Peptide cancer vaccine presenting the shared 36-amino-acid mutant calreticulin (CALR) C-terminal neoantigen to expand CALR-specific cytotoxic T cells targeting CALR-mutant malignant hematopoietic cells.
Synthetic peptide vaccine comprising the shared 36-amino-acid mutant calreticulin (CALR) C-terminal neoantigen. After uptake by antigen-presenting cells, the peptide is presented on MHC to prime and expand CALR-mutant–specific cytotoxic T cells (and helper T cells), leading to recognition and killing of CALR-mutant malignant hematopoietic cells; adjuvants (e.g., poly-ICLC) enhance dendritic cell activation and antigen presentation.
NO
INDIRECT
The vaccine primes CALR-mutant–specific cytotoxic T cells that kill CALR-mutant malignant cells via TCR recognition and perforin/granzyme pathways. A KLH helper peptide, if present, only provides CD4 T-cell help and is not a cytotoxic target, so cells expressing KLH are not killed.
Autologous gene-modified T cells engineered to express a chimeric antigen receptor targeting B7-H3 (CD276); upon antigen engagement, CAR signaling (CD3ζ with costimulatory domains) activates T cells to proliferate, release cytokines, and kill B7-H3–expressing tumor cells. Administered intraperitoneally or intravenously.
Autologous T cells are engineered to express a chimeric antigen receptor targeting B7-H3 (CD276). Upon binding B7-H3 on tumor cells, CAR signaling (CD3ζ with costimulatory domains) activates the T cells to proliferate, release cytotoxic cytokines, and mediate direct tumor cell lysis.
YES
DIRECT
CAR T cells bind B7-H3 on target cells, activating CD3ζ/costimulatory signaling to induce cytolysis via perforin/granzyme release and death-receptor pathways.
Anti-CD38 IgG1 monoclonal antibody that depletes CD38-positive cells via ADCC/CDC/ADCP and may reduce adenosine-mediated immunosuppression.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on tumor and immunosuppressive cells, inducing Fc-mediated cytotoxicity and phagocytosis (ADCC, CDC, ADCP) to deplete CD38+ cells and reduce adenosine-mediated immunosuppression.
YES
DIRECT
Daratumumab binds CD38 on target cells and via its Fc engages effector mechanisms—ADCC (NK cells), CDC (complement), and ADCP (macrophages)—resulting in lysis and phagocytosis of CD38+ cells.
Humanized IgG1 monoclonal antibody against EGFR/HER1 (ErbB1) that blocks ligand binding and receptor activation, inhibits downstream EGFR signaling, and may induce antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting EGFR (HER1) that binds the extracellular domain to block ligand binding and receptor activation/dimerization, suppressing downstream EGFR signaling (RAS/RAF/MEK/ERK and PI3K/AKT) to inhibit tumor-cell proliferation and survival; may also mediate ADCC.
YES
DIRECT
IgG1 anti‑EGFR antibody binds EGFR on target cells and its Fc engages FcγR on immune effectors (e.g., NK cells) to trigger ADCC, killing EGFR+ cells; signaling blockade is mainly cytostatic.
An off-the-shelf, allogeneic NK-92–derived CAR-NK cell therapy engineered to express an anti-CD19 CAR for direct killing of CD19+ B cells, secrete ER-retained IL-2 to support NK activation/persistence, and express high-affinity CD16a (FcγRIIIa V158) to enhance ADCC.
Allogeneic NK-92–derived CAR-NK cells engineered with an anti-CD19 chimeric antigen receptor to recognize and kill CD19+ B cells via NK cytotoxic mechanisms (perforin/granzyme). The cells secrete ER-retained IL-2 to support NK activation and persistence and express high-affinity CD16a (Fc-gamma RIIIa V158) to enhance antibody-dependent cellular cytotoxicity, enabling synergy with therapeutic antibodies.
YES
DIRECT
Anti-CD19 CAR on NK-92–derived cells binds CD19 and triggers NK degranulation (perforin/granzyme) to kill CD19+ cells; high-affinity CD16a can add ADCC when antibodies are present.