Monoclonal antibodies targeting BCMA conjugated to cytotoxic payloads to deliver chemotherapy directly to myeloma cells.
An anti-BCMA monoclonal antibody delivers a cytotoxic payload to BCMA-expressing myeloma cells. After binding BCMA and internalization, the linker is cleaved in the cell to release the toxin, causing microtubule disruption or DNA damage and inducing apoptosis; Fc-mediated effector functions may contribute.
ADC binds BCMA, is internalized, linker is cleaved to release a cytotoxic payload that disrupts microtubules or damages DNA, inducing apoptosis; Fc-mediated ADCC/CDC may contribute.
An intravenous anti-MET antibody–drug conjugate (ABBV-399) that targets MET-overexpressing tumor cells and delivers the microtubule toxin MMAE.
An anti-MET monoclonal antibody linked via a cleavable valine-citrulline linker to the microtubule toxin MMAE. After binding to c-MET on MET-overexpressing tumor cells and internalization, MMAE is released intracellularly to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis.
ADC binds MET on target cells, is internalized, linker cleavage releases MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis (with potential bystander effect).
Lentivirally engineered CAR T cells targeting CD123; administered IV at 2×10^6–1×10^7 CAR-T/kg with dose escalation; designed for MHC-independent cytotoxicity against CD123+ myeloid blasts.
Autologous/allogeneic T cells are lentivirally engineered to express an anti‑CD123 chimeric antigen receptor. Upon binding CD123 on myeloid blasts, the CAR provides MHC‑independent activation signaling that drives T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD123+ tumor cells.
Anti-CD123 CAR T cells bind CD123 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (MHC-independent).
An autologous, gene-modified T-cell therapy in which patient T cells are engineered to express chimeric antigen receptors targeting CD19 and a BAFF-based target, leading to antigen-dependent T-cell activation, cytokine release, and cytotoxic killing of malignant B cells in relapsed/refractory B-ALL and B-cell NHL.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes CD19 and a BAFF pathway target on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity to eliminate malignant B cells, addressing antigen escape in relapsed/refractory B-ALL and B-cell NHL.
CAR T cells recognize CD19 on target cells, become activated, and kill them via T‑cell cytotoxic pathways (perforin/granzyme-mediated lysis and Fas–FasL apoptosis) after antigen engagement.
An autologous, gene-modified T-cell therapy in which patient T cells are engineered to express chimeric antigen receptors targeting CD19 and a BAFF-based target, leading to antigen-dependent T-cell activation, cytokine release, and cytotoxic killing of malignant B cells in relapsed/refractory B-ALL and B-cell NHL.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes CD19 and a BAFF pathway target on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity to eliminate malignant B cells, addressing antigen escape in relapsed/refractory B-ALL and B-cell NHL.
CAR T cells bearing a BAFF-targeted CAR bind BAFF-R on target cells, become activated, and induce perforin/granzyme-dependent cytolysis to kill BAFF-R–positive cells.