An autologous, gene-modified T-cell therapy in which patient T cells are engineered to express chimeric antigen receptors targeting CD19 and a BAFF-based target, leading to antigen-dependent T-cell activation, cytokine release, and cytotoxic killing of malignant B cells in relapsed/refractory B-ALL and B-cell NHL.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes CD19 and a BAFF pathway target on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity to eliminate malignant B cells, addressing antigen escape in relapsed/refractory B-ALL and B-cell NHL.
A BAFF-based CAR binds TACI on B cells, triggering CAR T-cell activation and perforin/granzyme-mediated cytotoxicity that kills TACI-expressing cells.
An autologous, gene-modified T-cell therapy in which patient T cells are engineered to express chimeric antigen receptors targeting CD19 and a BAFF-based target, leading to antigen-dependent T-cell activation, cytokine release, and cytotoxic killing of malignant B cells in relapsed/refractory B-ALL and B-cell NHL.
Autologous T cells are gene-modified to express a chimeric antigen receptor that recognizes CD19 and a BAFF pathway target on B cells. Upon antigen engagement, the CAR T cells activate, proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity to eliminate malignant B cells, addressing antigen escape in relapsed/refractory B-ALL and B-cell NHL.
BAFF-ligand-based CAR on the engineered T cells binds BCMA, triggering T-cell activation and perforin/granzyme-mediated killing of the target cell.
Autologous, gene-modified BCMA-directed CAR T-cell therapy; engineered T cells express an anti-BCMA CAR with 4-1BB costimulatory and CD3ζ signaling domains to induce activation, proliferation, cytokine release, and cytotoxic killing of myeloma cells.
Autologous T cells genetically modified to express a BCMA-directed chimeric antigen receptor with CD3zeta activation and 4-1BB costimulatory domains. CAR engagement of BCMA on malignant plasma cells triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-expressing tumor cells.
BCMA-directed CAR T cells bind BCMA on target cells, activate, and induce perforin/granzyme-mediated cytolytic killing (with T-cell effector mechanisms).
An anti-HER2 antibody-drug conjugate composed of a humanized IgG1 anti-HER2 antibody (trastuzumab) linked via a cleavable linker to a membrane-permeable topoisomerase I inhibitor payload (DXd). It binds HER2/ERBB2 on tumor cells, mediates partial HER2 signaling blockade and ADCC, and after internalization releases DXd to inhibit topoisomerase I, causing DNA damage, apoptosis, and a bystander effect. Dosed at 5.4 mg/kg IV every 3 weeks.
Humanized anti‑HER2 (trastuzumab) antibody linked via a cleavable linker to a membrane‑permeable topoisomerase I inhibitor (DXd). Binds HER2 on tumor cells to enable internalization; linker cleavage releases DXd to inhibit topoisomerase I, causing DNA damage and apoptosis, with a bystander effect. The antibody component also partially blocks HER2 signaling and mediates Fc‑dependent ADCC.
The ADC binds HER2, is internalized, and releases a topoisomerase I inhibitor (DXd) that causes DNA damage and apoptosis; Fc-mediated ADCC and a bystander effect further kill HER2+ cells.
A recombinant anti-EGFR human/murine chimeric IgG1 monoclonal antibody (cetuximab biosimilar candidate) given as a single IV dose; binds EGFR (ErbB1/HER1), blocks EGF/TGF-α binding and receptor activation, promotes receptor internalization, inhibits RAS–RAF–MEK–ERK and PI3K–AKT signaling, and can mediate ADCC via its IgG1 Fc.
Chimeric IgG1 monoclonal antibody targeting EGFR (ErbB1/HER1); competitively blocks EGF/TGF-α binding, prevents receptor activation and promotes internalization, thereby inhibiting downstream RAS–RAF–MEK–ERK and PI3K–AKT signaling to suppress tumor cell proliferation and survival; Fc region can engage Fcγ receptors to mediate ADCC.
IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to mediate ADCC against EGFR-expressing cells; may also trigger complement-dependent lysis, while EGFR blockade is mainly antiproliferative.