Autologous, gene-modified CAR T-cell therapy; patient T cells engineered to express a chimeric antigen receptor targeting CD19 to induce targeted cytotoxicity.
Autologous T cells are genetically engineered to express an anti‑CD19 chimeric antigen receptor. Binding to CD19 on B‑lineage cells triggers MHC‑independent T‑cell activation (CD3ζ with costimulation), resulting in proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of CD19+ malignant B cells, with on‑target depletion of CD19+ cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells and trigger MHC-independent T-cell activation, leading to perforin/granzyme-mediated cytolysis (and death-receptor signaling) of CD19+ cells.
Oral small-molecule, highly selective BCL-2 inhibitor (BH3 mimetic) that restores mitochondrial apoptosis in CLL cells (also known as BGB-11417).
Oral BH3‑mimetic that selectively binds and inhibits the anti‑apoptotic protein BCL‑2, displacing pro‑apoptotic factors to trigger mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL‑2–dependent tumor cells (e.g., CLL).
YES
DIRECT
BH3-mimetic inhibition of BCL-2 displaces pro-apoptotic factors, activates BAX/BAK, triggers mitochondrial outer membrane permeabilization, caspase activation, and intrinsic apoptosis in BCL-2–dependent cells.
Oral BCL-2 inhibitor (BH3 mimetic) that induces apoptosis in CLL cells.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the BCL-2 hydrophobic groove, neutralizes its anti-apoptotic function, and restores mitochondrial apoptosis in malignant B cells; relatively spares BCL-XL, reducing thrombocytopenia risk.
YES
DIRECT
Venetoclax is a BH3-mimetic that binds and inhibits BCL-2, releasing pro-apoptotic effectors (BAX/BAK) to trigger mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.
Intravenous type II anti-CD20 monoclonal antibody that depletes B cells via ADCC, direct cell death, and complement-dependent cytotoxicity.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC, direct caspase-independent cell death, and complement-dependent cytotoxicity (CDC).
YES
DIRECT
Binds CD20 on B cells and induces killing via enhanced Fc gamma RIIIa–mediated ADCC by immune effectors, complement-dependent cytotoxicity (CDC), and direct caspase-independent cell death.