An EGFR-targeted antibody–drug conjugate that delivers the microtubule-disrupting payload MMAE; after binding EGFR and internalization, MMAE causes G2/M arrest and apoptosis.
EGFR-targeted antibody-drug conjugate (becotatug vedotin) linked to MMAE. After binding EGFR on tumor cells and internalization, MMAE is released to bind tubulin and inhibit polymerization, leading to microtubule disruption, G2/M cell-cycle arrest, and apoptosis in EGFR-expressing cells.
NO
INDIRECT
MRG003 binds EGFR, is internalized, and releases MMAE, which binds beta‑tubulin to disrupt microtubules and cause G2/M arrest and apoptosis. Beta‑tubulin expression alone does not confer killing without EGFR-mediated delivery.
Chimeric anti-EGFR monoclonal antibody that blocks ligand binding and receptor activation and mediates antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab is a chimeric monoclonal antibody against EGFR that blocks ligand binding and prevents receptor activation and dimerization, suppressing downstream signaling (e.g., RAS/RAF/MEK/ERK, PI3K/AKT) to inhibit tumor cell proliferation; it also mediates antibody‑dependent cellular cytotoxicity (ADCC) against EGFR-expressing cells.
YES
DIRECT
Cetuximab binds EGFR on target cells and engages immune effectors via its Fc to induce antibody‑dependent cellular cytotoxicity (ADCC) (and potentially complement-mediated lysis), killing EGFR+ cells; it also blocks EGFR signaling (antiproliferative).
An antibody–drug conjugate comprising an anti-HER3 monoclonal antibody linked to the topoisomerase I inhibitor DXd; binds HER3 (ERBB3), internalizes, and releases DXd to induce DNA damage with potential bystander effect.
Anti-HER3 (ERBB3) antibody–drug conjugate; binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor DXd via a cleavable linker, causing DNA damage/topoisomerase I inhibition and cytotoxicity with a membrane-permeable bystander effect.
YES
DIRECT
Anti-HER3 antibody–drug conjugate binds HER3, is internalized, and releases the topoisomerase I inhibitor DXd via a cleavable linker, causing DNA damage–mediated cell death; released payload can also produce a bystander effect.
An antibody–drug conjugate comprising an anti-HER3 monoclonal antibody linked to the topoisomerase I inhibitor DXd; binds HER3 (ERBB3), internalizes, and releases DXd to induce DNA damage with potential bystander effect.
Anti-HER3 (ERBB3) antibody–drug conjugate; binds HER3 on tumor cells, is internalized, and releases the topoisomerase I inhibitor DXd via a cleavable linker, causing DNA damage/topoisomerase I inhibition and cytotoxicity with a membrane-permeable bystander effect.
YES
INDIRECT
HER3-targeted ADC internalizes into HER3+ cells and releases DXd; DXd inhibits topoisomerase I, causing DNA damage and cell death (with a membrane-permeable bystander effect). Topoisomerase I is the intracellular payload target, not the binding antigen.
Autologous CD8+ T cells genetically engineered (gene-edited, TCR-transduced) with a personalized, multi-target, tumor-specific TCR set; administered as sequential IV infusions to redirect T-cell receptor specificity to patient-specific HLA class I–presented tumor antigens and drive cytotoxic effector activity (cytokine release, perforin/granzyme-mediated killing).
Autologous CD8+ T cells are gene-edited and TCR-transduced to express a personalized set of tumor-specific T-cell receptors that recognize patient-specific peptide–HLA class I complexes on tumor cells, activating TCR signaling and cytotoxic effector functions (cytokine release, perforin/granzyme-mediated killing) to eliminate cancer cells.
YES
DIRECT
Engineered CD8+ T cells recognize the patient-specific peptide–HLA class I complex via the introduced TCR and directly kill target cells through cytotoxic granule release (perforin/granzymes) and death-receptor pathways.