An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered subcutaneously or intravenously with dose escalation to define RP2R.
Fully human effector-silent Fc IgG1 trispecific antibody that binds CD79b and CD20 on B-cell tumors and CD3 on T cells, redirecting and activating cytotoxic T cells to kill malignant B cells via immune-synapse formation and granzyme/perforin-mediated lysis.
The trispecific T-cell engager binds CD3 on T cells and CD20 on B cells, creating an immune synapse that activates cytotoxic T cells to kill CD20-expressing cells via perforin/granzyme-mediated lysis.
Donor-derived antigen-specific CD4+ and CD8+ T lymphocytes selected by IFN-γ capture after brief stimulation with CMV, EBV, and adenovirus peptides; infused as adoptive cellular therapy to restore antiviral immunity in allo-HSCT recipients.
Donor-derived CD4+ and CD8+ T lymphocytes are briefly stimulated with CMV, EBV, and adenovirus peptides and IFN-γ–secreting cells are magnetically captured, enriching for virus-specific TCR specificities. After infusion, these unengineered T cells recognize HLA-presented viral epitopes via their native TCRs, secrete Th1 cytokines (e.g., IFN-γ), and kill infected cells through perforin/granzyme-mediated cytotoxicity, expanding in vivo to restore antiviral immunity in allo-HSCT recipients.
Virus-specific T cells recognize adenoviral peptide–HLA complexes via their native TCRs and kill the presenting infected cells through perforin/granzyme–mediated apoptosis (± Fas–FasL).
An investigational CD3 T‑cell engager bispecific antibody (protein immunotherapy) that binds CD3 on T cells and a B‑cell tumor antigen to redirect and activate cytotoxic T cells against malignant B cells in relapsed/refractory B‑cell NHL; administered at fixed subcutaneous dosing in combination with JNJ‑80948543.
A bispecific antibody that binds CD3 on T cells and CD22 on malignant B cells, crosslinking T cells to target cells to form an immune synapse, activate and redirect cytotoxic T-lymphocyte activity, and induce lysis of CD22-expressing B-cell lymphoma cells.
The bispecific antibody bridges CD3 on T cells to CD22 on target B cells, forming an immune synapse and triggering T‑cell–mediated cytolysis (perforin/granzyme-induced apoptosis) of CD22+ cells.
Anti-HER2 IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, inhibiting receptor phosphorylation and downstream PI3K/AKT and MAPK signaling (extracellular blockade).
Fc-engineered humanized IgG1 monoclonal antibody that binds the HER2 extracellular domain IV, blocking HER2-mediated receptor phosphorylation and downstream PI3K/AKT and MAPK signaling, and engaging immune effector functions to induce ADCC against HER2-overexpressing tumor cells.
Binds HER2 on tumor cells and engages Fcγ receptor–bearing immune cells to mediate ADCC, causing lysis/apoptosis of HER2+ cells (with additional growth inhibition via signaling blockade).
Autologous, fully human anti-CD19 CAR T-cell therapy; patient T cells are engineered to express a chimeric antigen receptor targeting CD19 to deplete CD19+ B-lineage cells and reset humoral immunity in refractory dermatomyositis.
Autologous T cells engineered with an anti-CD19 CAR (CD28 costimulatory and CD3ζ signaling domains) recognize CD19 and, upon engagement, become activated to kill CD19+ B-lineage cells (B cells and plasmablasts), depleting autoantibody-producing cells and resetting humoral immunity.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, and Fas-FasL pathways).