An antibody-drug conjugate (Trodelvy) comprising a humanized anti–Trop-2 IgG1 linked to SN-38 (a topoisomerase I inhibitor). It binds Trop-2 on tumor cells, is internalized, and releases SN-38 to inhibit topoisomerase I, causing DNA single-strand breaks, replication arrest, and apoptosis; the hydrolyzable linker supports a bystander effect.
Humanized anti-Trop-2 IgG1 antibody linked to SN-38. After binding Trop-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which inhibits topoisomerase I by stabilizing topo I-DNA complexes, causing DNA single-strand breaks, replication arrest, and apoptosis; the hydrolyzable linker enables a bystander cytotoxic effect.
The ADC binds TROP2, is internalized, and releases SN-38 intracellularly; SN-38 inhibits topoisomerase I, causing DNA damage, replication arrest, and apoptosis (with a hydrolyzable linker allowing some bystander killing).
Gene-modified T cells engineered with chimeric antigen receptors targeting GD2 and B7-H3; administered primarily as autologous cells with option for healthy-donor T cells if autologous cells are unsuitable. Designed for MHC-independent tumor recognition, T-cell activation, cytokine release, and cytotoxic killing to reduce antigen escape in GD2/B7-H3–expressing tumors.
Gene-modified T cells expressing CARs against GD2 and B7-H3 recognize these antigens on tumor cells independent of MHC, triggering T-cell activation, cytokine release, proliferation, and cytotoxic killing; dual-antigen targeting is intended to reduce antigen escape in GD2/B7-H3–expressing tumors.
CAR T cells recognize GD2 via the CAR, become activated, and kill GD2-expressing cells through perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis), with supportive cytokine release.
Gene-modified T cells engineered with chimeric antigen receptors targeting GD2 and B7-H3; administered primarily as autologous cells with option for healthy-donor T cells if autologous cells are unsuitable. Designed for MHC-independent tumor recognition, T-cell activation, cytokine release, and cytotoxic killing to reduce antigen escape in GD2/B7-H3–expressing tumors.
Gene-modified T cells expressing CARs against GD2 and B7-H3 recognize these antigens on tumor cells independent of MHC, triggering T-cell activation, cytokine release, proliferation, and cytotoxic killing; dual-antigen targeting is intended to reduce antigen escape in GD2/B7-H3–expressing tumors.
CAR T cells recognizing B7-H3 activate upon antigen binding and kill target cells via contact-dependent cytotoxicity (perforin/granzyme release and Fas–FasL apoptosis).
CD20×CD3 bispecific monoclonal antibody that redirects T cells via CD3 to lyse CD20-positive B cells.
CD20×CD3 bispecific monoclonal antibody that binds CD3 on T cells and CD20 on B cells, crosslinking them to redirect and activate T cells to form an immune synapse and lyse CD20-positive B cells via perforin/granzyme release and cytokine-mediated cytotoxicity.
Glofitamab bridges CD3+ T cells to CD20-expressing cells, forming an immune synapse; activated T cells kill CD20+ cells via perforin/granzyme release and cytokine-mediated cytotoxicity.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; gene-modified T cells target CD19+ B cells/plasmablasts to induce B-cell aplasia and reset humoral immunity.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with 4-1BB and CD3zeta signaling domains bind CD19 on B cells/plasmablasts and induce targeted cytotoxicity, causing B-cell aplasia and resetting humoral immunity (also cytotoxic to CD19+ tumor cells).
Anti-CD19 CAR T cells bind CD19 on target cells and induce T cell–mediated killing via perforin/granzyme (and Fas–FasL) apoptosis.