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.
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).
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.
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.
A Trop-2–directed antibody–drug conjugate (brand name Trodelvy) consisting of a humanized anti–Trop-2 IgG1 monoclonal antibody linked via a hydrolyzable linker to SN-38, the active metabolite of irinotecan and a topoisomerase I inhibitor. Binding to Trop-2 on tumor cells triggers internalization and intracellular release of SN-38, causing DNA damage and cell death with a bystander effect.
Trop-2-directed IgG1 antibody-drug conjugate linked via a hydrolyzable linker to SN-38 (a topoisomerase I inhibitor). Binding to Trop-2 on tumor cells triggers internalization and intracellular release of SN-38, which stabilizes Topo I-DNA complexes, causing DNA breaks, replication arrest, and apoptosis; the membrane-permeable payload produces a bystander killing effect.
ADC binds Trop-2, is internalized, and releases SN-38 (topoisomerase I inhibitor) intracellularly, causing DNA damage, replication arrest, and apoptosis; the membrane-permeable payload can also cause bystander killing.
An antibody–drug conjugate targeting NaPi2b (SLC34A2) that, after binding and internalization into tumor cells, releases a topoisomerase I inhibitor payload (exatecan/camptothecan class) to inhibit topo I, cause replication-associated DNA breaks, and induce cell death; administered IV every 3 weeks.
Humanized IgG1 antibody–drug conjugate targeting NaPi2b (SLC34A2). After binding and internalization, a cleavable linker releases exatecan, a camptothecin-class topoisomerase I inhibitor, which blocks topo I, induces replication-associated DNA breaks, and triggers cell cycle arrest and apoptosis, with potential bystander killing of adjacent tumor cells.
ADC binds NaPi2b, is internalized, and releases exatecan (topoisomerase I inhibitor) after linker cleavage, causing replication-associated DNA breaks, cell-cycle arrest, and apoptosis; can also cause bystander killing of neighboring cells.