Allogeneic CD19-directed CAR T-cell therapy using donor T cells engineered to target CD19 on B cells, leading to T-cell activation and cytotoxic elimination of malignant B cells and minimal residual disease.
Allogeneic donor T cells engineered to express a CD19‑specific chimeric antigen receptor recognize CD19 on B cells, leading to T‑cell activation, proliferation, and cytotoxic elimination of malignant B cells to eradicate minimal residual disease.
CD19-directed CAR T cells recognize CD19 on target B cells, activate, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas/FasL-mediated apoptosis).
Anti-CD52 monoclonal antibody that depletes CD52-positive immune cells (T, B, NK) to reduce rejection of allogeneic CAR T cells.
Unconjugated anti-CD52 monoclonal antibody that binds CD52 on T, B, and NK cells and depletes them via Fc-mediated effector functions (ADCC/CDC), achieving lymphodepletion to reduce host rejection of allogeneic CAR T cells.
Unconjugated anti-CD52 mAb binds CD52 and triggers Fc-mediated ADCC and complement-dependent cytotoxicity, leading to lysis/depletion of CD52+ lymphocytes.
Actinium-225–macropa–pelgifatamab (225Ac‑pelgi), a PSMA-targeted radioimmunoconjugate in which the anti‑PSMA monoclonal antibody pelgifatamab is chelated via macropa to the alpha-emitter actinium‑225 to deliver targeted alpha radiation; administered IV every 6 weeks for mCRPC.
An anti‑PSMA monoclonal antibody (pelgifatamab) is chelated via macropa to the alpha‑emitter actinium‑225. After binding PSMA on prostate cancer cells, the conjugate delivers short‑range, high‑LET alpha radiation that induces lethal DNA double‑strand breaks, leading to targeted tumor cell death.
Anti-PSMA antibody delivers actinium-225 alpha radiation to PSMA-expressing cells, causing high-LET DNA double-strand breaks and targeted cell death.
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal IgG1 that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via antibody-dependent cellular cytotoxicity (Fc-engaged NK cells/macrophages), complement-dependent cytotoxicity, and direct apoptosis.
HER2-targeted antibody–drug conjugate; anti-HER2 IgG1 linked to the topoisomerase I inhibitor deruxtecan. Binds HER2, internalizes, and releases a cytotoxic payload causing DNA damage with a bystander effect.
HER2-directed antibody–drug conjugate composed of trastuzumab linked to the topoisomerase I inhibitor deruxtecan (DXd). After binding HER2 on tumor cells and internalization, the payload is released to inhibit topoisomerase I, causing DNA damage, cell cycle arrest, and apoptosis, with a membrane-permeable bystander killing effect; the antibody component can also mediate ADCC.
The ADC binds HER2, is internalized, and releases the deruxtecan payload that inhibits topoisomerase I, causing DNA damage and apoptosis; the IgG1 Fc can also mediate ADCC, with some bystander killing from the membrane-permeable payload.