An allogeneic, off-the-shelf CAR T-cell therapy enriched for T stem cell memory (Tscm) cells. These engineered T cells express a dual CAR targeting CD19 and CD20 on B cells to drive activation, proliferation, and cytotoxic killing of malignant B cells. Administered as a single IV dose after lymphodepletion; the Tscm phenotype is intended to enhance persistence and self-renewal.
Allogeneic T cells enriched for T stem cell memory are engineered to express dual CARs targeting CD19 and CD20 on B cells. Antigen binding activates T-cell signaling leading to proliferation and cytotoxic killing of malignant B cells; dual targeting aims to limit antigen escape, while the Tscm phenotype supports persistence and self-renewal. Given after lymphodepletion; an optional rimiducid safety switch can induce rapid ablation of the cells if required.
Dual CAR T cells recognize CD20 on target cells, activate, and kill via cytotoxic T-cell mechanisms (perforin/granzyme release and death-receptor–mediated apoptosis).
A bispecific/biparatopic anti-HER2 IgG1 antibody that binds two HER2 epitopes, blocks dimerization and signaling, promotes receptor internalization, and mediates ADCC.
Bispecific/biparatopic anti-HER2 IgG1 that binds two non-overlapping HER2 epitopes (ECD2 and ECD4), blocks HER2 dimerization and downstream signaling, promotes receptor clustering, internalization and downregulation, and elicits Fc-mediated effector functions (ADCC/ADCP) against HER2-overexpressing tumor cells.
Binds HER2 and engages FcγR-bearing immune cells to mediate ADCC/ADCP (and possibly CDC), leading to killing of HER2+ cells; signaling blockade/internalization is primarily cytostatic.
A bispecific/biparatopic anti-HER2 IgG1 antibody that binds two HER2 epitopes, blocks dimerization and signaling, promotes receptor internalization, and mediates ADCC.
Bispecific/biparatopic anti-HER2 IgG1 that binds two non-overlapping HER2 epitopes (ECD2 and ECD4), blocks HER2 dimerization and downstream signaling, promotes receptor clustering, internalization and downregulation, and elicits Fc-mediated effector functions (ADCC/ADCP) against HER2-overexpressing tumor cells.
Binds HER2 on tumor cells and engages immune effector cells via its Fc region, inducing ADCC by NK cells and ADCP by macrophages (and possibly complement), leading to killing of HER2-expressing cells.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis; administered IV or as a subcutaneous co-formulation.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis.
Binds CD20 on B cells and kills via complement-dependent cytotoxicity and Fc-mediated ADCC; can also induce apoptosis upon CD20 engagement.
Subcutaneous CD20×CD3 bispecific T‑cell–engaging monoclonal antibody that binds CD20 on B cells and CD3 on T cells to redirect T‑cell cytotoxicity against malignant B cells.
Humanized bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells, cross-linking them to form an immune synapse and activate T-cell cytotoxicity (perforin/granzyme) to kill CD20+ malignant B cells.
The bispecific antibody links CD3 on T cells to CD20 on B cells, forming an immune synapse that activates T-cell killing (perforin/granzyme-mediated cytotoxicity) of CD20+ cells.