Autologous, gene-modified TCR T-cell therapy engineered to express an HLA-A*02:01–restricted TCR recognizing HPV16/52 antigens; mediates antigen-specific cytotoxicity and cytokine release against HPV-positive tumor cells; administered after lymphodepletion.
Autologous T cells genetically engineered to express an HLA-A*02:01–restricted TCR that recognizes HPV16/52-derived peptides on tumor cells; antigen/MHC engagement activates the T cells to release cytotoxic granules and cytokines, mediating targeted killing of HPV-positive tumor cells. Administered after lymphodepletion to promote expansion and persistence.
YES
DIRECT
Engineered TCR T cells recognize HPV52 peptide–HLA-A*02:01 complexes and kill target cells via perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis, with supportive cytokine effects.
An intravenous bispecific antibody-drug conjugate targeting EGFR and HER3. After binding and internalization, it releases the topoisomerase I inhibitor payload brengitecan, causing DNA damage and tumor cell death.
Bispecific ADC that binds EGFR and HER3 on tumor cells, is internalized, and releases the topoisomerase I–inhibitor payload brengitecan, leading to DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
YES
DIRECT
Bispecific ADC binds EGFR (and HER3), is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and tumor cell death (with possible bystander effect).
An intravenous bispecific antibody-drug conjugate targeting EGFR and HER3. After binding and internalization, it releases the topoisomerase I inhibitor payload brengitecan, causing DNA damage and tumor cell death.
Bispecific ADC that binds EGFR and HER3 on tumor cells, is internalized, and releases the topoisomerase I–inhibitor payload brengitecan, leading to DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
YES
DIRECT
The bispecific ADC binds HER3 (and EGFR) on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and tumor cell death (with possible bystander effect).
An intravenous bispecific antibody-drug conjugate targeting EGFR and HER3. After binding and internalization, it releases the topoisomerase I inhibitor payload brengitecan, causing DNA damage and tumor cell death.
Bispecific ADC that binds EGFR and HER3 on tumor cells, is internalized, and releases the topoisomerase I–inhibitor payload brengitecan, leading to DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
NO
INDIRECT
The ADC binds EGFR/HER3 (not Topoisomerase I), is internalized, and releases the topo I inhibitor brengitecan to cause DNA damage in EGFR/HER3-positive cells, with potential bystander killing.
Intravenous chimeric monoclonal antibody targeting CD20 on B cells; depletes B cells via ADCC/CDC and apoptosis to reduce autoreactive B-cell activity and autoantibody production.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing autoreactive B-cell activity and autoantibody production.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC (NK cells/macrophages) and complement-dependent cytotoxicity, and can also induce apoptosis of the target cells.