Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and recruits immune effectors via its Fc to mediate ADCC (e.g., NK cells/macrophages), activates complement for CDC/lysis, and can trigger apoptosis upon CD20 cross-linking.
An autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy given as a single IV infusion; patient T cells are engineered to express a CAR targeting CD19 to mediate cytotoxic killing and cytokine-driven clearance of malignant B cells, with expected on-target B-cell aplasia.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19. Upon infusion, CAR engagement of CD19 on malignant and normal B cells activates CD3ζ and costimulatory signaling, driving T-cell expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+ cells, resulting in on-target B-cell aplasia.
YES
DIRECT
CD19 CAR-T cells bind CD19 on targets, trigger CD3ζ/costimulatory signaling, form an immune synapse, and kill via perforin/granzyme release (and death-receptor pathways), lysing CD19+ cells.
Autologous gene-modified T lymphocytes engineered to express chimeric antigen receptors that recognize tumor antigens independently of MHC, leading to potent T-cell activation and antitumor activity; associated with cytokine release syndrome and potential cardiotoxic effects.
Autologous T lymphocytes are genetically engineered to express chimeric antigen receptors (scFv-based receptors with CD3ζ and costimulatory domains such as CD28 or 4-1BB) that bind tumor-associated surface antigens independently of MHC. Antigen engagement triggers potent T-cell activation, expansion, and cytotoxic killing of target cells via perforin/granzyme and cytokine release, which can cause cytokine release syndrome and potential cardiotoxic effects.
YES
DIRECT
CAR T cells recognize the tumor-associated surface antigen and directly kill antigen-positive cells via T-cell effector functions (perforin/granzyme-mediated apoptosis and death-receptor signaling) after CAR activation.
HER3-directed antibody–drug conjugate targeting ERBB3; internalization after receptor binding with subsequent release of a cytotoxic payload to kill HER3-expressing tumor cells.
HER3 (ERBB3)-targeted IgG1 ADC that binds HER3 on tumor cells, undergoes internalization and cleavable-linker processing to release a topoisomerase I inhibitor payload, stabilizing Topo I–DNA complexes and inducing DNA breaks, replication arrest, and apoptosis in HER3-expressing cells.
YES
DIRECT
ADC binds HER3 on target cells, is internalized, and releases a topoisomerase I inhibitor via a cleavable linker, causing DNA damage/replication arrest and apoptosis in HER3-expressing cells.
Anti-CD30 antibody–drug conjugate linked to MMAE; binds CD30 on Hodgkin Reed–Sternberg cells, internalizes, releases microtubule poison causing G2/M arrest and apoptosis.
Chimeric anti‑CD30 monoclonal antibody linked to the microtubule inhibitor MMAE via a protease‑cleavable valine‑citrulline linker; after binding CD30 on tumor cells and internalization, the linker is cleaved to release MMAE, which binds tubulin and blocks microtubule polymerization, causing G2/M arrest and apoptosis with selectivity for CD30‑positive cells.
YES
DIRECT
The anti‑CD30 ADC binds CD30, is internalized, and its linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis in CD30‑positive cells.