A targeted biologic HER2 dual antibody–drug conjugate (ADC) given IV every 3 weeks; two anti‑HER2 antibodies bind ERBB2 on tumor cells, drive receptor-mediated internalization, and release an intracellular cytotoxic payload to induce tumor cell death; binding may also inhibit HER2 signaling.
HER2-directed antibody–drug conjugate in which humanized anti-HER2 antibodies bind ERBB2 on tumor cells, trigger receptor-mediated internalization, and enzymatic cleavage of a linker to release a topoisomerase I inhibitor payload. The released payload inhibits Topo I, blocking DNA replication and causing cell-cycle arrest and apoptosis; antibody binding may also hinder HER2 signaling.
The ADC binds HER2 on target cells, is internalized, and enzymatic linker cleavage releases a topoisomerase I inhibitor payload that blocks DNA replication, causing DNA damage, cell-cycle arrest, and apoptosis (with possible additional HER2 signaling inhibition).
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 EBV peptide–HLA complexes via their native TCR and directly kill infected cells through perforin/granzyme-mediated cytotoxicity (and Fas–FasL).
A subcutaneous, humanized BCMA×CD3 bispecific monoclonal antibody (T‑cell–redirecting immunotherapy; brand name Elrexfio) that binds BCMA on plasma cells and CD3 on T cells to form an immune synapse, activate TCR/CD3 signaling, induce cytokine release, and mediate perforin/granzyme cytotoxic killing of BCMA+ plasma cells.
Humanized bispecific antibody that binds BCMA on plasma cells and CD3 on T cells, bringing them into proximity to form an immune synapse. This activates TCR/CD3 signaling, triggers T‑cell activation and cytokine release, and induces perforin/granzyme-mediated lysis of BCMA-positive plasma cells.
Elranatamab bridges CD3 on T cells to BCMA on target cells, activates TCR signaling, forms an immune synapse, and induces perforin/granzyme-mediated lysis of BCMA+ cells.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy (axi-cel). Patient T cells are engineered to express a CD19-targeted CAR with CD28 costimulatory and CD3ζ signaling domains; given once at 2.0×10^6 CAR+ cells/kg as consolidation in high-risk large B-cell lymphoma.
Autologous T cells are genetically engineered to express a CD19-directed chimeric antigen receptor containing a CD28 costimulatory and CD3ζ signaling domain. Upon binding CD19 on B-cell malignancies, the CAR T cells activate, proliferate, and mediate cytotoxicity (perforin/granzyme and cytokine-dependent killing), leading to elimination of CD19+ tumor cells and on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19 and, upon activation, directly kill CD19+ cells via T-cell cytotoxicity (perforin/granzyme release and cytokine-mediated apoptosis).
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 CD79b on B cells, forming an immune synapse that activates T cells to kill CD79b+ cells via perforin/granzyme-mediated lysis.