Human IgG1κ monoclonal antibody targeting CD38; depletes CD38+ plasma cells via ADCC, CDC, ADCP, and apoptosis, with additional immunomodulatory effects.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on plasma cells and other CD38+ immune cells, inducing cell death via ADCC, CDC, ADCP, and apoptosis, thereby depleting CD38+ pathogenic and immunosuppressive cells and exerting immunomodulatory effects.
YES
DIRECT
Binding of daratumumab to CD38 on cells triggers antibody-mediated killing via ADCC, CDC, ADCP, and can induce apoptosis of CD38+ cells.
Human anti-CD2 monoclonal antibody biologic that binds CD2 on T cells and NK cells, blocks LFA-3/CD2 costimulation, and preferentially depletes/modulates CD2hi effector-memory T cells while relatively sparing regulatory T cells.
Human anti-CD2 monoclonal antibody that binds CD2 on T cells and NK cells, blocks LFA-3/CD2 costimulation, and preferentially depletes/modulates CD2hi effector-memory T cells while relatively sparing regulatory T cells, suppressing alloreactive responses.
YES
DIRECT
Anti-CD2 IgG engages Fc effector functions to deplete CD2+ cells via ADCC/ADCP and possibly complement-mediated lysis; may also trigger apoptosis, while also blocking LFA-3/CD2 costimulation.
Armored, glypican-3 (GPC3)-targeted autologous CAR T-cell therapy for advanced/recurrent GPC3-positive hepatocellular carcinoma. Patient T cells are engineered to express a CAR that binds GPC3, triggering T-cell activation, cytokine release, and cytotoxic killing of GPC3+ tumor cells. The armored design is intended to enhance T-cell persistence and function within the solid tumor microenvironment. Administered as a single IV infusion.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds glypican-3 (GPC3) on tumor cells, leading to T-cell activation, cytokine release, and direct cytotoxic killing of GPC3-positive cells; the armored design enhances T-cell persistence and function within the immunosuppressive solid tumor microenvironment.
YES
DIRECT
GPC3-specific CAR T cells bind GPC3 on target cells, become activated, and kill them via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL–mediated apoptosis).
Autologous anti-CD19 CAR T-cell therapy (gene-modified T cells) for CD19+ B-cell malignancies.
Autologous T cells are genetically modified with a gamma-retroviral vector to express an anti-CD19 chimeric antigen receptor containing a CD28 costimulatory domain and CD3ζ signaling domain. After infusion, these CAR T cells recognize CD19 on B-cell malignancies, become activated, expand, secrete cytokines, and kill CD19+ tumor cells via perforin/granzyme-mediated cytotoxicity.
YES
DIRECT
Anti-CD19 CAR T cells recognize CD19 on target cells and kill them via immune-synapse–mediated perforin/granzyme cytotoxicity (and death-receptor pathways).
Chimeric anti-CD20 monoclonal antibody that depletes B cells via CDC/ADCC and apoptosis.
Chimeric anti‑CD20 IgG1 monoclonal antibody that binds CD20 on normal and malignant B cells and induces B‑cell depletion primarily via complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and direct apoptotic signaling.
YES
DIRECT
Rituximab binds CD20 on B cells, activating complement for CDC (MAC lysis) and engaging FcγR-bearing effectors (NK cells/macrophages) for ADCC/ADCP; cross-linking can also trigger apoptosis.