Anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes malignant and normal B cells via Fc-mediated ADCC and phagocytosis, complement-dependent cytotoxicity, and direct induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces Fc-mediated ADCC/phagocytosis by NK cells/macrophages, complement-dependent cytotoxicity, and direct apoptotic signaling.
CD20xCD3 bispecific T-cell–engaging antibody that recruits and activates T cells via CD3 to kill CD20+ B cells.
CD20xCD3 bispecific antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking them to activate T-cell signaling and cytotoxicity, leading to targeted lysis of CD20-positive malignant B cells.
YES
DIRECT
Glofitamab bridges CD3+ T cells to CD20+ cells, activating T-cell cytotoxicity that kills the CD20-expressing cells via perforin/granzyme-mediated lysis (and related effector pathways).
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
YES
DIRECT
Vγ9Vδ2 T cells use NKG2D to recognize ULBP4 on target cells, triggering activation and perforin/granzyme-mediated cytolysis.
An antibody–drug conjugate consisting of a humanized anti-B7-H3 (CD276) IgG1 monoclonal antibody linked via a cleavable linker to a deruxtecan (DXd) topoisomerase I inhibitor payload. After binding B7-H3 on tumor cells and internalization, the linker is cleaved to release DXd, inducing DNA damage and apoptosis with potential bystander effect; the antibody may also mediate Fc-dependent ADCC/ADCP.
Ifinatamab deruxtecan is a B7-H3–targeted antibody–drug conjugate. After binding B7-H3 on tumor cells and internalization, a cleavable linker releases the deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and apoptosis. The membrane-permeable payload can produce a bystander effect, and the IgG1 antibody may also mediate Fc-dependent ADCC/ADCP.
YES
INDIRECT
After the ADC binds B7-H3 and releases the DXd payload, DXd inhibits DNA topoisomerase I in exposed cells, causing DNA damage and apoptosis (including bystander killing).
CD20xCD3 bispecific T-cell–engaging antibody that recruits and activates T cells via CD3 to kill CD20+ B cells.
CD20xCD3 bispecific antibody that simultaneously binds CD20 on B cells and CD3 on T cells, crosslinking them to activate T-cell signaling and cytotoxicity, leading to targeted lysis of CD20-positive malignant B cells.
NO
INDIRECT
CD3 on T cells is engaged to activate T cells, which then kill CD20+ B cells via perforin/granzyme-mediated cytotoxicity; CD3+ T cells are not targeted for lysis.