Anti-CD79b antibody-drug conjugate delivering MMAE to B cells; microtubule toxin–mediated cytotoxicity.
Anti-CD79b antibody-drug conjugate that binds CD79b on B cells, is internalized, and releases the microtubule toxin MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
NO
INDIRECT
Polatuzumab vedotin binds CD79b on B cells, is internalized, and releases MMAE, which inhibits beta-tubulin polymerization to cause mitotic arrest and apoptosis. Beta-tubulin expression alone does not confer targeting.
Anti-CD20 monoclonal antibody causing B-cell depletion via ADCC and complement activation.
Unconjugated anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates cell depletion/killing via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptosis, eliminating CD20-positive malignant and normal B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by NK/macrophages, activates complement (CDC), and can directly induce apoptosis via CD20 signaling.
Selective BCL-2 inhibitor inducing apoptosis in malignant B cells.
Selective BCL-2 inhibitor (BH3-mimetic) that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, releases pro-apoptotic effectors (e.g., BAX/BAK), and induces mitochondrial apoptosis in malignant B cells; sparing BCL-XL reduces thrombocytopenia.
YES
DIRECT
BH3-mimetic binds and inhibits BCL-2, releasing BAX/BAK to induce mitochondrial outer membrane permeabilization and caspase-dependent intrinsic apoptosis in target-expressing cells.
An in vivo gene therapy using a lentiviral vector that delivers a CD20-specific chimeric antigen receptor (CAR20) transgene. Following a single IV infusion, it transduces the patient’s immune cells to generate CAR-T and CAR-NK cells in vivo, which bind CD20 on malignant B cells and mediate cytotoxic killing.
INT2104 is an in vivo lentiviral gene therapy that delivers a CD20-specific CAR transgene (CAR20) to the patient’s immune cells after IV infusion. The transduced T and NK cells express CAR20, recognize CD20 on malignant B cells, form an immune synapse, and mediate cytotoxic killing via perforin/granzyme release and cytokine-driven mechanisms, depleting CD20-positive tumor cells.
YES
DIRECT
CAR20-expressing T and NK cells recognize CD20, form an immune synapse, and kill target cells via perforin/granzyme-mediated cytolysis and cytokine-driven mechanisms.
An investigational anti-CD38 therapeutic monoclonal antibody administered intravenously (16 mg/kg weekly for 8 weeks) to deplete CD38-expressing long-lived plasma cells and plasmablasts, aiming to reduce pathogenic antiplatelet autoantibodies and improve platelet counts in refractory ITP.
Anti-CD38 monoclonal antibody that binds CD38 on long-lived plasma cells and plasmablasts, triggering ADCC, CDC, and ADCP to deplete these cells and reduce pathogenic antiplatelet autoantibodies; may also inhibit CD38 ectoenzyme activity.
YES
DIRECT
The anti-CD38 antibody binds CD38 on target cells and, via its Fc, recruits immune effectors to kill through ADCC, CDC, and ADCP; it may also induce apoptosis and inhibit CD38 ectoenzyme activity.