Small-molecule dimerizer that activates an inducible caspase-9 safety switch to ablate the engineered cells if required.
Rimiducid (AP1903) is a synthetic dimerizer that binds FKBP12-F36V domains on the inducible caspase-9 (iCasp9) safety switch in engineered cells, inducing caspase-9 dimerization and activation, triggering the apoptotic cascade and rapid ablation of the modified cells.
Rimiducid binds FKBP12-F36V on the iCasp9 safety switch in engineered cells, induces caspase-9 dimerization/activation, and triggers the apoptotic cascade, killing the engineered cells.
Personalized cellular immunotherapy using patient-derived tumor-resident T cells (primarily CD8+ and CD4+) expanded ex vivo and reinfused as a single IV infusion (e.g., 2.0×10^7 cells/kg) to recognize tumor/neoantigens via TCR–MHC interactions and mediate cytotoxicity through perforin/granzyme and cytokine release.
Autologous tumor-resident T cells (CD8+/CD4+) expanded ex vivo and reinfused; they recognize patient-specific tumor/neoantigens via native TCR–MHC I/II interactions and mediate cytotoxicity through perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF-α), enhancing antitumor immunity within the tumor microenvironment.
Autologous TILs recognize neoantigen peptides presented on tumor MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, with IFN-γ/TNF-α enhancing killing.
Anti-EGFR monoclonal antibody that blocks EGFR signaling; used as a rechallenge in RAS/NRAS/BRAF/EGFR wild-type disease.
Chimeric monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocks ligand binding and receptor dimerization, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling; can elicit Fc-mediated ADCC; results in antiproliferative effects, with activity primarily in RAS/NRAS/BRAF wild-type tumors.
Cetuximab binds EGFR on target cells and its Fc engages FcγR-expressing immune effectors (e.g., NK cells) to trigger ADCC (±CDC), killing EGFR+ cells; it also blocks EGFR signaling with antiproliferative effects.
Intravenous anti‑CD20 monoclonal antibody that depletes B cells via complement‑dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes CD20+ cells via complement‑dependent cytotoxicity (CDC), antibody‑dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) via FcγR-bearing effector cells, and can directly trigger apoptosis.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding, receptor activation and dimerization, thereby inhibiting downstream MAPK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its IgG1 Fc can also recruit immune effector functions to mediate antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-expressing effector cells (e.g., NK cells) to mediate ADCC (and possibly CDC), killing EGFR+ cells; EGFR blockade itself is mainly cytostatic.