Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC by NK cells/macrophages; CD20 crosslinking can also trigger apoptosis.
Human IgG1 monoclonal antibody targeting PD-L1, blocking PD-L1/PD-1 interactions to enhance T-cell responses; can mediate ADCC.
Human IgG1 monoclonal antibody that binds PD-L1 and blocks its interaction with PD-1, releasing inhibitory checkpoint signaling to restore and enhance T‑cell antitumor activity; its Fc can also mediate ADCC against PD‑L1–expressing tumor cells.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, engages Fcγ receptor–bearing effector cells (e.g., NK cells) to trigger ADCC that kills PD-L1–expressing cells; checkpoint blockade also indirectly enhances T-cell killing.
A bispecific T-cell–engaging antibody (PF-06863135) targeting BCMA on myeloma cells and CD3 on T cells to redirect T-cell cytotoxicity against BCMA-positive cells.
Elranatamab is a bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to form an immune synapse and activate cytotoxic T-cell killing of BCMA-positive myeloma cells.
Elranatamab bridges CD3 on T cells and BCMA on target cells, forming an immune synapse that activates T-cell cytotoxicity (perforin/granzyme-mediated killing) of BCMA-positive cells.
Autologous T cells genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells, enabling antigen-dependent T-cell activation and cytotoxic killing independent of the native TCR; designed to broaden AML coverage and reduce antigen escape.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) independent of the native TCR, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of AML blasts and leukemic stem/progenitor cells. Dual targeting is intended to broaden AML coverage and reduce antigen escape.
CAR-T cells recognize CLL1 on target cells, triggering CAR signaling and T‑cell effector functions that lyse the cells via perforin/granzyme-mediated cytotoxicity (and Fas/FasL pathways).
Autologous T cells genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells, enabling antigen-dependent T-cell activation and cytotoxic killing independent of the native TCR; designed to broaden AML coverage and reduce antigen escape.
Autologous T cells are genetically engineered to express chimeric antigen receptors that recognize CLL1 (CLEC12A) and CD38 on AML cells. Antigen binding triggers CAR signaling (CD3ζ with costimulatory domains) independent of the native TCR, leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of AML blasts and leukemic stem/progenitor cells. Dual targeting is intended to broaden AML coverage and reduce antigen escape.
CAR-T cells bind CD38 via the CAR, triggering T-cell activation and perforin/granzyme-mediated killing (and death receptor pathways) of CD38+ cells.