Rigosertib (ON-01910)

For research use only.

Catalog No.S1362

23 publications

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. Rigosertib inhibits PI3K/Akt pathway and activates oxidative stress signals. Rigosertib induces apoptosis in various cancer cells. Phase 3.

Size Price Stock Quantity  
10mM (1mL in DMSO) USD 320 In stock
USD 170 In stock
USD 320 In stock
USD 970 In stock
Bulk Discount
Bulk Inquiry

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

Selleck's Rigosertib (ON-01910) has been cited by 23 publications

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. Rigosertib inhibits PI3K/Akt pathway and activates oxidative stress signals. Rigosertib induces apoptosis in various cancer cells. 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 M4myTGN6fG:2b4jpZ:Kh[XO|YYm= NIDTVnQ6PiCq MoLvR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gT|U3OiClZXzsd{Bi\nSncjC5OkBpenNiYomgeJJ6eGGwIHLseYUh\XilbIXzbY9vKGG|c3H5MEBKSzVyPUeuOUBvVQ>? NUm3TIkxOjF6MUK0NlE>
human T47D cells M2q4bGN6fG:2b4jpZ:Kh[XO|YYm= M1fIWVczKGh? MV3DfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDUOFdFKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO|YYmsJGdKPTB;MUCgcm0> NUTxS493OjF2NkO5OFQ>
human HeLa cells Mmm0VJJwdGmoZYLheIlwdiCjc4PhfS=> M4TmPVczKGh? MmfaRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKZVzhJINmdGy|IHHzd4V{e2WmIHHzJINmdGxiZ4Lve5RpKGmwaHnibZRqd25iYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF0yOiCwTR?= M4riOVI1PDdzOEez
human MDA468 cells M3jjS2N6fG:2b4jpZ:Kh[XO|YYm= MWq3NkBp MWnDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNSGE1PjhiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2yNEBvVQ>? M2L4NFIyPDZ|OUS0
human LNCAP cells NVLwcY9[WHKxbHnm[ZJifGmxbjDhd5NigQ>? NHewSXI4OiCq NIS1TG1CdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGFTKHCxc3n0bZZmKGi3bXHuJGxPS0GSIHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwh\3Kxd4ToJIlvcGmkaYTpc44h[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME2yOUBvVQ>? M2HwV|I1PDdzOEez
human PANC1 cells MkTpVJJwdGmoZYLheIlwdiCjc4PhfS=> MlG0O|IhcA>? NH3zTYhCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGDBUmMyKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD1|OTDuUS=> NXPFR|hnOjR2N{G4O|M>
human MCF7 cells MoSwVJJwdGmoZYLheIlwdiCjc4PhfS=> NI\MeJg4OiCq NV3zTpQ4SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBGWiCyb4PpeIl3\SCqdX3hckBOS0Z5IHPlcIx{KGG|c3Xzd4VlKGG|IHPlcIwh\3Kxd4ToJIlvcGmkaYTpc44h[W[2ZYKgO|IhcHK|IHL5JG1VXCCjc4PhfUwhT0l3ME21NEBvVQ>? MoD6NlQ1PzF6N{O=
human HCT116 cells NEPRSJREgXSxdH;4bYPDqGG|c3H5 NF3udJg4OiCq NInJOFVEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJS1RzMU[gZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KE2WVDDhd5NigSxiR1m1NF02OCCwTR?= NYTqZ5ByOjF2NkO5OFQ>
human MCF7 cells NXLCS5V{S3m2b4TvfIlkyqCjc4PhfS=> MVW3NkBp Ml\pR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWNHPyClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUWwJI5O MV2yNVQ3Ozl2NB?=
human MDA-MB-231 cells Mo\JVJJwdGmoZYLheIlwdiCjc4PhfS=> MXW3NkBp MU\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IFXSJI5m\2G2aY\lJIh2dWGwIF3ERU1OSi1{M{GgZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdCCpcn;3eIghcW6qaXLpeIlwdiCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6 NXfoOot[OjR2N{G4O|M>
human A2780 cells MVnQdo9tcW[ncnH0bY9vKGG|c3H5 M3HhRlczKGh? NFntdGlCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFGyO|gxKGOnbHzzJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeTygS2k2OD14MjDuUS=> Mli2NlQ1PzF6N{O=
human HCT116 cells MUfQdo9tcW[ncnH0bY9vKGG|c3H5 MlGxO|IhcA>? MY\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiFVEGxOkBk\WyuczDhd5Nme3OnZDDhd{Bk\WyuIHfyc5d1cCCrbnjpZol1cW:wIHHmeIVzKDd{IHjyd{BjgSCPVGSgZZN{[XluIFfJOVA:PzBibl2= NX[2R49yOjR2N{G4O|M>
human DU145 cells MUHQdo9tcW[ncnH0bY9vKGG|c3H5 NIThd2U4OiCq M322ZWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgRXIhdmWpYYTpeoUhcHWvYX6gSHUyPDViY3XscJMh[XO|ZYPz[YQh[XNiY3XscEBoem:5dHigbY5pcWKrdHnvckBi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MEBIUTVyPUe1JI5O NWT0[pJ4OjR2N{G4O|M>
human DU145 cells MojzR5l1d3SxeHnjxsBie3OjeR?= MmPBPVYhcA>? NEL3TohEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBFXTF2NTDj[YxteyCjZoTldkA6PiCqcoOgZpkhfHK7cHHuJIJtfWViZYjjcJV{cW:wIHHzd4F6NCCLQ{WwQVc2KG6P NUX2TZd3OjF6MUK0NlE>
human MDA468 cells NH3OcWhEgXSxdH;4bYPDqGG|c3H5 Mne1OFghcA>? Ml[4R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWRCPDZ6IHPlcIx{KGGodHXyJFQ5KGi{czDifUBOXFRiYYPzZZktKEeLNUC9NE4{ODJizszN M4\wOFIyPDZ|OUS0
human MRC5 cells NIj3bJREgXSxdH;4bYPDqGG|c3H5 MWC3NkBp NV\kTnp7S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVVKFNTDj[YxteyCjZoTldkA4OiCqcoOgZpkhVVSWIHHzd4F6NCCJSUWwQVAvPzFizszN MXKyNVQ3Ozl2NB?=
human A2780 cells NXuyNFZbTnWwY4Tpc44h[XO|YYm= Mn3NNE4zPSEQvF2= NWHMcoZ1OjRiaB?= NF[z[5BT\WS3Y4Tpc44hcW5iTXPsNUBt\X[nbDDpckBpfW2jbjDBNlc5OCClZXzsd{BifCByLkK1JJVOKGGodHXyJFI1KGi{czDifUBY\XO2ZYLuJIJtd3RiYX7hcJl{cXN? NUDOWVBEOjR2N{G4O|M>

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
pAbl / Abl / PCrk-L / Crk-L / Cleaved caspase3 / Cleaved PARP / pHistone H2A.X; 

PubMed: 26008977     


Ba/F3 T315I cells were treated with rigosertib at the indicated concentrations for 24 h. Total extracts were examined via immunoblotting with anti-phospho ABL, phospho-Crk-L, phosphohistone H2A.X, cleaved caspase 3, cleaved-PARP, ABL, Crk-L, and β-actin antibodies (abs). ABL, Abelson; PARP, poly (ADP-ribose) polymerase; abs, antibodies.

26008977
Immunofluorescence
p-ATF / COX IV; 

PubMed: 27764820     


Representative confocal microscopy images of FaDu, UMSCC 47 and D-HMVEC cells treated with rigosertib (1.0 μM) or ON 01911.Na (1.0 μM) for 24 h before fixing, staining with indicated antibodies, and capturing images. Green: p-ATF; Red: Cox IV (mitochondrial marker); Blue: DAPI (nuclear marker).

27764820
Growth inhibition assay
GI50; 

PubMed: 29108241     


The GI50 values of BI2536, rigosertib, and poloxin were determined in both parental and volasertib-resistant R-MOLM14 and R-HL-60. Error bars represent the mean values ± S.D. of at least three independent experiments.

Cell viability; 

PubMed: 27764820     


Cell viability as measured by MTS. FaDu, Detroit 562, UMSCC 1, UMSCC 47 and UMSCC 104 cells were treated with increasing concentrations of rigosertib for 48 h, and cell viability was assessed. 50% growth inhibition (IC50) is recorded for each cell line in μM in the legend. Untreated cells were considered 100% viable and percent viability of cells treated with rigosertib was calculated vs. this control. Data represent the mean +/− SD of 3 independent experiments.

29108241 27764820
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]
- Collapse

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]
- Collapse
  • 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]
- Collapse
  • Animal Models: Mouse (female athymic, NCR-nu/nu) xenograft models of Bel-7402, MCF-7, and MIA-PaCa cells
  • 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
Smiles [Na+].COC1=CC(=C(\C=C\[S](=O)(=O)CC2=CC=C(OC)C(=C2)NCC([O-])=O)C(=C1)OC)OC

In vivo Formulation Calculator (Clear solution)

Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
Dosage mg/kg Average weight of animals g Dosing volume per animal ul Number of animals
Step 2: Enter the in vivo formulation ()
% DMSO % % Tween 80 % ddH2O
CalculateReset

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 (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)

  • Mass
    Concentration
    Volume
    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
    V1
    C2
    V2

* 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 interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04177498 Not yet recruiting Drug: Rigosertib Sodium|Other: Quality-of-Life Assessment Recessive Dystrophic Epidermolysis Bullosa Thomas Jefferson University|Onconova Therapeutics Inc. December 31 2019 Early Phase 1
NCT02075034 Suspended Drug: rigosertib Myelodysplastic Syndrome Onconova Therapeutics Inc. May 2014 Phase 1
NCT02030639 Completed Drug: rigosertib Healthy Onconova Therapeutics Inc. January 2014 Phase 1
NCT01928537 Active not recruiting Drug: rigosertib sodium Myelodysplastic Syndromes|Refractory Anemia With Excess Blasts|Chronic Myelomonocytic Leukemia|Cytopenia Onconova Therapeutics Inc. August 2013 Phase 3
NCT01807546 Completed Drug: rigosertib Head and Neck Squamous Cell Carcinoma|Anal Squamous Cell Carcinoma|Lung Squamous Cell Carcinoma|Cervical Squamous Cell Carcinoma|Esophageal Squamous Cell Carcinoma|Skin Squamous Cell Carcinoma|Penile Squamous Cell Carcinoma Onconova Therapeutics Inc. March 2013 Phase 2
NCT01168011 Completed Drug: rigosertib Solid Tumor Onconova Therapeutics Inc. July 2010 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
selleck catalog

PLK Signaling Pathway Map

PLK Inhibitors with Unique Features

  • Pan Plk Inhibitors

    BI 2536 : Pan-Plk1, Plk1, IC50=0.83 nM; Plk2, IC50=3.5 nM; Plk3, IC50=9 nM.

  • Most Potent Plk Inhibitor

    BI 2536 : Plk1, IC50=0.83 nM.

  • Plk Inhibitor in Clinical Trial

    Volasertib (BI 6727) : Phase III for acute myeloid leukaemia.

  • Newest Plk Inhibitor

    Ro3280 New : Potent, highly selective inhibitor of Polo-like kinase 1 (PLK1) with IC50 of 3 nM.

Related PLK Products

  • SBE 13 HCl New

    SBE 13 HCl is a potent and selective PLK1 inhibitor with IC50 of 200 pM, >4000-fold selectivity over Aurora A kinase, Plk2 and Plk3.

  • Ro-3306 New

    RO-3306 is an ATP-competitive, and selective CDK1 inhibitor with Ki of 20 nM, >15-fold selectivity against a diverse panel of human kinases. RO-3306 enhances p53-mediated Bax activation and mitochondrial apoptosis.

  • CCG-1423 New

    CCG-1423 is a specific RhoA pathway inhibitor, which inhibits SRF-mediated transcription.

  • BI 2536

    BI-2536 is a potent Plk1 inhibitor with IC50 of 0.83 nM in a cell-free assay. BI-2536 inhibits Bromodomain 4 (BRD4) with Kd of 37 nM and potently suppresses c-Myc expression. BI-2536 induces apoptosis and attenuates autophagy. Phase 2.

    Features:The first potent and selective Plk1 inhibitor that induces all hallmarks of Plk1 inhibition.

  • HMN-214

    HMN-214 is a prodrug of HMN-176, which alters the cellular spatial orientation of Plk1.

  • GSK461364

    GSK461364 inhibits purified Plk1 with Ki of 2.2 nM in a cell-free assay. It is more than 1000-fold selective against Plk2/3. Phase 1.

    Features:Demonstrates >390-fold selectivity for Plk1 relative to Plk2 and Plk3.

  • Volasertib (BI 6727)

    Volasertib (BI 6727) is a highly potent Plk1 inhibitor with IC50 of 0.87 nM in a cell-free assay. It shows 6- and 65-fold greater selectivity against Plk2 and Plk3. Volasertib induces cell cycle arrest and apoptosis in various cancer cells. Phase 3.

    Features:A high volume of distribution, indicating good tissue penetration, and a long terminal half-life.

  • MLN0905

    MLN0905 is a potent inhibitor of PLK1 with IC50 of 2 nM.

  • Ro3280

    RO3280 is a potent, highly selective inhibitor of Polo-like kinase 1 (PLK1) with IC50 of 3 nM.

    Features:A selective PLK1 inhibitor. Demonstrates greater potency than BI2536. Potential use in nasopharyngeal carcinomas.

  • onvansertib (NMS-P937)

    onvansertib (NMS-P937) is an orally available, selective Polo-like Kinase 1 (PLK1) inhibitor with IC50 of 2 nM, 5000-fold selectivity over PLK2/PLK3. Phase 1.

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