Rucaparib (AG-014699) phosphate

For research use only.

Catalog No.S1098 Synonyms: PF-01367338

77 publications

Rucaparib (AG-014699) phosphate Chemical Structure

CAS No. 459868-92-9

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 77 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 NH7GeHlHfW6ldHnvckBCe3OjeR?= M4jBSVAvOS9zL{WwNE8yODByIH7N NXTo[2J7cW6qaXLpeJMhWEGUUDDhZ5Rqfmm2eTDheEB{fGG{dHnu[{Bkd26lZYLueJJifGmxbjDv[kA2ODBibl2= M4PaTlI2OTJ6NEW1
BT474 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn3QOVAxKG6P M4HGZlEx6oDVMUZCpIQ> NULZVo5GemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? NYXsfmZXOjVzMki0OVU>
SKBR3 NWjrXldnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGTsWWE2ODBibl2= NWO0[JE2OTEkgKOxOeKh\A>? MnnTdoVlfWOnczDj[YxtKGe{b4f0bEBqdiC2aHWg[o92eiCuaX7ld{BidmRic3nncolncWOjboTsfS=> MnjLNlUyOjh2NUW=
AU565 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NELZPYY2ODBibl2= MnHmNVDjiJNzNdMg[C=> MXLy[YR2[2W|IHPlcIwh\3Kxd4ToJIlvKHSqZTDmc5VzKGyrbnXzJIFv\CC|aXfubYZq[2GwdHz5 Mn3VNlUyOjh2NUW=
EFM192A MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUHmZoxoPTByIH7N NIPKSWIyOOLCk{G1xsBl NVvGd2VkemWmdXPld{Bk\WyuIHfyc5d1cCCrbjD0bIUh\m:3cjDsbY5meyCjbnSgd4lodmmoaXPhcpRtgQ>? MlvaNlUyOjh2NUW=
MDA-MB-231 MWPGeY5kfGmxbjDBd5NigQ>? M121ZlExNzJyL{SwJO69VQ>? NXH5Xm9qOjRiaB?= MlHLbY5kemWjc3XzJJAuSUuWIHzleoVteyCrbjDhJIRwe2VvZHXw[Y5l\W62IH3hco5meg>? MWOyOFQzODF3Mh?=
MDA-MB-231 MmT1R4VtdCCYaXHibYxqfHliQYPzZZk> MkTkNE4yNTRyIN88US=> MY[yOEBp MXzJR|Ux6oDLPfMAjVE4Njd5wrFOwG0> NYTNZYVWOjR2MkCxOVI>
MDA-MB-231 MYfBdI9xfG:|aYOgRZN{[Xl? MXqxNE8zOC92MDFOwG0> NUfkelhFOjRiaB?= NFr6eWRqdmS3Y3XzJIFxd3C2b4Ppd{Bld3OnIHTldIVv\GWwdHz5 M4rZTlI1PDJyMUWy
MDA-MB-231 NX3tfmdrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3nNcVExNzJyL{SwJO69VQ>? MoPpNlQhcA>? MmjaZoxw[2u|IHPlcIwh[3mlbHWgdJJw\3Knc4Ppc44hcW5iR{KvUUBxcGG|ZR?= NFTjcZQzPDR{MEG1Ni=>
H460 NIi2WnBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NITtOYo1ODBibl2= NFHnV|gzPMLiaB?= M3HHXolv[3KnYYPld{Bk\WyudXzhdkBz[WSrb4PlcpNqfGm4aYT5 MYCyOFQyOTZzMR?=
A549  NU[5XXp4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWS0NFAhdk1? MmjHNlTDqGh? NELBfW1qdmO{ZXHz[ZMh[2WubIXsZZIhemGmaX;z[Y5{cXSrdnn0fS=> NVj0Rnk2OjR2MUG2NVE>
DT40 M4f6e2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGTkOopKSzVyPUKxJI5O NIrodVUzPDN3NkixNy=>
DU145 NWX2[Yx7T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1XaeGlEPTB;MUigcm0> NFfFWngzPDN3NkixNy=>
COLO704 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlnZTWM2OD1{LkWyJOKyKDBwNkeg{txO MkPKNlM4Ojl2MEK=
OVMANAb MnK1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NE\1U2tKSzVyPUKuOVghyrFiMD6zPEDPxE1? MV:yN|czQTRyMh?=
OV177 MnTKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mmr2TWM2OD1{Lke4JOKyKDBwN{Gg{txO MnLnNlM4Ojl2MEK=
OAW28 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4\aXGlEPTB;Mz62NUDDuSByLkK4JO69VQ>? NIXmUWgzOzd{OUSwNi=>
OVSAHO M3fRfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1fTVmlEPTB;Mz62OEDDuSByLkOzJO69VQ>? MVeyN|czQTRyMh?=
OVKATE NFPBZ5RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnzQTWM2OD1|Lk[0JOKyKDFwN{mg{txO NIfCOVIzOzd{OUSwNi=>
OVCAR3 M{jvdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoPhTWM2OD1|Lke0JOKyKDBwNECg{txO MV:yN|czQTRyMh?=
PEO14 M1fiVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmT5TWM2OD1|Lki0JOKyKDBwN{[g{txO MlzVNlM4Ojl2MEK=
A2780 NXXxOFhnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml;hTWM2OD1|Lkm0JOKyKDBwMkWg{txO MnKwNlM4Ojl2MEK=
OVTOKO NH\hUYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEC1RZVKSzVyPUSuNVQhyrFiMT61N{DPxE1? MoS0NlM4Ojl2MEK=
KURAMOCHIb NWrqOnU4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlPITWM2OD12LkO0JOKyKDBwMkmg{txO MnHBNlM4Ojl2MEK=
TOV21G M1jQUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXNTWM2OD13LkC3JOKyKDFwM{Cg{txO NFTRc|QzOzd{OUSwNi=>
OVISE Moe1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3f0fmlEPTB;NT62PEDDuSByLkKzJO69VQ>? Mnv1NlM4Ojl2MEK=
KK MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFrzeWlKSzVyPU[uNVUhyrFiMT60NkDPxE1? NWniPYx6OjN5Mkm0NFI>
RMUGS NELCNZlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlXXTWM2OD15LkCzJOKyKDFwOEOg{txO MmnsNlM4Ojl2MEK=
PEO6 NEjT[YFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4PvOGlEPTB;Nz6wOkDDuSByLke0JO69VQ>? M1rpblI{PzJ7NECy
OVCA429 M2\NW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnjkTWM2OD16LkK5JOKyKDFwNkSg{txO NWfjc4pvOjN5Mkm0NFI>
OV167 NFLzT3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV3Ffo1QUUN3ME24MlM{KMLzIEGuNVgh|ryP MlT6NlM4Ojl2MEK=
RMG1 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3PkWmlEPTB;OT6zNkDDuSB{LkO2JO69VQ>? NGXmSVgzOzd{OUSwNi=>
OVCAR5 M2PtT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUn4Uo9WUUN3ME25MlUxKMLzIEKuOVkh|ryP MVqyN|czQTRyMh?=
EFO21 NFnMSlBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml64TWM2OD17LkmyJOKyKDFwOEeg{txO MnH1NlM4Ojl2MEK=
ES2 MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXnJR|UxRTFyLkGyJOKyKDFwMkOg{txO MXeyN|czQTRyMh?=
Tyk-nu NEP3V3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17rOGlEPTB;MUCuNlAhyrFiMT6xNkDPxE1? MnjRNlM4Ojl2MEK=
CAOV3 MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH7heFZKSzVyPUGwMlM4KMLzIECuPFch|ryP NUS1SpdQOjN5Mkm0NFI>
OV207 MnTWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYXJR|UxRTF{LkK3JOKyKDBwM{Kg{txO MX:yN|czQTRyMh?=
HEY NYDUfppZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3fzUGlEPTB;MUOuNFEhyrFiMD63OUDPxE1? M1HXelI{PzJ7NECy
DOV13 NXHMOJZWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoDpTWM2OD5zNTFOwG0> NVW5b3htOjN5Mkm0NFI>
EFO27 NFezeFZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGX5bnpKSzVyPkG1JO69VQ>? NELZ[|EzOzd{OUSwNi=>
HEY C2 NHTjT2lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1\4UmlEPTB-MUWg{txO M3S5VlI{PzJ7NECy
KOC-7cc NXrpT|ltT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NIfpfWFKSzVyPkG1JO69VQ>? MYSyN|czQTRyMh?=
MCASb NIT0RVlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH;ySoNKSzVyPkG1JO69VQ>? Mn[2NlM4Ojl2MEK=
OAW42 MW\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1LNU2lEPTB-MUWg{txO NIq2W3EzOzd{OUSwNi=>
OV2008 NF3Y[4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRjF3IN88US=> MXKyN|czQTRyMh?=
OV90 M3WzW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWnrWWozUUN3ME6xOUDPxE1? MVSyN|czQTRyMh?=
OVCA420b MojWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2nTSWlEPTB-MUWg{txO Mn7UNlM4Ojl2MEK=
OVCA432 M17ybmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGXTXJBKSzVyPkG1JO69VQ>? M2TPfFI{PzJ7NECy
PEA2 MnHFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkPOTWM2OD5zNTFOwG0> NEjseVAzOzd{OUSwNi=>
SKOV3 MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIL3fnhKSzVyPkG1JO69VQ>? MYqyN|czQTRyMh?=
TOV112D MmX4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVSwMVMh|ryP NHLP[GRKSzVyPkG1JO69VQ>? MlH0NlM4Ojl2MEK=
C4-2 M33iUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rVdVAuOyEQvF2= M4KwN|E1KGR? NI\YR2FFVVOR M1fLVYRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M4[4XlI{PTZ3MkS0
PC3 M{fwfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVjhSoNKOC1|IN88US=> MoDONVQh\A>? M3LsdmROW09? NH71NIVl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 MlrONlM2PjV{NES=
DU145 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXXlW|ZtOC1|IN88US=> MXWxOEBl MXjEUXNQ NGX4SJhl\WO{ZXHz[ZMh[2:ub375JI52dWKncjDkc5NmKGSncHXu[IVvfGy7 NVXzSGFQOjN3NkWyOFQ>
VCaP  MofrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYDQT5I5OC1|IN88US=> NHrjZ2kyPCCm Mmq0SG1UVw>? M3K4ToRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? M{PXSFI{PTZ3MkS0
LNCaP  NUP0OZJ5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2PiV|AuOyEQvF2= NGHrSGgyPCCm M3rGcGROW09? M1nOVoRm[3KnYYPld{Bkd2yxbomgcpVu[mW{IHTvd4Uh\GWyZX7k[Y51dHl? NWezfJc{OjN3NkWyOFQ>
MDA-MB-468 NUD3ZZpRS2WubDDWbYFjcWyrdImgRZN{[Xl? M4XKZWlEPTB;OT63JO69VQ>? NXjocHRyOjJ4N{ixOlE>
MDA-MB-231 M3;vZmNmdGxiVnnhZoltcXS7IFHzd4F6 M1[4SGlEPTB;MUOg{txO NGjhUo4zOjZ5OEG2NS=>
Cal-51 MmTNR4VtdCCYaXHibYxqfHliQYPzZZk> MYHJR|UxRThwNjFOwG0> MlX5NlI3PzhzNkG=

... 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=C3C(=CC(=C4)F)N2.OP(=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, NSC 737664) 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, NSC-746045, IND-71677) 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