A Nectin-4–targeting antibody–drug conjugate (ADC) that delivers the microtubule-disrupting cytotoxic payload MMAE to tumor cells.
Bulumtatug fuvedotin (9MW2821) targets Nectin-4 on tumor cells; after binding and internalization, the linker is cleaved to release MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death (with potential bystander cytotoxicity).
The ADC binds Nectin-4, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptotic death (with possible bystander effect).
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.
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.
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.
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.
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.
Humanized IgG1 monoclonal antibody targeting EGFR (ErbB1); blocks ligand binding, inhibits MAPK/ERK and PI3K/AKT signaling, can trigger ADCC, and enhances radiosensitization of EGFR-expressing tumor cells.
Humanized IgG1 monoclonal antibody that binds EGFR (ErbB1), blocks ligand binding and receptor activation, suppressing downstream MAPK/ERK and PI3K/AKT signaling; can engage ADCC and enhances radiosensitization of EGFR-expressing tumor cells, leading to growth inhibition.
Anti-EGFR IgG1 mAb binds EGFR on target cells, blocks survival signaling (promoting growth arrest/apoptosis) and recruits FcγR+ effector cells to mediate ADCC against EGFR-expressing cells.