ELR510444

ELR510444 (48 h) potently inhibits the proliferation of various cancer cell lines and endothelial cell lines at low nanomolar concentrations, with relatively low relative resistance in βIII-tubulin-overexpressing HeLa cells (Rr = 1.4) and P-glycoprotein-overexpressing SK-OV-3 cells (Rr = 2.3)^[1].
ELR510444 (18 h) acts as a microtubule depolymerizing agent in rat embryonic aortic smooth muscle cells A-10, with an EC₅₀ of 21 nM for inducing cellular microtubule loss^[1].
ELR510444 (25 nM; 18 h) induces mitotic arrest and formation of compact abnormal multipolar spindles in HeLa cervical cancer cells^[1].
ELR510444 induces apoptosis in HCT-116 cells, with an EC₅₀ of 19 nM for activating caspase 3/7, which is consistent with its antiproliferative mechanism^[1].
ELR510444 (30 nM; 1 h) induces rapid morphological changes (retraction of intercellular junctions, formation of membrane vesicles) in 2H-11 mouse tumor endothelial cells upon treatment at 30 nM for 1 h, suggesting its potential vascular disrupting activity^[1].
ELR510444 (0-100 nM; 16 h) potently inhibits HIF-1α activity in VHL-deficient RCC4 cells, with nearly complete inhibition observed at concentrations ≥ 30 nM^[2].
ELR510444 (0-100 nM; 24 h) reduces the protein expression of HIF-1α and HIF-2α in VHL-deficient RCC4 cells in a dose-dependent manner^[2].
ELR510444 (10 nM; 24 h) significantly reduces the transcriptional level of HIF-1α in VHL-deficient RCC4 cells, as well as the transcriptional level of HIF-2α in VHL-deficient RCC4, 786-O and A498 cells^[2].
ELR510444 (10 nM; 16 h) significantly reduces VEGF secretion in VHL-deficient A498, RCC4 and 786-O renal cell carcinoma cells^[2].
ELR510444 (0-1000 nM; 72 h) reduces cell viability in all tested renal cell carcinoma cell lines, and exerts more significant efficacy in VHL-deficient A498, 786-O and RCC4 cells compared with VHL-proficient ACHN, Caki-1 and Caki-2 cells^[2].
ELR510444 (3-30 nM; 24 h) reduces the clonogenic survival rate of all tested renal cell carcinoma cell lines, and exerts more significant efficacy on VHL-deficient A498, 786-O and RCC4 cells compared with VHL-proficient ACHN, Caki-1 and Caki-2 cells^[2].
ELR510444 (10-30 nM; 24 h) induces apoptosis in all tested renal cell carcinoma cell lines; it exhibits selective activity against VHL-deficient A498, 786-O and RCC4 cells at a concentration of 10 nM, and acts on all cell lines at 30 nM^[2].
Studies show that introduction of VHL into VHL-deficient A498 and 786-O renal cell carcinoma cells significantly reduces the sensitivity of these cells to apoptosis induced by 10 nM ELR510444 (10 nM; 24 h)^[2].
ELR510444 (10 nM; 24 h) reduces the expression level of HIF-2α protein in vector-only-transfected and VHL-transfected A498 and 786-O renal cell carcinoma cells under both basal and hypoxic (CoCl₂-treated) conditions^[2].
ELR510444 (10 nM; 16 h) reduces VEGF secretion levels in vector-only-transfected and VHL-transfected A498 and 786-O renal cell carcinoma cells under both basal and hypoxic (CoCl₂-treated) conditions^[2].
ELR510444 (0-30 nM; 72 h) reduces the viability of vector-only transfected and VHL-transfected A498 and 786-O renal cell carcinoma cells, and its efficacy against VHL-transfected cells is enhanced under hypoxic conditions (treated with CoCl₂)^[2].
ELR510444 (10-30 nM; 24 h) induces mitotic arrest and apoptosis in all tested renal cell carcinoma cell lines at the concentration of 30 nM, while it preferentially induces apoptosis in VHL-deficient cell lines at 10 nM^[2].
ELR510444 (20-35 nM; 24 h) destabilizes microtubules in RCC4 renal cancer cells, with an EC₅₀ of 27 nM, and significant depolymerization is observed at concentrations ≥ 20 nM^[2].

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