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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2 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.

    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.

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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 MWrGeY5kfGmxbjDhd5NigQ>? NH[3OGtKdmirYnn0bY9vKG:oIGDBVnAhcW5iaInkdo9o\W5icHXyc5hq\GVvaX7keYNm\CCqdX3hckBJ\UyjIHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gSG5CNWSjbXHn[U1qdmS3Y3XkJHBCWnmuYYTpc44tKEWFNUC9NE4xODRizszN M{jTUlE6QDd|OUix
A549 cells NEizbJZEgXSxdH;4bYNqfHliYYPzZZk> NVTOVnFYPS15IHThfZM> M4DHWGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGE2PDliY3XscJMhfHKjboPm[YN1\WRid3n0bEBDWkODMjDzbHJPSSCjc4Pld5Nm\CCjczDpcohq[mm2aX;uJI9nKGOnbHygdJJwdGmoZYLheIlwdiCjZoTldkA2KHSxIEeg[IF6eyCkeTDD[YxtXGm2ZYKtRox2\SCjc4PhfUwhS0N3ME2wMlAyOSEQvF2= Mmm5NlU4PjFyOU[=
MDA-MB-436 cells NIKzd5dRem:uaX\ldoF1cW:wIHHzd4F6 NFHUZ3k3KGSjeYO= MUfBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2GQT3NRk01OzZiY3XscJMh\XiycnXzd4lv\yCEUlPBNUA2Ozl4IDugNWc,SSCvdYThcpQh[W[2ZYKgOkBl[Xm|IHL5JINmdGxidHn0[ZIu[my3ZTDhd5NigSxiQ1O1NF0yQCCwTR?= M2\zPFE6QDd|OUix
SUM1315MO2 cells NWrNfHIzS3m2b4TvfIlkcXS7IHHzd4F6 NUTC[48{OTJiZHH5dy=> MnnKR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV3VOOTNzNV3PNkBk\WyuczDjZZJzgWmwZzDCVmNCOSCvdYThcpQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgNVIh\GG7czDifUBE\WyuVHn0[ZIuSmy3ZTDhd5NigSxiQ1O1NF0xNjB{IN88US=> MU[yOVc3OTB7Nh?=
DoTc2-4510 cells Mly1R5l1d3SxeHnjbZR6KGG|c3H5 NFPmdo02NTdiZHH5dy=> MoXuR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gSI9V[zJvNEWxNEBk\WyuczDjZZJzgWmwZzDCVmNCOiCvdYThcpQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;MD6wNlMh|ryP M2DrXVI2PzZzMEm2
SUM149PT cells MkTaR5l1d3SxeHnjbZR6KGG|c3H5 MVK1MVch\GG7cx?= NF3FSllEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXU1zNEnQWEBk\WyuczDjZZJzgWmwZzDCVmNCOSCvdYThcpQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;MD6wNlQh|ryP M4LNUFI2PzZzMEm2
UWB1.289 cells NWjObmtRS3m2b4TvfIlkcXS7IHHzd4F6 MVS1MVch\GG7cx?= MUTDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDVW2IyNjJ6OTDj[YxteyClYYLyfYlv\yCEUlPBNUBufXSjboSgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDj[YxtKHC{b3zp[oVz[XSrb36gZYZ1\XJiNTD0c{A4KGSjeYOgZpkhS2WubGTpeIVzNUKudXWgZZN{[XluIFPDOVA:OC5yNU[g{txO Mmf2NlU4PjFyOU[=
Capan1 cells NFvI[JVEgXSxdH;4bYNqfHliYYPzZZk> NIKzT|JEgXSxdH;4bYNqfHliYXfhbY5{fCCEUlPBNk1l\W[rY3nlcpQhcHWvYX6gR4Fx[W5zIHPlcIx{NCCFQ{WwQVAvODlizszN MkLrNlU4PjFyOU[=
Jurkat cells MVzGeY5kfGmxbjDhd5NigQ>? NWD4XoxzUW6qaXLpeIlwdiCxZjDQRXJROSCrbjDoeY1idiCMdYLrZZQh[2WubIOgZZN{\XO|ZXSgZZMhemWmdXP0bY9vKG:oIHPlcIwhfmmjYnnsbZR6KGGodHXyJFk3KGi{czDifUBOXFNiYYPzZZkhcW5icILld4Vv[2Vib3[gNVAxKHWPIH;mJJRmdW:8b3zvcYll\SxiRVO1NF0xNjJizszN NHnQdZMzOzh3MEG5PS=>
BT20 cells MXfDfZRwfG:6aXPpeJkh[XO|YYm= MlvuOU04KGSjeYO= M1\0e2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGJVOjBiY3XscJMh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;Mj6yJO69VQ>? NF[1XmgzPTd4MUC5Oi=>
A2780 cells MknqSpVv[3Srb36gZZN{[Xl? NFnve4FKdmirYnn0bY9vKG:oIGDBVnAhcW5iaIXtZY4hSTJ5OECgZ4VtdHNiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iCqeXTyc4dmdiCyZYLvfIll\S2rbnT1Z4VlKFCDUonsZZRqd25iYomgZ4VtdC2kYYPl[EBie3OjeR?= NFzzOYkzPTd4MUC5Oi=>

... Click to View More Cell Line Experimental Data

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]
+ Expand
  • 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]
+ Expand
  • 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 Conditions Sponsor/Collaborators Start Date Phases
NCT03586661 Not yet recruiting Deleterious BRCA1 Gene Mutation|Deleterious BRCA2 Gene Mutation|Endometrial Adenocarcinoma|High Grade Ovarian Serous Adenocarcinoma|Primary Peritoneal High Grade Serous Adenocarcinoma|Recurrent Endometrial Carcinoma|Recurrent Fallopian Tube Carcinoma|Recurrent Ovarian Carcinoma|Recurrent Primary Peritoneal Carcinoma M.D. Anderson Cancer Center|National Cancer Institute (NCI) February 2019 Phase 1
NCT03651206 Not yet recruiting Ovarian Carcinosarcoma|Endometrial Carcinosarcoma ARCAGY/ GINECO GROUP|Tesaro Inc. January 2019 Phase 2|Phase 3
NCT03553004 Not yet recruiting Pancreatic Cancer Anup Kasi|Tesaro Inc.|University of Kansas Medical Center January 1 2019 Phase 2
NCT03695380 Not yet recruiting OVARIAN CANCER Hoffmann-La Roche December 31 2018 Phase 1
NCT03598270 Not yet recruiting Recurrent Ovarian Carcinoma Grupo Español de Investigación en Cáncer de Ovario|Hoffmann-La Roche|Apices Soluciones S.L.|Tesaro Inc. November 2018 Phase 3
NCT03368729 Not yet recruiting 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 November 1 2018 Phase 1|Phase 2

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Frequently Asked Questions

  • Question 1:

    How to reconstitute the compound for in vivo studies?

  • Answer:

    You can use the formulation 1% CMC-Na (suspension) for oral administration.

PARP Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID