Patient-derived T cells genetically engineered ex vivo to express a chimeric antigen receptor recognizing TM4SF1 on tumor cells, leading to T-cell activation, cytokine release, and cytotoxic killing of TM4SF1-expressing cancer cells. The CAR construct includes an EGFR-based safety switch. Administered via IV or local infusion with dose escalation (0.5–10×10^6 cells/kg).
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds TM4SF1 on tumor cells. Antigen engagement triggers CAR signaling, leading to T‑cell activation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of TM4SF1‑expressing cancer cells. An EGFR-based safety switch enables targeted elimination of the CAR T cells if required.
NO
INDIRECT
Not targeted. The CAR recognizes TM4SF1, not EGFR. EGFR is included only as a safety tag on the CAR T cells for their ablation by anti‑EGFR therapy; EGFR+ host cells are not killed by the CAR T product.
A humanized IgG monoclonal antibody given IV every 2 weeks that binds tumor-expressed CD24 to block the CD24–Siglec‑10 innate immune checkpoint, enhancing macrophage-mediated phagocytosis and potentially engaging Fc-dependent effector functions (ADCC/ADCP) in adults with advanced solid tumors.
Humanized IgG monoclonal antibody that binds CD24 on tumor cells to block the CD24–Siglec‑10 innate immune checkpoint, enhancing macrophage-mediated phagocytosis and potentially engaging Fc-dependent effector functions (ADCC/ADCP).
YES
DIRECT
Anti-CD24 IgG binds CD24 on tumor cells, blocks the CD24–Siglec-10 checkpoint and engages Fcγ receptors on effector cells, triggering macrophage phagocytosis (ADCP) and NK cell ADCC of CD24+ cells; complement lysis may also contribute.
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.
YES
DIRECT
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.
YES
DIRECT
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).
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.
NO
INDIRECT
TRL345 binds HCMV gB on infected cells; its Fc engages CD16A on NK cells to mediate ADCC and complement against gB-expressing cells. CD16A+ cells act as effectors and are not targeted for killing.