An autologous, ex vivo–expanded T‑cell therapy composed of cytotoxic T lymphocytes engineered/selected to recognize personalized tumor‑specific antigens (neoantigens) via native TCRs; administered intraventricularly to target pediatric embryonal brain tumors.
Autologous, ex vivo–expanded cytotoxic T cells selected for reactivity to patient-specific tumor antigens/neoantigens via native TCRs. After intraventricular administration, TCR recognition of peptide–MHC on tumor cells activates CTLs to kill targets through perforin/granzyme release and cytokine-mediated immune responses in the CNS.
TCR recognition of the neoantigen peptide–HLA-II complex on tumor cells activates the infused CTLs to kill the presenting cells via perforin/granzyme-mediated cytotoxicity.
TIGIT-targeting IgG1 monoclonal antibody with intact Fc; blocks TIGIT binding to CD155 (PVR) and CD112 (Nectin-2) to relieve TIGIT-mediated suppression, enhance CD8+ T-cell activity, and leverage Fc effector function for NK cell-mediated depletion of TIGIT-high intratumoral Tregs.
Humanized IgG1 anti-TIGIT immune checkpoint antibody that blocks TIGIT interaction with CD155 (PVR) and CD112 (Nectin-2), restoring CD226 co-stimulatory signaling and enhancing CD8+ T-cell and NK-cell activity; intact Fc enables ADCC/ADCP to deplete TIGIT-high intratumoral Tregs.
Anti-TIGIT IgG1 binds TIGIT on target cells and engages Fcγ receptors on NK cells/macrophages, inducing ADCC/ADCP that depletes TIGIT-high cells (e.g., intratumoral Tregs).
Anti-CD38 IgG1 monoclonal antibody (brand: Darzalex) that targets CD38 on AML cells, mediating ADCC, CDC, ADCP, and apoptosis, and depleting CD38+ immunosuppressive cells.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on tumor cells, inducing direct apoptosis and immune effector–mediated cytotoxicity (ADCC, CDC, ADCP), and depleting CD38+ immunosuppressive cells (e.g., Tregs, Bregs, MDSCs).
Binds CD38 on target cells and induces killing via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis.
An anti-CD38 antibody–drug conjugate comprising a human anti-CD38 monoclonal antibody covalently linked to a duostatin tubulin inhibitor; binds CD38 on malignant plasma cells, is internalized, and releases the duostatin payload to inhibit microtubule polymerization and induce apoptosis.
Fully human anti-CD38 antibody–drug conjugate that binds CD38 on malignant plasma cells, is internalized, and releases a duostatin/MMAF tubulin inhibitor payload to block microtubule polymerization, inducing G2/M arrest and apoptosis.
The anti-CD38 ADC binds CD38, is internalized, and releases an MMAF/duostatin payload that inhibits tubulin polymerization, causing G2/M arrest and apoptosis of CD38+ cells.
Gene-modified natural killer cells expressing a chimeric antigen receptor targeting CD19 to redirect NK cytotoxicity against CD19+ B cells; administered as cellular immunotherapy to deplete autoreactive B cells.
Gene-modified natural killer cells expressing an anti‑CD19 chimeric antigen receptor redirect NK cytotoxicity to CD19+ B cells in an MHC‑independent manner, inducing perforin/granzyme‑mediated killing of naive, memory, and plasmablast B‑cell subsets to deplete autoreactive B cells and reduce autoantibody production and B‑cell antigen presentation.
Anti-CD19 CAR NK cells recognize CD19 on target cells and directly kill them via MHC-independent degranulation with perforin/granzyme-mediated apoptosis (and potentially death-receptor pathways).