binds HER2 and its Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to trigger antibody-dependent cellular cytotoxicity (ADCC), with possible complement activation; signaling blockade itself is non-cytolytic.
Humanized anti-HER2 monoclonal antibody that binds HER2 subdomain II, inhibits ligand-dependent HER2 dimerization (notably HER2/HER3), downregulates downstream PI3K/AKT and MAPK signaling, and mediates ADCC.
Humanized monoclonal antibody against HER2 (ERBB2) subdomain II that blocks ligand-dependent HER2 dimerization—particularly HER2/HER3—thereby inhibiting downstream PI3K/AKT and MAPK signaling and mediating antibody-dependent cellular cytotoxicity (ADCC).
Fc-mediated ADCC by NK cells and other effector cells against HER2-expressing cells; additionally, HER2 dimerization blockade can induce growth inhibition and apoptosis.
Humanized anti-HER2 monoclonal antibody that binds HER2 subdomain IV, inhibits ligand-independent signaling, promotes HER2 downregulation, and mediates ADCC.
Humanized anti-HER2 monoclonal antibody that binds HER2 extracellular domain IV (ERBB2), inhibits ligand-independent HER2 signaling, promotes receptor internalization/downregulation, suppresses downstream PI3K/AKT and MAPK pathways, and engages Fc receptors to mediate ADCC against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 and its Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC (±ADCP/CDC), killing HER2-expressing cells; signaling blockade may also promote apoptosis.