Autologous anti-CD19 CAR T-cell therapy (brexu-cel) that redirects patient T cells to kill CD19-positive B-lymphoblasts, inducing cytotoxicity and B-cell aplasia.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are retrovirally transduced to express an anti-CD19 scFv linked to CD28 costimulatory and CD3 zeta signaling domains. After infusion, CAR engagement of CD19 on B-lineage cells activates the T cells to proliferate and kill CD19-positive malignant B cells, leading to tumor lysis and on-target B-cell aplasia.
Anti-CD19 CAR T cells bind CD19 on target cells and directly kill them via T-cell cytotoxicity (perforin/granzyme release and apoptosis via death receptor pathways).
Autologous, fully human anti-CD19 CAR T-cell therapy engineered to eliminate CD19+ B-lineage cells to suppress B cell–driven autoimmunity in progressive MS.
Autologous anti-CD19 CAR T cells engineered with an scFv targeting CD19 and CD8alpha hinge/transmembrane, CD28 costimulatory, and CD3zeta signaling domains. After infusion, they bind CD19 on B-lineage cells, become activated, proliferate, and kill targets via cytotoxic mechanisms, selectively depleting CD19+ B cells to suppress B cell–driven autoimmunity.
Anti-CD19 CAR T cells bind CD19 on target cells; CAR signaling activates T cells to kill via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
Autologous T cells engineered ex vivo to express a claudin 18.2-specific CAR; after infusion they bind CLDN18.2 on tumor cells and trigger MHC-independent T-cell activation, cytokine release, and cytotoxic killing in CLDN18.2-positive gastric/GEJ adenocarcinoma.
Autologous T cells are engineered ex vivo to express a CAR that binds claudin 18.2; upon encountering CLDN18.2 on tumor cells, the CAR triggers MHC-independent T-cell activation, cytokine release, and cytotoxic killing of CLDN18.2-positive cancer cells.
CAR-T cells recognize CLDN18.2 and, upon activation, directly lyse target cells via perforin/granzyme release (and Fas–FasL apoptosis).
Bicycle toxin conjugate targeting Nectin-4 that delivers the cytotoxic payload MMAE (a microtubule inhibitor), causing mitotic arrest and apoptosis.
A bicyclic peptide (Bicycle toxin conjugate) that binds Nectin-4 on tumor cells and is internalized to release the cytotoxic payload MMAE, which inhibits microtubule polymerization, leading to mitotic arrest and apoptosis in Nectin-4–expressing cells.
BT8009 binds Nectin-4 on tumor cells, is internalized, and releases MMAE, a microtubule inhibitor, causing mitotic arrest and apoptosis of Nectin-4–expressing cells.
Anti-PD-L1 monoclonal antibody that blocks PD-L1 to enhance antitumor T-cell responses.
Human IgG1 anti–PD-L1 monoclonal antibody that blocks PD-L1 from engaging PD-1, relieving checkpoint-mediated T-cell inhibition and restoring antitumor T-cell activity; its Fc can also mediate antibody-dependent cellular cytotoxicity (ADCC) against PD-L1–expressing tumor cells.
Avelumab binds PD-L1 on target cells and, via its IgG1 Fc, recruits FcγR-expressing effector cells (e.g., NK cells) to mediate ADCC against PD-L1–positive cells; PD-L1 blockade also restores T-cell killing.