DXL625

DXL625 (1-25 μg/mL; 24 h, 48 h) induces dose-dependent and time-dependent reductions in ATP content in Ramos Burkitt’s lymphoma cells, with greater potency than Rituxan at all tested concentrations (1, 5, 10, 25 μg/mL) after 24 and 48 hours of treatment^[1].
DXL625 (1-25 μg/mL; 24 h) induces dose-dependent caspase-mediated apoptosis in Ramos Burkitt’s lymphoma cells, with 30.0% of cells undergoing apoptosis at the highest tested concentration (25 μg/mL) after 24 hours of treatment^[1].
DXL625 (10 μg/mL; 24 h) induces caspase-mediated apoptosis in Ramos Burkitt’s lymphoma cells, with 24.2% of cells testing positive for activated caspases after 24 hours of treatment with 10 μg/mL DXL625^[1].
DXL625 (10 μg/mL; 2 h) induces complement-dependent cytotoxicity in Ramos Burkitt’s lymphoma cells, resulting in 56.5% cell death after 2 hours of treatment with 10 μg/mL DXL625 in the presence of 5% (v/v) rabbit complement sera^[1].
DXL625 (10 μg/mL; 2 h) retains complement-dependent cytotoxicity activity against primary CD19⁺ B-lymphocytes from healthy donor peripheral blood lymphocytes, reducing the CD19⁺ population to 3.1% after 2 hours of treatment with 10 μg/mL DXL625 in the presence of 5% (v/v) rabbit complement sera^[1].
DXL625 (10 μg/mL; 24 h) induces enhanced NK cell-mediated antibody-dependent cellular cytotoxicity in Ramos Burkitt’s lymphoma cells, reducing normalized cell viability to 0.56 after 24 hours of treatment with 10 μg/mL DXL625 at a 6:1 effector-to-target ratio^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.