Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1); activates NK cells and mediates antibody-dependent cellular cytotoxicity against myeloma cells.
Humanized IgG1 monoclonal antibody that binds SLAMF7 (CS1) on myeloma and NK cells; activates NK cells and induces Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) against SLAMF7-expressing myeloma cells.
Elotuzumab binds SLAMF7 on myeloma cells and engages/activates NK cells via Fc gamma receptors (CD16) and SLAMF7 on NK cells, triggering antibody-dependent cellular cytotoxicity to lyse SLAMF7+ tumor cells.
A CD19-targeting antibody-drug conjugate consisting of a human monoclonal IgG linked to a pyrrolobenzodiazepine (PBD) prodrug. Administered intravenously on Day 1 of 21-day cycles. The anti-CD19 antibody binds CD19 on B cells, is internalized, and releases an activated PBD payload that forms DNA interstrand crosslinks, blocking replication/transcription and inducing apoptosis in CD19-positive malignant B lymphocytes.
CD19-targeting monoclonal antibody-drug conjugate; after binding CD19 on B cells and internalization, a tumor-cleavable linker is processed to release a PBD payload that forms DNA interstrand crosslinks, blocking replication/transcription and inducing apoptosis in CD19-positive malignant B lymphocytes.
The ADC binds CD19 on target cells, is internalized, and the linker is cleaved in lysosomes to release a PBD payload that forms DNA interstrand crosslinks, blocking replication/transcription and triggering apoptosis of CD19+ cells.
Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated antibody-dependent cellular cytotoxicity; it can also trigger apoptosis of CD20+ cells.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting tumor-associated antigen(s); administered as a single IV infusion (~1–2×10^6 cells/kg) after fludarabine/cyclophosphamide lymphodepletion to enable expansion and persistence. Mechanism: MHC-independent antigen recognition via CAR with CD3ζ ± costimulatory domains, leading to T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxic killing.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that binds tumor-associated antigens independent of MHC, delivering CD3ζ signaling with costimulatory domains to activate T cells. Upon antigen engagement, CAR-T cells expand, release cytokines, and kill target cells via perforin/granzyme and apoptotic pathways. Lymphodepleting chemotherapy (fludarabine/cyclophosphamide) enhances CAR-T expansion and persistence after infusion.
CAR-T cells bind the selected tumor antigen via the CAR, become activated, and kill antigen-expressing cells through perforin/granzyme-mediated cytolysis and death-receptor–mediated apoptosis.
Natural killer cells genetically engineered to express a chimeric antigen receptor to enhance antigen-specific cytotoxicity; given as a single IV infusion (~1–2×10^6 cells/kg) following lymphodepleting chemotherapy. Mechanism: CAR-mediated target recognition combined with innate NK cytotoxic pathways (perforin/granzyme, Fas/TRAIL).
NK cells are genetically engineered to express a chimeric antigen receptor that enables antigen-specific, MHC-independent recognition of tumor cells. CAR engagement activates NK signaling and enhances innate NK cytotoxic mechanisms, leading to target-cell killing via perforin/granzyme release and death-receptor pathways (Fas/TRAIL), along with cytokine secretion to eliminate antigen-expressing tumor cells.
CAR on engineered NK cells binds the tumor antigen, triggering NK activation and killing antigen-positive cells via perforin/granzyme release and death-receptor pathways (FasL/TRAIL).