CAR T cells engineered via lentiviral vector to target CD5; IV administration with dose escalation; intended to eliminate CD5+ T-cell malignancies through CAR signaling and effector functions.
Autologous or allogeneic T cells are lentivirally engineered to express a CD5-specific chimeric antigen receptor. Upon binding CD5 on malignant T cells, the CAR provides MHC-independent activation, leading to T-cell expansion and perforin/granzyme-mediated cytotoxicity with cytokine release, eliminating CD5-positive tumor cells.
CAR T cells recognize CD5 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated cytotoxicity with associated cytokine release, eliminating CD5+ cells.
Humanized anti-CD20 IgG1 monoclonal antibody (Ocrevus) administered subcutaneously; depletes CD20+ B cells via ADCC, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation, costimulation, and pro-inflammatory cytokines while sparing stem cells and plasma cells; indirectly dampens T-cell activation and CNS inflammation.
Humanized anti-CD20 IgG1 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via ADCC, complement-dependent cytotoxicity, and apoptosis, reducing B-cell antigen presentation/costimulation and pro-inflammatory cytokines while sparing stem and plasma cells; indirectly dampens T-cell activation and CNS inflammation.
Anti-CD20 IgG1 binds CD20 on B cells and induces Fc-mediated effector killing (ADCC/ADCP) and complement-dependent cytotoxicity, leading to lysis/apoptosis of CD20+ cells.
Allogeneic, multiplex base-edited anti-CD7 CAR-T cell therapy with edits in TRAC, CD7, PDCD1 (PD-1), and CD52 to target CD7+ malignant T cells, reduce GVHD and fratricide, resist alemtuzumab, and enhance antitumor activity.
Allogeneic, multiplex base-edited anti-CD7 CAR T cells that bind CD7 on malignant T cells and mediate targeted cytotoxicity. Edits knock out TRAC (removes TCR to reduce GVHD), CD7 (prevents fratricide), PDCD1/PD-1 (limits checkpoint inhibition to enhance activity), and CD52 (confers resistance to alemtuzumab during conditioning), enabling effective killing of CD7+ T-cell malignancies.
Anti-CD7 CAR T cells recognize CD7 on target cells and kill them via T-cell effector functions, primarily perforin/granzyme-mediated cytolysis and death receptor signaling.
Anti-CD52 monoclonal antibody used for lymphodepletion to enhance CAR-T cell engraftment.
Humanized anti-CD52 IgG1 monoclonal antibody that binds CD52 on lymphocytes and other leukocytes and mediates complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, depleting CD52+ cells; used here for lymphodepletion to enhance CAR-T engraftment (with BEAM-201 edited to resist alemtuzumab).
Alemtuzumab binds CD52 on leukocytes and triggers complement-dependent cytotoxicity and Fc receptor–mediated antibody-dependent cellular cytotoxicity by NK cells/macrophages, lysing CD52+ cells.
An autologous, gene-modified CAR T-cell therapy (BMS-986393; CC-95266; “Arlo-cel”) targeting GPRC5D for relapsed/refractory multiple myeloma. Patient T cells are engineered to express a CAR that binds GPRC5D on myeloma cells, activating T cells and inducing cytokine release and perforin/granzyme-mediated cytotoxic killing.
Autologous T cells are gene-modified to express a chimeric antigen receptor targeting GPRC5D on myeloma cells. CAR engagement activates the T cells, triggering cytokine release, proliferation, and perforin/granzyme-mediated cytotoxic lysis of GPRC5D-expressing tumor cells.
CAR T cells recognize GPRC5D on target cells and, upon engagement, kill them via T‑cell cytotoxic mechanisms, primarily perforin/granzyme-mediated lysis (with possible Fas–FasL signaling).