Ianalumab (VAY736) is a fully human monoclonal IgG1 antibody that targets the BAFF receptor (BAFF-R; TNFRSF13C) on B cells, blocking BAFF/BLyS survival signaling and inducing antibody-dependent cellular cytotoxicity to deplete B cells. Administered subcutaneously to reduce autoreactive B-cell activity and autoantibody production in diffuse cutaneous systemic sclerosis.
Fully human IgG1 monoclonal antibody against BAFF-R (TNFRSF13C) on B cells that blocks BAFF/BLyS survival signaling and induces Fc-mediated cytotoxicity (e.g., ADCC), resulting in B-cell depletion and reduced autoreactive B-cell activity and autoantibody production.
YES
DIRECT
Ianalumab binds BAFF-R on B cells and engages Fc gamma receptors on effector cells to trigger ADCC, killing BAFF-R–positive cells; blockade of BAFF survival signaling also promotes apoptosis.
HER2-targeted biparatopic antibody–drug conjugate (ADC) that binds two non-overlapping HER2 extracellular epitopes (ECD2 and ECD4), enhances receptor internalization and downregulates surface HER2 to provide dual HER2 signaling blockade while delivering a cytotoxic payload.
TQB2102 is a HER2-directed biparatopic antibody-drug conjugate that binds two non-overlapping HER2 extracellular epitopes (ECD2 and ECD4), drives receptor internalization and surface HER2 downregulation to block HER2 signaling, and releases an intracellular cytotoxic payload to kill HER2-expressing tumor cells.
YES
DIRECT
HER2-directed ADC binds HER2, is internalized, and releases an intracellular cytotoxic payload that kills the HER2-expressing cell (with additional HER2 signaling blockade).
Cord blood–derived natural killer (NK) cells genetically engineered to express a CD19-directed chimeric antigen receptor for antigen-specific recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies.
Cord blood–derived NK cells are engineered to express a CD19-specific chimeric antigen receptor, enabling antigen-dependent recognition and cytotoxic killing of CD19-positive B cells in B-cell malignancies. In this construct, IL-15 supports NK activation, proliferation, and persistence, while IL-10 modulates inflammatory responses to enhance antitumor activity and potentially reduce toxicity.
NO
INDIRECT
The CAR-NK cells specifically recognize CD19 and lyse CD19+ cells via NK degranulation (perforin/granzyme). IL-10 receptor beta is not targeted, so its expression does not trigger killing.
An intravenous glyco-humanized polyclonal (polyspecific) antibody engineered for human-like glycosylation and multi-epitope binding to malignant T-cell surface antigens, aiming to eliminate tumor T cells via Fc-mediated effector functions (ADCC, CDC) and potential direct neutralization in PTCL subtypes.
Glyco-humanized polyspecific polyclonal antibody that binds multiple surface antigens on malignant T cells and induces their elimination via Fc-mediated effector functions (enhanced ADCC through FcγR-expressing NK cells/macrophages and complement-dependent cytotoxicity), with possible direct neutralization of target cells.
YES
DIRECT
Antibody binds malignant T‑cell surface antigens and recruits immune effector functions: Fc gamma receptor–mediated ADCC by NK cells/macrophages and complement-dependent cytotoxicity (CDC), leading to lysis/elimination of the bound target cells.
Humanized, afucosylated IgG1 monoclonal antibody that antagonizes the OX40 (CD134) costimulatory receptor and can deplete OX40+ activated T cells via ADCC, reducing T-cell activation, survival, memory, and type 2 inflammation relevant to atopic dermatitis. Administered as a single subcutaneous dose (via vial or prefilled syringe).
Humanized, afucosylated IgG1 monoclonal antibody against OX40 (CD134) that blocks OX40–OX40L costimulatory signaling and, via enhanced Fc-mediated ADCC, depletes OX40+ activated T cells, thereby reducing T‑cell activation, survival/memory, and type 2 inflammatory responses.
YES
DIRECT
Afucosylated IgG1 anti-OX40 engages Fc receptors (e.g., FcγRIIIa) on NK cells to trigger ADCC, with possible macrophage ADCP, depleting OX40+ activated T cells.