A bispecific antibody–drug conjugate (izalontamab brengitecan; iza-bren; BMS-986507) targeting EGFR and HER3 that, upon internalization, releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after binding and internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, inducing DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
YES
DIRECT
The ADC binds EGFR on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death (with possible bystander effect).
A bispecific antibody–drug conjugate (izalontamab brengitecan; iza-bren; BMS-986507) targeting EGFR and HER3 that, upon internalization, releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after binding and internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, inducing DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
YES
DIRECT
ADC binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor brengitecan, causing DNA damage and cell death (with potential bystander effect).
A bispecific antibody–drug conjugate (izalontamab brengitecan; iza-bren; BMS-986507) targeting EGFR and HER3 that, upon internalization, releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and tumor cell death.
Bispecific ADC targeting EGFR and HER3; after binding and internalization, it releases the camptothecin-class topoisomerase I inhibitor brengitecan, inducing DNA damage (via topo I inhibition) and tumor cell death, with potential bystander effect.
YES
INDIRECT
The ADC binds EGFR/HER3, is internalized, and releases brengitecan; the payload inhibits DNA topoisomerase I, causing DNA damage and cell death (with possible bystander effect).
Off-the-shelf, partially HLA-matched allogeneic anti-CD19 chimeric antigen receptor (CAR) T-cell therapy administered intravenously after lymphodepletion; donor-derived T cells engineered to express a CD19-specific CAR that binds CD19 on malignant B cells, triggering T-cell activation, cytokine release, and cytotoxic killing.
Allogeneic donor-derived T cells engineered with a CD19-specific chimeric antigen receptor (with 1XX CD3zeta signaling) bind CD19 on malignant B cells, inducing T-cell activation, cytokine release, proliferation, and cytotoxic lysis of CD19+ cells; the EBV-sensitized allogeneic platform is intended to reduce GVHD risk.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target B cells, become activated, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and apoptosis; Fas/FasL).
Humanized, defucosylated anti-CCR4 IgG1 monoclonal antibody that depletes CCR4-positive malignant T cells and regulatory T cells via enhanced antibody-dependent cellular cytotoxicity and complement-mediated cytotoxicity.
Humanized, defucosylated anti-CCR4 IgG1 that binds CCR4 (CD194) on malignant T cells and regulatory T cells, blocking CCR4 signaling and depleting CCR4-positive cells via enhanced antibody-dependent cellular cytotoxicity and complement-mediated cytotoxicity, leading to antitumor activity and reduction of Treg-mediated immunosuppression.
YES
DIRECT
Anti-CCR4 IgG1 binds CCR4 on target cells and recruits Fc effector functions, causing ADCC by NK/macrophages and complement-dependent cytotoxicity (CDC), depleting CCR4+ cells.