An antibody–drug conjugate targeting Nectin-4 (PVRL4); upon internalization it releases a monomethyl auristatin E (MMAE)-type microtubule-disrupting payload, inducing mitotic arrest, tumor cell death, and potentially immunogenic cell death.
Targets Nectin-4 on tumor cells; upon binding and internalization, releases the MMAE payload that inhibits tubulin polymerization, leading to G2/M mitotic arrest, apoptosis, and potential immunogenic cell death.
NO
INDIRECT
9MW2821 targets Nectin-4 on the cell surface; after internalization, the released MMAE binds beta-tubulin (vinca domain) to disrupt microtubules, causing G2/M arrest and apoptosis. Thus, killing is directed by Nectin-4 expression, not by beta-tubulin expression itself.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor used as background anticancer therapy.
Third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, exon 19 deletions, L858R), suppressing downstream signaling (e.g., MAPK/PI3K) and inducing death of EGFR-mutant tumor cells. Shows minimal activity against wild-type EGFR and penetrates the blood–brain barrier. Has also been reported to reduce PD-L1 expression and inflammatory cytokines in some EGFR-mutant contexts.
NO
DIRECT
Not killed. Lazertinib is a mutant‑selective EGFR TKI with minimal activity against wild‑type EGFR; cytotoxicity occurs only in EGFR‑mutant cells via direct blockade of EGFR signaling leading to apoptosis.
An autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy (second-generation CAR with CD28 costimulation) administered after lymphodepleting chemotherapy to promote CAR-T expansion in relapsed/refractory large B-cell lymphoma.
Autologous T cells engineered to express a CD19-specific chimeric antigen receptor with CD28 costimulation and CD3 zeta signaling selectively bind CD19 on B cells, become activated, expand after lymphodepletion, and mediate cytokine release and cytotoxic killing of CD19-positive malignant cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19, become activated, and kill target cells via perforin/granzyme-mediated cytolysis and death-receptor–mediated apoptosis.
Investigational, off-the-shelf allogeneic iPSC-derived natural killer (NK) cell therapy intended to kill tumor cells directly and augment antibody-dependent cellular cytotoxicity (ADCC) when paired with anti-CD20 antibodies.
Allogeneic iPSC-derived NK cells engineered with an anti-CD19 CAR to recognize and kill CD19+ tumor cells and release inflammatory cytokines. Includes a high-affinity, non-cleavable CD16 to enhance antibody-dependent cellular cytotoxicity with tumor-targeting antibodies (e.g., rituximab) and an IL-15/IL-15Rα fusion to support NK survival and persistence. An alloimmune defense receptor targeting 4-1BB eliminates alloreactive host immune cells, and CD38 knockout prevents NK fratricide and enables combination with anti-CD38 antibodies.
YES
DIRECT
Anti-CD19 CAR-engineered NK cells bind CD19 and directly kill target cells via NK degranulation (perforin/granzyme-mediated apoptosis); ADCC can augment killing when tumor-bound antibodies are present.
Investigational, off-the-shelf allogeneic iPSC-derived natural killer (NK) cell therapy intended to kill tumor cells directly and augment antibody-dependent cellular cytotoxicity (ADCC) when paired with anti-CD20 antibodies.
Allogeneic iPSC-derived NK cells engineered with an anti-CD19 CAR to recognize and kill CD19+ tumor cells and release inflammatory cytokines. Includes a high-affinity, non-cleavable CD16 to enhance antibody-dependent cellular cytotoxicity with tumor-targeting antibodies (e.g., rituximab) and an IL-15/IL-15Rα fusion to support NK survival and persistence. An alloimmune defense receptor targeting 4-1BB eliminates alloreactive host immune cells, and CD38 knockout prevents NK fratricide and enables combination with anti-CD38 antibodies.
YES
DIRECT
FT522 NK cells express an alloimmune defense receptor that binds 4-1BB (CD137) on activated alloreactive host immune cells, triggering NK activation and direct killing via perforin/granzyme-mediated cytolysis.