Veliparib (ABT-888)

For research use only. Not for use in humans.

Catalog No.S1004 Synonyms: NSC 737664

119 publications

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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Selleck's Veliparib (ABT-888) has been 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 M{DtTGtqdmG|ZTDBd5NigQ>? NF3TbWs{OCCvaX6= NXe4SnNDUW6qaXLpeIlwdiCxZjDQRXJROSC5aYToJGVEPTBib3[gNE4xODJizszN M{ixV|E6QDh6N{[w
Jurkat NG\ydGVMcW6jc3WgRZN{[Xl? NWf5[XdmQTZiaB?= Mn\hSG1UVw>? NVrhRZNvUW6qaXLpeIlwdiCxZjDQRXJROSCjc4Pld5Nm\CCjczDy[YR2[3Srb36gc4Yh[2WubDD2bYFjcWyrdImge4l1cCCHQ{WwJI9nKDNizszN MYqyN|g2ODF7OR?=
Capan1 NHnIXHBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF3XbWo4OiCq M2DM[WROW09? MVnBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IFLSR2EzKGenbnWgcZV1[XSnZDDoeY1idiCFYYDhclEh[2WubIOge4l1cCCLQ{WwJI9nKDN7Lkeg{txO MnTUNlQ{QTh|OEO=
DT40 MmL5R5l1d3SxeHnjJGF{e2G7 M1T2V|czKGh? M1\rV2ROW09? NViydGdCS3m2b4TvfIlkcXS7IHHnZYlve3RiY3jpZ4tmdiCEUlPBNk1l\W[rY3nlcpQhTFR2MDDj[Yxtew>? NXrGRZN2OjR7MkK1PFc>
ML-1 M3rtOmFxd3C2b4TpZ{BCe3OjeR?= MX[yMlUh|ryP MnzFNlQhcA>? NXPqcoNPTE2VTx?= M{nT[HN6dmW{Z3nzeIlk[WyueTDlcohidmOnczDUVmFKVC2rbnT1Z4VlKGGyb4D0c5NqeyCrbjDNUE0yKGOnbHzz NX\GcYpQOjR6OUWxN|U>
HCT-116 MYTLbY5ie2ViQYPzZZk> NHPQS|QxNjVizszN MmjqNlQhcA>? M13iUnBCWlBiYXP0bZZqfHliZHXjdoVie2W| M1zNflI{ODV2MkGz
UM-SCC1 Ml76R5l1d3SxeHnjJGF{e2G7 MoC5NVAh|ryP NUT5cJlvOjRiaB?= MWXS[YR2[2W|IITo[UBk\WyuII\pZYJqdGm2eR?= MnPNNlE6OTJ4MkC=
FaDu NUDUUJhFS3m2b4TvfIlkKEG|c3H5 NFziPWgyOCEQvF2= NXL1S41NOjRiaB?= NIPVSVVT\WS3Y3XzJJRp\SClZXzsJJZq[WKrbHn0fS=> MYCyNVkyOjZ{MB?=
PC-3 NX7sO3c1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mor4NVAh|ryP MmryTY5lfWOnczDhJJNq\26rZnnjZY51KGmwaHnibZRqd25iaX6gZ49td267IH\vdo1ifGmxbtMg NGnCZ5AzOTV5MUmxNi=>
EoL-1-cell NXTIUYw5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnvUTWM2OD1zLkC3PVgh|ryP MmPBV2FPT0WU
NCI-SNU-5 NXXsUnNCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEjrPY1KSzVyPUOuNVI5PDFizszN M3;PN3NCVkeHUh?=
BV-173 M33zfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHjLVZNKSzVyPUWuOFU1ODlizszN MVLTRW5ITVJ?
HCC1806 M3LCcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2XTNWlEPTB;NT63OVE4OyEQvF2= NXTTN|ZRW0GQR1XS
COLO-680 NIHoU49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWjzdo1LUUN3ME22MlIyPDB4IN88US=> M1TlVXNCVkeHUh?=
HCC2218 M1;u[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2\DOmlEPTB;Nz63PVcxPCEQvF2= NWPpbZdsW0GQR1XS
SK-MEL-24 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmDKTWM2OD15LkixPVI1KM7:TR?= NX\oeotVW0GQR1XS
NCI-H720 NYf6SFkzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFyzOVJKSzVyPUiuOFM3ODNizszN MYHTRW5ITVJ?
KASUMI-1 NFG1N|hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXnJR|UxRThwOEmyOlYh|ryP M2LMd3NCVkeHUh?=
HAL-01 MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIXEVGRKSzVyPUmuPFg3OiEQvF2= M2DU[nNCVkeHUh?=
CAL-33 NICxWoFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml7PTWM2OD1zMD60N|Qh|ryP NIfzR5pUSU6JRWK=
SK-MEL-1 MlnFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1\wV2lEPTB;MUKuOFY3OyEQvF2= NGHKNGJUSU6JRWK=
Ramos-2G6-4C10 MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1XHSWlEPTB;MUKuOFc2OiEQvF2= MWXTRW5ITVJ?
KY821 MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVTJR|UxRTF{LkS4OUDPxE1? NHjrOHJUSU6JRWK=
HEC-1 MmmzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWXJR|UxRTF{LkmxPVYh|ryP NIL3Z5dUSU6JRWK=
SK-NEP-1 M4m5eWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVrJR|UxRTF|LkG2OkDPxE1? M1uwVHNCVkeHUh?=
MN-60 MkHnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEX2fVNKSzVyPUGzMlU{QDlizszN MVXTRW5ITVJ?
DU-145 MmDXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJR|UxRTF|LkmwOVMh|ryP M1jEdXNCVkeHUh?=
EW-3 NVqwe5FPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MlLMTWM2OD1zND61OVY2KM7:TR?= MmSwV2FPT0WU
OS-RC-2 MnW4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYjYdGF2UUN3ME2xOU46PTh7IN88US=> Mni4V2FPT0WU
RPMI-8226 Ml[5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWLtT2Y3UUN3ME2xOk4zODR{IN88US=> NHPkXWJUSU6JRWK=
ChaGo-K-1 MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NV24eZR6UUN3ME2xOk42OzJ3IN88US=> MUHTRW5ITVJ?
DEL MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUPJR|UxRTF4Lk[3NVch|ryP M3Gy[nNCVkeHUh?=
GP5d NHzse|NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGf0e5hKSzVyPUG3MlA2OyEQvF2= MVLTRW5ITVJ?
COLO-668 MoHtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHnLRZFKSzVyPUG3MlYzQTRizszN M2LrTnNCVkeHUh?=
H9 NXOyR5NVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3TnUGlEPTB;MUiuNlg{OyEQvF2= MofRV2FPT0WU
NKM-1 MoHDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M4rSemlEPTB;MUiuOVEyQSEQvF2= MljiV2FPT0WU
KYSE-150 MorMS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFvTVWZKSzVyPUG4Mlk6QDZizszN NGrzdYxUSU6JRWK=
Daoy M{\6T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MnzKTWM2OD1zOT61OlQ6KM7:TR?= MUTTRW5ITVJ?
ECC10 NVH2[VBtT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnTHTWM2OD1{MD63OFU2KM7:TR?= M2n2UnNCVkeHUh?=
A388 NXy3UWpOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYjJR|UxRTJzLkmwPVEh|ryP NVnR[HdXW0GQR1XS
MHH-NB-11 M2O3Umdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGntWpJKSzVyPUKzMlE{PjNizszN MoizV2FPT0WU
HCC1937 NVnyNmxCT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWLUfopWUUN3ME2yOE44PDZizszN NVfiWVJ7W0GQR1XS
TGBC11TKB MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2jUdWlEPTB;MkWuOlg3OyEQvF2= MWrTRW5ITVJ?
CTV-1 NX\OeoM{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmXiTWM2OD1{NT64PVY6KM7:TR?= MkDXV2FPT0WU
NCI-H2029 NGf2RVZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmXoTWM2OD1{Nj60NlM5KM7:TR?= NWGwc5Z4W0GQR1XS
HLE MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mk\JTWM2OD1{Nz6wOVQh|ryP MmDEV2FPT0WU
NCI-H1693 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX;a[W9vUUN3ME2yO{4zQDl6IN88US=> NEfiSI5USU6JRWK=
HCC70 NUTzSINMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEX1ToJKSzVyPUK3MlczPDZizszN NF7GXopUSU6JRWK=
BEN MkfCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3nYcmlEPTB;MkeuPVU3PiEQvF2= M3jsbHNCVkeHUh?=
LB771 Ml\1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIj2emlKSzVyPUK4Mlg{PzNizszN MUXTRW5ITVJ?
697 M4\mVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MomwTWM2OD1{OT6wNlM2KM7:TR?= M130UHNCVkeHUh?=
LU-139 NYPCbYx3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmLaTWM2OD1{OT6zO|Q5KM7:TR?= NGjPUpNUSU6JRWK=
EW-13 MnzZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVLJR|UxRTJ7LkO4NVQh|ryP NXPlclJvW0GQR1XS
MOLT-13 NHzKSHZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3TXemlEPTB;MkmuN|gyPCEQvF2= NF\iNpBUSU6JRWK=
L-363 NUizNnd3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFvrbZRKSzVyPUK5MlQ4QThizszN NEPmSINUSU6JRWK=
EM-2 MmfXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1zwXGlEPTB;MkmuOFkxOSEQvF2= Mo\5V2FPT0WU
RS4-11 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHP6VY9KSzVyPUOwMlQzPDFizszN MWHTRW5ITVJ?
A2780 NF36OHVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoizTWM2OD1|MD63OFU4KM7:TR?= MmLoV2FPT0WU
KU812 M3TzW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUPJR|UxRTN{LkO2OFIh|ryP NXX3bmluW0GQR1XS
COLO-684 NVP5fotsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYnPTYZIUUN3ME2zN{4{PTl7IN88US=> MkjKV2FPT0WU
MFE-280 Mn;xS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFXvcmFKSzVyPUOzMlM5QDlizszN NHPqU2FUSU6JRWK=
KG-1 M{jLT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmjHTWM2OD1|Mz62NFAyKM7:TR?= NYX6fG1tW0GQR1XS
JVM-3 NU\kWmtJT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2nuTWlEPTB;M{WuOVg3QCEQvF2= NVPQS3RCW0GQR1XS
MV-4-11 M2j3SGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4\XfGlEPTB;M{WuPFQ6QSEQvF2= NITOUVlUSU6JRWK=
LAMA-84 NUfMfVR3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHjEcJJKSzVyPUO2Mlc{PDVizszN MlqwV2FPT0WU
MOLT-16 M1:2Wmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF\lcVFKSzVyPUO2Mlk2OiEQvF2= MkC2V2FPT0WU
H4 Mm\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF7tcWpKSzVyPUO3MlU3PyEQvF2= MUHTRW5ITVJ?
T47D MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MorvTWM2OD1|Nz63NFE5KM7:TR?= Mn7xV2FPT0WU
CAL-54 M3O2cGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MorJTWM2OD1|Nz65OlYh|ryP NYTlNVU4W0GQR1XS
SW982 MmnPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYTOWFFsUUN3ME2zPE4xQTl6IN88US=> MoDiV2FPT0WU
IGROV-1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYrJR|UxRTN7LkOzNFQh|ryP NXP1WWFOW0GQR1XS
NB14 NHfnS25Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXvJR|UxRTRyLkewN|Eh|ryP Mn7tV2FPT0WU
HCC1187 MkO5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVXJR|UxRTRzLkK3O|Eh|ryP M4jM[nNCVkeHUh?=
SBC-1 NFzwN4xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml;aTWM2OD12MT6zNFY{KM7:TR?= MUDTRW5ITVJ?
KARPAS-45 NH3UOFNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVHtS3RbUUN3ME20NU41QDF6IN88US=> NXzDTGoyW0GQR1XS
MOLT-4 NF7tUnVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYH4[I5PUUN3ME20Nk4zPTN6IN88US=> NID2fYZUSU6JRWK=
JVM-2 NV7nUopwT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGP4bolKSzVyPUSyMlkzODdizszN NFGxTZVUSU6JRWK=
A4-Fuk MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXrJR|UxRTR|LkW2PVEh|ryP M{DTVXNCVkeHUh?=
MDA-MB-361 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWnMVFh4UUN3ME20N{45PDF2IN88US=> M3XWW3NCVkeHUh?=
BALL-1 M2nZOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHT1U4hKSzVyPUSzMlk2OzJizszN NHPsRnpUSU6JRWK=
T98G M3HuTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4XvSmlEPTB;NESuPFUyPyEQvF2= MmrnV2FPT0WU
Mo-T NELvcWpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVnjTYZRUUN3ME20OU43Ozh7IN88US=> M{\ROHNCVkeHUh?=
MHH-PREB-1 NFPoZmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXrJR|UxRTR3Lke1PFUh|ryP NIe0XYVUSU6JRWK=
ALL-PO NF;KV2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVjHN2JXUUN3ME20O{4{PzlzIN88US=> M3W0eXNCVkeHUh?=
NCI-H510A MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MonkTWM2OD12Nz65NFM1KM7:TR?= MmDVV2FPT0WU
ML-2 NHjXOmhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MXHJR|UxRTR7Lke4OVYh|ryP MWDTRW5ITVJ?

... 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
Smiles CC1(CCCN1)C2=NC3=C(C=CC=C3[NH]2)C(N)=O

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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)

    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) 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