Autologous, gene-modified CAR T-cell therapy that dual-targets CD19 and CD20 to induce antigen-dependent T-cell activation, proliferation, cytokine release, and cytotoxic elimination of malignant B cells; administered as a single-dose infusion after lymphodepletion.
Autologous T cells genetically engineered to express chimeric antigen receptors that co-target CD19 and CD20; antigen engagement activates CAR signaling leading to T-cell activation, proliferation, cytokine release, and cytotoxic elimination of malignant B cells (on-target B-cell aplasia).
CAR T cells recognize CD19 and are activated via CAR signaling, then kill target cells through perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis), causing on-target B-cell aplasia.
An autologous NKG2D-based CAR T-cell therapy in which patient T cells are gene-engineered to express a chimeric antigen receptor using the NKG2D receptor ectodomain fused to intracellular activation/costimulatory domains (e.g., CD3ζ). The cells target stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumor cells to mediate cytotoxicity and cytokine release.
Autologous T cells are engineered to express an NKG2D-based CAR (NKG2D ectodomain fused to 4-1BB and CD3ζ signaling domains) that recognizes stress-induced NKG2D ligands (MICA, MICB, ULBP1–6) on tumors, activating T cells to release cytokines and mediate perforin/granzyme-dependent cytotoxicity against NKG2DL-positive cancer cells.
NKG2D CAR T cells bind ULBP6 on target cells, activating CD3ζ/4-1BB signaling and inducing perforin/granzyme-mediated lysis with cytokine release.
Autologous, gene-modified CAR T-cell therapy that dual-targets CD19 and CD20 to induce antigen-dependent T-cell activation, proliferation, cytokine release, and cytotoxic elimination of malignant B cells; administered as a single-dose infusion after lymphodepletion.
Autologous T cells genetically engineered to express chimeric antigen receptors that co-target CD19 and CD20; antigen engagement activates CAR signaling leading to T-cell activation, proliferation, cytokine release, and cytotoxic elimination of malignant B cells (on-target B-cell aplasia).
CAR T cells bind CD20 via the CAR, become activated, and directly kill CD20+ cells via perforin/granzyme-mediated cytolysis and apoptosis, with supportive cytokine release.
Anti-CD20 monoclonal antibody that depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes CD20+ cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (MAC formation), and CD20 cross-linking–induced apoptosis.
An anti-HER2 antibody–drug conjugate that binds ERBB2 and delivers monomethyl auristatin E (MMAE) to tumor cells, inhibiting microtubules and mediating HER2 blockade/ADCC.
Disitamab vedotin is an anti‑HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, blocks HER2 signaling and mediates ADCC, then is internalized and releases the cytotoxic payload monomethyl auristatin E (MMAE). MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis, with potential bystander killing of adjacent cells.
ADC binds HER2, is internalized, and releases MMAE to inhibit microtubules causing G2/M arrest and apoptosis; additionally mediates ADCC and possible bystander killing.