Oral small-molecule EGFR tyrosine kinase inhibitor designed to selectively inhibit EGFR exon 20 insertion mutants, suppressing MAPK/ERK and PI3K–AKT signaling in tumor cells.
Oral, irreversible EGFR tyrosine kinase inhibitor that selectively targets mutant EGFR—especially exon 20 insertion variants (also T790M, Ex19del, L858R)—to block EGFR phosphorylation and downstream MAPK/ERK and PI3K–AKT signaling, leading to tumor cell growth inhibition and death.
Irreversible small-molecule inhibition of mutant EGFR kinase blocks phosphorylation and downstream MAPK/ERK and PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
Vγ9Vδ2 T cells express NKG2D, which binds ULBP1 on target cells and triggers perforin/granzyme-mediated lysis.
Anti–claudin-1 (CLDN1) monoclonal antibody intended to inhibit CLDN1-driven pro-tumor signaling and invasion and enable immune effector engagement against CLDN1-positive cells.
Humanized anti-CLDN1 monoclonal antibody that binds an extracellular epitope on non-junctional CLDN1 on tumor cells, blocks CLDN1-driven pro-tumor signaling and ECM remodeling to improve immune-cell infiltration, and engages Fc effector functions to mediate ADCC, promoting NK- and T-cell-mediated killing of CLDN1-positive cells.
Anti-CLDN1 mAb binds non-junctional CLDN1 on tumor cells and, via its Fc region, recruits FcγR+ immune effectors to mediate ADCC (e.g., NK cell–mediated lysis) of CLDN1-positive cells.
Autologous anti-BCMA CAR T-cell therapy (engineered T cells targeting BCMA on myeloma cells).
Autologous T cells engineered with a BCMA-targeting chimeric antigen receptor (dual-epitope binder with 4-1BB costimulatory domain). After infusion, CAR T cells bind BCMA on malignant plasma cells, activate, expand, and induce targeted cytotoxicity against BCMA-expressing tumor cells.
Anti-BCMA CAR T cells bind BCMA on target cells, activate, and kill them via T cell cytotoxic mechanisms (perforin/granzyme-mediated apoptosis and related death receptor pathways).