Monoclonal antibody inhibitor of CCR8 that targets CCR8-expressing intratumoral regulatory T cells (Tregs) to block CCR8 signaling and/or deplete CCR8+ Tregs, aiming to relieve immunosuppression in the tumor microenvironment.
Humanized IgG1 anti-CCR8 monoclonal antibody that binds CCR8 on intratumoral regulatory T cells, blocks CCR8 signaling and depletes CCR8+ Tregs via ADCC, reducing immunosuppression in the tumor microenvironment and restoring antitumor immunity.
The IgG1 anti-CCR8 antibody binds CCR8 on target cells and recruits FcγR-expressing effector cells (e.g., NK cells) to mediate ADCC, depleting CCR8+ cells.
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), and can trigger apoptosis of the bound cells.
HER2-targeted antibody-drug conjugate composed of an anti-HER2 monoclonal antibody linked to a topoisomerase I/camptothecin-class cytotoxic payload; binds HER2 on tumor cells, is internalized, and releases the payload to cause DNA damage and tumor cell death; Fc-mediated ADCC may also contribute.
Anti-HER2 monoclonal antibody linked to a topoisomerase I (camptothecin-class) cytotoxic payload. Binds HER2 on tumor cells, is internalized, and releases the payload to induce DNA damage and tumor cell death; Fc-mediated ADCC may also contribute.
The anti-HER2 ADC binds HER2, is internalized, and releases a topoisomerase I (camptothecin-class) cytotoxic payload that causes DNA damage and apoptosis; Fc effector function may add ADCC.
Autologous anti-CD19 CAR T-cell therapy; patient T cells engineered to express a CD19-directed CAR (with CD3ζ and costimulatory signaling) to proliferate and kill CD19+ malignant B cells.
Autologous T cells engineered to express a CD19-directed chimeric antigen receptor containing CD3zeta and costimulatory signaling domains. Binding to CD19 on malignant B cells activates T-cell effector functions, driving proliferation, cytokine release, and cytolytic killing of CD19-positive cells.
Anti-CD19 CAR T cells bind CD19 on target cells, activate, form an immunologic synapse, and kill via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Polyclonal anti-T-cell antibody used in conditioning for T-cell depletion prior to HSCT.
Polyclonal anti-T-cell immunoglobulin that binds multiple T-cell surface antigens (e.g., CD2, CD3, CD4, CD8, HLA-DR), depleting T lymphocytes via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, resulting in profound T-cell immunosuppression and reduction of alloreactivity before HSCT.
ATG binds CD2 on T cells and depletes them via complement-dependent lysis and Fc-mediated ADCC, with additional apoptosis induction upon crosslinking.