Anti-HER2 antibody–drug conjugate (RC48) that delivers MMAE; binds HER2, internalizes, and releases MMAE to disrupt microtubules and kill tumor cells.
Anti-HER2 monoclonal antibody–drug conjugate that binds HER2, is internalized, and releases the microtubule inhibitor MMAE via a cleavable linker, inhibiting tubulin polymerization to induce G2/M arrest and apoptosis in HER2-expressing tumor cells.
NO
INDIRECT
Disitamab vedotin binds HER2 on the cell surface, is internalized, and releases MMAE; MMAE then binds beta‑tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. Tubulin expression alone does not confer targeting—killing occurs only in cells that take up the ADC via HER2.
An intravenous bispecific T‑cell–redirecting antibody (MUC16×CD3) that binds MUC16 on tumor cells and CD3 on T cells to recruit and activate cytotoxic T cells, inducing tumor cell lysis.
A bispecific MUC16×CD3 T‑cell–redirecting antibody that binds MUC16 on tumor cells and CD3 on T cells, crosslinking and activating cytotoxic T cells to drive targeted lysis of MUC16‑expressing cancer cells.
YES
DIRECT
Bispecific MUC16×CD3 antibody crosslinks T cells to MUC16+ cells, activating T cells to deliver perforin/granzymes and lyse the target cells.
An intravenous bispecific T‑cell–redirecting antibody (MUC16×CD3) that binds MUC16 on tumor cells and CD3 on T cells to recruit and activate cytotoxic T cells, inducing tumor cell lysis.
A bispecific MUC16×CD3 T‑cell–redirecting antibody that binds MUC16 on tumor cells and CD3 on T cells, crosslinking and activating cytotoxic T cells to drive targeted lysis of MUC16‑expressing cancer cells.
NO
INDIRECT
Ubamatamab binds CD3 on T cells to activate and redirect them to MUC16+ tumor cells; the activated T cells kill the MUC16-expressing cells (perforin/granzyme), not the CD3+ T cells.
Autologous CAR T-cell gene therapy in which patient T cells are engineered to express two fully human CARs: anti-CD19 with CD28/CD3ζ signaling and anti-CD20 with 4-1BB/CD3ζ signaling to enhance activation and persistence and reduce antigen-loss escape.
Autologous T cells are genetically engineered to express two CARs: an anti‑CD19 CAR with CD28/CD3ζ signaling and an anti‑CD20 CAR with 4‑1BB/CD3ζ signaling. Upon binding CD19 or CD20 on B cells, the CARs activate T‑cell cytotoxicity and cytokine release to kill malignant B cells; CD28 promotes rapid activation/expansion and 4‑1BB enhances persistence. Dual antigen targeting is intended to reduce antigen‑loss escape and results in on‑target B‑cell aplasia.
YES
DIRECT
CAR T cells recognize CD19 via the CAR, form an immunologic synapse, and kill CD19+ cells through perforin/granzyme-mediated lysis and death-receptor pathways.
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.
NO
INDIRECT
SHR-A2009 targets HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor that binds Topo I to cause DNA breaks and apoptosis; Topo I expression alone is not the selection target.