Anti-TIGIT Fc-enabled IgG1 monoclonal antibody that blocks TIGIT and can deplete TIGIT+ regulatory T cells, enhancing CD226 co-stimulation.
Fc-enabled anti-TIGIT IgG1 monoclonal antibody that blocks TIGIT interaction with CD155/CD112 to relieve inhibitory signaling and enhance CD226 (DNAM-1) co-stimulation on T and NK cells; additionally can deplete TIGIT+ regulatory T cells via Fc-mediated ADCC, collectively restoring antitumor immunity.
YES
DIRECT
Fc-enabled IgG1 binds TIGIT on target cells and engages FcγR-expressing effectors (e.g., NK cells, macrophages) to mediate ADCC/ADCP, depleting TIGIT+ cells (notably TIGIT+ Tregs).
Anti-TIGIT Fc-enabled IgG1 monoclonal antibody that blocks TIGIT and can deplete TIGIT+ regulatory T cells, enhancing CD226 co-stimulation.
Fc-enabled anti-TIGIT IgG1 monoclonal antibody that blocks TIGIT interaction with CD155/CD112 to relieve inhibitory signaling and enhance CD226 (DNAM-1) co-stimulation on T and NK cells; additionally can deplete TIGIT+ regulatory T cells via Fc-mediated ADCC, collectively restoring antitumor immunity.
NO
INDIRECT
Belrestotug binds TIGIT on target immune cells and its Fc engages CD16a on NK cells to mediate ADCC against TIGIT+ cells (e.g., Tregs). CD16a+ cells serve as effectors and are not killed by the drug.
Autologous, third-generation mesothelin-targeted chimeric antigen receptor T cells administered by endoscopic ultrasound–guided intratumoral injection as neoadjuvant therapy for resectable pancreatic ductal adenocarcinoma; the CAR engages mesothelin and signals via CD3ζ with dual co-stimulatory domains to drive cytotoxic killing and cytokine release.
Autologous, third-generation mesothelin-targeted chimeric antigen receptor T cells that bind mesothelin on tumor cells and signal via CD3z with dual co-stimulatory domains to activate T-cell effector functions, leading to proliferation, cytotoxic killing (perforin/granzyme), and cytokine release; delivered by intratumoral endoscopic ultrasound guidance as neoadjuvant therapy for resectable pancreatic ductal adenocarcinoma.
YES
DIRECT
Mesothelin-targeted CAR T cells bind mesothelin on tumor cells and induce T-cell cytotoxicity, primarily via perforin/granzyme-mediated apoptosis (with ancillary Fas–FasL and cytokine effects).
Autologous, genetically engineered chimeric antigen receptor (CAR) T-cell therapy targeting CD19; CAR engagement activates cytotoxic T-cell responses to eliminate CD19+ malignant B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor. After infusion, the CAR binds CD19 on malignant B cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, resulting in targeted elimination of CD19+ B-cell tumors.
YES
DIRECT
CAR-T cells recognize CD19 on target cells and directly kill them via T-cell cytotoxic mechanisms, primarily perforin/granzyme release (and death-receptor signaling).
Intravenous IgG1 monoclonal antibody targeting CD38 on malignant plasma cells; induces ADCC, CDC, ADCP, and direct apoptosis; inhibits CD38 ectoenzyme activity and depletes CD38+ immunosuppressive cells to enhance anti-myeloma immunity.
Isatuximab is an IgG1 monoclonal antibody targeting CD38 on malignant plasma cells. It induces antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP), and can trigger direct apoptosis. It also inhibits CD38 ectoenzyme activity and depletes CD38+ immunosuppressive cells, enhancing anti-myeloma immune responses.
YES
DIRECT
Isatuximab binds CD38 on target cells and mediates Fc-dependent ADCC and ADCP, activates complement (CDC), and can induce direct apoptosis, leading to killing of CD38+ cells.