A human IgG1 monoclonal antibody targeting OX40 (CD134) on activated T cells; blocks OX40–OX40L costimulatory signaling and can deplete OX40+ T cells via ADCC, reducing T‑cell survival and pathogenic type 2 inflammation.
Human IgG1 monoclonal antibody that binds OX40 (CD134) on activated T cells, blocks OX40-OX40L costimulatory signaling to suppress T-cell survival/activation and type 2 cytokine responses, and can deplete OX40+ T cells via ADCC.
IgG1 Fc engages effector cells to mediate ADCC (and related Fc-effector functions), depleting OX40+ T cells bound by the antibody.
A CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells to trigger targeted T‑cell–mediated cytotoxicity.
Humanized CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate T cells and induce targeted cytotoxic killing of CD20-positive B-cell malignancies via immune synapse formation and perforin/granzyme release.
Bispecific antibody crosslinks CD3 on T cells with CD20 on target B cells, forming an immune synapse that triggers T‑cell–mediated killing via perforin/granzyme release.
Humanized anti-EGFR IgG1 monoclonal antibody that blocks ligand binding, inhibits downstream EGFR signaling (RAS/RAF/MEK/ERK; PI3K/AKT), enhances radiosensitivity, and can induce ADCC.
Humanized IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor activation, suppressing downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit proliferation and survival; its Fc can mediate ADCC and it enhances radiosensitivity in EGFR-overexpressing tumors.
EGFR+ cells can be killed via Fc-mediated ADCC (primarily NK cells/macrophages; possible CDC), while EGFR signaling blockade is mainly cytostatic.
TROP-2–targeted antibody–drug conjugate that delivers SN-38, a topoisomerase I inhibitor.
TROP-2-targeted monoclonal antibody conjugated to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, the linker is cleaved to release SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA damage, inhibition of DNA replication, and apoptosis.
The ADC binds TROP-2, is internalized, and releases SN-38, which inhibits topoisomerase I, causing DNA damage, replication arrest, and apoptosis.
An autologous CD7-directed CAR T-cell therapy in which a patient’s T cells are engineered to express a CAR targeting CD7; engagement triggers cytotoxic activity to eliminate CD7-positive malignant T lymphoblasts and also depletes normal CD7+ T and NK cells.
Autologous T cells are engineered ex vivo to express a CD7-specific chimeric antigen receptor; after infusion, CAR T cells bind CD7 on target cells, activate, and mediate cytotoxic killing of CD7-positive malignant T lymphoblasts, with on-target depletion of normal CD7+ T and NK cells.
Anti-CD7 CAR T cells bind CD7 on target cells, activate, and induce T-cell cytotoxic killing (perforin/granzyme-mediated apoptosis, plus death receptor pathways).