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 64 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 NVfTRo97U2mwYYPlJGF{e2G7 MlXPN|AhdWmw MUjJcohq[mm2aX;uJI9nKFCDUmCxJJdqfGhiRVO1NEBw\iByLkCwNkDPxE1? MlvkNVk5QDh5NkC=
Jurkat M4XxOGtqdmG|ZTDBd5NigQ>? Mo[yPVYhcA>? NV3GRoNlTE2VTx?= M3TiWGlvcGmkaYTpc44hd2ZiUFHSVFEh[XO|ZYPz[YQh[XNicnXkeYN1cW:wIH;mJINmdGxidnnhZoltcXS7IIfpeIghTUN3MDDv[kA{KM7:TR?= NV\6c3R6OjN6NUCxPVk>
Capan1 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mn7sO|IhcA>? M1nzSmROW09? NF7wNoFCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JGJTS0F{IHflcoUhdXW2YYTl[EBpfW2jbjDDZZBidjFiY3XscJMhf2m2aDDJR|UxKG:oIEO5Mlch|ryP M2[zV|I1Ozl6M{iz
DT40 NID1eldEgXSxdH;4bYMhSXO|YYm= NXW4ZW5LPzJiaB?= NEf3SpZFVVOR NXu3ZXVQS3m2b4TvfIlkcXS7IHHnZYlve3RiY3jpZ4tmdiCEUlPBNk1l\W[rY3nlcpQhTFR2MDDj[Yxtew>? NXvHNpRyOjR7MkK1PFc>
ML-1 M3H1d2Fxd3C2b4TpZ{BCe3OjeR?= NY\HTmVXOi53IN88US=> NEnXXVMzPCCq MVPEUXNQ MXHTfY5memerc4TpZ4FtdHliZX7oZY5k\XNiVGLBTWwucW6mdXPl[EBieG:ydH;zbZMhcW5iTVytNUBk\Wyucx?= NXXNbFY1OjR6OUWxN|U>
HCT-116 NWXNcIRMU2mwYYPlJGF{e2G7 NFPh[5oxNjVizszN Mk\YNlQhcA>? NVfGeWx2WEGUUDDhZ5Rqfmm2eTDk[YNz\WG|ZYO= NYjKT|J2OjNyNUSyNVM>
UM-SCC1 Mn;xR5l1d3SxeHnjJGF{e2G7 NEKzbYMyOCEQvF2= NVqxXJkxOjRiaB?= MUfS[YR2[2W|IITo[UBk\WyuII\pZYJqdGm2eR?= NIfESIozOTlzMk[yNC=>
FaDu NXnJVVZ{S3m2b4TvfIlkKEG|c3H5 MmLQNVAh|ryP MUOyOEBp MUXS[YR2[2W|IITo[UBk\WyuII\pZYJqdGm2eR?= MmLWNlE6OTJ4MkC=
PC-3 M2\TS2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4[3SlExKM7:TR?= MYHJcoR2[2W|IHGgd4lodmmoaXPhcpQhcW6qaXLpeIlwdiCrbjDjc4xwdnliZn;ycYF1cW:wwrC= MXqyNVU4OTlzMh?=
EoL-1-cell Mm\IS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX3RUFdsUUN3ME2xMlA4QThizszN NFLtVZpUSU6JRWK=
NCI-SNU-5 MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Ml\tTWM2OD1|LkGyPFQyKM7:TR?= Mme1V2FPT0WU
BV-173 MorOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NVXJZmJVUUN3ME21MlQ2PDB7IN88US=> MX;TRW5ITVJ?
HCC1806 Mkm2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn\wTWM2OD13Lke1NVc{KM7:TR?= MUHTRW5ITVJ?
COLO-680 M2HmUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVvDcY5LUUN3ME22MlIyPDB4IN88US=> NF;0UoNUSU6JRWK=
HCC2218 NGW2WGVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFv6SXFKSzVyPUeuO|k4ODRizszN MoPWV2FPT0WU
SK-MEL-24 NILJT2tIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIDFd|FKSzVyPUeuPFE6OjRizszN MXfTRW5ITVJ?
NCI-H720 NF3sd|FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGLrd2xKSzVyPUiuOFM3ODNizszN MoDzV2FPT0WU
KASUMI-1 M4\lbGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXjLXVk1UUN3ME24Mlg6OjZ4IN88US=> NXroelg6W0GQR1XS
HAL-01 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVe4OIFmUUN3ME25Mlg5PjJizszN M{W0d3NCVkeHUh?=
CAL-33 NX64OJM1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVXGeFZiUUN3ME2xNE41OzRizszN M37kXHNCVkeHUh?=
SK-MEL-1 MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWLIdllLUUN3ME2xNk41PjZ|IN88US=> MojDV2FPT0WU
Ramos-2G6-4C10 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXvvU2JZUUN3ME2xNk41PzV{IN88US=> NVHzSJZPW0GQR1XS
KY821 NUeyW5NST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVTJR|UxRTF{LkS4OUDPxE1? NF\WfVJUSU6JRWK=
HEC-1 NUe0bYo2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoW3TWM2OD1zMj65NVk3KM7:TR?= M3;uOHNCVkeHUh?=
SK-NEP-1 NXfu[3lYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUT5cGRSUUN3ME2xN{4yPjZizszN NFvLNVNUSU6JRWK=
MN-60 MlXFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{fYSWlEPTB;MUOuOVM5QSEQvF2= MWXTRW5ITVJ?
DU-145 MnjNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXPJR|UxRTF|LkmwOVMh|ryP NWTrdGFTW0GQR1XS
EW-3 NEmwW3dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2nqTGlEPTB;MUSuOVU3PSEQvF2= NHzzcGtUSU6JRWK=
OS-RC-2 NGr0V4NIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MorvTWM2OD1zNT65OVg6KM7:TR?= Mn3vV2FPT0WU
RPMI-8226 MoL1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MYnJR|UxRTF4LkKwOFIh|ryP NFzXV45USU6JRWK=
ChaGo-K-1 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M3PldmlEPTB;MU[uOVMzPSEQvF2= NInyWW9USU6JRWK=
DEL NVH2TXJlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVjJR|UxRTF4Lk[3NVch|ryP NHuwfplUSU6JRWK=
GP5d Mk\RS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHW4UI1KSzVyPUG3MlA2OyEQvF2= MnzEV2FPT0WU
COLO-668 M3nTemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFvvZpFKSzVyPUG3MlYzQTRizszN NXjGUJE3W0GQR1XS
H9 NUDucGJiT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NEH4[IxKSzVyPUG4MlI5OzNizszN M4\ab3NCVkeHUh?=
NKM-1 MkC4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3fQTmlEPTB;MUiuOVEyQSEQvF2= NGjvVodUSU6JRWK=
KYSE-150 MkjFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXXneG9GUUN3ME2xPE46QTh4IN88US=> M4LOVnNCVkeHUh?=
Daoy NHXGSHpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXXEWngxUUN3ME2xPU42PjR7IN88US=> MYnTRW5ITVJ?
ECC10 NUDNWJpMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1\vb2lEPTB;MkCuO|Q2PSEQvF2= M{HFR3NCVkeHUh?=
A388 MoD6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NI\Xco5KSzVyPUKxMlkxQTFizszN MmDzV2FPT0WU
MHH-NB-11 MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2qyTmlEPTB;MkOuNVM3OyEQvF2= MmfEV2FPT0WU
HCC1937 MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnLETWM2OD1{ND63OFYh|ryP MnLoV2FPT0WU
TGBC11TKB MVXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NFfYdoVKSzVyPUK1MlY5PjNizszN NEfQPGZUSU6JRWK=
CTV-1 NEG2dmxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX3ZOY9PUUN3ME2yOU45QTZ7IN88US=> M2DPTHNCVkeHUh?=
NCI-H2029 NULIfGg6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUPJR|UxRTJ4LkSyN|gh|ryP NITnNWxUSU6JRWK=
HLE MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MoqyTWM2OD1{Nz6wOVQh|ryP NVrvXGlNW0GQR1XS
NCI-H1693 NWXydXRKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUiwPHNxUUN3ME2yO{4zQDl6IN88US=> NX7wTpIyW0GQR1XS
HCC70 M{\oVmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYPJR|UxRTJ5LkeyOFYh|ryP M3\Yd3NCVkeHUh?=
BEN M1PncWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXrqZVRpUUN3ME2yO{46PTZ4IN88US=> NYXYN5NLW0GQR1XS
LB771 M1Lzemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2TMfmlEPTB;MkiuPFM4OyEQvF2= MXPTRW5ITVJ?
697 MnfES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnT0TWM2OD1{OT6wNlM2KM7:TR?= M{C2fHNCVkeHUh?=
LU-139 NUm2TJlKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYHWPWpFUUN3ME2yPU4{PzR6IN88US=> MVnTRW5ITVJ?
EW-13 NFf6bIRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXjnbGY6UUN3ME2yPU4{QDF2IN88US=> Mmi0V2FPT0WU
MOLT-13 Ml;KS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWrJR|UxRTJ7LkO4NVQh|ryP M1LEc3NCVkeHUh?=
L-363 MkC5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUe3dWZRUUN3ME2yPU41Pzl6IN88US=> Mn:0V2FPT0WU
EM-2 MnTPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NY\RfldJUUN3ME2yPU41QTBzIN88US=> NXv3UnZlW0GQR1XS
RS4-11 MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEW1TGZKSzVyPUOwMlQzPDFizszN MmPVV2FPT0WU
A2780 NIWyR49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mk\mTWM2OD1|MD63OFU4KM7:TR?= MXXTRW5ITVJ?
KU812 M4nDd2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLWW2FKSzVyPUOyMlM3PDJizszN NIPsfGtUSU6JRWK=
COLO-684 Mnq2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NWL1[4FCUUN3ME2zN{4{PTl7IN88US=> MnvEV2FPT0WU
MFE-280 MWrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVXJR|UxRTN|LkO4PFkh|ryP MnL1V2FPT0WU
KG-1 NYrEWXRLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWnJR|UxRTN|Lk[wNFEh|ryP NEXxSoRUSU6JRWK=
JVM-3 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MofQTWM2OD1|NT61PFY5KM7:TR?= M1PJOHNCVkeHUh?=
MV-4-11 Ml;DS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NW\D[lJ{UUN3ME2zOU45PDl7IN88US=> NGjQVZlUSU6JRWK=
LAMA-84 NV7LfndlT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NW\hcHhuUUN3ME2zOk44OzR3IN88US=> M13TXHNCVkeHUh?=
MOLT-16 NWW4XoZoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MYPJR|UxRTN4Lkm1NkDPxE1? NWnEW21EW0GQR1XS
H4 NVy3[2dKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnnsTWM2OD1|Nz61Olch|ryP NGDFV4RUSU6JRWK=
T47D NXy3cIRLT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVLqdYR4UUN3ME2zO{44ODF6IN88US=> NUCwSWxPW0GQR1XS
CAL-54 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXfJR|UxRTN5Lkm2OkDPxE1? NI\mR2hUSU6JRWK=
SW982 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVThWIFjUUN3ME2zPE4xQTl6IN88US=> MU\TRW5ITVJ?
IGROV-1 Moj3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MljsTWM2OD1|OT6zN|A1KM7:TR?= NVjac48yW0GQR1XS
NB14 MnvNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M13LSmlEPTB;NECuO|A{OSEQvF2= M{HpZ3NCVkeHUh?=
HCC1187 M4PSN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYDJR|UxRTRzLkK3O|Eh|ryP NXHXXnRIW0GQR1XS
SBC-1 M3:5PWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLx[FFKSzVyPUSxMlMxPjNizszN MYTTRW5ITVJ?
KARPAS-45 NHvQNYdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEDwSVRKSzVyPUSxMlQ5OThizszN NFj3NYdUSU6JRWK=
MOLT-4 M{LUemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M373SWlEPTB;NEKuNlU{QCEQvF2= NHjReJBUSU6JRWK=
JVM-2 NV3DUWh{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2nRXGlEPTB;NEKuPVIxPyEQvF2= MVHTRW5ITVJ?
A4-Fuk MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEDpfYxKSzVyPUSzMlU3QTFizszN NITkSVJUSU6JRWK=
MDA-MB-361 MljDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmLBTWM2OD12Mz64OFE1KM7:TR?= Mli3V2FPT0WU
BALL-1 MlnkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXm5eWhEUUN3ME20N{46PTN{IN88US=> NGfUTIVUSU6JRWK=
T98G NH\p[JZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3y4e2lEPTB;NESuPFUyPyEQvF2= M3Hi[3NCVkeHUh?=
Mo-T M2TjSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGW0U2hKSzVyPUS1MlY{QDlizszN NF20SVhUSU6JRWK=
MHH-PREB-1 MlvkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHLXSYpKSzVyPUS1Mlc2QDVizszN NYO4UGNtW0GQR1XS
ALL-PO NIfkfWJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1z5TWlEPTB;NEeuN|c6OSEQvF2= MVHTRW5ITVJ?
NCI-H510A NX7qeGhET3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NITFUo5KSzVyPUS3MlkxOzRizszN M1jIU3NCVkeHUh?=
ML-2 MkXFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFS5WY1KSzVyPUS5Mlc5PTZizszN MWXTRW5ITVJ?

... 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]
+ Expand
  • 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 Conditions Sponsor/Collaborators Start Date Phases
NCT03400306 Not yet recruiting Cancer - Ovarian AbbVie May 10 2020 Phase 1
NCT03400306 Not yet recruiting Cancer - Ovarian AbbVie May 10 2020 Phase 1
NCT03044795 Not yet recruiting Cancer University Medical Center Groningen|AbbVie|Dutch Cancer Society November 2018 Phase 2
NCT03044795 Not yet recruiting Cancer University Medical Center Groningen|AbbVie|Dutch Cancer Society November 2018 Phase 2
NCT03581292 Recruiting Anaplastic Astrocytoma|Glioblastoma|Malignant Glioma National Cancer Institute (NCI) October 31 2018 Phase 2
NCT03581292 Recruiting Anaplastic Astrocytoma|Glioblastoma|Malignant Glioma National Cancer Institute (NCI) October 31 2018 Phase 2

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 Products5

  • 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