Rigosertib (ON-01910)

Catalog No.S1362

Rigosertib (ON-01910) Chemical Structure

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.

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In DMSO USD 320 In stock
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USD 320 In stock
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Cited by 8 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.

  • Rigosertib (ON-01910) purchased from Selleck.

    Dr. Antonino Maria Sparta, PhD University of Bologna. Rigosertib (ON-01910) purchased from Selleck.

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Biological Activity

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.
Targets
PLK1 [1]
(Cell-free assay)
PDGFR [1]
(Cell-free assay)
Bcr-Abl [1]
(Cell-free assay)
Flt1 [1]
(Cell-free assay)
Src [1]
(Cell-free assay)
9 nM 18 nM 32 nM 42 nM 155 nM
In vitro

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. [1] 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. [2] 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. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human K562 cells M4\0WWN6fG:2b4jpZ:Kh[XO|YYm= NGf5SG06PiCq M{\uO2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGs2PjJiY3XscJMh[W[2ZYKgPVYhcHK|IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCjc4PhfUwhUUN3ME23MlUhdk1? MorjNlE5OTJ2MkG=
human T47D cells NUnMRmhbS3m2b4TvfIlkyqCjc4PhfS=> NHLKWIM4OiCq M2K4cWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHQ1P0RiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2xNEBvVQ>? Mn\NNlE1PjN7NES=
human HeLa cells M1jrfHBzd2yrZnXyZZRqd25iYYPzZZk> Mlj3O|IhcA>? NWfPVHVRSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDI[WxiKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD1zMjDuUS=> MmfmNlQ1PzF6N{O=
human MDA468 cells M33yfWN6fG:2b4jpZ:Kh[XO|YYm= NIjB[XI4OiCq MlzuR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWRCPDZ6IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9NlAhdk1? MVKyNVQ3Ozl2NB?=
human LNCAP cells M{fBNXBzd2yrZnXyZZRqd25iYYPzZZk> Ml3mO|IhcA>? M{fO[GFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgRXIheG:|aYTpeoUhcHWvYX6gUG5ESVBiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEBoem:5dHigbY5pcWKrdHnvckBi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUK1JI5O MWOyOFQ4OTh5Mx?=
human PANC1 cells M1;IbHBzd2yrZnXyZZRqd25iYYPzZZk> MnKwO|IhcA>? MVHBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFCDTlOxJINmdGy|IHHzd4V{e2WmIHHzJINmdGxiZ4Lve5RpKGmwaHnibZRqd25iYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0{QSCwTR?= NV3FU5FQOjR2N{G4O|M>
human MCF7 cells M4e0R3Bzd2yrZnXyZZRqd25iYYPzZZk> MWG3NkBp NF\4fYNCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGVTKHCxc3n0bZZmKGi3bXHuJG1ETjdiY3XscJMh[XO|ZYPz[YQh[XNiY3XscEBoem:5dHigbY5pcWKrdHnvckBi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUWwJI5O M{PHcFI1PDdzOEez
human HCT116 cells NEnzcWZEgXSxdH;4bYPDqGG|c3H5 MX:3NkBp M1fzUWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGhEXDFzNjDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVUxKG6P M{DOblIyPDZ|OUS0
human MCF7 cells NWW1WGVbS3m2b4TvfIlkyqCjc4PhfS=> M37iSVczKGh? NEPvPXJEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOS0Z5IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9OVAhdk1? NH[zfIYzOTR4M{m0OC=>
human MDA-MB-231 cells NEPUdXlRem:uaX\ldoF1cW:wIHHzd4F6 NETTUWo4OiCq MUfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IFXSJI5m\2G2aY\lJIh2dWGwIF3ERU1OSi1{M{GgZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdCCpcn;3eIghcW6qaXLpeIlwdiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6 MnTZNlQ1PzF6N{O=
human A2780 cells NX:1e29MWHKxbHnm[ZJifGmxbjDhd5NigQ>? M4\vflczKGh? MlnERY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCDMke4NEBk\WyuczDhd5Nme3OnZDDhd{Bk\WyuIHfyc5d1cCCrbnjpZol1cW:wIHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFfJOVA:PjJibl2= MVmyOFQ4OTh5Mx?=
human HCT116 cells M3zSbnBzd2yrZnXyZZRqd25iYYPzZZk> NV3yd5VDPzJiaB?= M4DUfmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSFPUNVE3KGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD15MDDuUS=> Mn62NlQ1PzF6N{O=
human DU145 cells Mn3nVJJwdGmoZYLheIlwdiCjc4PhfS=> M321UFczKGh? M1zlPGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgRXIhdmWpYYTpeoUhcHWvYX6gSHUyPDViY3XscJMh[XO|ZYPz[YQh[XNiY3XscEBoem:5dHigbY5pcWKrdHnvckBi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUe1JI5O NF\TO5QzPDR5MUi3Ny=>
human DU145 cells NGrxe3ZEgXSxdH;4bYPDqGG|c3H5 M2TVc|k3KGh? MYHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDEWVE1PSClZXzsd{Bi\nSncjC5OkBpenNiYomgeJJ6eGGwIHLseYUh\XilbIXzbY9vKGG|c3H5MEBKSzVyPUe1JI5O NGf3ZY0zOThzMkSyNS=>
human MDA468 cells MWPDfZRwfG:6aXRCpIF{e2G7 NGm1V2I1QCCq Mnv5R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWRCPDZ6IHPlcIx{KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEeLNUC9NE4{ODJizszN NF:3flczOTR4M{m0OC=>
human MRC5 cells NVPLWXQ3S3m2b4TvfIlkyqCjc4PhfS=> MkDwO|IhcA>? NE\tSYFEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOWkN3IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9NE44OSEQvF2= MX:yNVQ3Ozl2NB?=
human A2780 cells NIPSU2lHfW6ldHnvckBie3OjeR?= NXPvOXdpOC5{NTFOwG0> MoTsNlQhcA>? MnnPVoVlfWO2aX;uJIlvKE2lbEGgcIV3\WxiaX6gbJVu[W5iQUK3PFAh[2WubIOgZZQhOC5{NTD1UUBi\nSncjCyOEBpenNiYomgW4V{fGW{bjDicI91KGGwYXz5d4l{ NHi1VYYzPDR5MUi3Ny=>

... Click to View More Cell Line Experimental Data

In vivo In mouse xenograft models of Bel-7402, MCF-7, and MIA-PaCa cells, Rigosertib (250 mg/kg) markedly inhibits tumor growth. [1] Rigosertib (200 mg/kg) shows inhibition on tumor growth in a mouse xengraft model of BT20 cells. [2]

Protocol

Kinase Assay:[1]
+ Expand

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.
Cell Research:[2]
+ Expand
  • Cell lines: A number of tumor cell lines, including BT20, MCF-7, DU145, PC3, U87, A549, H187, RF1, HCT15, HeLa, and Raji cells
  • Concentrations: 1 nM - 10 μM, dissolved in DMSO as stock solution.
  • Incubation Time: 96 hours
  • Method: Cells are grown in either DMEM or RPMI supplemented with 10% fetal bovine serum and 1 unit/mL penicillin-streptomycin solution. Tumor cells are plated into six-well dishes at a density of 1 × 105cells/mL/well, and Rigosertib is added 24 hours later at various concentrations. Cell counts are determined from duplicate wells after 96-hour of treatment. The total number of viable cells is determined by trypan blue exclusio
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Mouse (female athymic, NCR-nu/nu) xenograft models of Bel-7402, MCF-7, and MIA-PaCa cells
  • Formulation: Dissolved in PBS
  • Dosages: 250 mg/kg
  • Administration: Intraperitonially
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 95 mg/mL (200.64 mM)
Water 95 mg/mL (200.64 mM)
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
water
For best results, use promptly after mixing.
95mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 473.47
Formula

C21H24NNaO8S

CAS No. 1225497-78-8
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03786237 Not yet recruiting Epidermolysis Bullosa Dystrophica|Squamous Cell Carcinoma Prof. Johann Bauer|Salzburger Landeskliniken January 2019 Phase 1|Phase 2
NCT03786237 Not yet recruiting Epidermolysis Bullosa Dystrophica|Squamous Cell Carcinoma Prof. Johann Bauer|Salzburger Landeskliniken January 2019 Phase 1|Phase 2
NCT02730884 Recruiting Leukemia|Myelofibrosis|Anemia|Splenomegaly M.D. Anderson Cancer Center|Onconova Therapeutics Inc. August 16 2017 Phase 2
NCT02730884 Recruiting Leukemia|Myelofibrosis|Anemia|Splenomegaly M.D. Anderson Cancer Center|Onconova Therapeutics Inc. August 16 2017 Phase 2
NCT02562443 Recruiting Myelodysplastic Syndrome|MDS|Refractory Anemia With Excess Blasts|RAEB Onconova Therapeutics Inc. October 2015 Phase 3
NCT02562443 Recruiting Myelodysplastic Syndrome|MDS|Refractory Anemia With Excess Blasts|RAEB Onconova Therapeutics Inc. October 2015 Phase 3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID