Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG binds CD2 on T cells, leading to complement-dependent lysis and Fc receptor–mediated ADCC, with additional induction of apoptosis.
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.
Engineered TCR T cells recognize the HPV16 peptide-HLA-A*02:01 complex on target cells and induce cytolysis via perforin/granzyme release (with additional Fas-FasL/cytokine-mediated apoptosis).
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.
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.
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.
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).