An intravenous antibody–drug conjugate (RC48) consisting of an anti‑HER2 monoclonal antibody linked to the microtubule inhibitor MMAE; binds HER2, internalizes, and releases MMAE to disrupt microtubules, causing G2/M arrest, apoptosis, and bystander killing.
Disitamab vedotin is a humanized anti‑HER2 monoclonal antibody conjugated to the microtubule inhibitor monomethyl auristatin E (MMAE). It binds HER2 on tumor cells, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, disrupting microtubules and causing G2/M arrest and apoptosis; the membrane‑permeable payload can also produce bystander killing.
NO
INDIRECT
The ADC targets HER2 on tumor cells for uptake; after internalization, MMAE is released and binds beta‑tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis (with possible bystander killing). Tubulin expression alone does not determine targeting or killing.
Anti-EGFR antibody–drug conjugate delivering the microtubule-disrupting payload MMAE to EGFR-expressing tumor cells, causing mitotic arrest and apoptosis.
Anti-EGFR monoclonal antibody linked to MMAE; binds EGFR on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in EGFR-expressing cells.
YES
DIRECT
ADC binds EGFR, is internalized, and releases MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis of EGFR-expressing cells.
Anti-EGFR antibody–drug conjugate delivering the microtubule-disrupting payload MMAE to EGFR-expressing tumor cells, causing mitotic arrest and apoptosis.
Anti-EGFR monoclonal antibody linked to MMAE; binds EGFR on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in EGFR-expressing cells.
NO
INDIRECT
MRG003 targets EGFR on tumor cells; after internalization it releases MMAE, which binds the vinca site on beta-tubulin to inhibit microtubule polymerization, causing G2/M arrest and apoptosis. Tubulin expression alone is not directly targeted by the drug.
Autologous BCMA-directed CAR T-cell therapy (genetically modified CD3+ T cells expressing a chimeric antigen receptor targeting BCMA) for relapsed/refractory multiple myeloma.
Autologous CD3+ T cells are genetically modified to express a chimeric antigen receptor targeting BCMA on myeloma plasma cells. CAR binding to BCMA triggers T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity, leading to selective killing and clearance of BCMA-expressing malignant cells.
YES
DIRECT
BCMA-targeted CAR T cells bind BCMA on myeloma cells, become activated, and kill target cells via perforin/granzyme-mediated cytotoxicity (and related apoptotic pathways).
Autologous cell-based immunotherapy consisting of a patient’s fresh peripheral blood mononuclear cells (primarily T cells) armed ex vivo with an anti-CD3 x anti-EGFR bispecific antibody; upon reinfusion, redirects and activates T-cell cytotoxicity against EGFR-expressing tumor cells.
Autologous PBMCs (primarily T cells) are armed ex vivo with an anti-CD3×anti-EGFR bispecific antibody. After reinfusion, the bispecific antibody bridges CD3 on T cells to EGFR on tumor cells, activating and redirecting cytotoxic T-cell activity to lyse EGFR-expressing cancer cells without genetic modification.
YES
DIRECT
Anti-CD3×anti-EGFR bispecific-armed T cells bridge CD3 on T cells to EGFR on tumor cells, forming an immune synapse and inducing T-cell cytotoxicity (perforin/granzyme, Fas/FasL) against EGFR-expressing cells.