Anti-CLDN18.2 monoclonal antibody that binds claudin 18.2 on tumor cells and mediates immune cytotoxicity (ADCC/CDC).
ASKB589 is an anti-CLDN18.2 monoclonal antibody that binds claudin 18.2 on tumor cells and promotes immune-mediated killing via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of CLDN18.2-positive cancer cells.
Anti-CLDN18.2 antibody binds CLDN18.2 on tumor cells and triggers Fc-mediated ADCC by effector cells and complement-dependent cytotoxicity (CDC), leading to lysis of CLDN18.2-positive cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that induces direct cell death and potent ADCC/ADCP against CD20+ B cells.
Type II, glycoengineered anti-CD20 IgG1 that binds CD20 on B cells and, via enhanced FcγRIIIa affinity (afucosylated Fc), drives potent antibody-dependent cellular cytotoxicity and phagocytosis (ADCC/ADCP) and induces direct, caspase-independent cell death, leading to depletion of CD20+ malignant B cells.
Binds CD20 on B cells; afucosylated Fc engages FcγRIIIa on effector cells to mediate potent ADCC and ADCP, and the antibody itself induces direct, caspase‑independent cell death of CD20+ cells.
B7-H3 (CD276)–targeted chimeric antigen receptor gamma-delta T cell (CAR-γδ T) therapy; autologous engineered γδ T cells designed to mediate MHC-independent cytotoxicity against B7-H3–expressing solid tumors. Administered as a single infusion with dose escalation (1×10^8–1×10^9 CAR+ γδ T cells).
Autologous gamma-delta T cells are engineered to express a chimeric antigen receptor specific for B7-H3 (CD276). Upon binding B7-H3 on tumor cells, CAR signaling activates the γδ T cells to mediate MHC-independent cytotoxicity, leading to tumor cell killing via perforin/granzyme release and cytokine secretion, with expansion and persistence driven by CAR costimulatory/ζ signaling.
CAR γδ T cells bind B7‑H3 on target cells and, upon CAR activation, directly kill them via cytotoxic degranulation (perforin/granzyme) leading to apoptosis/lysis, with supportive cytokine effects.
Humanized IgG1 monoclonal antibody targeting OX40 (CD134); inhibits the OX40–OX40L T‑cell costimulatory pathway and depletes OX40+ activated T cells via Fc‑enhanced ADCC, reducing pathogenic effector/memory T‑cell activity and type 2 inflammatory cytokine signaling.
Humanized IgG1 monoclonal antibody against OX40 (CD134) that blocks OX40–OX40L costimulatory signaling and depletes OX40+ activated T cells via Fc-enhanced ADCC, reducing pathogenic effector/memory T-cell activity and type 2 inflammatory cytokine signaling.
The IgG1 antibody binds OX40 on activated T cells and its Fc engages Fcγ receptors on effector cells (e.g., NK cells), triggering Fc‑enhanced ADCC that lyses/depletes OX40+ cells.
Humanized anti-CD19 monoclonal antibody (Monjuvi) optionally used post-infusion to ablate transferred CAR Tregs as a safety measure.
Tafasitamab-cxix is a humanized anti-CD19 monoclonal antibody with an Fc-engineered region that enhances Fcγ receptor binding to promote antibody-dependent cellular cytotoxicity and phagocytosis, leading to depletion of CD19-expressing B cells (and any CD19-tagged engineered cells) for antineoplastic and immunomodulatory effects.
Binds CD19 on target cells and engages Fcγ receptor–bearing effector cells to mediate antibody-dependent cellular cytotoxicity and phagocytosis, depleting CD19+ cells.