Autologous, non–genetically modified tumor-infiltrating lymphocyte (TIL) therapy providing ex vivo expanded tumor‑reactive T cells to mediate cytotoxicity against tumor cells.
Autologous, non-genetically modified tumor-infiltrating lymphocytes expanded ex vivo; upon reinfusion, native TCRs recognize patient-specific tumor antigens and mediate cytotoxic killing of tumor cells via perforin/granzyme release and cytokine-driven immune activation.
Infused TILs use native TCRs to recognize tumor-derived peptide–HLA class I complexes on tumor cells and kill them via perforin/granzyme release and death-receptor pathways (e.g., Fas/FasL).
Autologous, non–genetically modified tumor-infiltrating lymphocyte (TIL) therapy providing ex vivo expanded tumor‑reactive T cells to mediate cytotoxicity against tumor cells.
Autologous, non-genetically modified tumor-infiltrating lymphocytes expanded ex vivo; upon reinfusion, native TCRs recognize patient-specific tumor antigens and mediate cytotoxic killing of tumor cells via perforin/granzyme release and cytokine-driven immune activation.
Reinfused TILs use native TCRs to recognize the tumor-derived peptide–HLA class II complex and directly kill the presenting cell via perforin/granzyme-mediated cytolysis, supported by cytokines (e.g., IFN-γ, TNF-α).
Anti-CD38 IgG1 monoclonal antibody that induces myeloma cell death via ADCC, CDC, and ADCP; can trigger direct apoptosis, inhibit CD38 ectoenzyme/adenosine signaling, and deplete CD38+ immunosuppressive cells.
Isatuximab is an anti‑CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells, inducing cell death via antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular phagocytosis (ADCP), and direct apoptosis. It also inhibits CD38 ectoenzyme/adenosine signaling and depletes CD38‑positive immunosuppressive cells, enhancing anti‑tumor immunity.
Isatuximab binds CD38 on target cells and induces Fc-mediated ADCC and ADCP, activates complement (CDC), and can trigger direct apoptosis.
Fourth-generation autologous gene-modified T cells expressing chimeric antigen receptors that co-target BCMA and CD19; administered as a single intravenous infusion (0.5–3 × 10^6 cells/kg) following lymphodepletion to deplete B-lineage cells in refractory autoimmune diseases.
Autologous, gene‑modified T cells engineered with chimeric antigen receptors that co-target CD19 on B cells and BCMA on plasmablasts/plasma cells. Antigen engagement triggers CAR signaling to activate T‑cell cytotoxicity and cytokine release, leading to depletion of B‑lineage cells and reduction of autoreactive B cells and autoantibody‑producing plasma cells.
CAR-T cells recognize CD19 via the CAR and directly kill CD19+ cells through perforin/granzyme-mediated cytolysis and apoptosis.
Fourth-generation autologous gene-modified T cells expressing chimeric antigen receptors that co-target BCMA and CD19; administered as a single intravenous infusion (0.5–3 × 10^6 cells/kg) following lymphodepletion to deplete B-lineage cells in refractory autoimmune diseases.
Autologous, gene‑modified T cells engineered with chimeric antigen receptors that co-target CD19 on B cells and BCMA on plasmablasts/plasma cells. Antigen engagement triggers CAR signaling to activate T‑cell cytotoxicity and cytokine release, leading to depletion of B‑lineage cells and reduction of autoreactive B cells and autoantibody‑producing plasma cells.
BCMA+ cells are recognized by the anti-BCMA CAR on infused T cells, which upon engagement activate cytotoxic effector functions (perforin/granzyme and Fas/FasL), causing apoptosis/lysis of BCMA-expressing plasmablasts/plasma cells.