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.
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.
Autologous, gene-modified CD19-directed CAR T-cell therapy. Patient T cells are engineered ex vivo to express an anti-CD19 CAR and, after infusion, selectively recognize and eliminate CD19+ B-lineage cells to deplete autoreactive B cells and suppress humoral autoimmunity in moderate to severe SLE.
Autologous T cells are gene-modified ex vivo to express an anti-CD19 chimeric antigen receptor; after infusion, the CAR T cells recognize CD19 on B-lineage cells and eliminate them via CAR-mediated cytotoxicity, depleting autoreactive B cells and suppressing humoral autoimmunity.
CD19-directed CAR T cells bind CD19 on target cells and kill them via T-cell cytotoxicity (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Type II, glycoengineered humanized anti-CD20 monoclonal antibody that induces B-cell depletion via direct cell death and enhanced ADCC/ADCP (with some CDC).
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes them via direct cell death and enhanced Fc gamma RIII–mediated ADCC and ADCP, with lesser complement-dependent cytotoxicity (CDC).
Obinutuzumab binds CD20 on B cells, triggering direct (type II) cell death and recruiting FcγRIII-expressing effector cells to mediate ADCC and ADCP; there is also some complement-dependent cytotoxicity.
Allogeneic, gene-edited CD70-directed CAR T-cell therapy (donor T cells engineered ex vivo with CRISPR-Cas9 to express an anti-CD70 chimeric antigen receptor) designed to recognize and kill CD70-positive malignant cells via CAR-mediated T-cell cytotoxicity; administered intravenously.
Allogeneic donor T cells are CRISPR-Cas9 edited to disrupt endogenous TCR and MHC class I to reduce graft-versus-host disease and enhance persistence, and are engineered to express a chimeric antigen receptor targeting CD70. After IV infusion, these CAR T cells recognize CD70 on malignant cells and mediate antigen-specific T-cell activation and cytotoxic killing of CD70-positive tumor cells independent of native MHC presentation.
Anti-CD70 CAR T cells bind CD70 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis and apoptosis of CD70-positive cells.
Subcutaneous bispecific T‑cell–engaging monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells to redirect T‑cell cytotoxicity against BCMA‑positive myeloma cells.
Bispecific T‑cell–engaging monoclonal antibody that binds BCMA on myeloma/plasma cells and CD3 on T cells, forming an immune synapse that activates and redirects T‑cell cytotoxicity (perforin/granzyme) to kill BCMA‑positive cells.
Bispecific antibody binds BCMA on target cells and CD3 on T cells, forming an immune synapse that redirects T-cell killing via perforin/granzyme-mediated apoptosis (and Fas/FasL).