Rucaparib (AG-014699) phosphate

For research use only.

Catalog No.S1098 Synonyms: PF-01367338

69 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 69 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 MlfVSpVv[3Srb36gRZN{[Xl? MlO2NE4yNzFxNUCwM|ExODBibl2= NEDiT2FqdmirYnn0d{BRSVKSIHHjeIl3cXS7IHH0JJN1[XK2aX7nJINwdmOncn70doF1cW:wIH;mJFUxOCCwTR?= M163UVI2OTJ6NEW1
BT474 M2m1TGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUf5VplWPTByIH7N NE[2SnEyOOLCk{G1xsBl MoXkdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> M{OxPFI2OTJ6NEW1
SKBR3 NF3vSnhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHe1dZo2ODBibl2= MYWxNQKBmzF3wrDk MUHy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 M{jLb|I2OTJ6NEW1
AU565 NEHtO4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoPCOVAxKG6P M2jKUFEx6oDVMUZCpIQ> NWfHc5ZVemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MVWyOVEzQDR3NR?=
EFM192A NXfWcXFsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXi1NFAhdk1? MorCNVDjiJNzNdMg[C=> NXrjWW8{emWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NWHYRYFTOjVzMki0OVU>
MDA-MB-231 MoDSSpVv[3Srb36gRZN{[Xl? M1\pPVExNzJyL{SwJO69VQ>? NUWwRXFsOjRiaB?= NF[wNpJqdmO{ZXHz[ZMheC2DS2SgcIV3\Wy|IHnuJIEh\G:|ZT3k[ZBmdmSnboSgcYFvdmW{ MVGyOFQzODF3Mh?=
MDA-MB-231 NGiwW4NE\WyuIG\pZYJqdGm2eTDBd5NigQ>? NGfNd4wxNjFvNECg{txO NFTTfHUzPCCq MnzGTWM2OOLCiU5ihKkyPy55N9Mg{txO M3OxV|I1PDJyMUWy
MDA-MB-231 MUTBdI9xfG:|aYOgRZN{[Xl? MVqxNE8zOC92MDFOwG0> NF;rcVMzPCCq Ml:zbY5lfWOnczDhdI9xfG:|aYOg[I9{\SCmZYDlcoRmdnSueR?= MVOyOFQzODF3Mh?=
MDA-MB-231 MlLpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4XjPVExNzJyL{SwJO69VQ>? NUDWRlBNOjRiaB?= M4S1[IJtd2OtczDj[YxtKGO7Y3zlJJBzd2e{ZYPzbY9vKGmwIFeyM20heGijc3W= M3ThT|I1PDJyMUWy
H460 NGTFO2tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml:2OFAxKG6P NGDse|YzPMLiaB?= NIrxRoVqdmO{ZXHz[ZMh[2WubIXsZZIhemGmaX;z[Y5{cXSrdnn0fS=> NEnoRlUzPDRzMU[xNS=>
A549  NHHDVldIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXS0NFAhdk1? MVuyOOKhcA>? M2DHTolv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 NYrlVpF6OjR2MUG2NVE>
DT40 MljkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUDJR|UxRTJzIH7N MXuyOFM2PjhzMx?=
DU145 NWTRcGdXT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWDOclJEUUN3ME2xPEBvVQ>? MUWyOFM2PjhzMx?=
COLO704 NHnLWYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWLJR|UxRTJwNUKgxtEhOC54NzFOwG0> NXHpU|ROOjN5Mkm0NFI>
OVMANAb Mmf2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MV3JR|UxRTJwNUigxtEhOC5|ODFOwG0> MYGyN|czQTRyMh?=
OV177 Mn7nS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoS4TWM2OD1{Lke4JOKyKDBwN{Gg{txO NX7tT5lUOjN5Mkm0NFI>
OAW28 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX\JR|UxRTNwNkGgxtEhOC5{ODFOwG0> M1zZUVI{PzJ7NECy
OVSAHO NYC1cIVsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUGzPFA2UUN3ME2zMlY1KMLzIECuN|Mh|ryP MkWyNlM4Ojl2MEK=
OVKATE MUDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXXJR|UxRTNwNkSgxtEhOS55OTFOwG0> NEfnb28zOzd{OUSwNi=>
OVCAR3 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUfmRZVXUUN3ME2zMlc1KMLzIECuOFAh|ryP NEjvV2YzOzd{OUSwNi=>
PEO14 MlHXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX;mZ4VNUUN3ME2zMlg1KMLzIECuO|Yh|ryP MUeyN|czQTRyMh?=
A2780 M3ruWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH7KOFBKSzVyPUOuPVQhyrFiMD6yOUDPxE1? M1q1bVI{PzJ7NECy
OVTOKO MkXFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEHvVpJKSzVyPUSuNVQhyrFiMT61N{DPxE1? NYrH[FhSOjN5Mkm0NFI>
KURAMOCHIb Mo[xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{XIRmlEPTB;ND6zOEDDuSByLkK5JO69VQ>? NFWy[3kzOzd{OUSwNi=>
TOV21G NGn2W2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUn0W2tMUUN3ME21MlA4KMLzIEGuN|Ah|ryP NFPQdZczOzd{OUSwNi=>
OVISE NGLkPWpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4jCZ2lEPTB;NT62PEDDuSByLkKzJO69VQ>? MXyyN|czQTRyMh?=
KK MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYXSZVlNUUN3ME22MlE2KMLzIEGuOFIh|ryP MXyyN|czQTRyMh?=
RMUGS NFvBXo5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MU\JR|UxRTdwMEOgxtEhOS56MzFOwG0> NUHLTlNVOjN5Mkm0NFI>
PEO6 NHKwR3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkPUTWM2OD15LkC2JOKyKDBwN{Sg{txO M2nVbFI{PzJ7NECy
OVCA429 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{XrZ2lEPTB;OD6yPUDDuSBzLk[0JO69VQ>? MVSyN|czQTRyMh?=
OV167 NFy1VWFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4fSbWlEPTB;OD6zN{DDuSBzLkG4JO69VQ>? MmrTNlM4Ojl2MEK=
RMG1 M3qyV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFLZb2ZKSzVyPUmuN|IhyrFiMj6zOkDPxE1? NF\IXlczOzd{OUSwNi=>
OVCAR5 M3vlZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVrJR|UxRTlwNUCgxtEhOi53OTFOwG0> MkHmNlM4Ojl2MEK=
EFO21 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXz3b|Q1UUN3ME25MlkzKMLzIEGuPFch|ryP NXSwT|BFOjN5Mkm0NFI>
ES2 NGXLTXpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXrhb29nUUN3ME2xNE4yOiEEsTCxMlI{KM7:TR?= MWKyN|czQTRyMh?=
Tyk-nu MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4j6PWlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? M1LEb|I{PzJ7NECy
CAOV3 NFezb45Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHXMfoRKSzVyPUGwMlM4KMLzIECuPFch|ryP NH3wT3YzOzd{OUSwNi=>
OV207 M1\EZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX7JR|UxRTF{LkK3JOKyKDBwM{Kg{txO M3zJbFI{PzJ7NECy
HEY MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mkj4TWM2OD1zMz6wNUDDuSByLke1JO69VQ>? NX65W49XOjN5Mkm0NFI>
DOV13 MmnNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF;BVWdKSzVyPkG1JO69VQ>? M{nQOlI{PzJ7NECy
EFO27 NVzVRXFwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIGwUHFKSzVyPkG1JO69VQ>? NHm2NZUzOzd{OUSwNi=>
HEY C2 M33Cbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NE\TXI1KSzVyPkG1JO69VQ>? MXGyN|czQTRyMh?=
KOC-7cc NWi4VIk6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlXZTWM2OD5zNTFOwG0> MUGyN|czQTRyMh?=
MCASb NXr3Vld4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV72enFRUUN3ME6xOUDPxE1? M1vJdVI{PzJ7NECy
OAW42 NXnEU4dGT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\UTWM2OD5zNTFOwG0> MV2yN|czQTRyMh?=
OV2008 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MY\JR|UxRjF3IN88US=> MkK2NlM4Ojl2MEK=
OV90 M4fpS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmPwTWM2OD5zNTFOwG0> NXzo[JFXOjN5Mkm0NFI>
OVCA420b MnS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYPoc3VJUUN3ME6xOUDPxE1? MkDJNlM4Ojl2MEK=
OVCA432 NEPMVHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlS2TWM2OD5zNTFOwG0> NH2wWZIzOzd{OUSwNi=>
PEA2 Mn72S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFvKdoRKSzVyPkG1JO69VQ>? NUGyNFZ[OjN5Mkm0NFI>
SKOV3 Mn7jS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml7HTWM2OD5zNTFOwG0> M2LqfFI{PzJ7NECy
TOV112D M1WyOGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MX2wMVMh|ryP MXXJR|UxRjF3IN88US=> NXj5dllyOjN5Mkm0NFI>
C4-2 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1H6NVAuOyEQvF2= M1rrS|E1KGR? M3u3ZWROW09? MY\k[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 M2DpSFI{PTZ3MkS0
PC3 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFvMR5gxNTNizszN NFrmWFgyPCCm NETPNWxFVVOR NVy5Vnhu\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= M1rLfFI{PTZ3MkS0
DU145 NFvKPYxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFzlTlQxNTNizszN NXT4d3p1OTRiZB?= MlLaSG1UVw>? NX20WYJj\GWlcnXhd4V{KGOxbH;ufUBvfW2kZYKg[I9{\SCmZYDlcoRmdnSueR?= NIHwO|IzOzV4NUK0OC=>
VCaP  NXTmelkzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIrpcYExNTNizszN M{nRVFE1KGR? Mm\DSG1UVw>? MV;k[YNz\WG|ZYOgZ49td267IH71cYJmeiCmb4PlJIRmeGWwZHXueIx6 MoLKNlM2PjV{NES=
LNCaP  NXXaVFBtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MY[wMVMh|ryP NXXy[nk3OTRiZB?= MWHEUXNQ NIrMfXhl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 Mn7PNlM2PjV{NES=
MDA-MB-468 MVfD[YxtKF[rYXLpcIl1gSCDc4PhfS=> MWDJR|UxRTlwNzFOwG0> M1nyOVIzPjd6MU[x
MDA-MB-231 NIrkRZhE\WyuIG\pZYJqdGm2eTDBd5NigQ>? MnPuTWM2OD1zMzFOwG0> NInY[mEzOjZ5OEG2NS=>
Cal-51 NXHrXpVKS2WubDDWbYFjcWyrdImgRZN{[Xl? NVHDSpJVUUN3ME24MlYh|ryP MUmyNlY4QDF4MR?=

... 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