Autologous tumor-infiltrating lymphocyte (TIL) cell therapy expanded ex vivo and infused IV after lymphodepletion to mediate tumor cell killing via TCR recognition of neoantigens.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepletion to recognize patient-specific tumor neoantigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine-driven immune activation and persistence.
Autologous TILs recognize the patient-specific neoantigen peptide–HLA class II complex via native TCRs and directly kill target cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
AZD0901 (CMG901) is an antibody–drug conjugate targeting CLDN18.2; it binds CLDN18.2 on tumor cells, is internalized, and releases a cytotoxic payload to kill CLDN18.2-expressing cells.
Claudin18.2-targeted monoclonal antibody linked via a cleavable linker to MMAE (vedotin). Binds CLDN18.2 on tumor cells, is internalized, and releases MMAE to inhibit tubulin polymerization, causing G2/M arrest and apoptosis in CLDN18.2-expressing cells.
The ADC binds CLDN18.2 on target cells, is internalized, and releases MMAE via a cleavable linker; MMAE disrupts microtubules, causing G2/M arrest and apoptosis of CLDN18.2-expressing cells.
Autologous, genetically modified CAR T-cell therapy targeting mesothelin, engineered with CD28 costimulation, a tuned 1XX CD3ζ signaling domain to balance activation and persistence, and a PD-1 dominant-negative receptor to resist PD-1/PD-L1–mediated inhibition; delivered intraperitoneally for mesothelin-positive esophagogastric adenocarcinoma with peritoneal carcinomatosis.
Autologous T cells engineered to express a mesothelin-specific CAR with CD28 costimulation and a tuned 1XX CD3ζ signaling domain to balance activation and persistence, plus a PD‑1 dominant‑negative receptor that abrogates PD‑1/PD‑L1–mediated inhibition. Upon intraperitoneal delivery, the cells recognize mesothelin on tumor cells and execute cytotoxic killing and cytokine release while resisting checkpoint suppression.
Mesothelin-specific CAR T cells bind mesothelin on target cells and kill via perforin/granzyme release and death-receptor (Fas/FasL) pathways, with cytokine-mediated effects; a PD-1 dominant-negative receptor blocks PD-1/PD-L1 inhibition.
Intravenous chimeric IgG1 monoclonal antibody against EGFR; blocks ligand binding and receptor dimerization, downregulates EGFR signaling, and can mediate ADCC.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream MAPK and PI3K–AKT signaling and tumor cell proliferation; its Fc region can also mediate NK cell–driven ADCC against EGFR-expressing cells.
IgG1 Fc engages Fcγ receptors on NK cells to mediate ADCC against EGFR-expressing cells (and can also activate complement-dependent cytotoxicity); signaling blockade is antiproliferative.
A bispecific EGFR/HER3-targeted antibody–drug conjugate that, after receptor binding and internalization, releases a camptothecin-class topoisomerase I inhibitor payload, causing DNA damage and apoptosis.
Bispecific EGFR/HER3-targeted antibody-drug conjugate that binds EGFR and HER3, undergoes receptor-mediated internalization, and releases a camptothecin-class topoisomerase I inhibitor payload, causing replication-associated DNA damage and apoptosis in tumor cells.
The bispecific ADC binds EGFR on target cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor that causes replication-associated DNA damage, leading to apoptosis.