Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG contains antibodies that bind CD8α on T cells, triggering complement-dependent lysis and Fc-mediated ADCC, with additional apoptosis, leading to direct depletion of CD8+ T cells.
Type II anti‑CD20 monoclonal antibody engineered to enhance antibody‑dependent cellular cytotoxicity; may be used for post‑response maintenance.
Humanized, glycoengineered type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them primarily via enhanced Fc gamma RIIIa (CD16a)-mediated antibody-dependent cellular cytotoxicity and direct, caspase-independent apoptosis, with relatively limited complement activation.
Binds CD20 on B cells and kills via Fc gamma RIIIa (CD16a)-mediated ADCC by NK cells and by inducing direct, caspase-independent apoptosis; complement activation is limited.
A HER3-targeted antibody-drug conjugate administered IV every 3 weeks in a Phase 1 dose escalation/expansion study. It is an anti-HER3 (ERBB3) monoclonal antibody that is internalized upon binding HER3 on tumor cells and releases a topoisomerase I inhibitor payload to induce DNA damage and apoptosis.
HER3-targeted monoclonal antibody binds ERBB3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that inhibits Topo I, causing DNA damage (replication-associated strand breaks) and apoptosis.
The HER3-targeted ADC binds ERBB3 on target cells, is internalized, and releases a topoisomerase I inhibitor payload that causes replication-associated DNA strand breaks leading to apoptosis.
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via ADCC, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (FcγR-expressing effector cells), complement-dependent cytotoxicity, and direct apoptosis signaling.
Second‑generation, irreversible pan‑HER tyrosine kinase inhibitor that covalently inhibits EGFR (HER1), HER2, and HER4, blocking downstream signaling (e.g., MAPK/PI3K‑AKT) to suppress proliferation and induce apoptosis in tumors driven by these receptors.
Irreversible inhibition of EGFR/HER family kinase activity blocks MAPK/PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-dependent tumor cells.