Investigational, off-the-shelf allogeneic iPSC-derived natural killer (NK) cell therapy intended to kill tumor cells directly and augment antibody-dependent cellular cytotoxicity (ADCC) when paired with anti-CD20 antibodies.
Allogeneic iPSC-derived NK cells engineered with an anti-CD19 CAR to recognize and kill CD19+ tumor cells and release inflammatory cytokines. Includes a high-affinity, non-cleavable CD16 to enhance antibody-dependent cellular cytotoxicity with tumor-targeting antibodies (e.g., rituximab) and an IL-15/IL-15Rα fusion to support NK survival and persistence. An alloimmune defense receptor targeting 4-1BB eliminates alloreactive host immune cells, and CD38 knockout prevents NK fratricide and enables combination with anti-CD38 antibodies.
Anti-CD19 CAR-engineered NK cells bind CD19 and directly kill target cells via NK degranulation (perforin/granzyme-mediated apoptosis); ADCC can augment killing when tumor-bound antibodies are present.
Investigational, off-the-shelf allogeneic iPSC-derived natural killer (NK) cell therapy intended to kill tumor cells directly and augment antibody-dependent cellular cytotoxicity (ADCC) when paired with anti-CD20 antibodies.
Allogeneic iPSC-derived NK cells engineered with an anti-CD19 CAR to recognize and kill CD19+ tumor cells and release inflammatory cytokines. Includes a high-affinity, non-cleavable CD16 to enhance antibody-dependent cellular cytotoxicity with tumor-targeting antibodies (e.g., rituximab) and an IL-15/IL-15Rα fusion to support NK survival and persistence. An alloimmune defense receptor targeting 4-1BB eliminates alloreactive host immune cells, and CD38 knockout prevents NK fratricide and enables combination with anti-CD38 antibodies.
FT522 NK cells express an alloimmune defense receptor that binds 4-1BB (CD137) on activated alloreactive host immune cells, triggering NK activation and direct killing via perforin/granzyme-mediated cytolysis.
Chimeric IgG1 monoclonal antibody targeting CD20 on B cells; mediates antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Chimeric IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Binds CD20 and eliminates target B cells via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (CDC), and apoptosis signaling.
Intravenous Nectin-4–directed antibody–drug conjugate delivering MMAE, a microtubule-disrupting cytotoxin.
Nectin-4–targeted monoclonal antibody linked via a cleavable linker to the cytotoxin MMAE. After binding Nectin-4 on tumor cells and internalization, linker cleavage releases MMAE, which binds tubulin to inhibit microtubule polymerization, causing G2/M cell-cycle arrest and apoptotic cell death in Nectin-4–expressing tumors.
ADC binds Nectin-4, is internalized, and releases MMAE, which disrupts microtubules (tubulin inhibition), causing G2/M arrest and apoptotic death of Nectin-4–expressing cells.
An anti-CD20 monoclonal antibody that depletes malignant B cells via complement activation, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via complement-dependent cytotoxicity and Fc-mediated ADCC by immune effector cells; it can also trigger apoptosis.