Autologous mesothelin-targeted CAR T-cell therapy in which a patient's T cells are lentivirally transduced to express an anti-mesothelin M5 scFv fused to 4-1BB and CD3ζ signaling domains; administered intratumorally (3e6 or 3e7 cells). Binding to mesothelin triggers T-cell activation and costimulation, leading to targeted cytotoxicity and local immune modulation.
Autologous T cells are lentivirally engineered to express an anti-mesothelin CAR (M5 scFv) with 4-1BB costimulatory and CD3ζ activation domains. Upon binding mesothelin on tumor cells, the CAR triggers T-cell activation, proliferation, and cytotoxic killing, with 4-1BB enhancing persistence; intratumoral delivery promotes localized immune modulation.
YES
DIRECT
Anti-mesothelin CAR T cells bind mesothelin, activating CD3ζ/4-1BB signaling and inducing T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, possibly Fas/FasL), killing mesothelin+ cells.
An antibody–drug conjugate (ADC) targeting Claudin 18.2; upon tumor binding and internalization, it releases the cytotoxic payload monomethyl auristatin E (MMAE) to disrupt microtubules and induce mitotic arrest/apoptosis in CLDN18.2-positive tumor cells.
RC118 is an anti‑CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE, which disrupts microtubule polymerization, causing G2/M arrest and apoptosis in CLDN18.2‑expressing cells.
YES
DIRECT
The ADC binds CLDN18.2 on target cells, is internalized, and releases the MMAE payload that disrupts microtubules, causing G2/M arrest and apoptosis.
An antibody–drug conjugate (ADC) targeting Claudin 18.2; upon tumor binding and internalization, it releases the cytotoxic payload monomethyl auristatin E (MMAE) to disrupt microtubules and induce mitotic arrest/apoptosis in CLDN18.2-positive tumor cells.
RC118 is an anti‑CLDN18.2 antibody–drug conjugate that binds CLDN18.2 on tumor cells, is internalized, and releases the cytotoxic payload MMAE, which disrupts microtubule polymerization, causing G2/M arrest and apoptosis in CLDN18.2‑expressing cells.
NO
INDIRECT
RC118 targets CLDN18.2, is internalized, and releases MMAE, which binds beta-tubulin (vinca site) to inhibit microtubule polymerization, causing G2/M arrest and apoptosis in CLDN18.2-positive cells; tubulin expression alone is not sufficient for targeting.
Autologous T-cell product expanded ex vivo; provides tumor-reactive lymphocytes that mediate TCR-dependent cytotoxicity as adoptive cell therapy.
Autologous tumor-draining lymph node–derived T cells expanded ex vivo and reinfused to provide tumor-reactive lymphocytes that recognize tumor antigens via native TCRs and kill target cells through perforin/granzyme cytotoxicity and cytokine-mediated immune activation.
YES
DIRECT
Adoptively transferred tumor-reactive T cells recognize the peptide–HLA class I complex via their native TCR and directly kill target cells through perforin/granzyme-mediated cytotoxicity (with possible Fas–FasL and cytokine contributions).
Autologous T-cell product expanded ex vivo; provides tumor-reactive lymphocytes that mediate TCR-dependent cytotoxicity as adoptive cell therapy.
Autologous tumor-draining lymph node–derived T cells expanded ex vivo and reinfused to provide tumor-reactive lymphocytes that recognize tumor antigens via native TCRs and kill target cells through perforin/granzyme cytotoxicity and cytokine-mediated immune activation.
YES
DIRECT
Adoptively transferred tumor-reactive T cells recognize the tumor antigen peptide–HLA-B complex via their native TCR and kill targets via perforin/granzyme cytolysis (and Fas–FasL apoptosis).