Rucaparib (AG-014699,PF-01367338) phosphate

Catalog No.S1098

Rucaparib (AG-014699,PF-01367338) phosphate Chemical Structure

Molecular Weight(MW): 421.36

Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with Ki of 1.4 nM for PARP1 in a cell-free assay, also showing binding affinity to eight other PARP domains. Phase 3.

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Cited by 25 Publications

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Biological Activity

Description Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with Ki of 1.4 nM for PARP1 in a cell-free assay, also showing binding affinity to eight other PARP domains. Phase 3.
Features The first PARP inhibitor used in clinical trials combined with temozolomide.
Targets
PARP [1]
(Cell-free assay)
1.4 nM(Ki)
In vitro

Rucaparib is a potent inhibitor of purified full-length human PARP-1 and shows higher inhibition of cellular PARP in LoVo and SW620 cells. Besides, Rucaparib binds detectably to eight other PARP domains, including PARP2, 3, 4, 10, 15, 16, TNKS1 and TNKS2. [1] [2] The radio-sensitization by Rucaparib is due to downstream inhibition of activation of NF-κB, and is independent of SSB repair inhibition. Rucaparib could target NF-κB activated by DNA damage and overcome toxicity observed with classical NF-κB inhibitors without compromising other vital inflammatory functions. [3] Rucaparib inhibits PARP-1 activity by 97.1% at a concentration of 1 μM in permeabilised D283Med cells. [4]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BT-474 NFL6WJFHfW6ldHnvckBCe3OjeR?= MYewMlEwOS93MECvNVAxOCCwTR?= M3\6XIlvcGmkaYTzJHBCWlBiYXP0bZZqfHliYYSgd5RienSrbnegZ49v[2W{boTyZZRqd25ib3[gOVAxKG6P Ml3vNlUyOjh2NUW=
BT474 M4P2WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXS1NFAhdk1? M4TPW|Ex6oDVMUZCpIQ> M2HCWpJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NIfZbJEzPTF{OES1OS=>
SKBR3 M1[xXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXheYx1PTByIH7N MVmxNQKBmzF3wrDk NUjYR4V6emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NHzaU2MzPTF{OES1OS=>
AU565 NU\1bJlnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVy1NFAhdk1? NUTmbYNsOTEkgKOxOeKh\A>? MnP6doVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M{PkWFI2OTJ6NEW1
EFM192A MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmCwOVAxKG6P NFHEfmoyOOLCk{G1xsBl M2rMXpJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> MVmyOVEzQDR3NR?=
MDA-MB-231 M3mxZWZ2dmO2aX;uJGF{e2G7 MYexNE8zOC92MDFOwG0> NGnkTYIzPCCq M3rlcIlv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? MYGyOFQzODF3Mh?=
MDA-MB-231 NFfZZ5RE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M4nMUFAvOS12MDFOwG0> M4jpSVI1KGh? Mm\wTWM2OOLCiU5ihKkyPy55N9Mg{txO M{PoblI1PDJyMUWy
MDA-MB-231 NGfkeGdCeG:ydH;zbZMhSXO|YYm= MljUNVAwOjBxNECg{txO MV2yOEBp NECxR|JqdmS3Y3XzJIFxd3C2b4Ppd{Bld3OnIHTldIVv\GWwdHz5 NFH0[HAzPDR{MEG1Ni=>
MDA-MB-231 M2CyOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUexNE8zOC92MDFOwG0> MVOyOEBp NUXNe3l4[myxY3vzJINmdGxiY4njcIUheHKxZ4Lld5Nqd25iaX6gS|IwVSCyaHHz[S=> NE\IdWYzPDR{MEG1Ni=>
H460 NWntfFIyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{TX[lQxOCCwTR?= NUjuNIhGOjUEoHi= M3\ZSIlv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 NETjTZQzPDRzMU[xNS=>
A549  MlrUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTqOFAxKG6P MXyyOOKhcA>? Mn\JbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= NUjIfGtrOjR2MUG2NVE>
DT40 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MW\JR|UxRTJzIH7N NXrYSGtjOjR|NU[4NVM>
DU145 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn\GTWM2OD1zODDuUS=> NIXXeoczPDN3NkixNy=>
COLO704 NV[y[mtQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnW1TWM2OD1{LkWyJOKyKDBwNkeg{txO NIK0[YczOzd{OUSwNi=>
OVMANAb NXnENFd[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIi0O3FKSzVyPUKuOVghyrFiMD6zPEDPxE1? MXKyN|czQTRyMh?=
OV177 M17WcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoLDTWM2OD1{Lke4JOKyKDBwN{Gg{txO MYSyN|czQTRyMh?=
OAW28 M3zwdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4TT[2lEPTB;Mz62NUDDuSByLkK4JO69VQ>? MoLxNlM4Ojl2MEK=
OVSAHO MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYnJR|UxRTNwNkSgxtEhOC5|MzFOwG0> M1:xUVI{PzJ7NECy
OVKATE NXn3bI52T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3zYSmlEPTB;Mz62OEDDuSBzLke5JO69VQ>? MoPqNlM4Ojl2MEK=
OVCAR3 MmjRS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYPJR|UxRTNwN{SgxtEhOC52MDFOwG0> NF62WmkzOzd{OUSwNi=>
PEO14 M{LmO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlXJTWM2OD1|Lki0JOKyKDBwN{[g{txO NGLoZ5IzOzd{OUSwNi=>
A2780 M2\nT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTNwOUSgxtEhOC5{NTFOwG0> NEfo[4szOzd{OUSwNi=>
OVTOKO M{XZVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml3aTWM2OD12LkG0JOKyKDFwNUOg{txO NX;jSHJQOjN5Mkm0NFI>
KURAMOCHIb M2m2fGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXXSS2tiUUN3ME20MlM1KMLzIECuNlkh|ryP NWDr[JRlOjN5Mkm0NFI>
TOV21G M37IdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoqwTWM2OD13LkC3JOKyKDFwM{Cg{txO NEPwR3czOzd{OUSwNi=>
OVISE NWjiN3MzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml:zTWM2OD13Lk[4JOKyKDBwMkOg{txO NYD0Wm9pOjN5Mkm0NFI>
KK NFL5PHlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRTZwMUWgxtEhOS52MjFOwG0> MVWyN|czQTRyMh?=
RMUGS MmS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3vEVmlEPTB;Nz6wN{DDuSBzLkizJO69VQ>? MnXMNlM4Ojl2MEK=
PEO6 NGfV[FNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkjQTWM2OD15LkC2JOKyKDBwN{Sg{txO M2PN[FI{PzJ7NECy
OVCA429 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVLJR|UxRThwMkmgxtEhOS54NDFOwG0> NUKzU2ZFOjN5Mkm0NFI>
OV167 NUiwW4lPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4Lre2lEPTB;OD6zN{DDuSBzLkG4JO69VQ>? NYT4NohwOjN5Mkm0NFI>
RMG1 NVjnUGxXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVnJR|UxRTlwM{KgxtEhOi5|NjFOwG0> Mo\DNlM4Ojl2MEK=
OVCAR5 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYXJR|UxRTlwNUCgxtEhOi53OTFOwG0> MlXQNlM4Ojl2MEK=
EFO21 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUXJR|UxRTlwOUKgxtEhOS56NzFOwG0> M3XRUFI{PzJ7NECy
ES2 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{n3VWlEPTB;MUCuNVIhyrFiMT6yN{DPxE1? MXuyN|czQTRyMh?=
Tyk-nu M3HFR2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWfJR|UxRTFyLkKwJOKyKDFwMUKg{txO MkDGNlM4Ojl2MEK=
CAOV3 NFTYUFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3vhR2lEPTB;MUCuN|chyrFiMD64O{DPxE1? MnPzNlM4Ojl2MEK=
OV207 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXrrcYxJUUN3ME2xNk4zPyEEsTCwMlMzKM7:TR?= MXGyN|czQTRyMh?=
HEY NGrRdoFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7JSZZ4UUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= M3XhS|I{PzJ7NECy
DOV13 NEO5[VFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWDJR|UxRjF3IN88US=> NXnyPYxuOjN5Mkm0NFI>
EFO27 NY[yXnRuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYjJR|UxRjF3IN88US=> NWW3TIN4OjN5Mkm0NFI>
HEY C2 M3XEfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1zaeGlEPTB-MUWg{txO NYXCNGpwOjN5Mkm0NFI>
KOC-7cc NELkZXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2HXXmlEPTB-MUWg{txO M2HBZ|I{PzJ7NECy
MCASb NGXFRY1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFGyS5lKSzVyPkG1JO69VQ>? M4jCN|I{PzJ7NECy
OAW42 M2Hadmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NInCc4FKSzVyPkG1JO69VQ>? MlLhNlM4Ojl2MEK=
OV2008 NXPCSJEzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV7JR|UxRjF3IN88US=> NXjz[I85OjN5Mkm0NFI>
OV90 M1uyXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVfk[GtlUUN3ME6xOUDPxE1? MXeyN|czQTRyMh?=
OVCA420b M1XWcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVflZmdCUUN3ME6xOUDPxE1? NX7SRZNDOjN5Mkm0NFI>
OVCA432 M1Prdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUf3bmY6UUN3ME6xOUDPxE1? NYPSZmJoOjN5Mkm0NFI>
PEA2 NWi3eItHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYXx[FZZUUN3ME6xOUDPxE1? MkXTNlM4Ojl2MEK=
SKOV3 NH7JdHFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{TkSGlEPTB-MUWg{txO NVL1TXRxOjN5Mkm0NFI>
TOV112D M4S5NWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4PFOlAuOyEQvF2= NIDY[plKSzVyPkG1JO69VQ>? NX7RZXFrOjN5Mkm0NFI>
C4-2 MlXtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX:wMVMh|ryP M1v1WlE1KGR? M4PKZmROW09? M17aXYRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NFPMcoEzOzV4NUK0OC=>
PC3 NIfTUVFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYOwMVMh|ryP M{H0PVE1KGR? MXnEUXNQ NH3GXJJl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M{nMPFI{PTZ3MkS0
DU145 MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3TQXVAuOyEQvF2= MnnPNVQh\A>? Mn7QSG1UVw>? M1LiXYRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? MWmyN|U3PTJ2NB?=
VCaP  M2LGV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mn\DNE0{KM7:TR?= Mn7SNVQh\A>? NYLsbFFVTE2VTx?= NGDyVpVl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NED5flIzOzV4NUK0OC=>
LNCaP  NITGU2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkC3NE0{KM7:TR?= MlzKNVQh\A>? NXW4O3Q2TE2VTx?= M1rLWoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NH63TYYzOzV4NUK0OC=>
MDA-MB-468 MoDqR4VtdCCYaXHibYxqfHliQYPzZZk> MmPXTWM2OD17Lkeg{txO NY\SZ|FmOjJ4N{ixOlE>
MDA-MB-231 MXnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MmrmTWM2OD1zMzFOwG0> M33jOlIzPjd6MU[x
Cal-51 M1[3UGNmdGxiVnnhZoltcXS7IFHzd4F6 MnnaTWM2OD16Lk[g{txO NHnoOW4zOjZ5OEG2NS=>

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
PAR; 

PubMed: 27960087     


MCF-7 cells were pretreated ± Rucaparib (15 µM, 2 hr), then ± Rucaparib (15 µM) or two different doses of β-lap (2.0 or 5.0 µM) for 2 hr. Levels of PAR (PARP hyperactivation) formation were assessed with α-tubulin as loading controls.

BRCA1; 

PubMed: 24085845     


MCF7 cells, MDA-MB-436 parental cells and resistant clones RR-1, RR-5, and RR-6 were treated with DMSO (−) or 1 µM rucaparib (+) for 24 h, and BRCA1 protein levels were assessed by using BRCA1 N- or C-terminal-specific antibodies by Western blot. 

27960087 24085845
Growth inhibition assay
Cell viability; 

PubMed: 31119062     


The effect of rucaparib on proliferation of keloid fibroblasts. (A) Keloid cell growth following treatment with rucaparib at various concentration (0, 2, 10, 20 μM) was evaluated by MTT assays. Data are expression as mean standard deviation of percent changes of triplicate optical densities. (B) Rucaparib (20 μM) significantly decreased proliferation of keloid fibroblasts. The combination of rucaparib (20 μM) and triamcinolone (50 μM) showed additive suppressive effect on keloid fibroblasts as compared with rucaparib single therapy. Data are expression as mean standard deviation of percent changes of triplicate optical densities. MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide.

31119062
Immunofluorescence
α-tubulin; 

PubMed: 30589644     


Representative immunofluorescence images of DMSO-, rucaparib- (Ruca-), and Ola-exposed A549-ERCC1(WT/WT) and A549-ERCC1(–/–) cells. Cells were exposed to 15 μM Ruca or 40 μM Ola during 72 hours. White arrows, CCFs; yellow arrows, micronuclei. Scale bar: 20 μm. 

PAR; 

PubMed: 27515310     


Cells were treated with 20 mM hydrogen peroxide (H2O2) in order to stimulate PARP-1 activity in the presence or absence of the PARP-1 inhibitors rucaparib and olaparib. Poly(ADP-ribose) (PAR) chain synthesis was detected using an anti-PAR monoclonal Alexa Fluor 488-conjugated antibody (green). The nucleus was visualised using the nuclear counterstain DAPI (blue). Representative images obtained from the analysis of anti-PAR staining of SK-N-BE(2c) cells are shown.

γH2AX; 

PubMed: 23565244     


γH2AX foci was determined by immunofluoresecence microscopy at 24 h following combined treatment with radiation and rucaparib in PC3 and LNCaP cells. 

53BP1; 

PubMed: 23565244     


53BP1 foci was determined by immunofluoresecence microscopy at 24 h following combined treatment with radiation and rucaparib in PC3 and LNCaP cells.

30589644 27515310 23565244
In vivo Rucaparib is not toxic but significantly enhances temozolomide-induced TGD in the DNA repair protein-competent D384Med xenografts. Pharmacokinetics studies also show that Rucaparib is detected in the brain tissue, which indicates that Rucaparib has potential in intra-cranial malignancy therapy. [4] Rucaparib significantly potentiates the cytotoxicity of topotecan and temozolomide in NB-1691, SH-SY-5Y, and SKNBE (2c) cells. Rucaparib enhances the antitumor activity of temozolomide and indicates complete and sustained tumor regression in NB1691 and SHSY5Y xenografts. [5]

Protocol

Kinase Assay:[1]
+ Expand

Ki Determination:

Inhibition of human full-length recombinant PARP-1 by [32P]NAD+ incorporation is measured. The [32P]ADP-ribose incorporated into acid insoluble material is quantified using a PhosphorImager. Ki is calculated by nonlinear regression analysis.
Cell Research:[4]
+ Expand
  • Cell lines: D425Med, D283Med and D384Med cells
  • Concentrations: 0.4 μM
  • Incubation Time: 3 or 5 days
  • Method: Medulloblastoma cell lines are seeded in 96-well plates at a density of 1 × 103, 3 × 103 and 3 × 103, respectively. At 24 hours (D384Med) or 48 hours (D283Med and D425Med) after seeding, the cells are exposed to various concentrations of temozolomide in the presence or absence of 0.4 μM Rucaparib. After 3 days (D425Med and D384Med) or 5 days (D283Med) of culture, cell viability is evaluated by a XTT cell proliferation kit assay. Cell growth is expressed as a percentage in relation to DMSO or 0.4 μM Rucaparib-alone controls. The concentration of temozolomide, alone or in combination with Rucaparib that inhibited growth by 50% (GI50) is calculated. The potentiation factor 50 (PF50) is defined as the ratio of the GI50 of temozolomide in the presence of Rucaparib to the GI50 of temozolomide alone.
    (Only for Reference)
Animal Research:[4]
+ Expand
  • Animal Models: CD-1 nude mice bearing established D283Med xenografts
  • Formulation: Normal saline
  • Dosages: 1 mg/kg
  • Administration: One or four daily by i.p.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 84 mg/mL (199.35 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing. 		10mg/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 421.36
Formula

C19H18FN3O.H3PO4
CAS No. 459868-92-9
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03694262 Not yet recruiting Endometrial Cancer Medical College of Wisconsin April 1 2019 Phase 2
NCT03694262 Not yet recruiting Endometrial Cancer Medical College of Wisconsin April 1 2019 Phase 2
NCT03840200 Not yet recruiting Breast Cancer|Prostate Cancer|Ovarian Cancer Hoffmann-La Roche March 22 2019 Phase 1|Phase 2
NCT03795272 Not yet recruiting Cervical Cancer Nordic Society for Gynaecologic Oncology|Institute of Cancer Research United Kingdom|Central and Eastern European Oncology Group|North Eastern Germany Society of Gynaecologic Oncology|Belgian Gynaecological Oncology Group|Princess Margaret Hospital Canada|PGOG (Polish Gynaecologic Oncology Group)|GSO Global Clinical Research BV|GCP-enhederne March 1 2019 Phase 2
NCT03639935 Recruiting Biliary Tract Cancer University of Michigan Rogel Cancer Center|Dana-Farber Cancer Institute|Vanderbilt University Medical Center March 2019 Phase 2
NCT03617679 Recruiting Metastatic Endometrial Cancer University of Colorado Denver|Clovis Oncology Inc.|National Cancer Institute (NCI) March 6 2019 Phase 2

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PARP Signaling Pathway Map

PARP Inhibitors with Unique Features

  • Selective PARP Inhibitors

    AG-14361 : PARP1-selective, Ki<5 nM.

  • Selective PARP Inhibitors

    UPF 1069 : PARP2-selective, IC50=0.3 μM.

  • Most Potent PARP Inhibitor

    MK-4827 (Niraparib) : PARP1, IC50=3.8 nM; PARP2, IC50=2.1 nM.

  • PARP Inhibitor in Clinical Trial

    Iniparib (BSI-201) : Phase III for solid tumors.

  • Newest PARP Inhibitor

    PJ34 HCl New : PARP inhibitor with EC50 of 20 nM and is equally potent to PARP1/2.

Related PARP Products5

  • G007-LK New

    G007-LK is a potent and selective tankyrase inhibitor with IC50 of 46 nM and 25 nM for TNKS1/2, respectively.

  • NU1025 New

    NU1025 is a potent PARP inhibitor with IC50 of 400 nM.

  • SCR7 New

    SCR7 is a specific DNA Ligase IV inhibitor, which blocks nonhomologous end-joining (NHEJ). It increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos.

  • Olaparib (AZD2281, Ku-0059436)

    Olaparib (AZD2281, KU0059436) is a selective inhibitor of PARP1/2 with IC50 of 5 nM/1 nM in cell-free assays, 300-times less effective against tankyrase-1.

    Features:A potent PARP inhibitor (currently in late stage clinical trials).

  • Veliparib (ABT-888)

    Veliparib (ABT-888) is a potent inhibitor of PARP1 and PARP2 with Ki of 5.2 nM and 2.9 nM in cell-free assays, respectively. It is inactive to SIRT2. Phase 3.

    Features:Increases the efficacy of common cancer therapies such as radiation and alkylating agents.

  • Talazoparib (BMN 673)

    Talazoparib (BMN 673) is a novel PARP inhibitor with IC50 of 0.57 nM for PARP1 in a cell-free assay. It is also a potent inhibitor of PARP-2, but does not inhibit PARG and is highly sensitive to PTEN mutation. Phase 3.

    Features:Most potent and selective PARPi reported thus far.

  • Iniparib (BSI-201)

    Iniparib (BSI-201) is a PARP1 inhibitor with demonstrated effectiveness in triple-negative breast cancer (TNBC). Phase 3.

  • PJ34 HCl

    PJ34 HCl is the hydrochloride salt of PJ34, which is a PARP inhibitor with EC50 of 20 nM and is equally potent to PARP1/2.

    Features:Water-soluble PARP1/2 inhibitor with >10,000-fold potentcy vs. 3-aminobenzamide (prototypical PARP inhibitor). Potential uses in cardiovascular diseases (stroke, cerebral ischemia, & myocardial ischemia).

  • AG-14361

    AG14361 is a potent inhibitor of PARP1 with Ki of <5 nM in a cell-free assay. It is at least 1000-fold more potent than the benzamides.

    Features:The 1st high-potency PARP-1 inhibitor with the specificity & in vivo activity to enhance chemotherapy and radiation therapy of human cancers.

  • A-966492

    A-966492 is a novel and potent inhibitor of PARP1 and PARP2 with Ki of 1 nM and 1.5 nM, respectively.

    Features:A promising, structurally diverse benzimidazole analogue that is being further characterized preclinically.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID