Anti-CD38 IgG1 monoclonal antibody that targets CD38 on myeloma and immune cells, mediating ADCC, CDC, ADCP, and immunomodulation.
Unconjugated anti-CD38 IgG1 monoclonal antibody that binds CD38 on myeloma and immune cells, inducing Fc-mediated antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP); also depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), enhancing antitumor immunity.
YES
DIRECT
Daratumumab binds CD38 on target cells and engages immune effectors via its Fc to mediate NK cell ADCC, complement-dependent cytotoxicity (CDC), and macrophage antibody-dependent cellular phagocytosis (ADCP), leading to lysis and clearance of CD38+ cells.
An autologous anti-mesothelin CAR T-cell therapy. Patient T cells are engineered ex vivo using circular mRNA to transiently express a mesothelin-targeting chimeric antigen receptor (no genomic integration) and administered by IV infusion weekly ×4 (dose escalation 1×10^8 to 2×10^9 cells). The CAR engages mesothelin on tumor cells to drive HLA-independent T-cell activation, cytotoxicity, cytokine release, and proliferation.
Autologous T cells are engineered ex vivo with circular mRNA to transiently express a mesothelin-targeting chimeric antigen receptor. Upon binding mesothelin on tumor cells, the CAR delivers HLA-independent activation signals (CD3ζ-based), triggering T‑cell cytotoxicity (perforin/granzyme), cytokine release, and clonal expansion without genomic integration.
YES
DIRECT
Anti-mesothelin CAR T cells bind mesothelin and, via CD3zeta signaling, directly lyse target cells through perforin/granzyme-mediated cytotoxicity (with cytokine release).
Gene-modified, allogeneic cord blood–derived natural killer (NK) cells engineered with a TROP2-specific chimeric antigen receptor and transduced to express IL-15; administered intraperitoneally to target TROP2-positive tumors and enhance NK survival and persistence.
Allogeneic cord blood-derived NK cells engineered with a TROP2-specific chimeric antigen receptor and IL-15 expression. CAR recognition of TROP2 on tumor cells triggers NK activation and cytolytic killing (perforin/granzyme), while IL-15 supports NK survival, proliferation, and persistence; delivered intraperitoneally to target TROP2-positive tumors.
YES
DIRECT
CAR-NK cells recognize TROP2 on target cells, triggering NK activation and degranulation with perforin/granzyme–mediated cytolysis (and death-receptor signaling), killing TROP2-positive cells.
Gene-modified, allogeneic cord blood–derived natural killer (NK) cells engineered with a TROP2-specific chimeric antigen receptor and transduced to express IL-15; administered intraperitoneally to target TROP2-positive tumors and enhance NK survival and persistence.
Allogeneic cord blood-derived NK cells engineered with a TROP2-specific chimeric antigen receptor and IL-15 expression. CAR recognition of TROP2 on tumor cells triggers NK activation and cytolytic killing (perforin/granzyme), while IL-15 supports NK survival, proliferation, and persistence; delivered intraperitoneally to target TROP2-positive tumors.
NO
INDIRECT
CAR-NK cells kill TROP2+ tumor cells via perforin/granzyme after CAR engagement. IL-15 interacts with IL-15Rα to support NK survival/persistence and does not mediate killing of IL-15Rα–expressing cells.
Gene-modified, allogeneic cord blood–derived natural killer (NK) cells engineered with a TROP2-specific chimeric antigen receptor and transduced to express IL-15; administered intraperitoneally to target TROP2-positive tumors and enhance NK survival and persistence.
Allogeneic cord blood-derived NK cells engineered with a TROP2-specific chimeric antigen receptor and IL-15 expression. CAR recognition of TROP2 on tumor cells triggers NK activation and cytolytic killing (perforin/granzyme), while IL-15 supports NK survival, proliferation, and persistence; delivered intraperitoneally to target TROP2-positive tumors.
NO
INDIRECT
The CAR-NK cells recognize TROP2, not CD122; they kill TROP2-positive tumor cells via perforin/granzyme. CD122 (IL-2Rβ) mediates IL-15 survival signaling for the NK cells and is not a cytotoxic target.