Recombinant humanized anti‑HER2 bispecific antibody–drug conjugate (ADC) that binds HER2 on tumor cells, is internalized, and releases the linked cytotoxic payload MMAE to inhibit tubulin polymerization; may also engage Fc‑mediated effector functions.
Bispecific anti-HER2 ADC that binds two non-overlapping HER2 extracellular epitopes (ECD2 and ECD4), is internalized, and releases the microtubule-disrupting payload MMAE to inhibit tubulin polymerization, leading to mitotic arrest and apoptosis; Fc-mediated effector functions may also contribute.
YES
DIRECT
KM501 binds HER2 (ECD2/ECD4), is internalized, and releases MMAE that disrupts microtubules, causing mitotic arrest and apoptosis; Fc effector functions may also mediate ADCC.
Recombinant humanized anti‑HER2 bispecific antibody–drug conjugate (ADC) that binds HER2 on tumor cells, is internalized, and releases the linked cytotoxic payload MMAE to inhibit tubulin polymerization; may also engage Fc‑mediated effector functions.
Bispecific anti-HER2 ADC that binds two non-overlapping HER2 extracellular epitopes (ECD2 and ECD4), is internalized, and releases the microtubule-disrupting payload MMAE to inhibit tubulin polymerization, leading to mitotic arrest and apoptosis; Fc-mediated effector functions may also contribute.
YES
DIRECT
ADC binds HER2 (ECD2/ECD4), is internalized, and releases MMAE to inhibit tubulin polymerization, causing mitotic arrest and apoptosis; Fc-mediated ADCC/CDC may also contribute.
Recombinant humanized anti‑HER2 bispecific antibody–drug conjugate (ADC) that binds HER2 on tumor cells, is internalized, and releases the linked cytotoxic payload MMAE to inhibit tubulin polymerization; may also engage Fc‑mediated effector functions.
Bispecific anti-HER2 ADC that binds two non-overlapping HER2 extracellular epitopes (ECD2 and ECD4), is internalized, and releases the microtubule-disrupting payload MMAE to inhibit tubulin polymerization, leading to mitotic arrest and apoptosis; Fc-mediated effector functions may also contribute.
NO
INDIRECT
KM501 binds HER2 on tumor cells, is internalized, and releases MMAE, which inhibits beta-tubulin polymerization to cause mitotic arrest and apoptosis; Fc effector functions may also contribute.
Autologous T cells engineered with a chimeric antigen receptor targeting CD19 to eliminate CD19-positive malignant B cells.
Autologous T cells genetically engineered to express a chimeric antigen receptor that binds CD19 on B cells, activating T-cell signaling (CD3ζ with co-stimulatory domains) to mediate perforin/granzyme-dependent cytotoxicity and eliminate CD19-positive malignant B cells.
YES
DIRECT
CAR T cells bind CD19 on target cells and, upon activation, kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL), inducing apoptosis/lysis of CD19+ cells.
A TROP-2–targeted antibody–drug conjugate (MK-2870/SKB264) that binds TROP-2 on tumor cells, is internalized, and releases a topoisomerase-I inhibitor payload to induce DNA damage and apoptosis.
TROP-2–targeted antibody–drug conjugate: the IgG1 antibody binds TROP-2 on tumor cells, is internalized, and a cleavable linker releases tirumotecan (a topoisomerase I–inhibiting belotecan derivative), leading to DNA replication inhibition, DNA damage, cell-cycle arrest, and apoptosis, with a bystander effect on neighboring tumor cells.
YES
INDIRECT
The ADC binds TROP-2 on tumor cells, is internalized, and releases the tirumotecan payload, which inhibits DNA topoisomerase I, causing DNA damage, cell-cycle arrest, and apoptosis; a bystander effect can also kill neighboring cells.