Anti-EGFR monoclonal antibody that blocks EGFR signaling; used as a rechallenge in RAS/NRAS/BRAF/EGFR wild-type disease.
Chimeric monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor dimerization, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling; can elicit Fc-mediated ADCC; results in antiproliferative effects, with activity primarily in RAS/NRAS/BRAF wild-type tumors.
YES
DIRECT
Cetuximab binds EGFR on target cells and its Fc engages FcγR-expressing immune effectors (e.g., NK cells) to trigger ADCC (±CDC), killing EGFR+ cells; it also blocks EGFR signaling with antiproliferative effects.
Intravenous anti‑CD20 monoclonal antibody that depletes B cells via complement‑dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes CD20+ cells via complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) via FcγR-bearing effector cells, and can directly trigger apoptosis.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding, receptor activation and dimerization, thereby inhibiting downstream MAPK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its IgG1 Fc can also recruit immune effector functions to mediate antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-expressing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC), killing EGFR+ cells; EGFR blockade itself is mainly cytostatic.
Autologous CD19-directed chimeric antigen receptor T-cell (CAR-T) therapy produced via the PrimeCAR platform (~3-day manufacturing) with a high T-naive cell fraction; administered as a single IV infusion after lymphodepletion to treat relapsed/refractory CD19+ B-cell non-Hodgkin lymphoma. Mechanism: engineered T cells expressing a CD19-binding CAR activate via CD3ζ, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity against CD19+ B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor; upon binding CD19 on B cells, the CAR signals via CD3ζ to activate and expand the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of CD19+ malignant and normal B cells.
YES
DIRECT
CD19 CAR-T cells bind CD19 on B cells, signal via CD3ζ, and directly lyse CD19+ cells through perforin/granzyme (and death receptor) pathways.
An antibody–drug conjugate composed of a humanized anti–Trop-2 monoclonal antibody linked to SN-38 (irinotecan’s active metabolite), delivering a topoisomerase I inhibitor to Trop-2–expressing tumor cells to induce DNA single-strand breaks and apoptosis.
Humanized anti–Trop-2 monoclonal antibody linked to SN-38 (irinotecan’s active metabolite). The antibody binds Trop-2 on tumor cells, is internalized, and 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; may also exert a bystander cytotoxic effect.
YES
DIRECT
ADC binds TROP2 on tumor cells, is internalized, and releases SN-38 intracellularly to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis (with possible bystander killing).