TROP2-directed antibody–drug conjugate (SKB264/MK-2870) delivering a topoisomerase I inhibitor to TROP2-positive tumor cells.
Humanized anti-TROP2 IgG1 ADC that binds TROP2 on tumor cells; following internalization and pH-sensitive/enzymatic cleavage of the linker, it releases the topoisomerase I inhibitor tirumotecan, inhibiting DNA replication and causing cell-cycle arrest and apoptosis, with a bystander effect on adjacent tumor cells.
The ADC binds TROP2 on target cells, is internalized, and releases the topoisomerase I inhibitor tirumotecan, inhibiting DNA replication and causing cell-cycle arrest and apoptosis (with possible bystander killing).
Bispecific T-cell–engager antibody (BCMA × CD3) that redirects T cells to kill BCMA-expressing myeloma cells.
Bispecific antibody that binds BCMA on myeloma cells and CD3 on T cells, forming an immune synapse that redirects and activates cytotoxic T cells to kill BCMA-expressing plasma cells via perforin/granzyme-mediated lysis, independent of MHC.
BCMA+ cells are bridged to CD3+ T cells by the bispecific, forming an immune synapse that triggers T‑cell–mediated killing via perforin/granzyme release (MHC-independent).
Anti-CD38 IgG1 monoclonal antibody that depletes CD38+ cells via ADCC, CDC, ADCP, and apoptosis.
Human IgG1κ monoclonal antibody targeting CD38 on myeloma and other CD38+ cells; induces tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis, and depletes CD38+ immunosuppressive cells (e.g., Tregs, B cells, MDSCs) to modulate the tumor microenvironment.
Binds CD38 on target cells and triggers Fc-mediated ADCC, CDC, and ADCP, and can induce direct apoptosis of CD38+ cells.
Autologous T cells engineered with a retroviral vector to express a single bispecific chimeric antigen receptor targeting CD19 and CD22, enabling TCR-independent activation, expansion, cytokine release, and cytotoxic killing of B-lineage leukemia; used to eradicate MRD and induce B-cell aplasia.
Autologous T cells are retrovirally engineered to express a single tandem (bispecific) CAR that recognizes CD19 and CD22 on B-lineage cells. Antigen binding triggers TCR-independent CD3ζ/costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19+/CD22+ leukemia, resulting in MRD clearance and B-cell aplasia.
CAR recognition of CD19 activates engineered T cells via CD3ζ/costimulatory signaling, inducing perforin/granzyme-mediated lysis of CD19+ cells (with associated cytokine release).
Anti-SLAMF7 monoclonal antibody that activates NK cells and mediates ADCC against SLAMF7+ myeloma cells.
Humanized anti‑SLAMF7 (CS1) monoclonal antibody that activates NK cells and induces Fc-mediated ADCC against SLAMF7-positive multiple myeloma cells, leading to targeted cytotoxicity with minimal effects on normal tissues.
Elotuzumab binds SLAMF7 on target cells and engages NK cells via its Fc (FcγRIIIa), triggering antibody-dependent cellular cytotoxicity; it also activates NK cells, leading to killing of SLAMF7+ cells.