Fully human anti-CD20 IgG1 monoclonal antibody (Kesimpta) administered subcutaneously; depletes CD20+ B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity/phagocytosis; may also induce apoptosis; spares stem cells and plasma cells.
Fully human anti-CD20 IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ B cells via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity/phagocytosis; may also induce apoptosis, while sparing hematopoietic stem cells and plasma cells.
Ofatumumab binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP; it may also induce apoptosis.
Autologous dual-target CAR T-cell therapy engineered to express CARs against BCMA and CD19; upon antigen engagement, T cells activate and kill BCMA+ plasma cells and CD19+ B cells to treat relapsed/refractory POEMS syndrome.
Autologous T cells engineered with dual chimeric antigen receptors targeting BCMA and CD19. Upon antigen binding, CAR signaling activates the T cells to proliferate and mediate cytotoxicity (perforin/granzyme, cytokine release), eliminating BCMA+ plasma cells and CD19+ B cells to deplete pathogenic clones in relapsed/refractory POEMS syndrome.
CAR T cells recognize BCMA via the CAR, activate, and kill BCMA-expressing cells through perforin/granzyme-mediated cytolysis (and death receptor/cytokine pathways).
Autologous dual-target CAR T-cell therapy engineered to express CARs against BCMA and CD19; upon antigen engagement, T cells activate and kill BCMA+ plasma cells and CD19+ B cells to treat relapsed/refractory POEMS syndrome.
Autologous T cells engineered with dual chimeric antigen receptors targeting BCMA and CD19. Upon antigen binding, CAR signaling activates the T cells to proliferate and mediate cytotoxicity (perforin/granzyme, cytokine release), eliminating BCMA+ plasma cells and CD19+ B cells to deplete pathogenic clones in relapsed/refractory POEMS syndrome.
CD19-specific CAR T cells bind CD19 on target cells, activate, and kill them via T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways).
Maplirpacept (PF-07901801; TTI-622) is an engineered SIRPα–IgG4 Fc fusion protein (myeloid checkpoint inhibitor) given IV weekly that binds CD47 on tumor cells to block the CD47–SIRPα “don’t-eat-me” signal, enhancing macrophage-mediated phagocytosis while using an IgG4 Fc to reduce off-target cytotoxicity.
Engineered SIRPα–IgG4 Fc fusion protein that binds CD47 on tumor cells to block the CD47–SIRPα myeloid checkpoint, releasing inhibitory “don’t‑eat‑me” signaling and enhancing macrophage-mediated phagocytosis; the IgG4 Fc is designed to limit off‑target cytotoxicity while permitting Fc receptor engagement.
Binds CD47 on target cells to block the CD47–SIRPα ‘don’t‑eat‑me’ checkpoint and, via its IgG4 Fc, engages Fcγ receptors on macrophages, triggering antibody-dependent cellular phagocytosis and macrophage-mediated killing.
Autologous TCR-engineered T-cell (TCR-T) therapy in which patient T cells are genetically modified to express an HLA-A*11:01–restricted, HBV-specific T-cell receptor targeting HBV antigen–expressing hepatocellular carcinoma cells; induces TCR signaling, cytokine release, and MHC class I–restricted cytotoxic killing. Administered with step-up induction followed by weekly maintenance infusions.
Autologous T cells are genetically engineered to express an HLA-A*11:01-restricted, HBV-specific T-cell receptor that recognizes HBV peptide–MHC class I complexes on hepatocellular carcinoma cells, activating TCR signaling, cytokine release, and perforin/granzyme-mediated cytotoxic killing.
Engineered TCR-T cells recognize the HBV peptide–HLA-A*11:01 complex on tumor cells and kill them via cytotoxic T-cell mechanisms, primarily perforin/granzyme-mediated lysis (and Fas–FasL apoptosis).