Patient-derived T lymphocytes activated and expanded ex vivo and reinfused to mediate anti-tumor cytotoxicity via TCR recognition of tumor neoantigens.
Autologous patient T lymphocytes are activated and expanded ex vivo to enrich neoantigen-specific TCR clones. Upon reinfusion, they recognize patient-specific tumor neoantigens presented on HLA and kill tumor cells via TCR-mediated cytotoxicity (perforin/granzyme and cytokine release). No genetic engineering is involved.
YES
DIRECT
Infused neoantigen-specific T cells recognize the tumor neoantigen peptide–HLA class II complex via their TCR and directly kill the presenting cells through perforin/granzyme release and Fas–FasL/cytokine-mediated apoptosis.
Chimeric IgG1 monoclonal antibody targeting EGFR; inhibits EGFR signaling and can induce antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody targeting EGFR; binds the extracellular domain to block ligand binding, receptor activation, and dimerization, thereby inhibiting downstream RAS-MAPK and PI3K-AKT signaling and suppressing tumor cell proliferation and survival; Fc-mediated ADCC can also contribute to antitumor activity.
YES
INDIRECT
Cetuximab binds EGFR on tumor cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC), killing EGFR+ cells; EGFR signaling blockade is mainly cytostatic.
First-in-human antibody-drug conjugate: an anti-HER3 (ERBB3) monoclonal antibody linked to a topoisomerase I–inhibiting exatecan-derivative payload. Binds HER3 on tumor cells, is internalized, releases the cytotoxic payload to inhibit topo I, causing DNA damage; may also dampen HER3 signaling.
Anti-HER3 (ERBB3) monoclonal antibody linked to a topoisomerase I–inhibiting exatecan-derivative payload; binds HER3 on tumor cells, is internalized, and releases the payload to inhibit topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis; may also reduce HER3 signaling.
YES
DIRECT
ADC binds HER3 on tumor cells, is internalized, and releases a topoisomerase I–inhibitor payload that causes DNA damage, cell‑cycle arrest, and apoptosis.
First-in-human antibody-drug conjugate: an anti-HER3 (ERBB3) monoclonal antibody linked to a topoisomerase I–inhibiting exatecan-derivative payload. Binds HER3 on tumor cells, is internalized, releases the cytotoxic payload to inhibit topo I, causing DNA damage; may also dampen HER3 signaling.
Anti-HER3 (ERBB3) monoclonal antibody linked to a topoisomerase I–inhibiting exatecan-derivative payload; binds HER3 on tumor cells, is internalized, and releases the payload to inhibit topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis; may also reduce HER3 signaling.
NO
INDIRECT
IBI133 targets HER3 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload that induces DNA damage and apoptosis. Topoisomerase I is the intracellular enzymatic target, but killing is directed by HER3 binding, not by topoisomerase I expression itself.
Oral small-molecule BCL-2 inhibitor that blocks anti-apoptotic BCL-2 to trigger mitochondrial apoptosis in MDS blasts.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, blocks its anti-apoptotic function, and releases pro-apoptotic effectors (BAX/BAK) to trigger mitochondrial apoptosis in MDS/tumor cells; relatively spares BCL-XL compared with navitoclax.
YES
DIRECT
Venetoclax is a BH3 mimetic that binds and inhibits BCL-2, releasing pro-apoptotic effectors (BAX/BAK) to trigger mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.