Veliparib (ABT-888)

Catalog No.S1004 Synonyms: NSC 737664

Veliparib (ABT-888) Chemical Structure

Molecular Weight(MW): 244.29

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.

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Cited by 119 Publications

Purity & Quality Control

Choose Selective PARP Inhibitors

Biological Activity

Description 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.
Targets
PARP2 [1]
(Cell-free assay)		 PARP1 [1]
(Cell-free assay)
2.9 nM(Ki) 5.2 nM(Ki)
In vitro

ABT-888 is inactive to SIRT2 (>5 μM). [1] ABT-888 inhibits the PARP activity with EC50 of 2 nM in C41 cells. [2] ABT-888 could decrease the PAR levels in both irradiated and nonirradiated H460 cells. ABT-888 also reduces clonogenic survival and inhibits DNA repair by PARP-1 inhibition in H460 cells. ABT-888 increases apoptosis and autophagy in H460 cells when combination with radiation. [3] ABT-888 also inhibits PARP activity in H1299, DU145 and 22RV1 cells and the inhibition is independent of p53 function. ABT-888 (10 μM) suppresses the surviving fraction (SF) by 43% in the clonogenic H1299 cells. ABT-888 shows effective radiosensitivity in oxic H1299 cells. Furthermore, ABT-888 could attenuate the SF of hypoxic-irradiated cells including H1299, DU145 and 22RV1. [4]
Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
C41 M4S1emtqdmG|ZTDBd5NigQ>? NY\uXJlrOzBibXnu NFG1dnlKdmirYnn0bY9vKG:oIGDBVnAyKHerdHigSWM2OCCxZjCwMlAxOiEQvF2= MkDPNVk5QDh5NkC=
Jurkat MVXLbY5ie2ViQYPzZZk> NInEO446PiCq MXfEUXNQ MmLGTY5pcWKrdHnvckBw\iCSQWLQNUBie3Onc4Pl[EBieyC{ZXT1Z5Rqd25ib3[gZ4VtdCC4aXHibYxqfHlid3n0bEBGSzVyIH;mJFMh|ryP NX73NHMyOjN6NUCxPVk>
Capan1 M3;T[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUXTV|F2PzJiaB?= NFrHeGhFVVOR MXzBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IFLSR2EzKGenbnWgcZV1[XSnZDDoeY1idiCFYYDhclEh[2WubIOge4l1cCCLQ{WwJI9nKDN7Lkeg{txO MXWyOFM6QDN6Mx?=
DT40 MUXDfZRwfG:6aXOgRZN{[Xl? M2CwZVczKGh? MUTEUXNQ NEG1RXlEgXSxdH;4bYNqfHliYXfhbY5{fCClaHnjb4VvKEKUQ1GyMYRm\mmlaXXueEBFXDRyIHPlcIx{ NWTQXZVyOjR7MkK1PFc>
ML-1 MXvBdI9xfG:2aXOgRZN{[Xl? Ml\VNk42KM7:TR?= NGXtNIozPCCq NXz0WGZFTE2VTx?= NFq3c3NUgW6ncnfpd5Rq[2GubImg[Y5p[W6lZYOgWHJCUUxvaX7keYNm\CCjcH;weI9{cXNiaX6gUWwuOSClZXzsdy=> M1zUNVI1QDl3MUO1
HCT-116 M3vnUmtqdmG|ZTDBd5NigQ>? NFH4WmMxNjVizszN Mn:zNlQhcA>? M4Li[XBCWlBiYXP0bZZqfHliZHXjdoVie2W| NIG5V3QzOzB3NEKxNy=>
UM-SCC1 NUHsbVJTS3m2b4TvfIlkKEG|c3H5 M{\xO|ExKM7:TR?= M1L3c|I1KGh? MUnS[YR2[2W|IITo[UBk\WyuII\pZYJqdGm2eR?= NXOyTlJROjF7MUK2NlA>
FaDu MYjDfZRwfG:6aXOgRZN{[Xl? M2LBXFExKM7:TR?= MmPKNlQhcA>? MljBVoVlfWOnczD0bIUh[2WubDD2bYFjcWyrdIm= MmDGNlE6OTJ4MkC=
PC-3 NIW3OW5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1rqPFExKM7:TR?= NEfQXoJKdmS3Y3XzJIEhe2mpbnnmbYNidnRiaX7obYJqfGmxbjDpckBkd2yxbomg[o9zdWG2aX;uxsA> NGfBc28zOTV5MUmxNi=>
EoL-1-cell NYD4SmtqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mmf5TWM2OD1zLkC3PVgh|ryP MYDTRW5ITVJ?
NCI-SNU-5 MkXaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUHJR|UxRTNwMUK4OFEh|ryP MmrhV2FPT0WU
BV-173 NEnUNoZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYTJR|UxRTVwNEW0NFkh|ryP M{DWXnNCVkeHUh?=
HCC1806 M3mzcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFm2V|lKSzVyPUWuO|UyPzNizszN Ml\aV2FPT0WU
COLO-680 NFnKVJpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3qxcGlEPTB;Nj6yNVQxPiEQvF2= NUXDWmIxW0GQR1XS
HCC2218 NI[zUVJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX\QU2xCUUN3ME23Mlc6PzB2IN88US=> M1HDUHNCVkeHUh?=
SK-MEL-24 NXr1bo5XT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnzXTWM2OD15LkixPVI1KM7:TR?= NImwe2ZUSU6JRWK=
NCI-H720 Mm[wS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWDCN3lmUUN3ME24MlQ{PjB|IN88US=> M1fZUnNCVkeHUh?=
KASUMI-1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEjZOolKSzVyPUiuPFkzPjZizszN MULTRW5ITVJ?
HAL-01 NXfQcW9ET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M13jNmlEPTB;OT64PFYzKM7:TR?= NUTJOIZbW0GQR1XS
CAL-33 NETuSHdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUPJR|UxRTFyLkSzOEDPxE1? MVvTRW5ITVJ?
SK-MEL-1 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUTC[opFUUN3ME2xNk41PjZ|IN88US=> MV3TRW5ITVJ?
Ramos-2G6-4C10 M{jmc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFj4S|FKSzVyPUGyMlQ4PTJizszN MnzpV2FPT0WU
KY821 NVX0dm5QT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3GzWGlEPTB;MUKuOFg2KM7:TR?= NYPXfZhrW0GQR1XS
HEC-1 NYLSUW5WT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUfJR|UxRTF{LkmxPVYh|ryP M1noWXNCVkeHUh?=
SK-NEP-1 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVm2NItKUUN3ME2xN{4yPjZizszN MWTTRW5ITVJ?
MN-60 NWTSZWJuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXKydop4UUN3ME2xN{42Ozh7IN88US=> MV7TRW5ITVJ?
DU-145 NH;SVndIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWjJXZdxUUN3ME2xN{46ODV|IN88US=> M{PHS3NCVkeHUh?=
EW-3 Mn[0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYm4VnFMUUN3ME2xOE42PTZ3IN88US=> NGjzbWFUSU6JRWK=
OS-RC-2 MlXoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MkHLTWM2OD1zNT65OVg6KM7:TR?= Ml3TV2FPT0WU
RPMI-8226 NVfGTld4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEPHXVZKSzVyPUG2MlIxPDJizszN M1\rZ3NCVkeHUh?=
ChaGo-K-1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGiwdYlKSzVyPUG2MlU{OjVizszN NIfpRpNUSU6JRWK=
DEL M2rnTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NED2VWFKSzVyPUG2MlY4OTdizszN M3TyNHNCVkeHUh?=
GP5d MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3\iXWlEPTB;MUeuNFU{KM7:TR?= NFvNPHFUSU6JRWK=
COLO-668 M1LsbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3TjO2lEPTB;MUeuOlI6PCEQvF2= MnLyV2FPT0WU
H9 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWnJR|UxRTF6LkK4N|Mh|ryP NX;TXmdrW0GQR1XS
NKM-1 NH;zOYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkP1TWM2OD1zOD61NVE6KM7:TR?= NHvMZlBUSU6JRWK=
KYSE-150 MnnhS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVTJR|UxRTF6Lkm5PFYh|ryP MlnlV2FPT0WU
Daoy M173cGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWDSdWhQUUN3ME2xPU42PjR7IN88US=> NIjRdVRUSU6JRWK=
ECC10 NYHre4Y4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFTicVdKSzVyPUKwMlc1PTVizszN Mn;vV2FPT0WU
A388 NFy0PGxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MVHJR|UxRTJzLkmwPVEh|ryP Ml35V2FPT0WU
MHH-NB-11 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXSy[286UUN3ME2yN{4yOzZ|IN88US=> MVjTRW5ITVJ?
HCC1937 NXLB[Y1QT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYnJR|UxRTJ2Lke0OkDPxE1? MlroV2FPT0WU
TGBC11TKB NFviVmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXzyOYhjUUN3ME2yOU43QDZ|IN88US=> NGP3[mxUSU6JRWK=
CTV-1 M2n4dmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjmTI5KSzVyPUK1Mlg6PjlizszN NIDqbo5USU6JRWK=
NCI-H2029 M1HKW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MljYTWM2OD1{Nj60NlM5KM7:TR?= NXvkUWRCW0GQR1XS
HLE MlvTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVW1N|dCUUN3ME2yO{4xPTRizszN Mn;jV2FPT0WU
NCI-H1693 NHe1V2RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWf4[IYxUUN3ME2yO{4zQDl6IN88US=> NFLPVo1USU6JRWK=
HCC70 MoewS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYfJR|UxRTJ5LkeyOFYh|ryP MnfXV2FPT0WU
BEN MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4HlW2lEPTB;MkeuPVU3PiEQvF2= NX3JSXE4W0GQR1XS
LB771 NWTY[IJ6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2TGOmlEPTB;MkiuPFM4OyEQvF2= NEDkcXBUSU6JRWK=
697 NHHoW2FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIHFOIFKSzVyPUK5MlAzOzVizszN MYrTRW5ITVJ?
LU-139 NIj0WoxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXTFfolyUUN3ME2yPU4{PzR6IN88US=> M1X5RXNCVkeHUh?=
EW-13 MmH2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHn6PFFKSzVyPUK5MlM5OTRizszN M1GyUHNCVkeHUh?=
MOLT-13 NXPzc4NPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXrReJk6UUN3ME2yPU4{QDF2IN88US=> NFfMdFZUSU6JRWK=
L-363 MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF3C[HRKSzVyPUK5MlQ4QThizszN NX3hRnA3W0GQR1XS
EM-2 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXjhO2d3UUN3ME2yPU41QTBzIN88US=> M3rmbnNCVkeHUh?=
RS4-11 NH:zUI9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnTFTWM2OD1|MD60NlQyKM7:TR?= NIjTfYxUSU6JRWK=
A2780 M1e5PGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnLNTWM2OD1|MD63OFU4KM7:TR?= MUnTRW5ITVJ?
KU812 Mnf3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NULxN4hSUUN3ME2zNk4{PjR{IN88US=> MVHTRW5ITVJ?
COLO-684 M1PHfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEPifWNKSzVyPUOzMlM2QTlizszN M2PxUHNCVkeHUh?=
MFE-280 MULHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWrhcYhiUUN3ME2zN{4{QDh7IN88US=> NHq1bJNUSU6JRWK=
KG-1 NFrrdIhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH\vZ41KSzVyPUOzMlYxODFizszN MV\TRW5ITVJ?
JVM-3 NFvOeJVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH;IN5pKSzVyPUO1MlU5PjhizszN MYrTRW5ITVJ?
MV-4-11 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlHETWM2OD1|NT64OFk6KM7:TR?= MmLMV2FPT0WU
LAMA-84 NGDESmlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmS0TWM2OD1|Nj63N|Q2KM7:TR?= M3PrRnNCVkeHUh?=
MOLT-16 NXKxfXBIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYHyVYxRUUN3ME2zOk46PTJizszN MmW0V2FPT0WU
H4 NVvLOZQzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1zscWlEPTB;M{euOVY4KM7:TR?= M3TyNXNCVkeHUh?=
T47D M2DFfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlfBTWM2OD1|Nz63NFE5KM7:TR?= Mn;EV2FPT0WU
CAL-54 NI\VOW5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUPUSmc{UUN3ME2zO{46PjZizszN NF;DN|JUSU6JRWK=
SW982 NETpflRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYnJR|UxRTN6LkC5PVgh|ryP M4LBe3NCVkeHUh?=
IGROV-1 Mkj1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGW5TGJKSzVyPUO5MlM{ODRizszN NXniN|RLW0GQR1XS
NB14 Mk\TS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnfXTWM2OD12MD63NFMyKM7:TR?= MkexV2FPT0WU
HCC1187 MkTTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGfVdXVKSzVyPUSxMlI4PzFizszN MkPSV2FPT0WU
SBC-1 NIPMW5RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVu1OlJpUUN3ME20NU4{ODZ|IN88US=> M2X4VnNCVkeHUh?=
KARPAS-45 MkLrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmjlTWM2OD12MT60PFE5KM7:TR?= MkfiV2FPT0WU
MOLT-4 NWX3OmlKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{TCSGlEPTB;NEKuNlU{QCEQvF2= MkLxV2FPT0WU
JVM-2 NXvzRphkT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3HTUmlEPTB;NEKuPVIxPyEQvF2= Mn7pV2FPT0WU
A4-Fuk MkLqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYr1O|NjUUN3ME20N{42PjlzIN88US=> MWrTRW5ITVJ?
MDA-MB-361 MVzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkC0TWM2OD12Mz64OFE1KM7:TR?= NFKxOXpUSU6JRWK=
BALL-1 NYe1dlNqT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4Czd2lEPTB;NEOuPVU{OiEQvF2= M3qyfXNCVkeHUh?=
T98G NIryUVBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlTsTWM2OD12ND64OVE4KM7:TR?= MlvDV2FPT0WU
Mo-T M3LPWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1jv[2lEPTB;NEWuOlM5QSEQvF2= MXnTRW5ITVJ?
MHH-PREB-1 M4jUbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXfrRXlyUUN3ME20OU44PTh3IN88US=> NHroNmZUSU6JRWK=
ALL-PO M2D3NGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjGTWM2OD12Nz6zO|kyKM7:TR?= M{HkeXNCVkeHUh?=
NCI-H510A NG\C[3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{mzRmlEPTB;NEeuPVA{PCEQvF2= NGPzTmVUSU6JRWK=
ML-2 M1fKNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWiz[4poUUN3ME20PU44QDV4IN88US=> MlKxV2FPT0WU

... Click to View More Cell Line Experimental Data
Assay
Methods Test Index PMID
Western blot
p-STAT3 / STAT3 / p-AKT(S473) / p-AKT(T308) / p-ERK / p-p38; 

PubMed: 22678161     


Effects of AG-014699, AZD-2281, ABT-888, or BSI-201 on the phosphorylation status of Stat3, Akt, ERK, and p38 in MDA-MB-468, MDA-MB-231, and Cal-51 cells after 72 h of treatment

22678161
Immunofluorescence
HuR; 

PubMed: 28687616     


Immunofluorescent images of HuR (green) in MIA PaCa-2 cells treated with PARPi for 12hr. Nuclei were stained with DAPI. Magnification 40X.

BRCA1; 

PubMed: 21917757     


Effects of ABT-888 and/or bortezomib on BRCA1 and RAD51 foci formation. BRCA1 and RAD1 foci induced by ABT-888 were completely resolved in cells cotreated with bortezomib. Image acquisition was performed with an epifluorescence microscope (BX51; Olympus) and multispectral color camera (Nuance FX; CRi) with a 60× or 100× magnification lens and oil immersion.

28687616 21917757
Growth inhibition assay
Cell viability (TNBC cell lines); 

PubMed: 27880910     


BRCA-proficient TNBC cell lines were treated with veliparib in the absence and presence of dinaciclib, demonstrating reduced IC50 values in the presence of dinaciclib.

Cell viability (melanoma cells); 

PubMed: 29956724     


Dose-dependent inhibitory effect of ABT-888 on melanoma cell proliferation. Human melanoma cell lines were exposed to diluents (control; CTRL) or increasing concentrations of ABT-888 for 72 h and their viability was assessed by MTT assay. Absorbance was detected at 540 nm with a microplate reader and data were expressed as a percentage of the CTRL. Data are the means ± SD of 3 experiments performed in triplicate. Statistical significance was calculated against the CTRL (*P<0.05; **P<0.01).

27880910 29956724
In vivo The oral bioavailability of ABT-888 is 56%-92% in mice, Sprague-Dawley rats, beagle dogs, and cynomolgus monkeys after oral administration. [1] ABT-888 (25 mg/kg i.p.) could improve tumor growth delay in a NCI-H460 xenograft model with well tolerated. Combination with radiation, ABT-888 decreases the tumor vessel formation. [3] ABT-888 reduces intratumor PAR levels by more than 95% at a dose of 3 and 12.5 mg/kg in A375 and Colo829 xenograft models and the suppression could be maintained over time. [4]

Protocol

Animal Research:

[1]
- Collapse
  • Animal Models: NCI-H460, H460, B16F10 and 9L xenografts in C57BL/6 mice
  • Formulation: Formulated in solution containing 0.9% NaCl adjusted to pH 4.0
  • Dosages: ~25 mg/kg
  • Administration: Orally administered
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 17 mg/mL (69.58 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
0.5% methylcellulose+0.2% Tween 80
For best results, use promptly after mixing. 		5 mg/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 244.29
Formula

C13H16N4O
CAS No. 912444-00-9
Storage powder
in solvent
Synonyms NSC 737664

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT03044795 Withdrawn Drug: Veliparib Cancer University Medical Center Groningen|AbbVie|Dutch Cancer Society November 2019 Phase 2
NCT02723864 Recruiting Drug: Veliparib + VX-970 + Cisplatin Neoplasms National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) August 9 2017 Phase 1
NCT02483104 Completed Drug: veliparib|Drug: carboplatin|Drug: paclitaxel Ovarian Cancer AbbVie July 2015 Phase 1
NCT01445522 Completed Drug: ABT-888|Drug: Cyclophosphamide Neoplasms|Lymphoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 3 2008 Phase 1
NCT00649207 Completed Drug: ABT-888|Radiation: Whole Brain Radiation Therapy Brain Diseases|Brain Neoplasms|Central Nervous System Diseases|Neoplasm Metastasis|Nervous System Neoplasms AbbVie (prior sponsor Abbott)|AbbVie March 2008 Phase 1
NCT00553189 Completed Drug: ABT-888|Drug: Topotecan Solid Tumors|Lymphomas National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) August 9 2007 Phase 1

Tech Support

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

    BMN 673 : Novel PARP inhibitor with IC50 of 0.58 nM. Also a potent inhibitor of PARP-2, but does not inhibit PARG and highly sensitive to PTEN mutation.

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, 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).

  • Rucaparib (AG-014699,PF-01367338) phosphate

    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.

  • 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