An intravenous biological immunotherapy in first-in-human monotherapy dose-escalation/expansion, likely targeting the CD47–SIRPα innate immune checkpoint (antibody or fusion protein) to block the “don’t-eat-me” signal and enhance macrophage-mediated phagocytosis and antitumor immunity, with focus on HER2-positive tumors.
Bispecific anti-CD47/anti-HER2 monoclonal antibody that targets HER2-positive tumor cells and blocks the CD47–SIRPα checkpoint to abrogate the tumor 'don't-eat-me' signal, enhancing macrophage-mediated phagocytosis and antigen presentation, with secondary activation of antitumor T-cell responses.
The bispecific antibody binds HER2 on tumor cells and blocks CD47–SIRPα, removing the “don’t‑eat‑me” signal and enabling macrophage-mediated phagocytosis (and Fc-driven ADCP), leading to killing of HER2+ cells; T‑cell responses are secondary.
Anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity.
Anti-CD20 chimeric monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, leading to elimination of malignant B cells.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP), resulting in lysis and apoptosis of CD20+ cells.
An autologous, genetically engineered T-cell therapy in which a patient’s T cells are modified to express chimeric antigen receptors targeting both BCMA (TNFRSF17) and GPRC5D. Engagement of these antigens triggers CD3ζ and costimulatory signaling, leading to T-cell activation, cytokine release, and perforin/granzyme-mediated lysis of multiple myeloma cells. Dual targeting is intended to reduce antigen escape in relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express chimeric antigen receptors targeting both BCMA (TNFRSF17) and GPRC5D. Binding to either antigen triggers CD3ζ and costimulatory signaling, leading to T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated lysis of multiple myeloma cells. Dual targeting is intended to reduce antigen escape in relapsed/refractory disease.
CAR-T cells bind BCMA on target cells, become activated, and kill them via immune synapse-mediated perforin/granzyme cytolysis (and Fas/FasL apoptosis).
An autologous, genetically engineered T-cell therapy in which a patient’s T cells are modified to express chimeric antigen receptors targeting both BCMA (TNFRSF17) and GPRC5D. Engagement of these antigens triggers CD3ζ and costimulatory signaling, leading to T-cell activation, cytokine release, and perforin/granzyme-mediated lysis of multiple myeloma cells. Dual targeting is intended to reduce antigen escape in relapsed/refractory multiple myeloma.
Autologous T cells are engineered to express chimeric antigen receptors targeting both BCMA (TNFRSF17) and GPRC5D. Binding to either antigen triggers CD3ζ and costimulatory signaling, leading to T‑cell activation, proliferation, cytokine release, and perforin/granzyme‑mediated lysis of multiple myeloma cells. Dual targeting is intended to reduce antigen escape in relapsed/refractory disease.
CAR-T cells recognize GPRC5D on target cells and, upon CAR activation, kill them via perforin/granzyme-mediated cytolysis (and death-receptor signaling).
Subcutaneous bispecific T‑cell–engaging monoclonal antibody targeting CD3 on T cells and CD20 on B cells to drive targeted T‑cell–mediated cytotoxicity.
Bispecific monoclonal antibody that simultaneously binds CD3 on T cells and CD20 on B cells, cross-linking T cells to CD20+ malignant B cells to form an immune synapse and activate T-cell–mediated cytotoxicity (perforin/granzyme release) against the target B cells.
Epcoritamab crosslinks CD3 on T cells to CD20 on target cells, forming an immune synapse and inducing perforin/granzyme-mediated T-cell killing of CD20+ cells.