Oral small-molecule BCL-2 inhibitor that restores mitochondrial apoptosis in AML cells.
Selective oral BH3 mimetic that inhibits BCL-2 by binding its hydrophobic groove, neutralizing its anti-apoptotic function and restoring mitochondrial apoptosis (via BAX/BAK activation) in tumor cells; spares BCL-XL.
Venetoclax directly binds and inhibits BCL-2, freeing proapoptotic signaling to activate BAX/BAK, trigger mitochondrial outer membrane permeabilization, cytochrome c release, caspase activation, and apoptotic death of BCL-2–dependent cells.
An investigational HER2-targeting antibody-drug conjugate comprising a humanized anti-HER2 monoclonal antibody linked via an enzyme-cleavable linker to a topoisomerase I inhibitor payload; after HER2 binding and internalization, the linker is cleaved intracellularly to release the cytotoxic payload, causing DNA damage and cell death.
A humanized anti-HER2 monoclonal antibody linked via an intracellularly cleavable linker to a topoisomerase I inhibitor. After HER2 binding and internalization, the linker is cleaved to release the payload, which inhibits topoisomerase I, induces DNA damage, and leads to tumor cell death.
Anti-HER2 ADC binds HER2, is internalized, linker is cleaved intracellularly to release a topoisomerase I inhibitor that causes DNA damage and kills the target cell.
HER2-targeted antibody–drug conjugate linking trastuzumab to a topoisomerase I inhibitor (DXd); binds HER2, mediates ADCC, internalizes and releases DXd to induce DNA damage (bystander effect).
HER2-targeted antibody–drug conjugate: trastuzumab binds HER2, inhibits signaling and mediates ADCC; the complex is internalized and releases the topoisomerase I inhibitor DXd, causing DNA damage and cell death with a bystander effect.
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; trastuzumab Fc can also mediate ADCC, with a membrane‑permeable payload enabling a bystander effect.
An anti–folate receptor alpha (FRα) antibody-drug conjugate administered IV every 3 weeks. The monoclonal antibody binds FRα on tumor cells, is internalized via FRα-mediated endocytosis, and releases a cytotoxic payload intracellularly (with potential bystander effect) to induce tumor-cell death, targeting FRα-overexpressing epithelial tumors in recurrent gynecologic cancers.
IMGN151 (opugotamig olatansine) is a biparatopic monoclonal antibody targeting folate receptor alpha (FRα) conjugated via a cleavable linker to the maytansinoid DM21 (a microtubule inhibitor). After binding FRα on tumor cells, the ADC is internalized and the payload is released intracellularly, binding tubulin to disrupt microtubule dynamics, leading to cell-cycle arrest and tumor-cell death, with potential bystander killing of adjacent cells.
An FRα-targeted ADC binds FRα, is internalized, and releases the maytansinoid DM21, which binds tubulin to disrupt microtubules, causing mitotic arrest and apoptosis (with possible bystander effect).
HER2-targeted antibody–drug conjugate linking trastuzumab to a cleavable topoisomerase I inhibitor (DXd) payload; blocks HER2 signaling, mediates ADCC, and delivers cytotoxic payload to HER2-expressing cells.
HER2-targeted trastuzumab linked via a cleavable linker to a topoisomerase I inhibitor payload (DXd). After binding HER2 and internalization, DXd is released to inhibit Top1, causing DNA damage and apoptosis; the antibody also blocks HER2 signaling, mediates ADCC, and enables bystander killing of neighboring tumor cells.
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; Fc-mediated ADCC and bystander killing can also contribute.