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.
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.
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.
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.
Human anti-CD38 monoclonal antibody for multiple myeloma that mediates ADCC, CDC, ADCP, and apoptosis of CD38+ plasma cells and depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), enhancing T/NK-cell responses.
Human anti-CD38 IgG1κ monoclonal antibody that binds CD38 on malignant plasma cells, inducing ADCC, CDC, ADCP, and direct apoptosis; also depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), thereby enhancing T- and NK-cell antitumor responses.
Daratumumab binds CD38 on target cells and triggers Fc-mediated ADCC by NK cells, complement-dependent cytotoxicity, antibody-dependent phagocytosis, and can induce direct apoptosis upon crosslinking.
Humanized anti-GD2 IgG1 monoclonal antibody that binds GD2 on tumor cells and mediates antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity.
Humanized anti-GD2 IgG1 monoclonal antibody that binds GD2 on tumor cells and induces immune-mediated killing via Fcγ receptor–driven antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of GD2-expressing cancer cells.
The anti-GD2 IgG1 binds GD2 on target cells and recruits immune effectors via its Fc to trigger ADCC (e.g., NK cell–mediated killing) and activates complement for CDC, leading to lysis of GD2-expressing cells.