Investigational IgG1 anti-CTLA-4 monoclonal antibody (checkpoint inhibitor) that blocks CTLA-4 to enhance T-cell priming and may deplete intratumoral regulatory T cells via Fc-mediated ADCC.
Humanized IgG1 monoclonal antibody against CTLA-4 that blocks CTLA-4-mediated inhibition of T-cell activation to enhance T-cell priming and effector function; Fc-enabled activity may deplete intratumoral regulatory T cells via ADCC, promoting antitumor cytotoxic T-lymphocyte responses.
IgG1 Fc enables Fcγ receptor-dependent ADCC/ADCP, depleting CTLA-4–expressing T cells (especially intratumoral Tregs) via NK cells/macrophages.
A fully human IgG1κ monoclonal antibody that binds the conserved AD-2 site I epitope on HCMV glycoprotein B (gB), neutralizing virus by blocking gB-mediated attachment/fusion and cell-to-cell spread, and engaging Fc-mediated effector functions (ADCC and complement).
Fully human IgG1κ monoclonal antibody that binds the conserved AD‑2 site I epitope on HCMV glycoprotein B (gB), neutralizing virus by blocking gB‑mediated attachment/fusion and cell‑to‑cell spread, while engaging Fc‑mediated effector functions (ADCC and complement) to enhance clearance.
IgG1 antibody binds gB on HCMV‑infected cells and engages Fc receptors to trigger ADCC and activates complement, leading to lysis of gB‑expressing cells (in addition to virion neutralization).
Autologous tumor-infiltrating lymphocyte (TIL) cellular therapy manufactured from a patient’s tumor, expanded ex vivo, and reinfused to mediate antitumor activity through native TCR recognition, cytotoxic mechanisms, and cytokine secretion.
Autologous TILs expanded ex vivo and reinfused; they recognize patient-specific tumor antigens via native TCR–MHC interactions and mediate antitumor effects through cytotoxic killing (perforin/granzymes) and cytokine secretion within the tumor microenvironment.
Autologous TILs recognize the peptide–HLA class II complex via native TCRs and kill the presenting cells through perforin/granzyme-mediated cytolysis and related T-cell effector pathways.
Murine IgG1 anti-CD66 (CEACAM) monoclonal antibody conjugated with the beta-emitting radionuclide Yttrium-90 to deliver targeted radiation to CD66+ myeloid/granulocytic cells in bone marrow and spleen for marrow-directed myeloablation.
Murine IgG1 anti-CD66 (CEACAM) monoclonal antibody conjugated to the beta-emitting radionuclide Yttrium-90; upon binding CD66+ myeloid/granulocytic cells in bone marrow and spleen, it delivers localized radiation that induces DNA damage and cell death, effecting marrow-directed myeloablation and reducing leukemic burden with limited exposure to other tissues.
The Y-90–labeled anti-CD66 antibody binds CEACAM8 (CD66b) on granulocytic cells and emits beta radiation that causes DNA double-strand breaks and lethal damage, directly ablating the bound target cells (with some local crossfire effect).
Murine IgG1 anti-CD66 (CEACAM) monoclonal antibody conjugated with the beta-emitting radionuclide Yttrium-90 to deliver targeted radiation to CD66+ myeloid/granulocytic cells in bone marrow and spleen for marrow-directed myeloablation.
Murine IgG1 anti-CD66 (CEACAM) monoclonal antibody conjugated to the beta-emitting radionuclide Yttrium-90; upon binding CD66+ myeloid/granulocytic cells in bone marrow and spleen, it delivers localized radiation that induces DNA damage and cell death, effecting marrow-directed myeloablation and reducing leukemic burden with limited exposure to other tissues.
The 90Y-labeled anti-CD66 antibody binds CD66/CEACAM antigens on myeloid cells; bound radionuclide emits beta radiation that causes DNA double-strand breaks and cell death in antigen-expressing cells (with some crossfire to nearby cells).