Olaparib (AZD2281)

Validation & Quality Control

Customer Reviews(10) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

Olaparib (AZD2281) is available in the following compound libraries:

Cambridge Cancer Compound Library(96-well) Chemical Library (96-well) Inhibitor Library (96-well)

Products used with Olaparib (AZD2281) in previous publications

Targets	Related Products	References	Purpose
PARP inhibitors	ABT-888 (Veliparib)	[1][2][3]	Positive Control. Compared to the PARP inhibition potency of Olaparib, ABT-888, PJ34, and Iniparib.
	PJ34	[4][6][7]
	Iniparib (BSI-201)	[1][9]
DNA/RNA Synthesis inhibitors	Cisplatin	[10][11][12]	The PARP inhibitors ABT-888 and Olaparib markedly synergize with the DNA/RNA synthesis inhibitors in cancer cell lines. Combining DNA/RNA synthesis inhibitors and PARP inhibitors may be an innovative therapeutic strategy for tumors.
	Fluorodeoxyuridine	[2][3]
	Gemcitabine	[2][3]
	Oxaliplatin	[2][10]
ATM/ATR inhibitors	KU-55933	[3][5][8]	The impact of ATM pathway on the sensitizing properties of PARP inhibition and ATM inhibitor KU-55933 increases effects of Olaparib.

Product Information

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Research Area
Research Area
Olaparib (AZD2281) Mechanism
Olaparib (AZD2281) Mechanism
Tankyrase-2 (TNKS2) is a protein with homology to the catalytic domain of poly(adenosine diphosphate–ribose) polymerase (PARP), containing 15 ANK repeats, 1 PARP catalytic domain, and 1 SAM (sterile alpha motif) domain. ^[1]
The crystal complex with TNKS2 and Olaparib shows that binding leads to a major conformational change of the D-loop residues (especially Asp1045, His1048, Ala1049, and Tyr1050). The His1048 that is blocking the cavity moves out. Indeed, the whole D-loop moves when Olaparib binds to TNKS2. At the nicotinamide-binding site, Olaparib forms similar hydrogen bonds with Ser1068 and Gly1032. The pyrimidine ring forms an offset π-stacking interaction with Tyr1071 as well as a hydrogen bond with a water molecule bound to the carbonyl of Gly1032. The fluorophenyl group stacks with Tyr1050 of the D-loop. The fluorine of the fluorophenyl group interacts unfavorably with the D-loop, as the electronegative fluorine produces van der Waals to carbonyls of His1048 and Ala1049. The carbonyl groups of Olaparib form hydrogen bonds with the amides of Tyr1060 and Asp1045. The cyclopropyl interacts with the hydrophobic face of the helix 1035–1042 which lines the donor site. The binding can be divided so that interactions at the upper nicotinamide binding site follow the lock-and-key model, whereas at the lower end of the cavity, it follows the induced-fit mechanism. ^[2]
References
[1] Smith S, et al. Science. 1998, 282(5393), 1484-1487.
[2] Narwal M, et al. J Med Chem. 2012, 55(3), 1360-1367.
Dr. Antonino Maria Sparta demonstrates a breakthrough in leukemia research by utilizing two inhibitors produced by Selleck Chemicals.

Cat.No.	Product Name	Solubility (25°C)
S1060	Olaparib (AZD2281)	<1 mg/mL	87 mg/mL	<1 mg/mL
S1004	ABT-888 (Veliparib)	<1 mg/mL	17 mg/mL	<1 mg/mL
S1098	Rucaparib (AG-014699 , PF-01367338)	<1 mg/mL	84 mg/mL	<1 mg/mL
S1087	Iniparib (BSI-201)	<1 mg/mL	58 mg/mL	28 mg/mL
S2197	A-966492	<1 mg/mL	65 mg/mL	<1 mg/mL
S2178	AG14361	<1 mg/mL	12 mg/mL	<1 mg/mL
S1132	INO-1001	<1 mg/mL	27 mg/mL	27 mg/mL
S8038	UPF 1069	<1 mg/mL	56 mg/mL	<1 mg/mL
S7048	BMN 673	<1 mg/mL	96 mg/mL	96 mg/mL

Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description	Olaparib (AZD2281, KU0059436) is a selective inhibitor of PARP1 and PARP2 with IC50 of 5 nM and 1 nM, respectively.
Targets	PARP1	PARP2
IC50	5 nM	1 nM ^[1]
In vitro	Olaparib would act against BRCA1 or BRCA2 mutations. Olaparib is not sensitive to tankyrase-1 (IC50 >1 μM). Olaparib could ablate the PARP-1 activity at concentrations of 30-100 nM in SW620 cells. Olaparib is hypersensitive to BRCA1-deficient cell lines (MDA-MB-463 and HCC1937), compared with BRCA1- and BRCA2-proficient cell lines (Hs578T, MDA-MB-231, and T47D). ^[1] Olaparib is strongly sensitive to KB2P cells due to suppression of base excision repair by PARP inhibition, which may result in the conversion of single-strand breaks to double-strand breaks during DNA replication, thus activating BRCA2-dependent recombination pathways. ^[2]
In vivo	Combining with temozolomide, Olaparib (10 mg/kg, p.o.) significantly suppresses tumor growth in SW620 xenografts. ^[1] Olaparib shows great response to Brca1^-/-;p53^-/- mammary tumors (50 mg/kg i.p. per day), while no responses to HR-deficient Ecad^-/-;p53^-/- mammary tumors. Olaparib even does not show dose-limiting toxicity in tumor-bearing mice. ^[3] Olaparib has been used to treat with BRCA mutated tumors, such as ovarian, breast and prostate cancers. Moreover, Olaparib shows selectively inhibition to ATM (Ataxia Telangiectasia Mutated)-deficient tumor cells, which indicates to be a potential agent for treating ATM mutant lymphoid tumors. ^[4]
Clinical Trials	Combining with cediranib, Olaparib is currently in Phase I/II study for treatment of recurrent papillary-serous ovarian, fallopian tube or peritoneal cancer or treatment of recurrent triple-negative breast cancer.
Features	Olaparib is one of the first PARP inhibitors.

Protocol(Only for Reference)

Kinase Assay:
^[1]

FlashPlate assay (96-well screening assay)	To columns 1 through 10, 1 μL of Olaparib (in DMSO) is added, and 1 μL DMSO only is added to the positive (POS) and negative (NEG) control wells (columns 11 and 12, respectively) of a pretreated FlashPlate. PARP-1 is diluted 1:40 in buffer (buffer B: 10% glycerol (v/v), 25 mM HEPES, 12.5 mM MgCl₂,50 mM KCl, 1 mM DTT, 0.01% NP-40 (v/v), pH 7.6) and 40 μL added to all 96 wells (final PARP-1 concentration in the assay is ~1 ng/μL). The plate is sealed and shaken at RT for 15 min. Following this, 10 μL of positive reaction mix (0.2 ng/μL of double-stranded oligonucleotide [M3/M4] DNA per well, 5 μM of NAD⁺ final assay concentration, and 0.075 μCi ³H-NAD⁺ per well) is added to the appropriate wells (columns 1-11). The negative reaction mix, lacking the DNA oligonucleotide, is added to column 12 (with the mean negative control value used as the background). The plate is resealed and shaken for a further 60 min at RT to allow the reaction to continue. Then, 50 μL of ice-cold acetic acid (30%) is added to each well to stop the reaction, and the plate is sealed and shaken for a further 60 min at RT. Tritiated signal bound to the FlashPlate is then determined in counts per minute (CPM) using the TopCount plate reader.
In vitro isolated enzyme assay	PARP-2 activity inhibition uses a variation of the PARP-1 assay in which PARP-2 protein (recombinant) is bound down by a PARP-2 specific antibody in a 96-well white-walled plate. PARP-2 activity is measured following ³H-NAD⁺ DNA additions. After washing, scintillant is added to measure ³H-incorporated ribosylations. For tankyrase-1, a α-Screen assay is developed in which HIS-tagged recombinant TANK-1 protein is incubated with biotinylated NAD⁺in a 384-well ProxiPlate assay. Alpha beads are added to bind the HIS and biotin tags to create proximity signal, whereas the inhibition of TANK-1 activity is directly proportional to the loss of this signal.

FlashPlate assay (96-well screening assay)

To columns 1 through 10, 1 μL of Olaparib (in DMSO) is added, and 1 μL DMSO only is added to the positive (POS) and negative (NEG) control wells (columns 11 and 12, respectively) of a pretreated FlashPlate. PARP-1 is diluted 1:40 in buffer (buffer B: 10% glycerol (v/v), 25 mM HEPES, 12.5 mM MgCl₂,50 mM KCl, 1 mM DTT, 0.01% NP-40 (v/v), pH 7.6) and 40 μL added to all 96 wells (final PARP-1 concentration in the assay is ~1 ng/μL). The plate is sealed and shaken at RT for 15 min. Following this, 10 μL of positive reaction mix (0.2 ng/μL of double-stranded oligonucleotide [M3/M4] DNA per well, 5 μM of NAD⁺ final assay concentration, and 0.075 μCi ³H-NAD⁺ per well) is added to the appropriate wells (columns 1-11). The negative reaction mix, lacking the DNA oligonucleotide, is added to column 12 (with the mean negative control value used as the background). The plate is resealed and shaken for a further 60 min at RT to allow the reaction to continue. Then, 50 μL of ice-cold acetic acid (30%) is added to each well to stop the reaction, and the plate is sealed and shaken for a further 60 min at RT. Tritiated signal bound to the FlashPlate is then determined in counts per minute (CPM) using the TopCount plate reader.

In vitro isolated enzyme assay

PARP-2 activity inhibition uses a variation of the PARP-1 assay in which PARP-2 protein (recombinant) is bound down by a PARP-2 specific antibody in a 96-well white-walled plate. PARP-2 activity is measured following ³H-NAD⁺ DNA additions. After washing, scintillant is added to measure ³H-incorporated ribosylations. For tankyrase-1, a α-Screen assay is developed in which HIS-tagged recombinant TANK-1 protein is incubated with biotinylated NAD⁺in a 384-well ProxiPlate assay. Alpha beads are added to bind the HIS and biotin tags to create proximity signal, whereas the inhibition of TANK-1 activity is directly proportional to the loss of this signal.

Cell Assay:
^[1]

Cell lines	Breast cancer cell lines including SW620 colon, A2780 ovarian, HCC1937, Hs578T, MDA-MB-231, MDA-MB-436, and T47D
Concentrations	1-300 nM
Incubation Time	7-14 days
Method	The cytotoxicity of Olaparib is measured by clonogenic assay. Olaparib is dissolved in DMSO and diluted by culture media before use. The cells are seeded in six well plates and left to attach overnight. Then Olaparib is added at various concentrations and the cells are incubated for 7-14 days. After that the surviving colonies are counted for calculating the IC50.

Animal Study:
^[3]

Animal Models	Brca1^-/-;p53^-/- mammary tumors are generated in K14cre;Brca1^F/F;p53^F/F mice.
Formulation	50 mg/mL stocks in DMSO with 10% 2-hydroxyl-propyl-β-cyclodextrine/PBS
Dosages	50 mg/kg
Administration	Administered via i.p. injection at 10 μL/g of body weight

1

References

Chemical Information

Download Olaparib (AZD2281) SDF

Molecular Weight (MW)	434.46
Formula	C₂₄H₂₃FN₄O₃
CAS No.	763113-22-0, 894104-70-2, 937799-91-2, 1021843-02-6
Synonyms	KU-0059436

Solubility (25°C) DMSO 87 mg/mL Water <1 mg/mL Ethanol <1 mg/mL
Storage	2 years -20°CPowder
	2 weeks4°Cin DMSO
	6 months-80°Cin DMSO

Chemical Name	4-(3-(1-(cyclopropanecarbonyl)piperazine-4-carbonyl)-4-fluorobenzyl)phthalazin-1(2H)-one

Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (10)

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Rating

Source

Nucl Med Commun, 2011, 32(11), 1046-51. Olaparib (AZD2281) purchased from Selleck

Method

Cell growth assay

Cell Lines

human Burkitt lymphoma cells

Concentrations

500 nmol/L

Incubation Time

0-5 d

Results

A volume of 500 nmol/l ABT-888 and AZD-2281 showed a moderate intrinsc effect on cell proliferation on days 3–5 (Fig. a). ABT-888 and AZD-2281 showed a significant ( P < 0.05) reduction in lymphoma cell growth on days 2–5 (Fig. b–d).

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Rating

Source

Nucl Med Commun, 2011, 32(11), 1046-51. Olaparib (AZD2281) purchased from Selleck

Method

PARP activity assay

Cell Lines

Raji lymphocyte tumor cells

Concentrations

500 nmol/L

Incubation Time

24 h

Results

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Rating

Source

Nuclear Medicine Communications, 2011, 32, 1046–1051 . Olaparib (AZD2281) purchased from Selleck

Method

Laser confocal microscopy/fluorescent H2AX Antibody Staining

Cell Lines

Epstein–Barr virus-infected Raji lymphocyte tumor cells

Concentrations

500 nM

Incubation Time

2 h

Results

The Fluor-647 anti-H2A.X-phosphorylated (Ser139) antibody stained significantly more double-stranded breaks in cells treated with ABT-888 and AZD-2281 compared with controls at 8 and 12 Gy (P<0.05).

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Rating

Source

EMBO Mol Med, 2012, 4, 1087–1096. Olaparib (AZD2281) purchased from Selleck

Method

Western Blot

Cell Lines

CAL51 cells

Concentrations

0-10 uM

Incubation Time

48 h

Results

As expected, H2AX phosphorylation could be detected by Western blotting when cells were exposed to 10 uM olaparib (Fig 5C). Whilst FK866 did not in itself induce H2AX phosphorylation, combining FK866 with olaparib caused detectable gH2AX as measured by Western blotting at concentrations of olaparib as low as 0.01 uM (Fig C).

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Rating

Source

HEPATOLOGY, 2012, 55, 1840-1851. Olaparib (AZD2281) purchased from Selleck

Method

Western Blot

Cell Lines

SNU398/SNU449 cells

Concentrations

3 uM

Incubation Time

48 h

Results

The results showed that coadministration of SAHA and olaparib resulted in a synergistic increase in the levels of the cleaved caspase-3 and cleaved PARP in SNU-398 cells as compared with SAHA or olaparib treatment alone. In contrast, the same effect in SNU-449 cells was only modest.

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Rating

Source

HEPATOLOGY, 2012, 55, 1840-1851. Olaparib (AZD2281) purchased from Selleck

Method

Western Blot

Cell Lines

SNU398/SNU449 cells

Concentrations

3 uM

Incubation Time

48 h

Results

Cotreatment with SAHA and olaparib synergistically down-regulated the protein levels of checkpoint protein 1 (Chk1), Chk2, and fanconi anemia group D2 protein (FANCD2) in SNU-398 but not SNU-449 Cells.

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Rating

Source

HEPATOLOGY, 2012, 55, 1840-1851 . Olaparib (AZD2281) purchased from Selleck

Method

Apoptosis assay

Cell Lines

SNU398/SNU449 cells

Concentrations

3 uM

Incubation Time

48 h

Results

Results showed that coadministration of SAHA and olaparib significantly increased apoptosis (12.8%) in SNU-398 cells compared with treatment with individual agent alone, whereas only a minor effect was observed in SNU-449 cells.

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Rating

Source

Dr David Schürmann from University of Basel. Olaparib (AZD2281) purchased from Selleck

Method

Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests, immuno-staining

Cell Lines

Primary human lung fibroblast cells (MRC-5)

Concentrations

0-100 nM

Incubation Time

2 h

Results

In vivo suppression of PAR formation by the PARP inhibitor AZD2281 upon induction of DNA damage Primary human lung fibroblast cells (MRC-5) were pre-treated with the indicated concentration of the PARP inhibitor AZD2281 for two hours. Oxidative DNA damage was induced by 500 µM H2O2 for 10 min and cellular PARP activity was measured by immuno-staining of poly(ADP)-ribose (PAR) (right panels). The in vivo effect of PARP inhibition was compared to cells without DNA damage induction and inhibitor (control) and H2O2-treated cells without inhibitor. Average nuclear PAR staining intensities of more than 50 cells were statistically analysed by Kruskal-Wallis and the post-hoc Dunn’s Multiple Comparison tests (left panel). Asterisks indicate highly significant (p<1%) differences to H2O2-treated cells without PARP inhibitor. Thick horizontal bars mark medians and error bars the interquartile range.

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Rating

Source

Dr Xiangbing Meng of University of Iowa. Olaparib (AZD2281) purchased from Selleck

Method

WST-1 method

Cell Lines

Hec50/Ishikawa/SKOV3/Caov3/PA-1 cell lines

Concentrations

0-12000 nM

Incubation Time

3 d

Results

Effect of AZD 2281 on the viability of endometrial cancer cell line Hec50 and Ishikawa and ovarian cancer cell line SKOV3,Caov3 and PA-1 was detected by WST-1 method after 3 days treatment.

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Rating

Source

JBC, 2011, 286, 12157–12165. Olaparib (AZD2281) purchased from Selleck

Method

Clonogenic Survival Assay

Cell Lines

HCT116+3+5 cells, HT29 cells

Concentrations

2 µM

Incubation Time

Results

As shown in Fig. A, MSH3-deficient G5 cells were more sensitive to olaparib than the MSH3-restored G5 cell line. These data clearly support the role of MSH3 in DSB repairs in CRC cells. Moreover, the combination of oxaliplatin and olaparib exhibited a synergistic effect in cytotoxicity in the MSH3-deficient G5 cells compared with the parental HCT116+3+5 cells. We also confirmed this effect in two other colon cancer cell lines HT29 (Fig. B) and SW480 (data not shown) in a transient knockdown system using MSH3 siRNA.

Product Citations (21)

Double-strand break repair-independent role for BRCA2 in blocking stalled replication fork degradation by MRE11. [Schlacher K, et al. Cell 2011;145(4), 529-542]
PubMed: 21565612
Synthetic lethality of PARP and NAMPT inhibition in triple‐negative breast cancer cells. [Winter GE, et al. Nat Chem Biol 2012;8(11):905-12]
PubMed: 23023260
Topoisomerase I poisoning results in PARP-mediated replication fork reversal. [Ray Chaudhuri A, et al. Nat Struct Mol Biol 2012;19(4):417-23]
PubMed: 22388737

Synergistic inhibition of hepatocellular carcinoma growth by cotargeting chromatin modifying enzymes and poly (ADP-ribose) polymerases. [Zhang JX, et al. Hepatology 2012;55(6):1840-51]
PubMed: 22223166
Nanoparticle-mediated measurement of target-drug binding in cancer cells. [Ullal AV, et al. ACS Nano 2011;5(11), 9216-9224]
PubMed: 21962084
The Forkhead Box M1 protein regulates BRIP1 expression and DNA damage repair in epirubicin treatment. [Monteiro LJ, et al. Oncogene 2012;ahead of print]
PubMed: 23108394
The USP1/UAF1 complex promotes double-strand break repair through homologous recombination. [Murai J, et al. Mol Cell Biol 2011;31(12), 2462-2469]
PubMed: 21482670
Imaging Therapeutic PARP Inhibition In Vivo through Bioorthogonally Developed Companion Imaging Agents. [Reiner T, et al. Neoplasia 2012;14(3):169-77]
PubMed: 22496617
PARP inhibition selectively increases sensitivity to cisplatin in ERCC1-low non-small cell lung cancer cells. [Cheng H, et al. Carcinogenesis 2013;ahead of print]
PubMed: 23275151
MSH3 mediates sensitization of colorectal cancer cells to cisplatin, oxaliplatin, and a poly(ADP-ribose) polymerase inhibitor. [Takahashi M, et al. JBC 2011;286(14), 12157-12165]
PubMed: 21285347
Inhibition of homologous recombination in human cells by targeting RAD51 recombinase. [Huang F, et al. J Med Chem 2012;55(7):3011-20]
PubMed: 22380680
Co-targeting of the PI3K pathway improves the response of BRCA1 deficient breast cancer cells to PARP1 inhibition. [Kimbung S, et al. Cancer Lett 2012;319(2), 232-241]
PubMed: 22266096
Poly (ADP-ribose) polymerase inhibitors combined with external beam and radioimmunotherapy to treat aggressive lymphoma. [King BS, et al. J Biol Chem 2012;287(47):39824-33]
PubMed: 23038248
Induction of Cancerous Stem Cells during Embryonic Stem Cell Differentiation. [Fujimori H, et al. J Biol Chem 2012;287(44):36777-91]
PubMed: 22961983
ATM is dispensable for I-SceI-induced homologous recombination in mouse embryonic stem cells. [Rass E, et al. J Biol Chem 2013;ahead of print]
PubMed: 23355489
A novel role of Krüppel-like factor 8 in DNA repair in breast cancer cells. [Lu H, et al. J Biol Chem 2012;287(52):43720-9]
PubMed: 23105099
Rad51 and BRCA2 - New molecular targets for sensitizing glioma cells to alkylating anticancer Drugs. [Quiros S, et al. Plos ONE 2011;6(11), e27183]
PubMed: 22073281
RECQ1 plays a distinct role in cellular response to oxidative DNA damage. [Sharma S, et al. DNA Repair 2012;11(6), 537-549]
PubMed: 22542292
Garcinol, a histone acetyltransferase inhibitor, radiosensitizes cancer cells by inhibiting non-homologous end joining. [Oike T, et al. Int J Radiat Oncol Biol Phys 2012;84(3):815-21]
PubMed: 22417805
Human monocytes undergo excessive apoptosis following temozolomide activating the ATM/ATR pathway while dendritic cells and macrophages are resistant. [Bauer M, et al. PLoS One 2012;7(6):e39956]
PubMed: 22768182
Radiosensitization effect of poly(ADP-ribose) polymerase inhibition in cells exposed to low and high liner energy transfer radiation. [Hirai T, et al. Cancer Sci 2012;103(6), 1045-50]
PubMed: 22404155

Tech Support & FAQs

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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Related PARP Inhibitors

ABT-888 (Veliparib)

ABT-888 (Veliparib, NSC 737664) is a potent inhibitor of PARP1 and PARP2 with K_i of 5.2 nM and 2.9 nM, respectively.
Iniparib (BSI-201)

BSI-201 (Iniparib, SAR240550) is a PARP1 inhibitor.
Rucaparib (AG-014699 , PF-01367338)

Rucaparib (AG-014699, PF-01367338) is an inhibitor of PARP with K_i of 1.4 nM.
INO-1001
INO-1001 is a potent inhibitor of PARP with IC50 of 50 nM and a mediator of oxidant-induced myocyte dysfunction during reperfusion.
AG14361
AG14361 is a potent inhibitor of PARP1 with K_i of < 5 nM.
A-966492
A-966492 is a novel and potent inhibitor of PARP1 and PARP2 with K_i of 1 nM and 1.5 nM, respectively.
MK-4827
MK-4827 is an selective inhibitor of PARP1 and PARP2 with IC50 of 3.8 nM and 2.1 nM, respectively.
PJ34
PJ-34 is a potent PARP inhibitor with EC50 of 20 nM.
BMN 673
BMN 673 is a novel PARP inhibitor with IC50 of 0.58 nM.
UPF 1069
UPF 1069 is a selective PARP2 inhibitor with IC50 of 0.3 μM.

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Validation & Quality Control

Product Citations(21)

Customer Reviews(10) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

Olaparib (AZD2281) is available in the following compound libraries:

Products used with Olaparib (AZD2281) in previous publications

Product Information

Compare PARP Inhibitors

Research Area

Olaparib (AZD2281) Mechanism

Product Description

Biological Activity

Protocol(Only for Reference)

Kinase Assay:
^[1]

Cell Assay:
^[1]

Animal Study:
^[3]

References

Chemical Information

Research Area

Customer Reviews (10)

Product Citations (21)

Tech Support & FAQs

If you have any other enquiries, please leave a message.

Related PARP Inhibitors

Cell Cycle and DNA Damage Related Products

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Cat.No.	Product Name	Solubility (25°C)
Cat.No.	Product Name	Water	DMSO	Ethanol
S1060	Olaparib (AZD2281)	<1 mg/mL	87 mg/mL	<1 mg/mL
S1004	ABT-888 (Veliparib)	<1 mg/mL	17 mg/mL	<1 mg/mL
S1098	Rucaparib (AG-014699 , PF-01367338)	<1 mg/mL	84 mg/mL	<1 mg/mL
S1087	Iniparib (BSI-201)	<1 mg/mL	58 mg/mL	28 mg/mL
S2197	A-966492	<1 mg/mL	65 mg/mL	<1 mg/mL
S2178	AG14361	<1 mg/mL	12 mg/mL	<1 mg/mL
S1132	INO-1001	<1 mg/mL	27 mg/mL	27 mg/mL
S8038	UPF 1069	<1 mg/mL	56 mg/mL	<1 mg/mL
S7048	BMN 673	<1 mg/mL	96 mg/mL	96 mg/mL

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Olaparib (AZD2281)

Validation & Quality Control

Product Citations(21)

Customer Reviews(10) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

Olaparib (AZD2281) is available in the following compound libraries:

Products used with Olaparib (AZD2281) in previous publications

Product Information

Compare PARP Inhibitors

Research Area

Olaparib (AZD2281) Mechanism

Product Description

Biological Activity

Protocol(Only for Reference)

Kinase Assay: [1]

Cell Assay: [1]

Animal Study: [3]

References

Chemical Information

Research Area

Customer Reviews (10)

Product Citations (21)

Tech Support & FAQs

If you have any other enquiries, please leave a message.

Related PARP Inhibitors

Cell Cycle and DNA Damage Related Products

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Kinase Assay:
^[1]

Cell Assay:
^[1]

Animal Study:
^[3]