Type II anti-CD20 monoclonal antibody that enhances antibody-dependent cellular cytotoxicity and induces direct B-cell death.
Glycoengineered humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; enhanced Fc gamma RIII affinity increases antibody-dependent cellular cytotoxicity and it induces direct, caspase-independent B-cell death, depleting malignant CD20-positive B cells.
YES
DIRECT
Binds CD20 on B cells and causes killing via Fc gamma RIII–mediated antibody-dependent cellular cytotoxicity; also induces direct, caspase-independent B-cell death (with some complement-mediated lysis).
Type II anti-CD20 monoclonal antibody that enhances antibody-dependent cellular cytotoxicity and induces direct B-cell death.
Glycoengineered humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells; enhanced Fc gamma RIII affinity increases antibody-dependent cellular cytotoxicity and it induces direct, caspase-independent B-cell death, depleting malignant CD20-positive B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its Fc engages CD16a (FcγRIIIa) on NK cells to trigger ADCC killing of CD20+ B cells. CD16a-expressing cells are effectors, not killed by the drug.
Type I anti-CD20 monoclonal antibody mediating complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Chimeric type I anti-CD20 monoclonal antibody that binds CD20 on B cells and induces cell death via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, depleting CD20-positive B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and induces cell death via complement-dependent cytotoxicity, Fc-mediated ADCC by immune effector cells, and apoptosis.
Autologous, genetically engineered T cells expressing a chimeric antigen receptor that targets CD19 on B cells to mediate cytotoxicity in relapsed/refractory diffuse large B-cell lymphoma.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor. CAR binding to CD19 on malignant and normal B cells triggers MHC-independent T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, resulting in elimination of CD19-positive cells (e.g., in DLBCL).
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 and kill target cells via MHC-independent T-cell activation with perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).
Oral small-molecule BH3-mimetic BCL-2 inhibitor (Venclexta) that induces apoptosis of BCL-2–dependent plasma cells; particularly relevant in t(11;14) AL amyloidosis where BCL-2 expression is high.
Selective BH3-mimetic BCL-2 inhibitor that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, and restores mitochondrial apoptosis in BCL-2–dependent tumor/plasma cells; does not inhibit BCL-XL, reducing thrombocytopenia risk.
YES
DIRECT
Venetoclax is a BH3-mimetic that binds and inhibits BCL-2, displacing pro-apoptotic factors and enabling BAX/BAK activation, mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.