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 115 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 NFi0UY9McW6jc3WgRZN{[Xl? M4HNc|MxKG2rbh?= NGjmd4dKdmirYnn0bY9vKG:oIGDBVnAyKHerdHigSWM2OCCxZjCwMlAxOiEQvF2= MXyxPVg5QDd4MB?=
Jurkat MkD2T4lv[XOnIFHzd4F6 NGi0XlM6PiCq NVvN[mg4TE2VTx?= MUnJcohq[mm2aX;uJI9nKFCDUmCxJIF{e2W|c3XkJIF{KHKnZIXjeIlwdiCxZjDj[YxtKH[rYXLpcIl1gSC5aYToJGVEPTBib3[gN{DPxE1? M1TiUVI{QDVyMUm5
Capan1 M4XleGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEnuUVY4OiCq NGDW[3VFVVOR M{[yVWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgRnJESTJiZ3Xu[UBufXSjdHXkJIh2dWGwIFPhdIFvOSClZXzsd{B4cXSqIFnDOVAhd2ZiM{muO{DPxE1? NV23eYVnOjR|OUizPFM>
DT40 NHvvbZVEgXSxdH;4bYMhSXO|YYm= Mn7NO|IhcA>? MVvEUXNQ MlrqR5l1d3SxeHnjbZR6KGGpYXnud5Qh[2irY3vlckBDWkODMj3k[YZq[2mnboSgSHQ1OCClZXzsdy=> NHPxZpIzPDl{MkW4Oy=>
ML-1 NXTEXIQ{SXCxcITveIlkKEG|c3H5 NGTKd24zNjVizszN MWeyOEBp MYLEUXNQ NXTaUWV1W3mwZYLnbZN1cWOjbHz5JIVvcGGwY3XzJHRTSUmOLXnu[JVk\WRiYYDvdJRwe2m|IHnuJG1NNTFiY3XscJM> M3\LVVI1QDl3MUO1
HCT-116 NHnLR4tMcW6jc3WgRZN{[Xl? MXywMlUh|ryP MUmyOEBp NHPWbYdRSVKSIHHjeIl3cXS7IHTlZ5Jm[XOncx?= M33GVlI{ODV2MkGz
UM-SCC1 NF2xWVlEgXSxdH;4bYMhSXO|YYm= NIfKSGkyOCEQvF2= M1\3bVI1KGh? Mn;2VoVlfWOnczD0bIUh[2WubDD2bYFjcWyrdIm= MkPkNlE6OTJ4MkC=
FaDu MoW5R5l1d3SxeHnjJGF{e2G7 NW\iXoRUOTBizszN M{njelI1KGh? MnLxVoVlfWOnczD0bIUh[2WubDD2bYFjcWyrdIm= MW[yNVkyOjZ{MB?=
PC-3 MmnlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVPFZXdzOTBizszN NYCxW5dqUW6mdXPld{BiKHOrZ37p[olk[W62IHnubIljcXSrb36gbY4h[2:ub375JIZwem2jdHnvcuKh NF7EcIYzOTV5MUmxNi=>
EoL-1-cell NELB[ppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYjJR|UxRTFwMEe5PEDPxE1? M{LFRnNCVkeHUh?=
NCI-SNU-5 NW\VRplQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnrzTWM2OD1|LkGyPFQyKM7:TR?= NFmy[2RUSU6JRWK=
BV-173 M2DTOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkjGTWM2OD13LkS1OFA6KM7:TR?= NFLBNZdUSU6JRWK=
HCC1806 Ml\SS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Ml;5TWM2OD13Lke1NVc{KM7:TR?= NUTafm5IW0GQR1XS
COLO-680 M1LiXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkO1TWM2OD14LkKxOFA3KM7:TR?= NXjUSoU{W0GQR1XS
HCC2218 NXrPNFF[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmnKTWM2OD15Lke5O|A1KM7:TR?= NIe0NJNUSU6JRWK=
SK-MEL-24 MnzTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXrJR|UxRTdwOEG5NlQh|ryP M2m0N3NCVkeHUh?=
NCI-H720 MnHMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4HofWlEPTB;OD60N|YxOyEQvF2= MoXCV2FPT0WU
KASUMI-1 NFflc2FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIXzRYNKSzVyPUiuPFkzPjZizszN NInvZXNUSU6JRWK=
HAL-01 NV7q[mlTT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvjZ446UUN3ME25Mlg5PjJizszN Mo\YV2FPT0WU
CAL-33 M3XtVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3j4TmlEPTB;MUCuOFM1KM7:TR?= NHHCXGhUSU6JRWK=
SK-MEL-1 M4PjWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoTGTWM2OD1zMj60OlY{KM7:TR?= NUTOfppXW0GQR1XS
Ramos-2G6-4C10 NHvaZ29Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX7X[WZmUUN3ME2xNk41PzV{IN88US=> MXPTRW5ITVJ?
KY821 NFT5RW9Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml7BTWM2OD1zMj60PFUh|ryP M17JeXNCVkeHUh?=
HEC-1 M{DBVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2TSNWlEPTB;MUKuPVE6PiEQvF2= NEK3[IdUSU6JRWK=
SK-NEP-1 NHe2TVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUiyRo42UUN3ME2xN{4yPjZizszN MX\TRW5ITVJ?
MN-60 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUXJR|UxRTF|LkWzPFkh|ryP NFrY[ZFUSU6JRWK=
DU-145 NYHhNnBUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVLJR|UxRTF|LkmwOVMh|ryP NWCyWm11W0GQR1XS
EW-3 NYnBeoI2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnPXTWM2OD1zND61OVY2KM7:TR?= NYPTeoprW0GQR1XS
OS-RC-2 NIHqcGtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEHXdFZKSzVyPUG1Mlk2QDlizszN M{f3UXNCVkeHUh?=
RPMI-8226 NVe0O|dPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2DBcWlEPTB;MU[uNlA1OiEQvF2= M2XXbHNCVkeHUh?=
ChaGo-K-1 M2j2UGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2rZc2lEPTB;MU[uOVMzPSEQvF2= NFjwXJlUSU6JRWK=
DEL Ml3MS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHTuO5FKSzVyPUG2MlY4OTdizszN NFjZfWlUSU6JRWK=
GP5d M3zCdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{HifmlEPTB;MUeuNFU{KM7:TR?= Mn\sV2FPT0WU
COLO-668 NUfrPXRrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NE[5WmFKSzVyPUG3MlYzQTRizszN NInrboxUSU6JRWK=
H9 MoHVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUDCfYdjUUN3ME2xPE4zQDN|IN88US=> NWTDW5lYW0GQR1XS
NKM-1 NVLhd5lQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVvRbGVCUUN3ME2xPE42OTF7IN88US=> NGi1SmZUSU6JRWK=
KYSE-150 MkDDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnXLTWM2OD1zOD65PVg3KM7:TR?= NH3OT3JUSU6JRWK=
Daoy M2\HZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjyXolKSzVyPUG5MlU3PDlizszN NEDKdlJUSU6JRWK=
ECC10 M1r6cmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVXJR|UxRTJyLke0OVUh|ryP NYCyOHpHW0GQR1XS
A388 NFTJW4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF3mVGZKSzVyPUKxMlkxQTFizszN MX;TRW5ITVJ?
MHH-NB-11 NVnLV4Y2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{HsTGlEPTB;MkOuNVM3OyEQvF2= MYLTRW5ITVJ?
HCC1937 MnPJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NInFN|NKSzVyPUK0Mlc1PiEQvF2= M{fsN3NCVkeHUh?=
TGBC11TKB NYq1[IJPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUfsT|BKUUN3ME2yOU43QDZ|IN88US=> NHTrO|dUSU6JRWK=
CTV-1 M{jl[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnnXTWM2OD1{NT64PVY6KM7:TR?= Mkf0V2FPT0WU
NCI-H2029 NI\wb|lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml;wTWM2OD1{Nj60NlM5KM7:TR?= M3Sxb3NCVkeHUh?=
HLE NWnyV4J1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoKyTWM2OD1{Nz6wOVQh|ryP MlPpV2FPT0WU
NCI-H1693 Mn\qS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF3aWlBKSzVyPUK3MlI5QThizszN NWLzSXAxW0GQR1XS
HCC70 NI\4RZdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFzCcGZKSzVyPUK3MlczPDZizszN Mln0V2FPT0WU
BEN NVnCUZJmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEXMeopKSzVyPUK3Mlk2PjZizszN NEXBN5JUSU6JRWK=
LB771 M4TPfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{i4[mlEPTB;MkiuPFM4OyEQvF2= M3fWO3NCVkeHUh?=
697 M33PO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFrKWY1KSzVyPUK5MlAzOzVizszN MULTRW5ITVJ?
LU-139 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHLoPZlKSzVyPUK5MlM4PDhizszN NFu3OplUSU6JRWK=
EW-13 NYrNcmg6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmnKTWM2OD1{OT6zPFE1KM7:TR?= NXjVTHV7W0GQR1XS
MOLT-13 NV;NT2hoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGHFZnpKSzVyPUK5MlM5OTRizszN NVfSWm9JW0GQR1XS
L-363 M3ztcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUHJR|UxRTJ7LkS3PVgh|ryP MXfTRW5ITVJ?
EM-2 M3jnSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWXJR|UxRTJ7LkS5NFEh|ryP MlnHV2FPT0WU
RS4-11 NFvmOGZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEnm[ZVKSzVyPUOwMlQzPDFizszN Mn:0V2FPT0WU
A2780 NH;Sc5BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M17iPWlEPTB;M{CuO|Q2PyEQvF2= NHH0eYNUSU6JRWK=
KU812 NUXVXoZNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV3hVJNkUUN3ME2zNk4{PjR{IN88US=> M1XONnNCVkeHUh?=
COLO-684 MkezS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4HTcGlEPTB;M{OuN|U6QSEQvF2= NFy5SopUSU6JRWK=
MFE-280 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIPuR|RKSzVyPUOzMlM5QDlizszN M2XJNXNCVkeHUh?=
KG-1 MlL6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV\rbpVEUUN3ME2zN{43ODBzIN88US=> NHOySWpUSU6JRWK=
JVM-3 NU[2SmdyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX:0[5dmUUN3ME2zOU42QDZ6IN88US=> MVrTRW5ITVJ?
MV-4-11 MlH5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYjjUFV[UUN3ME2zOU45PDl7IN88US=> MlrYV2FPT0WU
LAMA-84 MVPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn2xTWM2OD1|Nj63N|Q2KM7:TR?= NEC0dYJUSU6JRWK=
MOLT-16 MmPVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUfm[GVuUUN3ME2zOk46PTJizszN MkDWV2FPT0WU
H4 NHPkTnhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn\wTWM2OD1|Nz61Olch|ryP NWnsO5VuW0GQR1XS
T47D NGjN[m1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWHJR|UxRTN5LkewNVgh|ryP M3fmUXNCVkeHUh?=
CAL-54 M4G4c2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3O3[mlEPTB;M{euPVY3KM7:TR?= MX;TRW5ITVJ?
SW982 NX6zdYhxT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3rabmlEPTB;M{iuNFk6QCEQvF2= NXqzZmt6W0GQR1XS
IGROV-1 NUHwXmFFT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYDJNJN4UUN3ME2zPU4{OzB2IN88US=> NXGxUYkzW0GQR1XS
NB14 MnjES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn;5TWM2OD12MD63NFMyKM7:TR?= M175S3NCVkeHUh?=
HCC1187 M{\mSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Ml7lTWM2OD12MT6yO|cyKM7:TR?= NEDrdIFUSU6JRWK=
SBC-1 MoXrS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYfrWFVvUUN3ME20NU4{ODZ|IN88US=> NVTEWYtzW0GQR1XS
KARPAS-45 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4r6[GlEPTB;NEGuOFgyQCEQvF2= M2PDfXNCVkeHUh?=
MOLT-4 NF7rW4tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{na[GlEPTB;NEKuNlU{QCEQvF2= MXnTRW5ITVJ?
JVM-2 NVLPfnFKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHzGTnhKSzVyPUSyMlkzODdizszN NW\nXJlXW0GQR1XS
A4-Fuk MmrYS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoLNTWM2OD12Mz61OlkyKM7:TR?= MX7TRW5ITVJ?
MDA-MB-361 Mli0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVnJR|UxRTR|Lki0NVQh|ryP MYXTRW5ITVJ?
BALL-1 MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{fUZmlEPTB;NEOuPVU{OiEQvF2= MWjTRW5ITVJ?
T98G M{Czdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4m5cWlEPTB;NESuPFUyPyEQvF2= NU\mSGVqW0GQR1XS
Mo-T MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFLzOW1KSzVyPUS1MlY{QDlizszN M3z3fnNCVkeHUh?=
MHH-PREB-1 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1mzOWlEPTB;NEWuO|U5PSEQvF2= Ml;JV2FPT0WU
ALL-PO M3HhTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MonpTWM2OD12Nz6zO|kyKM7:TR?= MULTRW5ITVJ?
NCI-H510A NVvDW4ZtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFf4c4tKSzVyPUS3MlkxOzRizszN NGThd4xUSU6JRWK=
ML-2 NYPIU|FrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV7JR|UxRTR7Lke4OVYh|ryP MVjTRW5ITVJ?

... 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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Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

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