Off-the-shelf allogeneic CAR NK cell therapy with a logic-gated NOT design targeting CD33 and/or FLT3 and an inhibitory CAR to spare healthy cells; includes IL-15 support to enhance NK persistence/function for AML/MDS.
Off-the-shelf allogeneic NK cells engineered with an OR-gated activating CAR targeting CD33 and/or FLT3 and a NOT-gated inhibitory CAR recognizing EMCN to spare healthy hematopoietic stem cells; includes calibrated-release IL-15 to enhance NK persistence and function. Antigen engagement triggers NK activation and cytolytic killing of CD33/FLT3-positive AML/MDS cells while minimizing on-target/off-tumor toxicity.
CAR NK cells bind FLT3 via the activating CAR, triggering NK activation and degranulation (perforin/granzymes) to lyse/apoptose FLT3+ cells; an inhibitory CAR for EMCN spares healthy HSCs.
Therapeutic monoclonal antibody–drug conjugates that bind cell-surface Trop2, internalize, and release a cytotoxic payload to kill Trop2-positive tumor cells.
Monoclonal antibody binds cell-surface Trop2 on tumor cells, undergoes receptor-mediated internalization, and linker cleavage releases an intracellular cytotoxic payload (e.g., topoisomerase I inhibitor), causing DNA damage and tumor cell death with potential bystander effect in Trop2-positive cancers.
ADC binds Trop-2 on the cell surface, is internalized, and releases a cytotoxic payload (e.g., topoisomerase I inhibitor) that causes DNA damage and tumor cell death, with potential bystander killing.
Autologous CD19-directed CAR T-cell therapy (Relma-cel) in which patient T cells are gene-modified to express an anti-CD19 chimeric antigen receptor, leading to activation and lysis of CD19+ B-lineage cells to deplete B cells and modulate autoimmunity.
Autologous T cells are genetically engineered to express an anti-CD19 chimeric antigen receptor with costimulatory domains. After infusion, the CAR T cells recognize CD19 on B-lineage cells, activate, proliferate, secrete cytotoxic molecules and cytokines, and lyse CD19+ cells, leading to profound B-cell depletion (for malignant or autoreactive B-cell elimination).
CD19-directed CAR T cells bind CD19 on target B cells, activate, and kill them via perforin/granzyme-mediated cytolysis (and related effector mechanisms).
Anti-CD38 monoclonal antibody that targets CD38 on plasma cells, inducing ADCC, CDC, and apoptosis.
Human IgG1κ monoclonal antibody against CD38 that binds CD38 on malignant plasma cells, inducing antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis; also depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs) to enhance anti-tumor immunity.
Anti-CD38 antibody binds CD38 on target cells and triggers ADCC (NK cells), complement-mediated lysis (CDC), antibody-dependent cellular phagocytosis (ADCP), and can induce direct apoptosis.
A subcutaneous bispecific T cell–engaging antibody that binds CD20 on malignant B cells and engages CD8/TCR on T cells, redirecting cytotoxic T cells to CD20+ targets to induce immune synapse formation, TCR signaling, cytokine release, and perforin/granzyme-mediated killing, leading to depletion of CD20+ B cells in CD20+ mature B-cell malignancies (LBCL, FL, MCL, CLL/SLL).
An IgG-like T cell–engaging antibody that binds CD20 on malignant B cells and CD3/CD8 on CD8+ T cells, crosslinking them to form an immune synapse, activating TCR signaling, cytokine release, and perforin/granzyme-mediated killing to deplete CD20+ B cells in B-cell malignancies.
AZD5492 bridges CD20 on B cells with CD3/CD8 on CD8+ T cells, forming an immune synapse that activates TCR signaling and triggers perforin/granzyme-mediated killing of CD20+ cells.