Antibody–drug conjugate targeting CD30; internalized upon binding and releases MMAE to disrupt microtubules and induce apoptosis; may also engage immune effector functions.
CD30-targeted monoclonal antibody linked via a protease-cleavable valine–citrulline linker to the microtubule toxin MMAE. After binding CD30 on tumor cells and internalization, MMAE is released intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also recruit immune effector functions (e.g., ADCC).
YES
DIRECT
ADC binds CD30, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
Antibody–drug conjugate targeting CD30; internalized upon binding and releases MMAE to disrupt microtubules and induce apoptosis; may also engage immune effector functions.
CD30-targeted monoclonal antibody linked via a protease-cleavable valine–citrulline linker to the microtubule toxin MMAE. After binding CD30 on tumor cells and internalization, MMAE is released intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also recruit immune effector functions (e.g., ADCC).
NO
INDIRECT
The ADC binds CD30 on target cells and is internalized; the linker is cleaved to release MMAE, which binds β‑tubulin (vinca site) to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. Tubulin itself is not the selective binding target of the drug.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on plasmablasts/plasma cells and depletes them via ADCC, CDC, ADCP, and apoptosis to reduce factor VIII–neutralizing autoantibodies.
Human IgG1-kappa anti-CD38 monoclonal antibody that binds CD38 on plasmablasts/plasma cells and other CD38+ cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and apoptosis, thereby reducing pathogenic autoantibody production (e.g., factor VIII inhibitors).
YES
DIRECT
Daratumumab binds CD38 on target cells and induces killing via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis.
Autologous, genetically modified anti-CD19 chimeric antigen receptor (CAR) T-cell therapy made from a patient’s T cells; engineered to express an anti-CD19 CAR that, upon binding CD19 on B cells, induces antigen-dependent T-cell activation, proliferation, and cytotoxic killing, with expected on-target B-cell aplasia and risk of cytokine release.
Autologous patient T cells engineered to express an anti‑CD19 chimeric antigen receptor. Binding CD19 on malignant and normal B cells triggers CAR signaling, activating and expanding the T cells and inducing cytokine release and perforin/granzyme‑mediated cytotoxic killing, resulting in depletion of CD19+ cells (on‑target B‑cell aplasia).
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells and directly kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, with possible Fas/FasL involvement), causing depletion of CD19+ cells.
Gene-modified autologous T cells engineered to express a chimeric antigen receptor that recognizes VEGFR1 and PD-L1; upon antigen engagement, the CAR T cells exert cytotoxic activity against VEGFR1+ and/or PD-L1+ cells, aiming to disrupt VEGF/VEGFR1-driven angiogenesis and overcome PD-L1–mediated immune suppression. Administered regionally into the pleural or peritoneal cavity.
Autologous T cells genetically engineered to express a chimeric antigen receptor recognizing VEGFR1 and PD-L1. Binding to either antigen triggers T‑cell activation, cytotoxicity, and cytokine release to kill VEGFR1+ vascular/endothelial cells and PD‑L1+ tumor and immunosuppressive stromal/immune cells, disrupting VEGF/VEGFR1‑driven angiogenesis and overcoming PD‑L1–mediated immune evasion. Administered regionally into the pleural or peritoneal cavity.
YES
DIRECT
VEGFR1-specific CAR-T cells bind VEGFR1 on target cells, activate, and kill via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL), with supportive cytokine-mediated effects.