Oncolytic viral immunotherapy (PVSRIPO), a live-attenuated poliovirus type 1 Sabin/rhinovirus chimera that targets CD155/Necl-5 on tumor and antigen-presenting cells, replicates to cause oncolysis and antigen release, and induces type I IFN and dendritic-cell activation to drive tumor-specific T-cell responses.
Live-attenuated poliovirus type 1 Sabin/human rhinovirus HRV2 IRES chimera that targets CD155 (Necl-5) on tumor and antigen-presenting cells; selectively replicates in CD155+ nonneuronal tumor cells causing oncolysis and antigen release, which triggers type I interferon signaling and dendritic-cell activation to drive tumor-specific T-cell responses and systemic antitumor immunity.
YES
DIRECT
The oncolytic poliovirus binds CD155 to enter CD155+ tumor cells, selectively replicates inside them, and causes lytic cell death (oncolysis); immune activation occurs secondarily.
Engineered protein cytotoxin that binds integrin αvβ3 and induces apoptosis in αvβ3-expressing cells to remodel the tumor microenvironment.
Engineered protein cytotoxin that binds integrin αvβ3 and induces caspase-mediated apoptosis in αvβ3-expressing stromal, endothelial, and tumor cells, depleting these populations and remodeling the tumor microenvironment.
YES
DIRECT
Binds integrin αvβ3 on target cells and triggers caspase-mediated apoptosis, directly killing αvβ3-expressing cells.
Engineered protein cytotoxin that binds integrin αvβ3 and induces apoptosis in αvβ3-expressing cells to remodel the tumor microenvironment.
Engineered protein cytotoxin that binds integrin αvβ3 and induces caspase-mediated apoptosis in αvβ3-expressing stromal, endothelial, and tumor cells, depleting these populations and remodeling the tumor microenvironment.
YES
DIRECT
ProAgio binds integrin αvβ3 on target cells and directly triggers caspase-dependent apoptosis, killing αvβ3-expressing stromal, endothelial, and tumor cells.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR signaling (RAS–RAF–MEK–ERK and PI3K–AKT) and can trigger antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor dimerization, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling and inducing Fc-mediated ADCC.
YES
DIRECT
Cetuximab binds EGFR on target cells and its Fc engages Fcγ receptors on immune effectors (e.g., NK cells), inducing ADCC (and some CDC), leading to killing of EGFR+ cells; signaling blockade itself is mainly cytostatic.
An autologous anti‑CD19 CAR T‑cell therapy that targets CD19 on malignant B cells to trigger T‑cell activation and cytotoxic killing; administered after lymphodepleting chemotherapy to support CAR‑T expansion.
Autologous T cells genetically engineered to express an anti-CD19 chimeric antigen receptor (scFv-CD28-CD3zeta) recognize CD19 on malignant B cells, leading to T-cell activation, proliferation, cytokine release, and cytotoxic killing; lymphodepleting chemotherapy is given to enhance in vivo CAR-T expansion.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on target cells, activate, and kill via T-cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and Fas–FasL).