Autologous T cells engineered to express a CD19-directed chimeric antigen receptor (CAR) with CD3ζ and costimulatory signaling; metabolically armed to enhance CAR-T metabolic fitness, expansion, and persistence. Given as a single infusion to target CD19+ B-ALL cells.
Autologous T cells engineered with a CD19‑directed CAR (CD3ζ signaling plus costimulatory domains) bind CD19 on malignant B cells, triggering T‑cell activation and perforin/granzyme‑mediated cytotoxicity and cytokine release to eliminate CD19+ cells. The cells are metabolically armed to enhance metabolic fitness, expansion, and persistence in vivo, improving antitumor activity.
YES
DIRECT
CD19 CAR-T cells bind CD19 on target cells and, upon activation, kill them via perforin/granzyme-mediated cytolysis (and death-receptor pathways), eliminating CD19+ cells.
A human afucosylated IgG1 monoclonal antibody (AMG 451/KHK4083) targeting OX40 (CD134). It blocks OX40–OX40L signaling to reduce T‑cell activation, proliferation, survival, and cytokine production, and enhances ADCC-mediated depletion of OX40+ T cells; administered subcutaneously for atopic dermatitis.
Rocatinlimab is a human afucosylated IgG1 monoclonal antibody that binds OX40 (CD134), blocking OX40–OX40L costimulatory signaling to suppress T‑cell activation, proliferation, survival, and cytokine production. Its afucosylated Fc enhances ADCC, promoting depletion of OX40+ activated/memory T cells, thereby reducing inflammatory responses in atopic dermatitis.
YES
DIRECT
Afucosylated IgG1 anti‑OX40 binds OX40 on activated T cells and engages FcγRIIIa on NK cells/macrophages to drive ADCC (and ADCP), depleting/killing OX40+ T cells.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks ligand binding to EGFR, inhibiting MAPK/ERK and PI3K/AKT signaling and potentially mediating ADCC.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, thereby inhibiting downstream MAPK/ERK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its Fc region can also trigger antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab coats EGFR-expressing cells and its IgG1 Fc engages Fcγ receptors on effector cells (e.g., NK cells) to trigger ADCC (and some CDC), leading to target-cell lysis; EGFR blockade is mainly antiproliferative.
An antibody–drug conjugate (ADC) also known as iza-bren, izalontamab brengitecan (BMS-986507). The antibody targets a tumor-associated surface antigen, is internalized, and releases a 'gitecan' topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
Dual-targeting anti-EGFR/anti-HER3 antibody–drug conjugate. The antibody binds EGFR (HER1) and HER3 (ErbB3) on tumor cells, is internalized, and releases a 'gitecan' topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
YES
DIRECT
The ADC binds EGFR on tumor cells, is internalized, and releases a topoisomerase I inhibitor (gitecan) payload that induces DNA damage, killing EGFR-expressing cells.
An antibody–drug conjugate (ADC) also known as iza-bren, izalontamab brengitecan (BMS-986507). The antibody targets a tumor-associated surface antigen, is internalized, and releases a 'gitecan' topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
Dual-targeting anti-EGFR/anti-HER3 antibody–drug conjugate. The antibody binds EGFR (HER1) and HER3 (ErbB3) on tumor cells, is internalized, and releases a 'gitecan' topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
YES
DIRECT
The ADC binds HER3 on tumor cells, is internalized, and releases a topoisomerase I inhibitor (“gitecan”) that causes DNA damage leading to tumor cell death.