Rucaparib (AG-014699) phosphate

For research use only.

Catalog No.S1098 Synonyms: PF-01367338

68 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 68 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 MnfhSpVv[3Srb36gRZN{[Xl? NWLmRYtjOC5zL{GvOVAxNzFyMECgcm0> NYfCRYhEcW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= NHvJTHozPTF{OES1OS=>
BT474 MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYPzO|U5PTByIH7N NGq1VlkyOOLCk{G1xsBl NUDHNYxyemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NV;BUVAxOjVzMki0OVU>
SKBR3 M3rGUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{Ho[VUxOCCwTR?= Mni2NVDjiJNzNdMg[C=> MVzy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M4fBV|I2OTJ6NEW1
AU565 MlrlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX[1NFAhdk1? M1jVWVEx6oDVMUZCpIQ> M2XwR5Jm\HWlZYOgZ4VtdCCpcn;3eIghcW5idHjlJIZwfXJibHnu[ZMh[W6mIIPp[45q\mmlYX70cJk> NXXlNId6OjVzMki0OVU>
EFM192A NYTzfIZvT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHXhcWU2ODBibl2= Ml\3NVDjiJNzNdMg[C=> NVG3[lR1emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MkjJNlUyOjh2NUW=
MDA-MB-231 M3;zcmZ2dmO2aX;uJGF{e2G7 M4fhWVExNzJyL{SwJO69VQ>? NHHTOYEzPCCq MmfpbY5kemWjc3XzJJAuSUuWIHzleoVteyCrbjDhJIRwe2VvZHXw[Y5l\W62IH3hco5meg>? NELJNFAzPDR{MEG1Ni=>
MDA-MB-231 MkK5R4VtdCCYaXHibYxqfHliQYPzZZk> NIn0NZIxNjFvNECg{txO MlHGNlQhcA>? MoHjTWM2OOLCiU5ihKkyPy55N9Mg{txO NGXyR3IzPDR{MEG1Ni=>
MDA-MB-231 MmXYRZBweHSxc3nzJGF{e2G7 MYexNE8zOC92MDFOwG0> MXiyOEBp NYP3OWxzcW6mdXPld{BieG:ydH;zbZMh\G:|ZTDk[ZBmdmSnboTsfS=> NYj5NmVkOjR2MkCxOVI>
MDA-MB-231 MkP4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlOwNVAwOjBxNECg{txO MV2yOEBp MUDicI9kc3NiY3XscEBkgWOuZTDwdo9oemW|c3nvckBqdiCJMj;NJJBp[XOn MnS5NlQ1OjBzNUK=
H460 Mn7BS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYnKW5BQPDByIH7N M3vrRVI1yqCq NVHVRmkxcW6lcnXhd4V{KGOnbHz1cIFzKHKjZHnvd4Vve2m2aY\peJk> MmTONlQ1OTF4MUG=
A549  MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVS0NFAhdk1? MoPCNlTDqGh? M3vPcIlv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 NEPlNYYzPDRzMU[xNS=>
DT40 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIDkZWZKSzVyPUKxJI5O M4jyNVI1OzV4OEGz
DU145 M{e3Smdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEDEW|JKSzVyPUG4JI5O NFP1SoMzPDN3NkixNy=>
COLO704 NF[1VFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NULtdZh2UUN3ME2yMlUzKMLzIECuOlch|ryP NXHZd4QzOjN5Mkm0NFI>
OVMANAb MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEfhXIhKSzVyPUKuOVghyrFiMD6zPEDPxE1? MVSyN|czQTRyMh?=
OV177 M{PjdWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnnGTWM2OD1{Lke4JOKyKDBwN{Gg{txO M{LGRlI{PzJ7NECy
OAW28 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkHLTWM2OD1|Lk[xJOKyKDBwMkig{txO MX:yN|czQTRyMh?=
OVSAHO NWK2THNMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXroe4RrUUN3ME2zMlY1KMLzIECuN|Mh|ryP MUOyN|czQTRyMh?=
OVKATE MnvCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYXJR|UxRTNwNkSgxtEhOS55OTFOwG0> MYOyN|czQTRyMh?=
OVCAR3 NEm0WWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVv3Xm5mUUN3ME2zMlc1KMLzIECuOFAh|ryP M2DtOlI{PzJ7NECy
PEO14 MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEj0SldKSzVyPUOuPFQhyrFiMD63OkDPxE1? NYX5XldUOjN5Mkm0NFI>
A2780 M3X1[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NULwPZNrUUN3ME2zMlk1KMLzIECuNlUh|ryP Mny0NlM4Ojl2MEK=
OVTOKO NYW4eWtPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVPJR|UxRTRwMUSgxtEhOS53MzFOwG0> NVWzRVFpOjN5Mkm0NFI>
KURAMOCHIb Ml31S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYfuZ3VjUUN3ME20MlM1KMLzIECuNlkh|ryP NGnrWmUzOzd{OUSwNi=>
TOV21G NXTTbFlzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm[1TWM2OD13LkC3JOKyKDFwM{Cg{txO MV6yN|czQTRyMh?=
OVISE MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXfJR|UxRTVwNkigxtEhOC5{MzFOwG0> NE\0NWczOzd{OUSwNi=>
KK NEPUNoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFTmWXNKSzVyPU[uNVUhyrFiMT60NkDPxE1? NF7XRW0zOzd{OUSwNi=>
RMUGS NV;5fGx{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYi5[3pLUUN3ME23MlA{KMLzIEGuPFMh|ryP M4m2OlI{PzJ7NECy
PEO6 MmntS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3HSfWlEPTB;Nz6wOkDDuSByLke0JO69VQ>? MYGyN|czQTRyMh?=
OVCA429 MmPmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVrJR|UxRThwMkmgxtEhOS54NDFOwG0> MlO2NlM4Ojl2MEK=
OV167 NWTkSWh2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{XvbGlEPTB;OD6zN{DDuSBzLkG4JO69VQ>? MUCyN|czQTRyMh?=
RMG1 MnfqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1Wz[GlEPTB;OT6zNkDDuSB{LkO2JO69VQ>? MnTrNlM4Ojl2MEK=
OVCAR5 NIPEU4hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnrCTWM2OD17LkWwJOKyKDJwNUmg{txO MWiyN|czQTRyMh?=
EFO21 NHyx[JlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnzTTWM2OD17LkmyJOKyKDFwOEeg{txO NWHyXnd{OjN5Mkm0NFI>
ES2 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUDJR|UxRTFyLkGyJOKyKDFwMkOg{txO NIf6fVgzOzd{OUSwNi=>
Tyk-nu M1XXe2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnXCTWM2OD1zMD6yNEDDuSBzLkGyJO69VQ>? NYnVU2VsOjN5Mkm0NFI>
CAOV3 NWTEfWpyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlOyTWM2OD1zMD6zO{DDuSByLki3JO69VQ>? M2\uXlI{PzJ7NECy
OV207 M3zRUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUXJR|UxRTF{LkK3JOKyKDBwM{Kg{txO NI\CcFczOzd{OUSwNi=>
HEY NE\uWlhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWixRlgzUUN3ME2xN{4xOSEEsTCwMlc2KM7:TR?= M1vzXVI{PzJ7NECy
DOV13 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVL5R2JpUUN3ME6xOUDPxE1? Mne5NlM4Ojl2MEK=
EFO27 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVrJR|UxRjF3IN88US=> NYLvdGQ2OjN5Mkm0NFI>
HEY C2 NHO3bGxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVvye2doUUN3ME6xOUDPxE1? NEfKRWQzOzd{OUSwNi=>
KOC-7cc MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWPJR|UxRjF3IN88US=> MU[yN|czQTRyMh?=
MCASb NE\LXoNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2[zRWlEPTB-MUWg{txO M3vjelI{PzJ7NECy
OAW42 M37IRWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVLJR|UxRjF3IN88US=> M{\5dFI{PzJ7NECy
OV2008 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MULJR|UxRjF3IN88US=> MmLwNlM4Ojl2MEK=
OV90 MmHCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2fYZmlEPTB-MUWg{txO Ml;uNlM4Ojl2MEK=
OVCA420b MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml;aTWM2OD5zNTFOwG0> MXuyN|czQTRyMh?=
OVCA432 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnzkTWM2OD5zNTFOwG0> NFX0V5UzOzd{OUSwNi=>
PEA2 NIjVT45Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRjF3IN88US=> M3nvSlI{PzJ7NECy
SKOV3 NHLLeHlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1\hbWlEPTB-MUWg{txO NFzPdXUzOzd{OUSwNi=>
TOV112D NUjjV2FtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVi3NWNbOC1|IN88US=> MX;JR|UxRjF3IN88US=> NGX6[lQzOzd{OUSwNi=>
C4-2 Mmr3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFfrUoYxNTNizszN NH72dooyPCCm NFG3flZFVVOR M1XDXoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? MYKyN|U3PTJ2NB?=
PC3 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUXJcogxOC1|IN88US=> M2LUc|E1KGR? MYDEUXNQ NY\M[mxS\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M3T5UVI{PTZ3MkS0
DU145 NIPySHhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1\uN|AuOyEQvF2= MmTyNVQh\A>? MmDHSG1UVw>? M3O4fIRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? MlTONlM2PjV{NES=
VCaP  NXToXVlQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVfiTph1OC1|IN88US=> MWSxOEBl M3jib2ROW09? M3nyOYRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NVXqPY1HOjN3NkWyOFQ>
LNCaP  MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NI[4doQxNTNizszN M3flTVE1KGR? NVjSfYk6TE2VTx?= NHfNdZJl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NIPaPXozOzV4NUK0OC=>
MDA-MB-468 NGiwV|FE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MlXtTWM2OD17Lkeg{txO NFHQb4IzOjZ5OEG2NS=>
MDA-MB-231 NYrUTmd[S2WubDDWbYFjcWyrdImgRZN{[Xl? M3HwdmlEPTB;MUOg{txO NEPqVoczOjZ5OEG2NS=>
Cal-51 MXnD[YxtKF[rYXLpcIl1gSCDc4PhfS=> NIjkNGJKSzVyPUiuOkDPxE1? MnjjNlI3PzhzNkG=

... 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
  • 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
NCT04179396 Recruiting Drug: Rucaparib|Drug: Enzalutamide|Drug: Abiraterone Metastatic Castration Resistant Prostate Cancer Clovis Oncology Inc. December 5 2019 Phase 1
NCT04171700 Recruiting Drug: Rucaparib Solid Tumor Clovis Oncology Inc. November 21 2019 Phase 2
NCT03954366 Active not recruiting Drug: Rucaparib|Drug: Rosuvastatin|Drug: Oral Contraceptives Neoplasms Clovis Oncology Inc. May 8 2019 Phase 1
NCT03824704 Active not 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

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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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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. Olaparib induces significant autophagy that is associated with mitophagy in cells with BRCA mutations.

    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. Veliparib increases autophagy and apoptosis. 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