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.
IL-3 moiety binds CD123, the fusion protein is internalized, and the diphtheria toxin domain ADP-ribosylates EF-2 to block protein synthesis, causing cell death.
Subcutaneous bispecific T‑cell–engaging antibody (BCMA×CD3) that redirects cytotoxic T cells to BCMA-expressing myeloma cells to induce lysis.
Bispecific antibody targeting BCMA on myeloma cells and CD3 on T cells; crosslinks T cells to BCMA-positive plasma cells to form an immune synapse, activate cytotoxic T lymphocytes, and induce perforin/granzyme-mediated tumor cell lysis.
Elranatamab bridges CD3 on T cells to BCMA on target cells, forming an immune synapse and activating cytotoxic T cells to kill BCMA+ cells via perforin/granzyme-mediated lysis.
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.
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.
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.
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.