CLDN18.2-targeting antibody-drug conjugate that binds CLDN18.2 on tumor cells, internalizes, and delivers a cytotoxic payload to kill cancer cells.
Monoclonal antibody targets CLDN18.2 on tumor cells, is internalized, and releases the linked cytotoxic payload MMAE via a cleavable linker; MMAE binds tubulin and inhibits microtubule polymerization, inducing G2/M arrest and apoptosis in CLDN18.2-positive tumor cells.
YES
DIRECT
ADC binds CLDN18.2 on target cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis of CLDN18.2-positive cells.
HER2-targeted antibody–drug conjugate (RC48) comprising a humanized anti-HER2 IgG1 linked to the microtubule-disrupting payload MMAE; internalized upon HER2 binding and can mediate ADCC.
HER2-targeted IgG1 antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases the microtubule inhibitor MMAE, which disrupts tubulin polymerization to induce G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC.
NO
INDIRECT
Disitamab vedotin targets HER2, not beta-tubulin. After HER2-mediated internalization, the MMAE payload binds the β-tubulin (vinca) site, inhibiting microtubule polymerization and causing G2/M arrest and apoptosis; tubulin expression alone does not determine killing.
CLDN18.2-targeting antibody-drug conjugate that binds CLDN18.2 on tumor cells, internalizes, and delivers a cytotoxic payload to kill cancer cells.
Monoclonal antibody targets CLDN18.2 on tumor cells, is internalized, and releases the linked cytotoxic payload MMAE via a cleavable linker; MMAE binds tubulin and inhibits microtubule polymerization, inducing G2/M arrest and apoptosis in CLDN18.2-positive tumor cells.
NO
INDIRECT
LM-302 binds CLDN18.2 on tumor cells, is internalized, and releases MMAE; MMAE binds beta-tubulin to block microtubule polymerization, causing G2/M arrest and apoptosis in CLDN18.2-positive cells. Beta-tubulin expression alone does not determine killing.
Autologous, ex vivo–expanded tumor-infiltrating lymphocyte (TIL) product composed of polyclonal T cells that recognize patient-specific tumor neoantigens via the TCR and mediate cytotoxicity (perforin/granzyme and IFN-γ).
Autologous, ex vivo–expanded polyclonal TILs that are CRISPR/Cas9-edited to remove immunoregulatory targets; they recognize patient-specific tumor neoantigens via TCR–HLA interactions and kill tumor cells through perforin/granzyme release and IFN-γ–mediated cytotoxicity, enhancing TIL proliferation and function.
YES
DIRECT
Autologous CRISPR-edited TILs recognize the neoantigen–HLA class I complex via their TCR and directly lyse target cells through perforin/granzyme-mediated apoptosis, with IFN-γ/Fas–FasL contributions.
Autologous, ex vivo–expanded tumor-infiltrating lymphocyte (TIL) product composed of polyclonal T cells that recognize patient-specific tumor neoantigens via the TCR and mediate cytotoxicity (perforin/granzyme and IFN-γ).
Autologous, ex vivo–expanded polyclonal TILs that are CRISPR/Cas9-edited to remove immunoregulatory targets; they recognize patient-specific tumor neoantigens via TCR–HLA interactions and kill tumor cells through perforin/granzyme release and IFN-γ–mediated cytotoxicity, enhancing TIL proliferation and function.
YES
DIRECT
TILs recognize the neoantigen–HLA class II complex via their TCR and directly kill the target cell through perforin/granzyme release and IFN-γ–mediated cytotoxicity.