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.

Size Price Stock Quantity  
In DMSO USD 320 In stock
USD 170 In stock
USD 320 In stock
USD 970 In stock
Bulk Discount

Free Overnight Delivery on orders over $ 500
Next day delivery by 10:00 a.m. Order now.

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.

Purity & Quality Control

Choose Selective PLK Inhibitors

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.
PLK1 [1]
(Cell-free assay)
9 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 NV[2NJY6S3m2b4TvfIlkyqCjc4PhfS=> NUXRV4FVQTZiaB?= M3nNfGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGs2PjJiY3XscJMh[W[2ZYKgPVYhcHK|IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCjc4PhfUwhUUN3ME23MlUhdk1? M3TROVIyQDF{NEKx
human T47D cells MY\DfZRwfG:6aXRCpIF{e2G7 M16xT|czKGh? MV3DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDUOFdFKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;MUCgcm0> NVPnXJZnOjF2NkO5OFQ>
human HeLa cells NXH6THNIWHKxbHnm[ZJifGmxbjDhd5NigQ>? M4POflczKGh? NG\XW5NCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjlUIEh[2WubIOgZZN{\XO|ZXSgZZMh[2WubDDndo94fGhiaX7obYJqfGmxbjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDHTVUxRTF{IH7N MYmyOFQ4OTh5Mx?=
human MDA468 cells MknzR5l1d3SxeHnjxsBie3OjeR?= NE\MNWU4OiCq M{nTcWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1FSTR4ODDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVIxKG6P NF\0UWEzOTR4M{m0OC=>
human LNCAP cells M1zI[HBzd2yrZnXyZZRqd25iYYPzZZk> NELJeZA4OiCq MYnBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IFHSJJBwe2m2aY\lJIh2dWGwIFzOR2FRKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD1{NTDuUS=> NIfoc4kzPDR5MUi3Ny=>
human PANC1 cells M1O3UXBzd2yrZnXyZZRqd25iYYPzZZk> MXG3NkBp NI\SZ5ZCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGDBUmMyKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD1|OTDuUS=> M{\PUVI1PDdzOEez
human MCF7 cells Ml\kVJJwdGmoZYLheIlwdiCjc4PhfS=> NFzwRnE4OiCq Mo\1RY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDFVkBxd3OrdHn2[UBpfW2jbjDNR2Y4KGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD13MDDuUS=> NEnU[4wzPDR5MUi3Ny=>
human HCT116 cells NWCzSpRnS3m2b4TvfIlkyqCjc4PhfS=> Mlm3O|IhcA>? Mlm2R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTGNVOTF4IHPlcIx{KGGodHXyJFczKGi{czDifUBOXFRiYYPzZZktKEeLNUC9OVAhdk1? Mnn4NlE1PjN7NES=
human MCF7 cells NUnicYZHS3m2b4TvfIlkyqCjc4PhfS=> NXrrTmdjPzJiaB?= NXfXemQ4S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUOINzDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVUxKG6P NXrxeIJnOjF2NkO5OFQ>
human MDA-MB-231 cells MmTyVJJwdGmoZYLheIlwdiCjc4PhfS=> MmjvO|IhcA>? NInpPYpCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGVTKG6nZ3H0bZZmKGi3bXHuJG1FSS2PQj2yN|Eh[2WubIOgZZN{\XO|ZXSgZZMh[2WubDDndo94fGhiaX7obYJqfGmxbjDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7 M2\5elI1PDdzOEez
human A2780 cells M3m2SHBzd2yrZnXyZZRqd25iYYPzZZk> M3nUblczKGh? NHmxVGtCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFGyO|gxKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD14MjDuUS=> NUjYeJhoOjR2N{G4O|M>
human HCT116 cells NHTPUYFRem:uaX\ldoF1cW:wIHHzd4F6 MkfSO|IhcA>? NFnrO5JCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjDWFEyPiClZXzsd{Bie3Onc4Pl[EBieyClZXzsJIdzd3e2aDDpcohq[mm2aX;uJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;N{Cgcm0> NYnQeG1ZOjR2N{G4O|M>
human DU145 cells NWOyclFvWHKxbHnm[ZJifGmxbjDhd5NigQ>? MoXOO|IhcA>? NGHnNlZCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGFTKG6nZ3H0bZZmKGi3bXHuJGRWOTR3IHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwh\3Kxd4ToJIlvcGmkaYTpc44h[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME23OUBvVQ>? MXKyOFQ4OTh5Mx?=
human DU145 cells MYTDfZRwfG:6aXRCpIF{e2G7 M2D3blk3KGh? MVTDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDEWVE1PSClZXzsd{Bi\nSncjC5OkBpenNiYomgeJJ6eGGwIHLseYUh\XilbIXzbY9vKGG|c3H5MEBKSzVyPUe1JI5O NIfiXI4zOThzMkSyNS=>
human MDA468 cells MmLIR5l1d3SxeHnjxsBie3OjeR?= MkXoOFghcA>? NHHsR4dEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOTEF2NkigZ4VtdHNiYX\0[ZIhPDhiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0xNjNyMjFOwG0> NH3OU|UzOTR4M{m0OC=>
human MRC5 cells MoLUR5l1d3SxeHnjxsBie3OjeR?= MnTiO|IhcA>? NXfaT5VCS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVAvPzFizszN MVKyNVQ3Ozl2NB?=
human A2780 cells NEPLXnlHfW6ldHnvckBie3OjeR?= MYiwMlI2KM7:TR?= NXzDNmlxOjRiaB?= NXPJZ4U1WmWmdXP0bY9vKGmwIF3jcFEhdGW4ZXygbY4hcHWvYX6gRVI4QDBiY3XscJMh[XRiMD6yOUB2VSCjZoTldkAzPCCqcoOgZpkhX2W|dHXyckBjdG:2IHHuZYx6e2m| MUOyOFQ4OTh5Mx?=

... 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]


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 individually and in order:

* 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


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

Bio Calculators

Molarity Calculator

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

  • Mass
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

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

Tech Support

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.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

  • * Indicates a Required Field

PLK Signaling Pathway Map

PLK Inhibitors with Unique Features

Related PLK Products

Tags: buy Rigosertib (ON-01910) | Rigosertib (ON-01910) supplier | purchase Rigosertib (ON-01910) | Rigosertib (ON-01910) cost | Rigosertib (ON-01910) manufacturer | order Rigosertib (ON-01910) | Rigosertib (ON-01910) distributor
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID