An IV IgG-based bispecific immunotherapy antibody that conditionally agonizes CD28 on T cells when co-engaged with EGFR on tumor cells, localizing CD28 costimulation to EGFR-positive tumors to boost T-cell activation, proliferation, cytokine release, and cytotoxicity while limiting systemic immune activation.
IgG-based bispecific antibody that binds EGFR on tumor cells and CD28 on T cells to provide conditional CD28 costimulation only when both targets are engaged at the tumor site, enhancing T-cell activation, proliferation, cytokine release, and cytotoxicity against EGFR-positive tumors while limiting systemic immune activation.
NO
INDIRECT
The bispecific antibody bridges CD28 on T cells with EGFR on tumor cells to deliver localized CD28 costimulation, boosting T‑cell–mediated killing of EGFR-positive tumor cells (perforin/granzyme, cytokines); CD28-expressing T cells are not targeted for killing.
PBMC-derived chimeric antigen receptor macrophage (CAR-M) cell therapy targeting mesothelin; designed to recognize mesothelin-positive tumor cells, enhance phagocytosis, secrete inflammatory cytokines, and present tumor antigens to T cells.
PBMC-derived macrophages engineered to express an anti-mesothelin chimeric antigen receptor that recognizes mesothelin-positive tumor cells, enhances phagocytosis, secretes pro-inflammatory cytokines, and presents tumor antigens to activate T cells and remodel the tumor microenvironment.
YES
DIRECT
Anti-mesothelin CAR-engineered macrophages bind mesothelin on target cells and directly kill them via CAR-triggered phagocytosis and macrophage cytotoxic effector functions; inflammatory cytokines may augment this.
Long-peptide therapeutic cancer vaccine derived from CMV pp65 (26-aa) containing MHC I/II epitopes to induce CMV-specific CD8+ and CD4+ T-cell responses against CMV-expressing glioblastoma cells.
Long-peptide vaccine derived from CMV pp65 (26-aa) containing MHC I/II epitopes; following administration, antigen-presenting cells present these epitopes to activate and expand CMV-specific CD8+ cytotoxic and CD4+ helper T cells, enabling immune recognition and killing of CMV-expressing glioblastoma cells.
YES
INDIRECT
The vaccine primes CMV pp65–specific T cells; activated CTLs recognize pp65 peptides on MHC I of target cells and kill them via perforin/granzyme (and Fas–FasL) pathways.
Long-peptide therapeutic cancer vaccine derived from CMV pp65 (26-aa) containing MHC I/II epitopes to induce CMV-specific CD8+ and CD4+ T-cell responses against CMV-expressing glioblastoma cells.
Long-peptide vaccine derived from CMV pp65 (26-aa) containing MHC I/II epitopes; following administration, antigen-presenting cells present these epitopes to activate and expand CMV-specific CD8+ cytotoxic and CD4+ helper T cells, enabling immune recognition and killing of CMV-expressing glioblastoma cells.
YES
INDIRECT
The vaccine induces/expands CMV pp65–specific T cells; CTLs recognize pp65-derived peptides on MHC I of CMV-expressing cells and kill them via perforin/granzyme cytotoxicity (with CD4+ T-cell help).
Allogeneic cord blood–derived NK cells engineered to express a CD5-directed chimeric antigen receptor and constitutive IL-15 with an inducible caspase 9 (iC9) safety switch; redirects NK cytotoxicity to CD5+ malignant lymphocytes and supports NK survival and persistence.
Allogeneic cord blood–derived NK cells engineered with a CD5-specific chimeric antigen receptor to redirect NK cytotoxicity against CD5+ malignant lymphocytes. A constitutive IL-15 transgene enhances NK survival, proliferation, and persistence, while an inducible caspase-9 (iC9) safety switch enables rapid elimination of the cells if severe toxicity occurs.
YES
DIRECT
CD5-specific CAR on engineered NK cells binds CD5 on target cells, triggering NK degranulation (perforin/granzyme-mediated cytolysis and apoptosis) leading to direct killing of CD5+ cells.