Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via Fc-gamma receptor IIIa (CD16)-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via FcγRIIIa-mediated ADCC, complement-dependent cytotoxicity (C1q activation), and direct apoptosis upon CD20 cross-linking.
Allogeneic CD45RA− memory T cells engineered with an anti-CD19 chimeric antigen receptor containing 4-1BB/CD3ζ signaling domains to target and kill CD19+ B-lineage leukemia cells.
Allogeneic CD45RA− memory T cells engineered to express an anti‑CD19 chimeric antigen receptor with 4‑1BB costimulation and CD3ζ signaling recognize CD19 on B‑lineage leukemia cells, triggering T‑cell activation and cytotoxic killing; 4‑1BB enhances proliferation and persistence, and use of memory (CD45RA−) T cells aims to improve durability and reduce GVHD risk.
Anti-CD19 CAR T cells bind CD19 on target B cells, become activated via 4-1BB/CD3zeta signaling, and kill them through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
CD20×CD3 bispecific monoclonal antibody (T‑cell engager) that redirects T‑cell cytotoxicity against CD20+ B cells.
Humanized CD20×CD3 bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells, crosslinking and activating T cells to mediate targeted cytotoxic killing of CD20-positive B-cell malignancies.
Bispecific antibody bridges CD3 on T cells to CD20 on B cells, activating T cells to form an immunologic synapse and kill CD20+ cells via perforin/granzyme-mediated apoptosis.
Anti‑CD79b antibody–drug conjugate that delivers MMAE (vedotin), a microtubule inhibitor, to induce apoptosis in CD79b+ B cells.
Anti-CD79b monoclonal antibody–drug conjugate; binds CD79b on B cells, is internalized, and a protease-cleavable linker releases MMAE (vedotin), which inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ malignant B cells.
The ADC binds CD79b on B cells, is internalized, and releases MMAE intracellularly; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD79b+ cells.
An allogeneic, off-the-shelf CAR T-cell therapy enriched for T stem cell memory (Tscm) cells. These engineered T cells express a dual CAR targeting CD19 and CD20 on B cells to drive activation, proliferation, and cytotoxic killing of malignant B cells. Administered as a single IV dose after lymphodepletion; the Tscm phenotype is intended to enhance persistence and self-renewal.
Allogeneic T cells enriched for T stem cell memory are engineered to express dual CARs targeting CD19 and CD20 on B cells. Antigen binding activates T-cell signaling leading to proliferation and cytotoxic killing of malignant B cells; dual targeting aims to limit antigen escape, while the Tscm phenotype supports persistence and self-renewal. Given after lymphodepletion; an optional rimiducid safety switch can induce rapid ablation of the cells if required.
Anti-CD19 CAR T cells bind CD19 on target cells; CAR signaling activates cytotoxic T-cell effector functions, leading to perforin/granzyme-mediated apoptosis (and Fas/FasL killing) of CD19+ cells.