An anti-CD19 IgG monoclonal antibody–drug conjugate (Zynlonta; ADCT-402) that delivers the PBD dimer cytotoxic payload tesirine to CD19-expressing B cells. After binding and internalization, tesirine is released to create DNA interstrand crosslinks, triggering DNA damage responses, cell-cycle arrest, and apoptosis. Administered IV every 21 days for relapsed/refractory B-cell malignancies.
Humanized anti-CD19 monoclonal antibody linked via a cleavable linker to tesirine (a pyrrolobenzodiazepine dimer). After binding CD19 and internalization, the payload is released to form DNA minor-groove interstrand crosslinks (at N2-guanine), inhibiting DNA replication and inducing DNA damage response, cell-cycle arrest, and apoptosis in CD19-expressing B cells.
ADC binds CD19, is internalized, and releases the tesirine (PBD dimer) payload, which forms DNA interstrand crosslinks (N2-guanine), inhibiting replication and triggering DNA damage–mediated cell-cycle arrest and apoptosis in CD19+ cells.
Autologous CMV-specific T cells genetically modified via lentiviral transduction to express a chimeric antigen receptor (CAR) targeting HIV-1 gp120, incorporating an EGFR tag for selection/safety. Administered intravenously (5–50 million EGFR+ cells). CAR engagement triggers T-cell activation and cytotoxic killing of HIV-infected cells; endogenous CMV-specific TCR signaling supports expansion and persistence.
Autologous CMV-specific T cells are lentivirally engineered to express a CAR that binds HIV-1 gp120. Upon recognizing gp120 on HIV-infected cells, the CAR activates the T cells to proliferate and kill targets via perforin/granzyme cytotoxicity and cytokine release. The cells retain their endogenous CMV-specific TCR, enabling CMV-driven stimulation to enhance expansion and persistence in vivo. An EGFR tag allows cell selection and potential safety depletion.
CAR T cells bind gp120 on infected cells and directly lyse them via perforin/granzyme-mediated cytotoxicity.
Autologous CMV-specific T cells genetically modified via lentiviral transduction to express a chimeric antigen receptor (CAR) targeting HIV-1 gp120, incorporating an EGFR tag for selection/safety. Administered intravenously (5–50 million EGFR+ cells). CAR engagement triggers T-cell activation and cytotoxic killing of HIV-infected cells; endogenous CMV-specific TCR signaling supports expansion and persistence.
Autologous CMV-specific T cells are lentivirally engineered to express a CAR that binds HIV-1 gp120. Upon recognizing gp120 on HIV-infected cells, the CAR activates the T cells to proliferate and kill targets via perforin/granzyme cytotoxicity and cytokine release. The cells retain their endogenous CMV-specific TCR, enabling CMV-driven stimulation to enhance expansion and persistence in vivo. An EGFR tag allows cell selection and potential safety depletion.
Endogenous CMV-specific TCR on the engineered T cells recognizes CMV peptide–HLA class I complexes and triggers cytotoxic T-cell killing via perforin/granzyme (and related apoptosis pathways).
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and induces B‑cell depletion via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity, and direct induction of apoptosis.
A HER2-directed antibody–drug conjugate in which an anti-HER2 monoclonal antibody binds ERBB2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload, leading to tumor cell death; also attenuates HER2-driven signaling and may exert a bystander effect on neighboring HER2-low cells.
HER2-directed antibody–drug conjugate: an anti-HER2 monoclonal antibody binds ERBB2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor payload that induces DNA damage and apoptosis; additionally attenuates HER2 signaling and may exert a bystander effect on neighboring HER2-low cells.
Anti-HER2 ADC binds HER2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor that causes DNA breaks and apoptosis; may also produce a bystander effect.