Molecular Weight(MW): 473.47
Rigosertib (ON-01910) is a non-ATP-competitive inhibitor of PLK1 with IC50 of 9 nM in a cell-free assay. It shows 30-fold greater selectivity against Plk2 and no activity to Plk3. Phase 3.
Cited by 6 Publications
4 Customer Reviews
(A) Rigosertib induced increased apoptosis in CD34+ cells from MDS patients. Especially those from high-grade MDS (Left), in a dose-dependent manner (Right); (B) rigosertib also induced increased apoptosis in MDS and leukemia cell lines, including MDS-L, SKM1, U937, K562, Kasumi-1 and KG1a (Left), in a dose-dependent manner (Right); (C) rigosertib could not induce apoptosis in CD34+ cells from normal controls; (D) the LD50 values were lower in patients with high-grade MDS than in those with low-grade MDS (left). Patients with a normal and abnormal karyotype did not differ;
Sci Rep, 2014, 4:7310. Rigosertib (ON-01910) purchased from Selleck.
Along with cell death, immunoblotting shows ON 01910.Na induces hyperphosphorylation of RanGAP1, increased expression of RanGAP1.SUMO1 but decreased expression of free unmodified RanGAP1. No viable SU-DHL-5 cells were available for immunoblotting at 0.5 uM of ON 01910.Na.
PLoS One 2013 8(11), e79863. Rigosertib (ON-01910) purchased from Selleck.
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|Description||Rigosertib (ON-01910) is a non-ATP-competitive inhibitor of PLK1 with IC50 of 9 nM in a cell-free assay. It shows 30-fold greater selectivity against Plk2 and no activity to Plk3. Phase 3.|
Rigosertib is non-ATP-competitive inhibitor to PLK1 with IC50 of 9 nM. Rigosertib also exhibits inhibition against PLK2, PDGFR, Flt1, BCR-ABL, Fyn, Src, and CDK1, with IC50 of 18-260 nM. Rigosertib shows cell killing activity against 94 different tumor cell lines with IC50 of 50-250 nM, including BT27, MCF-7, DU145, PC3, U87, A549, H187, RF1, HCT15, SW480, and KB cells. While in normal cells, such as HFL, PrEC, HMEC, and HUVEC, Rigosertib has little or no effect unless its concentration is greater than 5-10 μM. In HeLa cells, Rigosertib (100-250 nM) induces spindle abnormalities and apoptosis.  Rigosertib also inhibits several multidrug resistant tumor cell lines, including MES-SA, MES-SA/DX5a, CEM, and CEM/C2a, with IC50 of 50-100 nM. In DU145 cells, Rigosertib (0.25-5 μM) blocks cell cycle progression in G2/M phase, results in an accumulation of cells containing subG1 content of DNA, and activates apoptotic pathways. In A549 cells, Rigosertib (50 nM-0.5 μM) induces loss of viability and caspase 3/7 activation.  In a recent study, Rigosertib induces apoptosis in chronic lymphocytic leukemia (CLL) cells without toxicity against T-cells or normal B-cells. Rigosertib also abrogates the pro-survival effect of follicular dendritic cells on CLL cells and reduces SDF-1-induced migration of leukemic cells. 
|In vivo||In mouse xenograft models of Bel-7402, MCF-7, and MIA-PaCa cells, Rigosertib (250 mg/kg) markedly inhibits tumor growth.  Rigosertib (200 mg/kg) shows inhibition on tumor growth in a mouse xengraft model of BT20 cells. |
In vitro enzyme assays for PLK1:Recombinant PLK1 (10 ng) is incubated with different concentrations of Rigosertib in a 15 µL reaction mixture (50 mM HEPES, 10 mM MgCl2, 1 mM EDTA, 2 mM Dithiothreitol, 0.01% NP-40 [pH 7.5]) for 30 min at room temperature. Kinase reactions are performed for 20 min at 30 °C in a volume of 20 µL (15 µL enzyme + inhibitor, 2 µL 1 mM ATP), 2 µL of γ32P-ATP (40 μCi), and 1 µL of recombinant Cdc25C (100 ng) or casein (1 μg) substrates. Reactions are terminated by boiling for 2 min in 20 µL of 2× Laemmli buffer. Phosphorylated substrates are separated by 18% SDS-PAGE. The gels are dried and exposed to X-ray film for 3-10 min.
|In vitro||DMSO||95 mg/mL (200.64 mM)|
|Water||95 mg/mL (200.64 mM)|
|Ethanol||slightly soluble or insoluble|
|In vivo||Add solvents individually and in order:
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT00861510||Completed||Lymphoma, Mantle-cell|Leukemia, Lymphocytic, Chronic, B-Cell|Leukemia, Hairy Cell|Waldenstrom Macroglobulinemia|Multiple Myeloma||National Heart, Lung, and Blood Institute (NHLBI)|National Institutes of Health Clinical Center (CC)||March 5, 2009||Phase 1|
|NCT02730884||Not yet recruiting||Leukemia|Myelofibrosis|Anemia|Splenomegaly||M.D. Anderson Cancer Center|Onconova Therapeutics, Inc.||December 2016||Phase 2|
|NCT02562443||Recruiting||Myelodysplastic Syndrome|MDS|Refractory Anemia With Excess Blasts|RAEB||Onconova Therapeutics, Inc.||October 2015||Phase 3|
|NCT02075034||Suspended||Myelodysplastic Syndrome||Onconova Therapeutics, Inc.||May 2014||Phase 1|
|NCT02030639||Completed||Healthy||Onconova Therapeutics, Inc.||January 2014||Phase 1|
|NCT02107235||Completed||Head and Neck Neoplasms|Carcinoma, Squamous Cell||Onconova Therapeutics, Inc.||January 2014||Phase 1|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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