An anti–PD-L1 IgG1 monoclonal antibody (checkpoint inhibitor) that blocks PD-1/PD-L1 signaling to restore cytotoxic T-cell activity and can mediate ADCC. Brand name: Bavencio.
Avelumab is an IgG1 anti–PD-L1 monoclonal antibody that blocks PD-1/PD-L1 checkpoint signaling to restore cytotoxic T-cell activity and can also mediate antibody-dependent cellular cytotoxicity (ADCC) against PD-L1–expressing tumor cells.
Avelumab binds PD-L1 and its IgG1 Fc engages Fc-gamma receptors on NK cells to trigger ADCC (and possibly ADCP), directly killing PD-L1–expressing cells; it also restores T-cell killing via PD-1/PD-L1 blockade.
Autologous CD19-directed CAR T-cell therapy with CD28 costimulation; gene-modified T cells recognize CD19 on malignant B cells to drive T-cell activation and cytotoxic killing.
Autologous T cells are genetically engineered to express a CD19-directed chimeric antigen receptor with CD28 costimulation. Upon binding CD19 on malignant B cells, CAR signaling activates and expands the T cells, triggering perforin/granzyme-mediated cytotoxicity and cytokine release to eliminate CD19+ B cells.
CD19-directed CAR T cells bind CD19 on target cells, form an immune synapse, and induce apoptosis via perforin/granzyme (and Fas–FasL) after CAR activation.
T-cell–engaging bispecific antibody (CD20×CD3) that bridges CD3 on T cells to CD20 on B cells, inducing T-cell–mediated B-cell lysis; administered with step-up dosing.
CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T cells for perforin/granzyme-mediated lysis of CD20+ B-cell malignancies; step-up dosing used to mitigate cytokine release.
Bispecific antibody links CD3 on T cells to CD20 on target cells, forming an immune synapse and inducing perforin/granzyme-mediated T‑cell killing of CD20+ cells.
Glycoengineered type II anti-CD20 monoclonal antibody used as pre-treatment to deplete peripheral B cells and mitigate CRS; mediates ADCC and direct cell death.
Glycoengineered type II anti-CD20 IgG1 that binds CD20 on B cells and, through enhanced Fc-gamma RIIIa (CD16a) engagement from afucosylated Fc glycans, induces strong ADCC (and phagocytosis) and triggers direct, caspase-independent cell death to deplete B cells.
Binds CD20 on B cells; afucosylated Fc enhances FcγRIIIa engagement to trigger strong NK cell–mediated ADCC and macrophage phagocytosis, and the type II antibody also induces direct, caspase‑independent cell death.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy administered intravenously after lymphodepleting chemotherapy to mediate TCR-dependent cytotoxicity against tumor cells.
Autologous TILs expanded ex vivo are reinfused after lymphodepleting chemotherapy. They recognize patient-specific tumor antigens via TCR-MHC and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, with IL-2 supporting T-cell activation, proliferation, and persistence.
Infused autologous TILs recognize tumor neoantigen peptide–MHC I via their TCR and directly kill target cells through perforin/granzyme-mediated apoptosis (and Fas–FasL), supported by IL-2.