Niraparib (MK-4827)

Catalog No.S2741

Niraparib (MK-4827) Chemical Structure

Molecular Weight(MW): 320.39

Niraparib (MK-4827) is a selective inhibitor of PARP1/2 with IC50 of 3.8 nM/2.1 nM, with great activity in cancer cells with mutant BRCA-1 and BRCA-2. It is >330-fold selective against PARP3, V-PARP and Tank1. Phase 3.

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Cited by 17 Publications

4 Customer Reviews

  • PARP1 silencing rescues PARP1/2 inhibitor sensitivity in the ERCC1-deficient population. Effect of PARP1 knockdown by siRNA on sensitivity of ERCC1-isogenic cell lines to niraparib. Cells were reverse-transfected with PARP1 siRNA and drug was added 48 h after transfection. Cells were exposed to the drug for 5 days. Error bars represent the s.d. from the mean of three independent experiments.

    Oncogene 2013 32(47):5377-87. Niraparib (MK-4827) purchased from Selleck.

  • Western Blot data testing protein expression after treatment with Olaparib, Niraparib, and Talazoparib on Brca1-deficient cell line in W780 cells.

    Theranostics, 2017, 7(17):4340-4349. Niraparib (MK-4827) purchased from Selleck.

  • Co-treatment of miR-489-3p with olaparib or niraparib followed by SDS-PAGE analysis to detect MEK1 expression shows that MEK1 and pMEK1 are reduced with 25 μM olaparib or niraparib treatment alone. Since miR-489-3p targets MEK1, this phenomenon is amplified in co-treatment conditions for both PARP inhibitors in OVCAR-3 and MDA-MB-231.

    Cancer Lett, 2018, 432:84-92. Niraparib (MK-4827) purchased from Selleck.

  • PAR synthesis is detected by immunofluorescence staining in A2780 and HO8910 treated with different concentration of berberine alone or in combination with niraparib (10 μM) for 48 h. Representative examples of immunofluorescence staining of PAR. Scale bar, 20 μm.

    Cell Death Dis, 2017, 8(10):e3070. Niraparib (MK-4827) purchased from Selleck.

Purity & Quality Control

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Biological Activity

Description Niraparib (MK-4827) is a selective inhibitor of PARP1/2 with IC50 of 3.8 nM/2.1 nM, with great activity in cancer cells with mutant BRCA-1 and BRCA-2. It is >330-fold selective against PARP3, V-PARP and Tank1. Phase 3.
PARP2 [1]
(Cell-free assay)
PARP1 [1]
(Cell-free assay)
2.1 nM 3.8 nM
In vitro

In a whole cell assay, MK-4827 inhibited PARP activity with EC50 = 4 nM and inhibited proliferation of cancer cells with mutant BRCA-1 and BRCA-2 with CC50 in the 10-100 nM range. It was demonstrated to be a potent and selective PARP-1 and PARP-2 inhibitor with IC50=3.8 and 2.1 nM, respectively. Furthermore, it displayed at least a 100-fold selectivity over PARP-3, V-PARP, and tankyrase-1, with IC50 = 1300, 330, and 570 nM, respectively. As well as inhibiting the growth of HeLa cell lacking BRCA-1 because of silencing by RNA interference, MK-4827 is able to inhibit the proliferation of cancer cell lines carrying natural BRCA-1 or BRCA-2 mutations. In MDA-MB-436 human mammary gland adenocarcinoma cells carrying BRCA-1 mutations, MK-4827 displayed CC50 = 18 nM, while in CAPAN-1 human pancreatic adenocarcinoma cells, which are BRCA-2 mutant, MK-4827 displayed CC50 = 90 nM. In contrast, normal human prostate and mammary epithelial cells are resistant to MK-4827, displaying antiproliferative effects in the micromolar range, thereby demonstrating the very high selective cytotoxicity from these PARP inhibitors in BRCA-1 and -2 mutant cancer cells compared to surrounding tissue[2].

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HeLa cells M2DHOGZ2dmO2aX;uJIF{e2G7 MXnJcohq[mm2aX;uJI9nKFCDUmCgbY4hcHmmcn;n[Y4heGW{b4jp[IUucW6mdXPl[EBpfW2jbjDI[WxiKGOnbHzzJIF{e2W|c3XkJIF{KGmwaHnibZRqd25iRF7BMYRidWGpZT3pcoR2[2WmIGDBVplt[XSrb36sJGVEPTB;MD6wNFQh|ryP NV7HN4xjOTl6N{O5PFE>
A549 cells M{nCe2N6fG:2b4jpZ4l1gSCjc4PhfS=> MYC1MVch\GG7cx?= MYjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJJRz[W6|ZnXjeIVlKHerdHigRnJESTJic3jSUmEh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;MD6wNVEh|ryP M1PGTlI2PzZzMEm2
MDA-MB-436 cells MVHQdo9tcW[ncnH0bY9vKGG|c3H5 NE\sSYM3KGSjeYO= MUfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2GQT3NRk01OzZiY3XscJMh\XiycnXzd4lv\yCEUlPBNUA2Ozl4IDugNWc,SSCvdYThcpQh[W[2ZYKgOkBl[Xm|IHL5JINmdGxidHn0[ZIu[my3ZTDhd5NigSxiQ1O1NF0yQCCwTR?= NUfTNldiOTl6N{O5PFE>
SUM1315MO2 cells M2rnVWN6fG:2b4jpZ4l1gSCjc4PhfS=> M4DiUVEzKGSjeYO= NYLqW4tsS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW1WPMUOxOW1QOiClZXzsd{Bk[XK{eXnu[{BDWkODMTDteZRidnRiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iClZXzsJJBzd2yrZnXyZZRqd25iYX\0[ZIhOTJiZHH5d{BjgSCFZXzsWIl1\XJvQnz1[UBie3OjeTygR2M2OD1yLkCyJO69VQ>? NYT5N4pTOjV5NkGwPVY>
DoTc2-4510 cells NUCyRmlHS3m2b4TvfIlkcXS7IHHzd4F6 NIHWdYQ2NTdiZHH5dy=> M3KwVWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGRwXGN{LUS1NVAh[2WubIOgZ4FzenmrbnegRnJESTJibYX0ZY51KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4Yh[2WubDDwdo9tcW[ncnH0bY9vKGGodHXyJFUhfG9iNzDkZZl{KGK7IFPlcIxVcXSncj3CcJVmKGG|c3H5MEBESzVyPUCuNFI{KM7:TR?= MWqyOVc3OTB7Nh?=
SUM149PT cells NUjOeJJMS3m2b4TvfIlkcXS7IHHzd4F6 MkiyOU04KGSjeYO= NEjxT5ZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXU1zNEnQWEBk\WyuczDjZZJzgWmwZzDCVmNCOSCvdYThcpQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;MD6wNlQh|ryP MXmyOVc3OTB7Nh?=
UWB1.289 cells MYLDfZRwfG:6aXPpeJkh[XO|YYm= NIXzNoM2NTdiZHH5dy=> NXnUfHQ2S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hXVeEMT6yPFkh[2WubIOgZ4FzenmrbnegRnJESTFibYX0ZY51KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4Yh[2WubDDwdo9tcW[ncnH0bY9vKGGodHXyJFUhfG9iNzDkZZl{KGK7IFPlcIxVcXSncj3CcJVmKGG|c3H5MEBESzVyPUCuNFU3KM7:TR?= NIKwPIszPTd4MUC5Oi=>
Capan1 cells MV7DfZRwfG:6aXPpeJkh[XO|YYm= MVPDfZRwfG:6aXPpeJkh[WejaX7zeEBDWkODMj3k[YZq[2mnboSgbJVu[W5iQ3HwZY4yKGOnbHzzMEBESzVyPUCuNFkh|ryP MVKyOVc3OTB7Nh?=
Jurkat cells NIjhXotHfW6ldHnvckBie3OjeR?= Mn;TTY5pcWKrdHnvckBw\iCSQWLQNUBqdiCqdX3hckBLfXKtYYSgZ4VtdHNiYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJI9nKGOnbHygeoli[mmuaYT5JIFnfGW{IEm2JIhzeyCkeTDNWHMh[XO|YYmgbY4heHKnc3XuZ4Uhd2ZiMUCwJJVOKG:oIITlcY97d2yxbXnk[UwhTUN3ME2wMlIh|ryP MV2yN|g2ODF7OR?=
BT20 cells NHnWV5FEgXSxdH;4bYNqfHliYYPzZZk> NYDQfFl3PS15IHThfZM> NHzLWVBEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBDXDJyIHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4Yh[2WubDDwdo9tcW[ncnH0bY9vKGGodHXyJFUhfG9iNzDkZZl{KGK7IFPlcIxVcXSncj3CcJVmKGG|c3H5MEBESzVyPUKuNkDPxE1? NHG4N3QzPTd4MUC5Oi=>
A2780 cells NXXmN45iTnWwY4Tpc44h[XO|YYm= NHPVVlFKdmirYnn0bY9vKG:oIGDBVnAhcW5iaIXtZY4hSTJ5OECgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iCqeXTyc4dmdiCyZYLvfIll\S2rbnT1Z4VlKFCDUonsZZRqd25iYomgZ4VtdC2kYYPl[EBie3OjeR?= M3jFNVI2PzZzMEm2

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
c-PARP /c-caspase 3 / γ-H2AX; 

PubMed: 29158830     

Western Blot data testing protein expression after treatment with Olaparib, Niraparib, and Talazoparib on Brca1-deficient cell line in W0069 cells.

Rad51 / Geminin; 

PubMed: 27614696     

Immunofluorescence microscopy of niraparib-treated PDX cells (PH039) and irradiated cells showing RAD51 foci (arrow) within geminin positive cells and lack of RAD51 foci formation in control cells. 

In vivo MK-4827, a novel, orally bioavailable, PARP-1 and PARP-2 inhibitor, strongly enhanced the effect of radiation on a variety of human tumor xenografts, both p53 wild type and p53 mutant[1]. It was well tolerated in vivo and demonstrated efficacy as a single agent in a xenograft model of BRCA-1 deficient cancer[2].


Cell Research:[2]
- Collapse
  • Cell lines: HeLa BRCA1-silenced cells
  • Concentrations: serial dilutions
  • Incubation Time: 7 days
  • Method: Proliferation assays were conducted in 96-well black viewplates, and 300 cells/well (250 cell/well for BRCA-1 wt) in culture medium, 190 μL/well (DMEM containing 10% FCS, 0.1 mg/mL penicillin-streptomycin, and 2 mM L-glutamine), were plated and incubated for 4 h at 37℃ under 5% CO2 atmosphere. Inhibitors were then added with serial dilutions, 10 μL/well to obtain the desired final compound concentration in 0.5% DMSO. The cells were then incubated for 7 days at 37℃ in 5% CO2 after which time viability was assessed. Briefly, with CellTiter-Blue solution prediluted 1:10 in medium, 100 μL/well was added and the cells left for 45 min at 37℃ under 5% CO2 and then a further 15 min at room temperature in the dark. The number of living cells was determined by reading the plate at fluorimeter, excitation at 550 nm and emission at 590 nm. Cell growth was expressed as the percentage growth with respect to vehicle treated cells. The concentration required to inhibit cell growth by 50% (CC50) was determined.
    (Only for Reference)
Animal Research:[1]
- Collapse
  • Animal Models: Female nude mice
  • Formulation: 0.5% Methocel in deionized water
  • Dosages: 25 mg/kg twice daily or 50 mg/kg once daily
  • Administration: oral administration
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 64 mg/mL (199.75 mM)
Ethanol 64 mg/mL (199.75 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
10% DMSO+40% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.

* 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 320.39


CAS No. 1038915-60-4
Storage powder
in solvent

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03368729 Not yet recruiting Drug: Niraparib|Drug: Trastuzumab Metastatic Breast Cancer|HER2 Positive Breast Carcinoma University of Alabama at Birmingham|Translational Breast Cancer Research Consortium|Tesaro Inc.|Susan G. Komen Breast Cancer Foundation|Breast Cancer Research Foundation of Alabama|VFoundation November 2019 Phase 1|Phase 2
NCT03644342 Recruiting Drug: Nirapaib Metastatic Carcinoma of the Cervix Michelle S Ludwig|Tesaro Inc.|Baylor College of Medicine July 15 2019 Phase 1|Phase 2
NCT03891615 Not yet recruiting Drug: Niraparib|Drug: Osimertinib Lung Cancer Massachusetts General Hospital|Tesaro Inc. April 30 2019 Phase 1
NCT03752216 Recruiting Drug: Niraparib Ovarian Cancer ARCAGY/ GINECO GROUP|Tesaro Inc. April 3 2019 Phase 4

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  • Answer:

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PARP Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID