An anti-CD19 antibody–drug conjugate (Zynlonta) that delivers a pyrrolobenzodiazepine dimer to CD19+ B cells, causing DNA crosslinking and apoptosis.
Anti-CD19 antibody–drug conjugate that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer payload via a cleavable linker; the PBD binds the DNA minor groove to form interstrand crosslinks, blocking DNA replication and inducing apoptosis in CD19-expressing tumor cells.
NO
INDIRECT
The ADC targets CD19 (not DNA) for cell entry; after CD19-mediated internalization, the PBD payload binds the DNA minor groove (guanine N2) to form interstrand crosslinks, blocking replication and inducing apoptosis in CD19+ cells.
Chimeric IgG1 monoclonal antibody against EGFR that inhibits downstream signaling to reduce proliferation and survival and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR that binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its Fc region also mediates antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on immune effector cells (e.g., NK cells), triggering antibody‑dependent cellular cytotoxicity; complement‑dependent cytotoxicity may also occur, and EGFR signaling blockade can promote apoptosis.
CAR T cells engineered via lentiviral vector to target CD5; IV administration with dose escalation; intended to eliminate CD5+ T-cell malignancies through CAR signaling and effector functions.
Autologous or allogeneic T cells are lentivirally engineered to express a CD5-specific chimeric antigen receptor. Upon binding CD5 on malignant T cells, the CAR provides MHC-independent activation, leading to T-cell expansion and perforin/granzyme-mediated cytotoxicity with cytokine release, eliminating CD5-positive tumor cells.
YES
DIRECT
CAR T cells recognize CD5 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated cytotoxicity with associated cytokine release, eliminating CD5+ cells.
Humanized anti-CD20 IgG1 monoclonal antibody (Ocrevus) administered subcutaneously; depletes CD20+ B cells via ADCC, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation, costimulation, and pro-inflammatory cytokines while sparing stem cells and plasma cells; indirectly dampens T-cell activation and CNS inflammation.
Humanized anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via ADCC, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation/costimulation and pro-inflammatory cytokines while sparing stem and plasma cells; indirectly dampens T-cell activation and CNS inflammation.
YES
DIRECT
Anti-CD20 IgG1 binds CD20 on B cells and induces Fc-mediated effector killing (ADCC/ADCP) and complement-dependent cytotoxicity, leading to lysis/apoptosis of CD20+ cells.
Chimeric IgG1 monoclonal antibody against EGFR that inhibits downstream signaling to reduce proliferation and survival and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR that binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its Fc region also mediates antibody-dependent cellular cytotoxicity (ADCC).
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a (FcγRIIIa) on NK cells to trigger ADCC that kills EGFR-positive targets. CD16a-expressing immune cells serve as effectors and are not killed by the drug.