A human afucosylated IgG1 monoclonal antibody (HZN-7734) that binds ILT7 (LILRA4) on plasmacytoid dendritic cells, depleting them via enhanced ADCC to reduce type I interferon signaling; administered subcutaneously.
Afucosylated IgG1 monoclonal antibody that binds ILT7 (LILRA4) on plasmacytoid dendritic cells, enhancing FcγRIIIa-mediated ADCC to deplete pDCs and thereby reduce type I interferon production and downstream inflammatory signaling.
Antibody-bound ILT7+ plasmacytoid dendritic cells are killed via enhanced FcγRIIIa-mediated ADCC, primarily by NK cells (perforin/granzyme-mediated lysis).
Autologous 4th-generation chimeric antigen receptor T-cell therapy engineered to target glypican-3 (GPC3) on hepatocellular carcinoma cells; administered intravenously. Antigen engagement triggers CAR signaling leading to T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor that binds glypican-3 (GPC3) on hepatocellular carcinoma cells; antigen engagement triggers CAR signaling (CD3ζ with costimulatory domains) leading to T‑cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of GPC3-positive tumor cells.
GPC3-specific CAR-T cells bind GPC3 on target cells, triggering CAR signaling and T-cell cytotoxicity with perforin/granzyme release (apoptotic lysis).
Autologous, lentiviral-transduced, gene-modified T-cell therapy expressing a CAR targeting the BT-001 tumor surface antigen; given via multiple IV infusions without lymphodepleting chemotherapy to redirect T cells to kill BT-001–positive solid tumor cells.
Autologous T cells are lentivirally transduced to express a chimeric antigen receptor that binds the BT-001 tumor surface antigen. Antigen engagement triggers CAR signaling (CD3ζ with costimulation), activating and expanding the T cells to mediate perforin/granzyme-dependent cytotoxicity and cytokine release, selectively killing BT-001–positive solid tumor cells; given as repeat IV infusions without lymphodepleting chemotherapy.
CAR-T cells recognize BT-001 on tumor cells; CAR signaling activates T cells to kill targets via perforin/granzyme cytolysis (and death‑receptor pathways), lysing BT-001–positive cells.
Autologous CD19/CD20-directed chimeric antigen receptor (CAR) T-cell therapy; patient T cells are genetically engineered to express CARs targeting CD19 and CD20 on B cells to mediate cytotoxic killing of lymphoma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor recognizing CD19 and CD20 on B cells; antigen binding activates CAR signaling to expand and activate the T cells, leading to cytokine release and perforin/granzyme-mediated cytotoxic killing of malignant B cells, with on-target depletion of normal B cells.
CAR-T cells recognize CD20 on target cells; CAR engagement activates T-cell effector functions leading to perforin/granzyme release (and Fas/FasL signaling), causing apoptosis/lysis of CD20-expressing cells.
Bispecific T-cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B cells to induce T cell–mediated cytotoxicity; used in B-ALL.
Bispecific T-cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on B cells, forming an immune synapse that activates and redirects T cells to kill CD19-positive B cells via perforin/granzyme-mediated cytotoxicity; used in B-ALL.
Blinatumomab links CD3 on T cells to CD19 on target B cells, activating T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity.