Oral small-molecule BCL-2 inhibitor (BH3 mimetic) that restores mitochondrial apoptosis in BCL-2–dependent CLL cells.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, neutralizes its anti-apoptotic function, and restores mitochondrial apoptosis in BCL-2–dependent tumor cells; spares BCL-XL, reducing thrombocytopenia risk.
YES
DIRECT
Venetoclax directly inhibits BCL-2, freeing pro-apoptotic BH3-only proteins to activate BAX/BAK, inducing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL‑2–dependent cells.
Intravenous chimeric monoclonal antibody against CD20 that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and depletes them via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates ADCC, CDC, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and induces Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct apoptotic signaling, resulting in depletion of CD20-positive B cells.
YES
DIRECT
Rituximab binds CD20 on B cells and induces Fc-mediated ADCC (NK/macrophages), complement-dependent cytotoxicity, and can trigger direct apoptotic signaling, leading to targeted killing of CD20+ cells.
Autologous genetically engineered T cells expressing an anti-CD19 chimeric antigen receptor; administered as a single IV infusion with 3+3 dose escalation (1×10^5, 3×10^5, 1×10^6 CAR+ cells/kg) after lymphodepletion. The CAR redirects patient T cells to recognize CD19 on B cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with expected on-target B-cell depletion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes CD19 on B cells, leading to antigen-dependent T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+ malignant and normal B cells (on-target B-cell aplasia).
YES
DIRECT
Anti-CD19 CAR-T cells engage CD19 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytotoxicity (and death-receptor pathways), causing on-target B-cell lysis.
An autologous anti-CD19 chimeric antigen receptor T-cell (CAR-T) therapy in which a patient's T cells are genetically engineered to express a CD19-specific CAR. CAR engagement activates CD3ζ signaling with costimulation (e.g., CD28/4-1BB), leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-expressing B-cell leukemia cells.
Autologous T cells genetically engineered to express a CD19-targeted chimeric antigen receptor; CD19 engagement activates CD3zeta and costimulatory (CD28/4-1BB) signaling, driving T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated killing of CD19-positive B-cell leukemia cells.
YES
DIRECT
CD19-specific CAR-T cells bind CD19 on target cells, become activated (CD3zeta with costimulation) and kill via perforin/granzyme-mediated cytotoxicity leading to apoptosis/lysis.