Rucaparib (AG-014699) phosphate

For research use only. Not for use in humans.

Catalog No.S1098 Synonyms: PF-01367338

57 publications

Rucaparib (AG-014699) 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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Selleck's Rucaparib (AG-014699) phosphate has been cited by 57 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 M4LvdGZ2dmO2aX;uJGF{e2G7 MXOwMlEwOS93MECvNVAxOCCwTR?= M2PhR4lvcGmkaYTzJHBCWlBiYXP0bZZqfHliYYSgd5RienSrbnegZ49v[2W{boTyZZRqd25ib3[gOVAxKG6P NGfBeoczPTF{OES1OS=>
BT474 MoflS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3LLd|UxOCCwTR?= MlvhNVDjiJNzNdMg[C=> NFzOOIpz\WS3Y3XzJINmdGxiZ4Lve5RpKGmwIITo[UBnd3W{IHzpcoV{KGGwZDDzbYdvcW[rY3HueIx6 MlnINlUyOjh2NUW=
SKBR3 M1\BXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MofFOVAxKG6P M2CyR|Ex6oDVMUZCpIQ> MYfy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M1TGSFI2OTJ6NEW1
AU565 Mk\6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYHkeJhuPTByIH7N M4Plb|Ex6oDVMUZCpIQ> M1rwfJJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> M3u2[|I2OTJ6NEW1
EFM192A Ml21S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3LXOFUxOCCwTR?= NHrsSlgyOOLCk{G1xsBl M3jSUJJm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NUThR5RIOjVzMki0OVU>
MDA-MB-231 NF;0cINHfW6ldHnvckBCe3OjeR?= MWOxNE8zOC92MDFOwG0> M37iT|I1KGh? M4DVcIlv[3KnYYPld{BxNUGNVDDs[ZZmdHNiaX6gZUBld3OnLXTldIVv\GWwdDDtZY5v\XJ? MmTNNlQ1OjBzNUK=
MDA-MB-231 M4S2bmNmdGxiVnnhZoltcXS7IFHzd4F6 M1\Id|AvOS12MDFOwG0> NETEZ|czPCCq NHnj[YNKSzVy4pEJQgKBkTF5Lke3xsDPxE1? NWnLTHEyOjR2MkCxOVI>
MDA-MB-231 NIrIdpVCeG:ydH;zbZMhSXO|YYm= MUexNE8zOC92MDFOwG0> NXntT4xCOjRiaB?= Mn36bY5lfWOnczDhdI9xfG:|aYOg[I9{\SCmZYDlcoRmdnSueR?= Mn3oNlQ1OjBzNUK=
MDA-MB-231 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYj3fnlkOTBxMkCvOFAh|ryP NYfE[Zl1OjRiaB?= M17iV4Jtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9vKGmwIFeyM20heGijc3W= M1HqU|I1PDJyMUWy
H460 NGLZ[mdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk\COFAxKG6P MUCyOOKhcA>? Mn;rbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= MnW2NlQ1OTF4MUG=
A549  MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2fGRVQxOCCwTR?= MnrDNlTDqGh? Mn3SbY5kemWjc3XzJINmdGy3bHHyJJJi\Gmxc3Xud4l1cX[rdIm= NYCwUGhGOjR2MUG2NVE>
DT40 NGnXUI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX3JR|UxRTJzIH7N M3nvWVI1OzV4OEGz
DU145 M4\VNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIXIUWFKSzVyPUG4JI5O NF[yPJIzPDN3NkixNy=>
COLO704 NEH5O3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmjOTWM2OD1{LkWyJOKyKDBwNkeg{txO MmPHNlM4Ojl2MEK=
OVMANAb Ml3tS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFroU25KSzVyPUKuOVghyrFiMD6zPEDPxE1? NYDTV45SOjN5Mkm0NFI>
OV177 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MU\JR|UxRTJwN{igxtEhOC55MTFOwG0> M4rQT|I{PzJ7NECy
OAW28 NEi4WJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1TseWlEPTB;Mz62NUDDuSByLkK4JO69VQ>? MX:yN|czQTRyMh?=
OVSAHO NX3NSo16T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVfJR|UxRTNwNkSgxtEhOC5|MzFOwG0> NVXPRnlyOjN5Mkm0NFI>
OVKATE M2Tnemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MofOTWM2OD1|Lk[0JOKyKDFwN{mg{txO MWqyN|czQTRyMh?=
OVCAR3 NUPuR4FJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MofHTWM2OD1|Lke0JOKyKDBwNECg{txO M2DNZVI{PzJ7NECy
PEO14 M{LQWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2nZWmlEPTB;Mz64OEDDuSByLke2JO69VQ>? NVLlR2JzOjN5Mkm0NFI>
A2780 NYfmWHlDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWTyNZF6UUN3ME2zMlk1KMLzIECuNlUh|ryP NULoVZVbOjN5Mkm0NFI>
OVTOKO MljVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUTBOIRGUUN3ME20MlE1KMLzIEGuOVMh|ryP NYHGV2gxOjN5Mkm0NFI>
KURAMOCHIb NE[1ZYxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkXuTWM2OD12LkO0JOKyKDBwMkmg{txO NH3zdGEzOzd{OUSwNi=>
TOV21G M2nnPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlT2TWM2OD13LkC3JOKyKDFwM{Cg{txO NFLobmMzOzd{OUSwNi=>
OVISE MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3f0NWlEPTB;NT62PEDDuSByLkKzJO69VQ>? Mm\aNlM4Ojl2MEK=
KK M4LrUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHETWM2OD14LkG1JOKyKDFwNEKg{txO NHTofmkzOzd{OUSwNi=>
RMUGS MoOzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MU\JR|UxRTdwMEOgxtEhOS56MzFOwG0> M2K2XlI{PzJ7NECy
PEO6 Ml:5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3zrOmlEPTB;Nz6wOkDDuSByLke0JO69VQ>? M120TFI{PzJ7NECy
OVCA429 M3fFPGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFPxU|dKSzVyPUiuNlkhyrFiMT62OEDPxE1? NUXndXBjOjN5Mkm0NFI>
OV167 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUHJR|UxRThwM{OgxtEhOS5zODFOwG0> NFzPdpIzOzd{OUSwNi=>
RMG1 M4\vO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MorsTWM2OD17LkOyJOKyKDJwM{[g{txO MlTBNlM4Ojl2MEK=
OVCAR5 NVXheHF3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mlr5TWM2OD17LkWwJOKyKDJwNUmg{txO MVSyN|czQTRyMh?=
EFO21 NX:zfoNpT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmP6TWM2OD17LkmyJOKyKDFwOEeg{txO M4rjV|I{PzJ7NECy
ES2 NV;kXXU6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX3iXHZGUUN3ME2xNE4yOiEEsTCxMlI{KM7:TR?= NF3jV40zOzd{OUSwNi=>
Tyk-nu NEnKS5BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnzQTWM2OD1zMD6yNEDDuSBzLkGyJO69VQ>? NYfu[XFEOjN5Mkm0NFI>
CAOV3 NHKzdGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFTIb|ZKSzVyPUGwMlM4KMLzIECuPFch|ryP Ml:1NlM4Ojl2MEK=
OV207 M1\iOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWfyVW97UUN3ME2xNk4zPyEEsTCwMlMzKM7:TR?= MmDUNlM4Ojl2MEK=
HEY M2HLbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{\R[GlEPTB;MUOuNFEhyrFiMD63OUDPxE1? M3nrb|I{PzJ7NECy
DOV13 NITBNIFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGC3fFRKSzVyPkG1JO69VQ>? NYC4ZWVjOjN5Mkm0NFI>
EFO27 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV7JR|UxRjF3IN88US=> MW[yN|czQTRyMh?=
HEY C2 NX3JOWdtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M373TWlEPTB-MUWg{txO M3PH[lI{PzJ7NECy
KOC-7cc MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH3EcnVKSzVyPkG1JO69VQ>? MWqyN|czQTRyMh?=
MCASb NX7r[2R[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX7JR|UxRjF3IN88US=> NEjuOIEzOzd{OUSwNi=>
OAW42 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVHJR|UxRjF3IN88US=> MUKyN|czQTRyMh?=
OV2008 NGGyclFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1fGR2lEPTB-MUWg{txO MUCyN|czQTRyMh?=
OV90 MmnoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoDwTWM2OD5zNTFOwG0> MlzQNlM4Ojl2MEK=
OVCA420b MlTuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlXJTWM2OD5zNTFOwG0> M4HicFI{PzJ7NECy
OVCA432 NXXiZ4RmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mmf4TWM2OD5zNTFOwG0> MYmyN|czQTRyMh?=
PEA2 MnPqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH:xOmRKSzVyPkG1JO69VQ>? NVLJW5lPOjN5Mkm0NFI>
SKOV3 MnHhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnLaTWM2OD5zNTFOwG0> MVmyN|czQTRyMh?=
TOV112D M{DF[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHzjO2QxNTNizszN MYHJR|UxRjF3IN88US=> MmHCNlM4Ojl2MEK=
C4-2 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXXteHJGOC1|IN88US=> M1fwO|E1KGR? NYrDO2U2TE2VTx?= NVj3S|hW\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NGXCO2QzOzV4NUK0OC=>
PC3 M4jGWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NITjbI8xNTNizszN M4j1NlE1KGR? MXfEUXNQ NGfNU2Vl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 M2Tab|I{PTZ3MkS0
DU145 NVOze2JlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1frNVAuOyEQvF2= NXH4VFlvOTRiZB?= MonVSG1UVw>? NFrFfWll\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NFTYTVYzOzV4NUK0OC=>
VCaP  MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn\ZNE0{KM7:TR?= NYHqcVFSOTRiZB?= M{O3eGROW09? NUDzV5dY\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= MWeyN|U3PTJ2NB?=
LNCaP  MljUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXOwMVMh|ryP NIGwS|EyPCCm MnrNSG1UVw>? M4DheoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M2PPdlI{PTZ3MkS0
MDA-MB-468 NYSz[IVkS2WubDDWbYFjcWyrdImgRZN{[Xl? NH:yWFlKSzVyPUmuO{DPxE1? MoHsNlI3PzhzNkG=
MDA-MB-231 Mm\ER4VtdCCYaXHibYxqfHliQYPzZZk> MVnJR|UxRTF|IN88US=> NWnVdINTOjJ4N{ixOlE>
Cal-51 NIW2PZNE\WyuIG\pZYJqdGm2eTDBd5NigQ>? M3HGVGlEPTB;OD62JO69VQ>? MUiyNlY4QDF4MR?=

... 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]
- Collapse

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]
- Collapse
  • 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]
- Collapse
  • 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 PF-01367338
Smiles CNCC1=CC=C(C=C1)C2=C3CCNC(=O)C4=CC(=CC(=C34)[NH]2)F.O[P](O)(O)=O

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03954366 Recruiting Drug: Rucaparib|Drug: Rosuvastatin|Drug: Oral Contraceptives Neoplasms Clovis Oncology Inc. May 8 2019 Phase 1
NCT03824704 Recruiting Drug: Rucaparib|Drug: Nivolumab Epithelial Ovarian Cancer|Fallopian Tube Cancer|Primary Peritoneal Carcinoma|High Grade Serous Carcinoma|Endometrioid Adenocarcinoma Clovis Oncology Inc.|Bristol-Myers Squibb|Foundation Medicine May 15 2019 Phase 2
NCT03413995 Recruiting Drug: Rucaparib Prostate Cancer Metastatic Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins|Clovis Oncology Inc. September 10 2018 Phase 2
NCT03572478 Recruiting Drug: Rucaparib|Drug: Nivolumab Prostate Cancer|Endometrial Cancer University of Chicago|Bristol-Myers Squibb|Clovis Oncology Inc. August 14 2018 Phase 1|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 Products

  • 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)

    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