Autologous tumor-infiltrating lymphocytes (TILs) expanded/activated ex vivo and reinfused as cellular immunotherapy targeting patient-specific tumor antigens.
Autologous tumor-infiltrating lymphocytes are expanded and activated ex vivo and reinfused; they recognize patient-specific tumor antigens via endogenous TCRs and mediate cytotoxicity through perforin/granzyme release and proinflammatory cytokines (e.g., IFN-gamma), leading to targeted tumor cell killing.
Infused TILs use their endogenous TCRs to recognize the tumor-associated peptide–MHC on target cells and directly kill them via perforin/granzyme-mediated cytolysis (and Fas–FasL), with cytokines (e.g., IFN-γ) supporting the response.
Subcutaneous anti-CD38 IgG1 monoclonal antibody that targets CD38 on myeloma cells, mediating ADCC, CDC, and ADCP, and depleting CD38+ immunosuppressive cells.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on malignant plasma cells and mediates Fc-dependent cytotoxicity (ADCC, CDC, ADCP) and apoptosis, resulting in lysis of CD38-expressing tumor cells; also depletes CD38+ immunosuppressive cells and can inhibit CD38 ectoenzyme activity, reducing adenosine-mediated immunosuppression.
Isatuximab binds CD38 on target cells and engages effector functions via its Fc to induce NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), and macrophage ADCP; it can also trigger apoptosis upon receptor crosslinking.
IgG1 monoclonal antibody targeting CD38 on myeloma/plasma cells; mediates ADCC, CDC, ADCP, induces direct apoptosis, and inhibits CD38 ectoenzyme activity.
Humanized IgG1 anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, triggers ADCC, CDC, and ADCP, induces direct apoptosis, and inhibits CD38 ectoenzyme activity, resulting in depletion of CD38-expressing cells.
Isatuximab binds CD38 on target cells and mediates Fc-dependent killing (ADCC by NK cells, CDC via complement, ADCP by macrophages) and can induce direct apoptosis of CD38+ cells.
Autologous, gene-modified CD19-directed CAR T-cell therapy metabolically enhanced to improve T-cell fitness, persistence, and antitumor activity.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor recognize CD19 on malignant B cells, triggering T‑cell activation, in vivo expansion, and cytotoxic killing via perforin/granzyme and cytokine release. Metabolic enhancements are incorporated to improve T‑cell fitness, persistence, and function within the tumor microenvironment, increasing antitumor durability.
CD19-directed CAR T cells recognize CD19 on target cells and kill them via perforin/granzyme-mediated apoptosis and cytokine/Fas–FasL signaling.
A PD-L1–blocking monoclonal antibody immune checkpoint inhibitor that prevents PD-1/PD-L1 interaction to reinvigorate T-cell activity.
Avelumab is a human IgG1 monoclonal antibody that binds PD-L1, blocking its interaction with PD-1 to inhibit PD-1 signaling, thereby restoring T-cell activation and antitumor cytotoxicity; its Fc region can also mediate ADCC against PD-L1-expressing tumor cells.
Avelumab binds PD-L1 on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to trigger ADCC (and possibly ADCP), directly killing PD-L1–expressing cells; it also indirectly enhances T‑cell killing via PD‑1/PD‑L1 blockade.