Anti-EGFR IgG1 monoclonal antibody that blocks upstream receptor signaling.
Chimeric IgG1 monoclonal antibody against EGFR that binds the extracellular domain to block ligand binding and receptor dimerization/activation, thereby suppressing downstream MAPK and PI3K-AKT signaling and inhibiting tumor cell proliferation; its IgG1 Fc can also mediate ADCC.
Cetuximab binds EGFR and its IgG1 Fc engages FcγR-bearing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC), killing EGFR+ cells; it also blocks EGFR signaling to inhibit proliferation.
Selective small-molecule BCL-2 inhibitor that promotes apoptosis.
Selective BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, neutralizing its anti-apoptotic function and freeing pro-apoptotic effectors (e.g., BAX/BAK) to trigger mitochondrial outer membrane permeabilization and caspase-dependent apoptosis; does not inhibit BCL-XL.
Venetoclax directly inhibits BCL-2, freeing pro-apoptotic effectors to activate BAX/BAK, causing mitochondrial outer membrane permeabilization and caspase-dependent apoptosis in BCL-2–dependent cells.
An anti–Trop-2 antibody–drug conjugate composed of a humanized monoclonal antibody targeting TACSTD2 (Trop-2) linked to a cytotoxic payload; it binds Trop-2 on tumor cells, is internalized, and releases the payload intracellularly to induce tumor cell death.
Humanized anti-Trop-2 monoclonal antibody linked via a cleavable linker to a camptothecin analog; binds TROP-2 (TACSTD2) on tumor cells, is internalized, and releases the topoisomerase I-inhibiting payload intracellularly to block DNA replication, causing cell-cycle arrest and apoptosis in TROP-2–expressing tumors.
An anti–TROP-2 antibody–drug conjugate binds TROP-2, is internalized, and releases a camptothecin (topoisomerase I–inhibiting) payload that blocks DNA replication, causing cell-cycle arrest and apoptosis of TROP-2–expressing cells.
Anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule inhibitor MMAE to induce mitotic arrest and apoptosis; may also mediate ADCC.
Anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE. Binds HER2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; may also mediate ADCC via the antibody Fc.
The ADC binds HER2, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.
An intravenous CD19-directed, T-cell–redirecting biologic immunotherapy given with step-up dosing; binds CD19 on B cells to engage and activate T cells for cytotoxic killing of malignant B cells, with expected on-target depletion of normal CD19+ B cells. Studied in CD19+ B-cell malignancies (B-NHL, B-ALL, CLL).
A trispecific T-cell engager antibody that binds CD19 on B cells and CD3/CD28 on T cells to crosslink and costimulate T cells, redirecting cytotoxic activity against CD19+ malignant B cells; on-target depletion of normal CD19+ B cells is expected.
Trispecific T‑cell engager binds CD19 on B cells and CD3/CD28 on T cells, crosslinking and costimulating T cells to kill CD19+ cells via perforin/granzyme-mediated cytolysis.