An antibody-drug conjugate targeting integrin beta-6 (ITGB6) that is internalized into tumor cells and releases the microtubule inhibitor monomethyl auristatin E (MMAE), leading to microtubule disruption and tumor cell death.
Monoclonal antibody targets integrin beta-6 (ITGB6) on tumor cells, is internalized, and releases the cytotoxic payload monomethyl auristatin E (MMAE). Released MMAE inhibits tubulin polymerization, disrupting microtubules, inducing mitotic arrest, and causing tumor cell death.
ADC binds ITGB6 on tumor cells, is internalized, and releases MMAE that inhibits tubulin polymerization, causing mitotic arrest and cell death.
An investigational anti-HER2 (ERBB2) antibody–drug conjugate administered intravenously every 21 days (1–8 mg/kg). The monoclonal antibody targets HER2 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor cell death; payload not disclosed.
Monoclonal antibody binds HER2 (ERBB2) on tumor cells, is internalized, and releases a linked cytotoxic payload intracellularly to kill the cancer cell; payload type not disclosed.
An anti-HER2 antibody–drug conjugate binds HER2, is internalized, and releases an intracellular cytotoxic payload that kills the target cell.
An anti-ROR1/CD3/HSA tri-specific antibody (biologic T-cell engager) that binds ROR1 on tumor cells and CD3 on T cells to activate cytotoxic T-cell killing of ROR1-positive cancers; the anti-HSA arm binds human serum albumin to extend half-life via FcRn recycling.
Tri‑specific antibody that binds ROR1 on tumor cells and CD3 on T cells to form an immune synapse and activate cytotoxic T‑cell killing of ROR1‑positive cancers; the anti‑HSA arm binds human serum albumin to extend half‑life via FcRn recycling.
Tri-specific T‑cell engager binds ROR1 on tumor cells and CD3 on T cells, forming an immune synapse that activates CTLs to kill ROR1+ cells via perforin/granzyme-mediated apoptosis; HSA binding only extends half-life.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
Polyclonal anti-thymocyte IgG binds CD45 on leukocytes, activating complement (CDC) and Fc-mediated ADCC, and can induce apoptosis via crosslinking, leading to target-cell depletion.
Small-molecule BH3-mimetic BCL-2 inhibitor that restores intrinsic mitochondrial apoptosis in CLL cells.
Selective oral BH3-mimetic that inhibits the anti-apoptotic protein BCL-2 by binding its hydrophobic groove, displacing BH3-only proteins (e.g., BIM) and enabling BAX/BAK-mediated mitochondrial outer membrane permeabilization, thereby restoring intrinsic apoptosis in BCL-2–dependent tumor cells such as CLL.
Venetoclax directly inhibits BCL-2 (BH3 mimetic), releasing pro-apoptotic BH3-only proteins to activate BAX/BAK, leading to mitochondrial outer membrane permeabilization, caspase activation, and apoptosis in BCL-2–dependent cells.