An autologous, genetically engineered T-cell therapy in which patient T cells are modified to express a chimeric antigen receptor targeting Claudin 18.2, with an iPD-1 design intended to counter PD-1/PD-L1–mediated inhibition. Administered as a single intravenous infusion to promote tumor cell killing via T-cell activation and cytotoxicity.
Autologous T cells genetically engineered to express a CAR targeting Claudin 18.2. Antigen engagement triggers T‑cell activation, proliferation, and cytotoxic killing of tumor cells. The iPD‑1 design counteracts PD‑1/PD‑L1–mediated inhibition in the tumor microenvironment to enhance T‑cell function and persistence.
YES
DIRECT
CAR-T cells recognize Claudin 18.2 and, upon engagement, directly kill target cells via perforin/granzyme-mediated cytolysis and death-receptor pathways; the iPD-1 design sustains activity in PD-1/PD-L1–rich tumors.
An autologous, genetically engineered T-cell therapy in which patient T cells are modified to express a chimeric antigen receptor targeting Claudin 18.2, with an iPD-1 design intended to counter PD-1/PD-L1–mediated inhibition. Administered as a single intravenous infusion to promote tumor cell killing via T-cell activation and cytotoxicity.
Autologous T cells genetically engineered to express a CAR targeting Claudin 18.2. Antigen engagement triggers T‑cell activation, proliferation, and cytotoxic killing of tumor cells. The iPD‑1 design counteracts PD‑1/PD‑L1–mediated inhibition in the tumor microenvironment to enhance T‑cell function and persistence.
NO
INDIRECT
CAR-T cells kill Claudin18.2+ tumor cells via perforin/granzyme; the iPD-1 feature counters PD-1/PD-L1 inhibition to enhance this killing but does not target or directly kill PD-L1+ cells.
Fully human anti-EGFR monoclonal antibody that binds EGFR on tumor epithelial cells, blocking downstream MAPK/PI3K signaling and inhibiting proliferation.
Fully human IgG1 monoclonal antibody targeting EGFR; binds and blocks EGFR activation to inhibit downstream MAPK/ERK and PI3K/AKT signaling, suppressing tumor cell proliferation and survival; may also induce ADCC and CDC against EGFR-expressing cells.
YES
DIRECT
Binds EGFR on target cells and, via its IgG1 Fc, recruits immune effectors to mediate ADCC and complement-dependent cytotoxicity (CDC), causing lysis/apoptosis; also blocks EGFR survival signaling.
Intravenous CD20×CD3 bispecific antibody that redirects T-cell cytotoxicity against CD20-positive B cells; administered with step-up dosing to reduce cytokine release syndrome.
CD20xCD3 bispecific antibody that simultaneously binds CD3 on T cells and CD20 on B cells, crosslinking them to activate T-cell cytotoxicity (immune synapse formation, perforin/granzyme release) and kill CD20-positive B-cell malignancies.
YES
DIRECT
Glofitamab links CD3 on T cells to CD20 on target cells, forming an immune synapse and inducing T‑cell cytotoxicity (perforin/granzyme-mediated apoptosis, +/- Fas/FasL).
Intravenous CD20×CD3 bispecific antibody that redirects T-cell cytotoxicity against CD20-positive B cells; administered with step-up dosing to reduce cytokine release syndrome.
CD20xCD3 bispecific antibody that simultaneously binds CD3 on T cells and CD20 on B cells, crosslinking them to activate T-cell cytotoxicity (immune synapse formation, perforin/granzyme release) and kill CD20-positive B-cell malignancies.
NO
INDIRECT
Glofitamab engages CD3 on T cells to activate them and crosslink to CD20 on B cells; activated T cells kill CD20+ cells via perforin/granzyme. CD3+ T cells are not the cytotoxic targets.