Investigational bispecific T‑cell–engaging monoclonal antibody (IV) that binds HLA‑G on tumor cells and CD3 on T cells to redirect cytotoxicity and overcome HLA‑G–mediated immune suppression.
Bispecific antibody that binds HLA-G on tumor cells and CD3 on T cells, bringing them into proximity to activate and redirect cytotoxic T-cell killing of HLA-G-expressing tumor cells while counteracting HLA-G-mediated immune suppression.
YES
DIRECT
The bispecific antibody binds HLA-G on target cells and CD3 on T cells, activating and redirecting cytotoxic T cells to kill HLA-G–expressing cells via perforin/granzyme (and Fas/FasL)–mediated apoptosis.
Investigational bispecific T‑cell–engaging monoclonal antibody (IV) that binds HLA‑G on tumor cells and CD3 on T cells to redirect cytotoxicity and overcome HLA‑G–mediated immune suppression.
Bispecific antibody that binds HLA-G on tumor cells and CD3 on T cells, bringing them into proximity to activate and redirect cytotoxic T-cell killing of HLA-G-expressing tumor cells while counteracting HLA-G-mediated immune suppression.
NO
INDIRECT
The drug binds CD3 on T cells to activate and redirect them; the activated T cells kill HLA-G–positive tumor cells, not the CD3+ T cells.
Autologous, second-generation CD19-directed CAR-T cell therapy; patient T lymphocytes are lentivirally transduced to express an anti-CD19 scFv with 4-1BB co-stimulatory and CD3zeta signaling domains, leading to activation, expansion, cytokine release, and cytotoxic killing of CD19+ B cells (with expected B-cell aplasia).
Autologous T cells are lentivirally transduced to express a CD19-directed chimeric antigen receptor with 4-1BB co-stimulatory and CD3zeta signaling domains. CAR engagement of CD19 on B cells triggers T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19+ malignant cells, leading to on-target B-cell aplasia.
YES
DIRECT
CD19 CAR-T cells bind CD19 on target B cells, triggering T-cell activation and cytotoxic killing via perforin/granzyme release and death receptor pathways, causing on‑target lysis of CD19+ cells.
Investigational HER2-directed antibody–drug conjugate given IV every 3 weeks; binds HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce cell death while retaining HER2 signaling blockade and Fc-mediated ADCC.
HER2-targeted monoclonal antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and releases a cytotoxic payload to kill HER2-expressing cells, while maintaining HER2 signaling blockade and Fc-mediated ADCC.
YES
DIRECT
The HER2-targeted ADC binds HER2, is internalized, and releases a cytotoxic payload that kills HER2-expressing cells; Fc-mediated ADCC can also contribute.
Approved HER2-directed antibody–drug conjugate that, after binding and internalization via HER2, releases the microtubule inhibitor DM1; preserves trastuzumab’s HER2 blockade and Fc-mediated ADCC.
HER2-targeted monoclonal antibody (trastuzumab) linked to the maytansinoid DM1. After binding HER2 on tumor cells and internalization, lysosomal processing releases DM1, a microtubule inhibitor that induces mitotic arrest and apoptosis; concurrently retains trastuzumab’s HER2 signaling blockade and Fc-mediated ADCC.
YES
DIRECT
T-DM1 binds HER2, is internalized, and releases the DM1 payload that inhibits microtubules, causing mitotic arrest and apoptosis; trastuzumab Fc can also mediate ADCC.