Recombinant fusion protein immunotoxin (IL-3 linked to truncated diphtheria toxin) that targets CD123 (IL-3Rα) on AML cells, is internalized, and ADP-ribosylates EF-2 to halt protein synthesis and induce cell death.
IL-3–diphtheria toxin recombinant fusion that targets CD123 (IL-3R alpha) on leukemic cells; following receptor-mediated endocytosis, the diphtheria toxin domain ADP-ribosylates EF-2, halting protein synthesis and causing cell death.
NO
INDIRECT
The drug binds CD123 on target cells, is endocytosed, and its diphtheria toxin domain ADP-ribosylates EF-2 to halt protein synthesis, causing cell death; EF-2 is an intracellular substrate, not the targeted antigen determining specificity.
Genetically modified autologous T lymphocytes engineered to express a chimeric antigen receptor targeting Trop-2 (TACSTD2) for adoptive cell therapy in advanced head and neck cancers.
Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor specific for Trop-2 (TACSTD2). CAR binding to Trop-2 on tumor cells triggers CD3 zeta/costimulatory signaling, activating the T cells to release cytokines and mediate perforin/granzyme-dependent lysis of Trop-2-positive head and neck cancer cells.
YES
DIRECT
CAR T cells bind Trop-2 on target cells, activate via CD3 zeta/co-stimulatory signaling, and kill through perforin/granzyme-mediated cytolysis (with cytokine release).
Allogeneic iPSC-derived CAR NK-cell therapy engineered with CD38 knockout, a MICA/MICB-targeting CAR, high-affinity non-cleavable CD16 (FcγRIIIa) to enhance ADCC, and an IL-15/IL-15Rα fusion to support NK survival and persistence; administered intraperitoneally.
Allogeneic iPSC-derived NK cells engineered to express a CAR targeting the alpha-3 domain of MICA/MICB for direct recognition and lysis of MICA/B+ tumor cells, a high‑affinity non‑cleavable CD16 to enhance antibody‑dependent cellular cytotoxicity (ADCC), and an IL‑15/IL‑15Rα fusion to support NK survival and persistence; CD38 knockout prevents NK fratricide and improves function, especially with anti‑CD38 antibodies. The cells mediate direct cytotoxicity and cytokine release, augmenting antitumor immunity.
YES
DIRECT
FT536 CAR NK cells bind the alpha-3 domain of MICA on target cells, triggering NK activation and degranulation (perforin/granzyme-mediated lysis). CD16 can further augment killing via ADCC when tumor-bound antibodies are present.
Allogeneic iPSC-derived CAR NK-cell therapy engineered with CD38 knockout, a MICA/MICB-targeting CAR, high-affinity non-cleavable CD16 (FcγRIIIa) to enhance ADCC, and an IL-15/IL-15Rα fusion to support NK survival and persistence; administered intraperitoneally.
Allogeneic iPSC-derived NK cells engineered to express a CAR targeting the alpha-3 domain of MICA/MICB for direct recognition and lysis of MICA/B+ tumor cells, a high‑affinity non‑cleavable CD16 to enhance antibody‑dependent cellular cytotoxicity (ADCC), and an IL‑15/IL‑15Rα fusion to support NK survival and persistence; CD38 knockout prevents NK fratricide and improves function, especially with anti‑CD38 antibodies. The cells mediate direct cytotoxicity and cytokine release, augmenting antitumor immunity.
YES
DIRECT
CAR NK cells bind the alpha-3 domain of MICB on target cells, activating NK degranulation and perforin/granzyme-mediated lysis; hnCD16 can also drive ADCC when targets are antibody-opsonized.
Allogeneic iPSC-derived CAR NK-cell therapy engineered with CD38 knockout, a MICA/MICB-targeting CAR, high-affinity non-cleavable CD16 (FcγRIIIa) to enhance ADCC, and an IL-15/IL-15Rα fusion to support NK survival and persistence; administered intraperitoneally.
Allogeneic iPSC-derived NK cells engineered to express a CAR targeting the alpha-3 domain of MICA/MICB for direct recognition and lysis of MICA/B+ tumor cells, a high‑affinity non‑cleavable CD16 to enhance antibody‑dependent cellular cytotoxicity (ADCC), and an IL‑15/IL‑15Rα fusion to support NK survival and persistence; CD38 knockout prevents NK fratricide and improves function, especially with anti‑CD38 antibodies. The cells mediate direct cytotoxicity and cytokine release, augmenting antitumor immunity.
NO
INDIRECT
FT536 NK cells use hnCD16 to bind the Fc region of therapeutic antibodies coating tumor cells, triggering ADCC against the antibody‑opsonized cells. The IgG Fc region itself is not a cellular antigen targeted for killing; direct killing is via the CAR to MICA/MICB on tumor cells.