Niraparib (MK-4827)

For research use only.

Catalog No.S2741

31 publications

Niraparib (MK-4827) Chemical Structure

CAS No. 1038915-60-4

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. Niraparib can form PARP–DNA complexes resulting in DNA damage, apoptosis, and cell death. Phase 3.

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Selleck's Niraparib (MK-4827) has been cited by 31 publications

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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. Niraparib can form PARP–DNA complexes resulting in DNA damage, apoptosis, and cell death. 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 NWn6NXQ1TnWwY4Tpc44h[XO|YYm= MlvjTY5pcWKrdHnvckBw\iCSQWLQJIlvKGi7ZILv[4VvKHCncn;4bYRmNWmwZIXj[YQhcHWvYX6gTIVN[SClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIFTORU1l[W2jZ3WtbY5lfWOnZDDQRXJ6dGG2aX;uMEBGSzVyPUCuNFA1KM7:TR?= MXqxPVg4Ozl6MR?=
A549 cells NIjJ[JFEgXSxdH;4bYNqfHliYYPzZZk> MUS1MVch\GG7cx?= MXzDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJJRz[W6|ZnXjeIVlKHerdHigRnJESTJic3jSUmEh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;MD6wNVEh|ryP MmfHNlU4PjFyOU[=
MDA-MB-436 cells M3X2THBzd2yrZnXyZZRqd25iYYPzZZk> MYe2JIRigXN? MVzBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2GQT3NRk01OzZiY3XscJMh\XiycnXzd4lv\yCEUlPBNUA2Ozl4IDugNWc,SSCvdYThcpQh[W[2ZYKgOkBl[Xm|IHL5JINmdGxidHn0[ZIu[my3ZTDhd5NigSxiQ1O1NF0yQCCwTR?= MmjiNVk5PzN7OEG=
SUM1315MO2 cells NEXDU4tEgXSxdH;4bYNqfHliYYPzZZk> MUOxNkBl[Xm| MYXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDTWW0yOzF3TV:yJINmdGy|IHPhdpJ6cW6pIFLSR2EyKG23dHHueEBie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJINmdGxicILvcIln\XKjdHnvckBi\nSncjCxNkBl[Xm|IHL5JGNmdGyWaYTldk1DdHWnIHHzd4F6NCCFQ{WwQVAvODJizszN MY[yOVc3OTB7Nh?=
DoTc2-4510 cells M4rLUGN6fG:2b4jpZ4l1gSCjc4PhfS=> MlPiOU04KGSjeYO= NXvSOVBFS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hTG:WY{KtOFUyOCClZXzsd{Bk[XK{eXnu[{BDWkODMjDteZRidnRiYYPz[ZN{\WRiYYOgbY5pcWKrdHnvckBw\iClZXzsJJBzd2yrZnXyZZRqd25iYX\0[ZIhPSC2bzC3JIRigXNiYomgR4VtdFSrdHXyMWJtfWViYYPzZZktKEOFNUC9NE4xOjNizszN NIiyfnozPTd4MUC5Oi=>
SUM149PT cells MlrjR5l1d3SxeHnjbZR6KGG|c3H5 MUe1MVch\GG7cx?= NGS5[I9EgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUXU1zNEnQWEBk\WyuczDjZZJzgWmwZzDCVmNCOSCvdYThcpQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBk\WyuIIDyc4xq\mW{YYTpc44h[W[2ZYKgOUB1dyB5IHThfZMh[nliQ3XscHRqfGW{LVLseYUh[XO|YYmsJGNEPTB;MD6wNlQh|ryP NHX1S5czPTd4MUC5Oi=>
UWB1.289 cells MVPDfZRwfG:6aXPpeJkh[XO|YYm= MYK1MVch\GG7cx?= M4rZNmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHVYSjFwMki5JINmdGy|IHPhdpJ6cW6pIFLSR2EyKG23dHHueEBie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJINmdGxicILvcIln\XKjdHnvckBi\nSncjC1JJRwKDdiZHH5d{BjgSCFZXzsWIl1\XJvQnz1[UBie3OjeTygR2M2OD1yLkC1OkDPxE1? NXz3XGdPOjV5NkGwPVY>
Capan1 cells NEC3eIdEgXSxdH;4bYNqfHliYYPzZZk> MnTwR5l1d3SxeHnjbZR6KGGpYXnud5QhSlKFQUKt[IVncWOrZX70JIh2dWGwIFPhdIFvOSClZXzsd{whS0N3ME2wMlA6KM7:TR?= NGTsUpIzPTd4MUC5Oi=>
Jurkat cells NYfoOXR5TnWwY4Tpc44h[XO|YYm= MWDJcohq[mm2aX;uJI9nKFCDUmCxJIlvKGi3bXHuJGp2emujdDDj[YxteyCjc4Pld5Nm\CCjczDy[YR2[3Srb36gc4Yh[2WubDD2bYFjcWyrdImgZYZ1\XJiOU[gbJJ{KGK7IF3UV{Bie3OjeTDpckBxemW|ZX7j[UBw\iBzMECgeW0hd2ZidHXtc5pwdG:vaXTlMEBGSzVyPUCuNkDPxE1? MV2yN|g2ODF7OR?=
BT20 cells MWfDfZRwfG:6aXPpeJkh[XO|YYm= MkPPOU04KGSjeYO= Mnz5R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRnQzOCClZXzsd{Bie3Onc4Pl[EBieyCrbnjpZol1cW:wIH;mJINmdGxicILvcIln\XKjdHnvckBi\nSncjC1JJRwKDdiZHH5d{BjgSCFZXzsWIl1\XJvQnz1[UBie3OjeTygR2M2OD1{LkKg{txO NH;JeWEzPTd4MUC5Oi=>
A2780 cells M2D5c2Z2dmO2aX;uJIF{e2G7 MoLoTY5pcWKrdHnvckBw\iCSQWLQJIlvKGi3bXHuJGEzPzhyIHPlcIx{KGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhcHmmcn;n[Y4heGW{b4jp[IUucW6mdXPl[EBRSVK7bHH0bY9vKGK7IHPlcIwu[mG|ZXSgZZN{[Xl? MVmyOVc3OTB7Nh?=

... 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]
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  • 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]
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  • Animal Models: Female nude mice
  • 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
Smiles C1CC(CNC1)C2=CC=C(C=C2)N3C=C4C=CC=C(C4=N3)C(=O)N

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04149145 Not yet recruiting Drug: M4344+Niraparib Ovarian Cancer Recurrent University of Alabama at Birmingham December 1 2020 Phase 1
NCT04475939 Not yet recruiting Drug: Niraparib|Drug: Pembrolizumab|Drug: Placebo Lung Cancer Non-Small Cell GlaxoSmithKline September 7 2020 Phase 3
NCT04392102 Not yet recruiting Drug: ZL-2306(Niraparib) Ovarian Cancer Zai Lab (Shanghai) Co. Ltd. July 31 2020 Phase 2
NCT04240106 Recruiting Drug: Niraparib 100 MG|Drug: Aromatase Inhibitors Breast Cancer|Breast Cancer Metastatic MedSIR|GlaxoSmithKline June 15 2020 Phase 2
NCT04235101 Recruiting Drug: SYD985 + Niraparib Solid Tumor Byondis B.V. June 22 2020 Phase 1

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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