An antibody–drug conjugate consisting of patritumab (anti-HER3 monoclonal antibody) linked to the deruxtecan topoisomerase I inhibitor payload (DXd). It binds HER3 on tumor cells, is internalized, and releases DXd to inhibit Topo I, causing DNA damage and cell death, with a potential bystander effect.
Human anti-HER3 monoclonal antibody (patritumab) linked via a cleavable linker to a deruxtecan (DXd) topoisomerase I inhibitor payload. Binds HER3 (ERBB3) on tumor cells, is internalized, and releases DXd intracellularly; DXd inhibits Topo I by stabilizing the Topo I–DNA cleavage complex and blocking religation, causing DNA damage, replication arrest, and apoptosis. The membrane-permeable payload can produce a bystander effect.
YES
DIRECT
ADC binds HER3 on target cells, is internalized, linker is cleaved to release the DXd topoisomerase I inhibitor; DXd stabilizes the Topo I–DNA cleavage complex causing DNA damage, replication arrest, and apoptosis, with a membrane-permeable payload enabling a bystander effect.
An antibody–drug conjugate consisting of patritumab (anti-HER3 monoclonal antibody) linked to the deruxtecan topoisomerase I inhibitor payload (DXd). It binds HER3 on tumor cells, is internalized, and releases DXd to inhibit Topo I, causing DNA damage and cell death, with a potential bystander effect.
Human anti-HER3 monoclonal antibody (patritumab) linked via a cleavable linker to a deruxtecan (DXd) topoisomerase I inhibitor payload. Binds HER3 (ERBB3) on tumor cells, is internalized, and releases DXd intracellularly; DXd inhibits Topo I by stabilizing the Topo I–DNA cleavage complex and blocking religation, causing DNA damage, replication arrest, and apoptosis. The membrane-permeable payload can produce a bystander effect.
YES
INDIRECT
The ADC binds HER3, is internalized, and releases the deruxtecan payload, which inhibits DNA topoisomerase I, stabilizing cleavage complexes and causing DNA damage and apoptosis; the membrane‑permeable payload can also kill nearby cells via a bystander effect.
An mRNA therapeutic (injection) that encodes a bispecific T‑cell engager targeting CD19 and CD3. After in vivo translation, the expressed CD19×CD3 engager redirects and activates T cells to kill CD19+ B cells, depleting autoreactive B-cell compartments and reducing autoantibody-producing cells (BiTE-like mechanism).
Injected mRNA is translated in vivo into a bispecific CD19xCD3 T‑cell engager that links CD3 on T cells to CD19 on B cells, redirecting and activating T cells to kill CD19+ B cells and deplete autoreactive, autoantibody‑producing compartments.
YES
DIRECT
An in vivo–expressed CD19xCD3 bispecific engages CD3 on T cells and CD19 on B cells, creating an immune synapse that redirects T cells to kill CD19+ cells via perforin/granzyme-mediated apoptosis.
An mRNA therapeutic (injection) that encodes a bispecific T‑cell engager targeting CD19 and CD3. After in vivo translation, the expressed CD19×CD3 engager redirects and activates T cells to kill CD19+ B cells, depleting autoreactive B-cell compartments and reducing autoantibody-producing cells (BiTE-like mechanism).
Injected mRNA is translated in vivo into a bispecific CD19xCD3 T‑cell engager that links CD3 on T cells to CD19 on B cells, redirecting and activating T cells to kill CD19+ B cells and deplete autoreactive, autoantibody‑producing compartments.
NO
INDIRECT
The mRNA expresses a CD19×CD3 bispecific that binds CD3ε on T cells to recruit/activate them against CD19+ B cells; T cells (CD3ε+) are not killed, they mediate killing of CD19+ targets via cytotoxic synapse and perforin–granzyme release.
Antibody–drug conjugate that binds a tumor-associated antigen, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and tumor cell death; potential bystander effect.
Nectin-4–targeted IgG1 antibody–drug conjugate; after binding and internalization, a cleavable linker releases a topoisomerase I inhibitor payload that inhibits topo I, causing DNA damage during replication and leading to cell-cycle arrest and apoptosis in antigen-expressing tumor cells, with potential bystander effect.
NO
INDIRECT
SHR-A2102 binds Nectin-4 (not topoisomerase I), is internalized, and releases a topoisomerase I inhibitor that causes DNA damage, cell-cycle arrest, and apoptosis. Expression of DNA topoisomerase I alone does not make cells targeted for killing.