Intravenous natural killer cell engager (NKCE) that binds CD123 on leukemic cells and co-engages activating receptors on NK cells to induce NK cell–mediated cytotoxicity.
Engineered tri-specific NK cell engager that binds CD123 on leukemic cells and co-engages NKp46 and CD16 (FcγRIIIa) on NK cells, bringing NK cells into contact with CD123+ targets and activating NK-mediated cytotoxicity to lyse tumor cells.
YES
DIRECT
The tri-specific NK cell engager binds CD123 on target cells and NKp46/CD16 on NK cells, bringing them together and activating NK cells to degranulate (perforin/granzymes) and lyse CD123-positive cells.
Intravenous natural killer cell engager (NKCE) that binds CD123 on leukemic cells and co-engages activating receptors on NK cells to induce NK cell–mediated cytotoxicity.
Engineered tri-specific NK cell engager that binds CD123 on leukemic cells and co-engages NKp46 and CD16 (FcγRIIIa) on NK cells, bringing NK cells into contact with CD123+ targets and activating NK-mediated cytotoxicity to lyse tumor cells.
NO
INDIRECT
NKp46 is on NK cells; the drug engages NKp46 and CD16 on NK cells while binding CD123 on tumor cells, activating NK-mediated cytotoxicity (perforin/granzyme) against CD123+ targets, not NKp46+ cells.
Intravenous natural killer cell engager (NKCE) that binds CD123 on leukemic cells and co-engages activating receptors on NK cells to induce NK cell–mediated cytotoxicity.
Engineered tri-specific NK cell engager that binds CD123 on leukemic cells and co-engages NKp46 and CD16 (FcγRIIIa) on NK cells, bringing NK cells into contact with CD123+ targets and activating NK-mediated cytotoxicity to lyse tumor cells.
NO
INDIRECT
The drug binds CD16A on NK cells (and NKp46) to activate them while simultaneously binding CD123 on tumor cells, bridging NK cells to CD123+ targets and inducing NK-mediated lysis (perforin/granzyme) of the CD123-expressing tumor cells; CD16A+ NK cells are not the cells killed.
Small-molecule BCL-2 inhibitor (BH3 mimetic) that promotes mitochondrial apoptosis in malignant cells.
Selective BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, neutralizes its anti-apoptotic function, and releases pro-apoptotic effectors (e.g., BAX/BAK) to trigger mitochondrial apoptosis in BCL-2-dependent malignant cells, with minimal BCL-XL inhibition.
YES
DIRECT
Venetoclax binds and inhibits BCL-2, releasing pro-apoptotic effectors (e.g., BAX/BAK) to trigger mitochondrial outer-membrane permeabilization and caspase-dependent intrinsic apoptosis in BCL-2–dependent cells.
An anti-HER2 antibody–drug conjugate (RC48) that binds HER2, is internalized, and releases the microtubule toxin MMAE to disrupt microtubules, causing G2/M arrest and apoptosis; may also mediate ADCC and a bystander effect.
HER2-targeted ADC that binds HER2, is internalized, and releases MMAE to inhibit tubulin polymerization, leading to G2/M arrest and apoptosis; may also trigger ADCC and a bystander killing effect.
YES
DIRECT
The ADC binds HER2, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis; ADCC and a bystander effect may also contribute.