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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
A recombinant human broadly neutralizing monoclonal antibody that targets the HIV-1 gp120 V3-glycan (N332) supersite to inhibit viral entry; neutralizes diverse HIV-1 strains and can mediate Fc-dependent effector functions (ADCC/ADCP). The LS Fc mutations enhance FcRn binding and extend serum half-life.
10-1074-LS is a broadly neutralizing human monoclonal antibody that binds the HIV-1 Env gp120 V3-glycan (N332) supersite, blocking Env–CD4 interactions and viral attachment/entry to neutralize diverse HIV-1 strains. Its Fc region can engage Fcγ receptors to mediate effector functions such as ADCC and ADCP, aiding clearance of virions/infected cells. LS Fc mutations (M428L/N434S) enhance FcRn binding, extending serum half-life.
NO
INDIRECT
10-1074-LS binds HIV-1 Env (gp120) on virions/infected cells and engages Fcγ receptors such as CD32A on effector cells to mediate ADCC/ADCP against Env+ targets. CD32A-expressing cells are not targeted or killed; they serve as effectors.
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.
NO
INDIRECT
Mosunetuzumab engages CD3ε on T cells to redirect them to CD20+ B cells; activated T cells kill CD20+ targets via perforin/granzyme. CD3ε+ T cells are effectors, not killed.