olaparib profile

ID Source	ID
PubMed CID	23725625
CHEMBL ID	521686
CHEBI ID	83766
SCHEMBL ID	426568
MeSH ID	M0537510

Synonym
HY-10162
BB 0260909
4-(3-(4-(cyclopropanecarbonyl)piperazine-1-carbonyl)-4-fluorobenzyl)phthalazin-1(2h)-one
4-{[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorophenyl]methyl}-1,2-dihydrophthalazin-1-one
4-({3-[(4-cyclopropanecarbonylpiperazin-1-yl)carbonyl]-4-fluorophenyl}methyl)-1,2-dihydrophthalazin-1-one
bdbm27566
olaparib ,
ku-59436
ku-0059436
azd-2281
AKOS005145764
4-[3-(4-cyclopropanecarbonyl-piperazine-1-carbonyl)-4-fluoro-benzyl]-2h-phthalazin-1-one
763113-22-0
az-2281
chebi:83766 ,
keylynk-010 component olaparib
azd2281
nsc-747856
olaparib component of keylynk-010
az2281
CHEMBL521686
4-[[3-[[4-(cyclopropylcarbonyl)-1-piperazinyl]carbonyl]-4-fluorophenyl]methyl]-1(2h)-phthalazinone
FT-0651458
olaparibum
nsc747856
4-[(3-{[4-(cyclopropylcarbonyl)piperazin-1-yl]carbonyl}-4-fluorophenyl)methyl]phthalazin-1(2h)-one
A9666
4-(3-(1-(cyclopropanecarbonyl)piperazine-4-carbonyl)-4-fluorobenzyl)phthalazin-1(2h)-one
NCGC00238451-02
EX-7210
azd 2281
09l ,
lynparza
4-(3-{[4-(cyclopropylcarbonyl)piperazin-1-yl]carbonyl}-4-fluorobenzyl)phthalazin-1(2h)-one
azd221
4-[(3-{[4-cyclopropylcarbonyl)piperazin-4-yl]carbonyl}-4-fluorophenyl)methyl]phtalazin-1(2h)-one
1-(cyclopropylcarbonyl)-4-[5-[(3,4-dihydro-4-oxo-1-phthalazinyl)methyl]-2-fluorobenzoyl]piperazine
D09730
lynparza (tn)
olaparib (jan/usan/inn)
ku 59436
unii-woh1jd9ar8
woh1jd9ar8 ,
nsc 747856
4-((3-{(4-(cyclopropylcarbonyl)piperazin-1-yl)carbonyl}-4-fluorophenyl)methyl)phthalazin-1(2h)-one
(2h)-phthalazinone, 4-((3-((4-(cyclopropylcarbonyl)-1-piperazinyl)carbonyl)-4-fluorophenyl)methyl)-
olaparib [usan:inn]
olaparib cpd
BCP9000363
ku0059436
olaparib (azd2281, ku-0059436)
c24h23fn4o3
BCPP000360
azd2281,olaparib, ku-0059436
NCGC00238451-01
CS-0075
S1060
BRD-K02113016-001-09-7
BRD-K02113016-001-08-9
FDLYAMZZIXQODN-UHFFFAOYSA-N
SCHEMBL426568
smr004701291
MLS006010185
ku59436
olaparib (azd2281) ,
gtpl7519
4-[[3-[4-(cyclopropanecarbonyl)piperazine-1-carbonyl]-4-fluorophenyl]methyl]-2h-phthalazin-1-one
SS-4573
olaparib [mi]
olaparib [orange book]
olaparib [usan]
olaparib [who-dd]
olaparib [mart.]
olaparib [jan]
olaparib [vandf]
1(2h)-phthalazinone, 4-[[3-[[4-(cyclopropylcarbonyl)-1-piperazinyl]carbonyl]-4-fluorophenyl]methyl]-
olaparib [inn]
piperazine, 1-(cyclopropylcarbonyl)-4-(5-((3,4-dihydro-4-oxo-1-phthalazinyl)methyl)-2-fluorobenzoyl)-
J-503540
mfcd13185161
EX-A002
AC-7939
HMS3654G13
NCGC00238451-09
SW218142-2
azd-2281 (olaparib)
DB09074
DTXSID60917988
olaparib (azd-2281)
SY040527
4-[3-[4-(cyclopropanecarbonyl)piperazine-1-carbonyl]-4-fluorobenzyl]phthalazin-1(2h)-one
763113-22-0, lynparza,
1021843-02-6
BCP01872
Q7083106
AMY10295
olaparib (azd2281; ku-0059436)
SB14617
HMS3870H03
HMS3295I09
HMS3426C03
HMS3746K07
CCG-264799
NCGC00238451-11
NCGC00238451-08
1-(cyclopropylcarbonyl)-4-[5-[(3,4-dihydro-4-oxo-1-phthalazine
olaparib(azd2281,kudosku-0059436)
nsc753686
nsc-753686
BO164169
olaparib- bio-x
4-(3-((4-(cyclopropylcarbonyl)piperazin-1-yl)carbonyl)-4-fluorobenzyl)phthalazin-1(2h)-one
parp inhibitor azd2281
olaparib (mart.)
l01xx46
4-((3-((4-(cyclopropylcarbonyl)piperazin-1-yl)carbonyl)-4-fluorophenyl)methyl)phthalazin-1(2h)-one
1(2h)-phthalazinone, 4-((3-((4-(cyclopropylcarbonyl)-1-piperazinyl)carbonyl)-4-fluorophenyl)methyl)-
EN300-7542225
Z2227698469

Excerpt	Reference	Relevance
"Olaparib is a PARPi, already used in some tumors but not tested in canine species."	( Treatment of Triple Negative Cell Lines with Olaparib to Block DNA Repair. Colombo, J; de Campos Zuccari, DAP; de Souza Tuckumantel, M; Moschetta-Pinheiro, MG; Rebolho, GK, 2022)	1.7
"Olaparib is a PARP1 inhibitor that blocks polyADP-ribosylation, which is involved in the epithelial-mesenchymal transition (EMT) characteristic of tumor recurrence."	( Possible Action of Olaparib for Preventing Invasion of Oral Squamous Cell Carcinoma In Vitro and In Vivo. Fujihara, H; Hamada, Y; Kawaguchi, K; Kishi, Y; Masutani, M; Nakamura, N; Nakayama, R; Yamada, H; Yasukawa, M, 2022)	1.77
"Olaparib is a PARP1 inhibitor used in clinical practice to treat homologous recombination-deficient tumors."	( [Effect of Usnic Acid-Derived Tyrosyl-DNA Phosphodiesterase 1 Inhibitor Used as Monotherapy or in Combination with Olaparib on Transplanted Tumors In Vivo]. Chepanova, AA; Dyrkheeva, NS; Filimonov, AS; Ilina, ES; Kornienko, TE; Lavrik, OI; Luzina, OA; Nikolin, VP; Popova, NA; Salakhutdinov, NF; Zakharenko, AL; Zakharova, OD, )	1.06
"Olaparib is an important drug with minor adverse events compared to chemotherapeutic drugs."	( [Olaparib Could Be Re-Administered after Chemotherapy]. Hayashi, M; Hirata, A; Kimura, K; Morita, S; Takashima, Y; Terasawa, R, 2023)	2.54
"Olaparib is a Poly (ADP-ribose) Polymerase (PARP) inhibitor which has been developed as an anti-cancer agent. "	( In vitro metabolism of olaparib in liver microsomes by liquid chromatography/electrospray ionization high-resolution mass spectrometry. Wang, L; Wang, M, 2020)	2.31
"Olaparib is a PARP inhibitor with a favourable safety profile in comparison to clinically used radiosensitisers including cisplatin when used as single agent."	( Study protocols of three parallel phase 1 trials combining radical radiotherapy with the PARP inhibitor olaparib. de Haan, R; Elkhuizen, P; Peulen, HMU; Schellens, JHM; Sonke, GS; Tesselaar, MET; van den Brekel, MWM; van den Heuvel, MM; van Triest, B; van Werkhoven, E; Vens, C; Verheij, M, 2019)	1.45
"Olaparib is a PARP inhibitor approved for maintenance therapy following platinum-based chemotherapy."	( Biguanides in combination with olaparib limits tumorigenesis of drug-resistant ovarian cancer cells through inhibition of Snail. Amin, O; Baloch, T; Bithras, J; Kessous, R; Kogan, L; Laskov, I; López-Ozuna, VM; Wang, Q; Yasmeen, A, 2020)	1.57
"Olaparib is a first-in-class PARP inhibitor that has demonstrated efficacy as maintenance therapy in patients with ovarian cancer. "	( Pharmacological issues concerning olaparib capsule and tablet formulations in treating ovarian cancer: Are they really the same drug? Cabiddu, M; Castelli, EA; Nozza, R; Oggionni, E; Omati, E; Perego, G; Petrelli, F; Scolari, C, 2020)	2.28
"Olaparib is a PARP1/2 inhibitor recently FDA-approved for treatment of BRCA1 and BRCA2 mutation carriers with metastatic breast cancer."	( The PARP inhibitor, olaparib, depletes the ovarian reserve in mice: implications for fertility preservation. Griffiths, M; Hutt, KJ; Lliberos Requesens, C; Phillips, KA; Sarma, U; Winship, AL, 2020)	1.6
"Olaparib is a potent inhibitor of poly(ADP-ribose) polymerase (PARP)-1, 2, and 3 with potential activity in endometrial cancer (EC)."	( An olaparib window-of-opportunity trial in patients with early-stage endometrial carcinoma: POLEN study. Coronado, P; Cortés, A; Cueva, JF; Gómez, L; Guerra, EM; Llombart-Cussac, A; Malfettone, A; Matias-Guiu, X; Medina, M; Minig, L; Poveda, A; Romero, I; Rubio, MJ; Sampayo, M; Santacana, M; Schoenenberger, JA, 2020)	2.62
"Olaparib (Ola) is a PARP inhibitor that is involved in preventing the release of PARP from RT-induced damaged DNA to potentiate the effect of RT."	( Enhanced Anti-Cancer Effect of Folate-Conjugated Olaparib Nanoparticles Combined with Radiotherapy in Cervical Carcinoma. Chen, Y; Fu, SZ; Hu, C; Li, D; Liao, Y; Wu, JB; Yang, J, 2020)	1.53
"Olaparib is an oral inhibitor of Poly (ADP-Ribose) polymerase (PARP) and has demonstrated optimal efficacy and clinical activity in trials."	( Combination of talaporfin photodynamic therapy and Poly (ADP-Ribose) polymerase (PARP) inhibitor in gastric cancer. Kataoka, H; Nishie, H; Sasaki, M; Suzuki, T; Tanaka, M, 2021)	1.34
"Olaparib is a poly-adenosine diphosphate-ribose polymerase inhibitor, which has been reported to inhibit glioma in preclinical and clinical trials."	( Successful treatment of an adult patient with diffuse midline glioma employing olaparib combined with bevacizumab. Luo, N; Qi, C; Tao, R; Wang, Y; Xu, J, 2021)	1.57
"Olaparib is an oral poly-adenosine diphosphate-ribose polymerase (PARP) inhibitor, which has been proven to treat BRCA-mutated tumors effectively, especially breast and ovarian cancer."	( Response to olaparib in metastatic lung adenocarcinoma with germline BRCA2 mutation: a case report. Fan, M; Hu, Y; Wu, C, 2022)	1.82
"Olaparib is an oral inhibitor of polyadenosine 5'-diphosphoribose polymerization (PARP) that has previously shown signs of activity in patients with BRCA mutations and pancreatic ductal adenocarcinoma (PDAC)."	( Olaparib in combination with irinotecan, cisplatin, and mitomycin C in patients with advanced pancreatic cancer. Azad, NS; De Jesus-Acosta, A; Donehower, RC; Fine, RL; Goggins, M; Jaffee, EM; Johnson, BA; Laheru, DA; Le, DT; Myzak, MC; Oberstein, PE; Yarchoan, M; Zheng, L, 2017)	3.34
"Olaparib is an oral poly(adenosine diphosphate-ribose) polymerase inhibitor that has promising antitumor activity in patients with metastatic breast cancer and a germline BRCA mutation."	( Olaparib for Metastatic Breast Cancer in Patients with a Germline BRCA Mutation. Armstrong, A; Conte, P; Delaloge, S; Domchek, SM; Goessl, C; Im, SA; Li, W; Masuda, N; Robson, M; Runswick, S; Senkus, E; Tung, N; Wu, W; Xu, B, 2017)	3.34
"Olaparib is a potent orally bioavailable poly(ADP-ribose) polymerase inhibitor (PARPi), approved for BRCA-mutated ovarian and breast cancers. "	( The poly(ADP-ribose) polymerase inhibitor olaparib induces up-regulation of death receptors in primary acute myeloid leukemia blasts by NF-κB activation. Aloisio, F; Consalvo, MI; De Gabrieli, A; Faraoni, I; Graziani, G; Lavorgna, S; Lo-Coco, F; Voso, MT, 2018)	2.19
"Olaparib is a poly(ADP-ribose) polymerase enzyme inhibitor that is approved for use in patients with advanced ovarian cancer (OC) and genetic "	( Administration of the Tablet Formulation of Olaparib in Patients with Ovarian Cancer: Practical Guidance and Expectations. Birrer, MJ; Moore, KN, 2018)	2.18
"Olaparib was shown to be a weak inhibitor of CYP3A (1.6-fold increase in exposure of a sensitive CYP3A probe) and to have no effect on P-glycoprotein or UGT1A1 substrates."	( Physiologically Based Pharmacokinetic Modeling for Olaparib Dosing Recommendations: Bridging Formulations, Drug Interactions, and Patient Populations. Bui, K; Learoyd, M; Pilla Reddy, V; Scarfe, G; Zhou, D, 2019)	1.49
"Olaparib is an orally active inhibitor of poly(ADP-ribose) polymerase (PARP) which has demonstrated anti-tumor activity in ovarian cancer."	( Olaparib for the treatment of relapsed ovarian cancer with a BRCA1/2 mutation. Banerjee, S; George, A; Stewart, J, 2018)	2.64
"Olaparib is a new treatment option for patients with a gBRCAm who have metastatic HER2-negative breast cancer."	( Olaparib tablets for the treatment of germ line BRCA-mutated metastatic breast cancer. Gelmon, KA; Le, D, 2018)	2.64
"Olaparib is a poly (adenosine diphosphate‑ribose) polymerase (PARP) 1 inhibitor, which has promising antitumor activity in patients with metastatic breast cancer and germline BRCA mutations."	( PARP inhibitor re‑sensitizes Adriamycin resistant leukemia cells through DNA damage and apoptosis. Huang, L; Li, Q; Ouyang, Y; Wu, J; Wu, W; Xiao, G; Xiao, S; Yao, C; Yuan, M, 2019)	1.24
"Olaparib is a poly ADP-ribose polymerase inhibitor that induces synthetic lethality in tumors with deficient homologous recombination repair. "	( Efficacy and Safety Exposure-Response Analyses of Olaparib Capsule and Tablet Formulations in Oncology Patients. Al-Huniti, N; Berges, A; Bui, K; Learoyd, M; Li, J; Milenkova, T; Tomkinson, H; Xu, H; Zhou, D, 2019)	2.21
"Olaparib (Ola) is a PARP inhibitor that is involved in arresting PARP release from radiotherapy (RT)-induced damaged DNA to potentiate the effect of RT."	( Olaparib nanoparticles potentiated radiosensitization effects on lung cancer. Chen, Y; Fu, S; Hu, C; Li, D; Liu, J; Wu, J; Wu, M; Wu, Z; Yang, J; Yang, L, 2018)	2.64
"Olaparib is a PARP inhibitor (PARPi). "	( Rad51/BRCA2 disruptors inhibit homologous recombination and synergize with olaparib in pancreatic cancer cells. Bagnolini, G; Balboni, A; Cavalli, A; De Franco, F; Di Stefano, G; Falchi, F; Farabegoli, F; Giacomini, E; Girotto, S; Manerba, M; Milano, D; Minucci, S; Pallavicini, I; Pellicciari, R; Roberti, M; Robertson, J; Schipani, F, 2019)	2.19
"Olaparib is a poly(ADP-ribose) polymerase inhibitor and cediranib is an oral anti-angiogenic. "	( Overall survival and updated progression-free survival outcomes in a randomized phase II study of combination cediranib and olaparib versus olaparib in relapsed platinum-sensitive ovarian cancer. Barry, WT; Birrer, M; Buckanovich, RJ; Buss, MK; Curtis, J; Fleming, GF; Hurteau, J; Ivy, SP; Kohn, EC; Lee, JM; Liu, JF; Luo, W; Matulonis, UA; Nattam, SR; Rimel, BJ; Whalen, C, 2019)	2.16
"Olaparib is an inhibitor of poly ADP ribose polymerase 1 (PARP-1). "	( Development and validation of a high-performance liquid chromatography-tandem mass spectrometry assay quantifying olaparib in human plasma. Beijnen, JH; Lucas, L; Nijenhuis, CM; Rosing, H; Schellens, JH, 2013)	2.04
"Olaparib is a poly(ADP-ribose) polymerase inhibitor and cediranib is an anti-angiogenic agent with activity against VEGF receptor (VEGFR) 1, VEGFR2, and VEGFR3. "	( Combination cediranib and olaparib versus olaparib alone for women with recurrent platinum-sensitive ovarian cancer: a randomised phase 2 study. Barry, WT; Birrer, M; Buckanovich, RJ; Buss, MK; Fleming, GF; Hurteau, J; Ivy, SP; Kohn, EC; Lee, H; Lee, JM; Liu, JF; Luo, W; Matulonis, UA; Nattam, S; Obermayer, L; Quy, P; Rimel, B; Whalen, C; Winer, EP, 2014)	2.15
"Olaparib is an oral poly (ADP-ribose) polymerase inhibitor with activity in germline BRCA1 and BRCA2 (BRCA1/2) -associated breast and ovarian cancers. "	( Olaparib monotherapy in patients with advanced cancer and a germline BRCA1/2 mutation. Audeh, MW; Balmaña, J; Bowen, K; Domchek, SM; Fielding, A; Fried, G; Friedlander, M; Hubert, A; Kaufman, B; Loman, N; Mitchell, G; Rosengarten, O; Schmutzler, RK; Shapira-Frommer, R; Steiner, M; Stemmer, SM, 2015)	3.3
"Olaparib is a potent new generation PARP inhibitor that has been approved for human testing."	( PARP inhibitor, olaparib ameliorates acute lung and kidney injury upon intratracheal administration of LPS in mice. Kapoor, K; Naura, AS; Sahu, B; Singla, E, 2015)	1.48
"Olaparib (Lynparza) is an oral poly(adenosine diphosphate [ADP]-ribose) polymerase inhibitor that induces synthetic lethality in cancers with homologous recombination defects."	( Phase I study of olaparib plus gemcitabine in patients with advanced solid tumours and comparison with gemcitabine alone in patients with locally advanced/metastatic pancreatic cancer. Bendell, J; Burke, W; Burris, H; Chau, I; Fielding, A; Hochster, H; Middleton, MR; O'Reilly, EM, 2015)	2.2
"Olaparib (Lynparza™) is an oral, small molecule, poly (ADP-ribose) polymerase inhibitor being developed by AstraZeneca for the treatment of solid tumours. "	( Olaparib: first global approval. Deeks, ED, 2015)	3.3
"Olaparib (Lynparza™) is a first-in-class, orally-active, small molecule, poly (ADP-ribose) polymerase inhibitor that induces synthetic lethality in homozygous BRCA-deficient cells. "	( Olaparib: a review of its use as maintenance therapy in patients with ovarian cancer. Frampton, JE, 2015)	3.3
"Olaparib (Lynparza®) is an oral, small molecule, poly (ADP-ribose) polymerase inhibitor that has become the first 'personalized' therapy available for patients with BRCA mutation-positive ovarian cancer (OC). "	( Safety evaluation of olaparib for treating ovarian cancer. Bowering, V; Karakasis, K; Lheureux, S; Oza, AM, 2015)	2.18
"Olaparib is a novel PARP inhibitor that is efficacious and well tolerated in patients with BRCA-mutated advanced ovarian cancers who have received three or more lines of prior treatment."	( Olaparib for the treatment of BRCA-mutated advanced ovarian cancer. Kolesar, J; Munroe, M, 2016)	3.32
"Olaparib is an FDA-approved PARP inhibitor (PARPi) that has shown promise as a synthetic lethal treatment approach for BRCA-mutant castration-resistant prostate cancer (CRPC) in clinical use. "	( Targeting Plk1 to Enhance Efficacy of Olaparib in Castration-Resistant Prostate Cancer. Broman, MM; Carlock, C; Chen, L; Farah, E; Kong, Y; Li, J; Li, Z; Liu, X; Ratliff, TL; Wang, R, 2017)	2.17
"Olaparib is an oral PARP inhibitor that blocks DNA repair pathway and coupled with BRCA mutated-disease results in tumor cell death."	( Defective DNA repair mechanisms in prostate cancer: impact of olaparib. De Felice, F; Marampon, F; Marchetti, C; Musella, A; Tombolini, V, 2017)	1.42
"Olaparib is a potent, oral PARP inhibitor that is well tolerated, with antitumor activity in BRCA1/2 mutation carriers."	( Poly(ADP)-ribose polymerase inhibition: frequent durable responses in BRCA carrier ovarian cancer correlating with platinum-free interval. A'Hern, R; Ashworth, A; Boss, DS; Carden, CP; Carmichael, J; de Bono, JS; De Greve, J; Fong, PC; Gourley, C; Kaye, SB; Lubinski, J; Mergui-Roelvink, M; Messiou, C; Schellens, JH; Shanley, S; Stone, J; Tutt, A; Yap, TA, 2010)	1.08
"Olaparib is a novel, orally active poly(ADP-ribose) polymerase (PARP) inhibitor that induces synthetic lethality in homozygous BRCA-deficient cells. "	( Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial. Audeh, MW; Bell-McGuinn, KM; Carmichael, J; Friedlander, M; Loman, N; Lu, K; Matulonis, U; Oaknin, A; Penson, RT; Powell, B; Schmutzler, RK; Scott, C; Tutt, A; Weitzel, JN; Wickens, M, 2010)	2.07
"Olaparib (AZD2281) is a small-molecule, potent oral poly(ADP-ribose) polymerase (PARP) inhibitor. "	( Olaparib in patients with recurrent high-grade serous or poorly differentiated ovarian carcinoma or triple-negative breast cancer: a phase 2, multicentre, open-label, non-randomised study. Carmichael, J; Clemons, M; Gelmon, KA; Gilks, B; Hirte, H; Huntsman, D; Mackay, H; Macpherson, E; Oza, A; Robidoux, A; Swenerton, K; Tischkowitz, M; Tonkin, K; Yerushalmi, R, 2011)	3.25
"Olaparib (AZD2281) is an orally active Poly(ADP-ribose) polymerase (PARP) inhibitor with favorable antitumor activity in advanced ovarian and breast cancers with BRCA1/2 mutations in Western (USA and European) studies. "	( A Phase I, dose-finding and pharmacokinetic study of olaparib (AZD2281) in Japanese patients with advanced solid tumors. Asahina, H; Goto, Y; Kawata, T; Nokihara, H; Shi, X; Shibata, T; Tamura, T; Tanioka, M; Yamada, K; Yamada, Y; Yamamoto, N, 2012)	2.07
"Olaparib (AZD2281) is a potent oral poly(ADP-ribose) polymerase inhibitor with anti-tumour activity and acceptable toxicity as monotherapy in patients with BRCA-deficient cancers. "	( Phase I study to assess the safety and tolerability of olaparib in combination with bevacizumab in patients with advanced solid tumours. Carmichael, J; Dean, E; Goodege-Kunwar, P; Middleton, MR; Pwint, T; Ranson, M; Swaisland, H, 2012)	2.07
"Olaparib (AZD2281) is an oral poly(adenosine diphosphate [ADP]-ribose) polymerase inhibitor that has shown antitumor activity in patients with high-grade serous ovarian cancer with or without BRCA1 or BRCA2 germline mutations."	( Olaparib maintenance therapy in platinum-sensitive relapsed ovarian cancer. Carmichael, J; Friedlander, M; Gourley, C; Harter, P; Ledermann, J; Macpherson, E; Matei, D; Matulonis, U; Meier, W; Rustin, G; Safra, T; Scott, C; Shapira-Frommer, R; Vergote, I; Watkins, C, 2012)	3.26
"Olaparib is an orally bioavailable inhibitor of PARP-1 and PARP-2 that has been tested in multiple clinical trials."	( The combination of olaparib and camptothecin for effective radiosensitization. Hareyama, M; Matsumoto, H; Matsumoto, Y; Miura, K; Sakata, K; Someya, M; Takahashi, A, 2012)	1.43
"Olaparib (AZD2281) is an oral poly(ADP-ribose) polymerase (PARP) inhibitor with antitumour activity in cancer patients with BRCA1/2 germline mutations and in patients with homologous recombination deficiency. "	( Evaluation of the pharmacodynamics and pharmacokinetics of the PARP inhibitor olaparib: a phase I multicentre trial in patients scheduled for elective breast cancer surgery. Bundred, N; Carmichael, J; Cavallin, M; Dixon, JM; Eglitis, J; Gardovskis, J; Jaskiewicz, J; McCormack, P; Paramonov, V; Parry, T; Swaisland, H, 2013)	2.06

Excerpt	Reference	Relevance
"Olaparib has a high potential of being a cost-effective maintenance treatment versus RS for patients with "	( Cost-effectiveness of olaparib versus routine surveillance in the maintenance setting for patients with Chan, JJ; Ghosh, W; Hettle, R; Tan, DS; Viswambaram, A; Yu, CC, 2021)	2.38
"Olaparib has shown significant clinical benefit as maintenance therapy in women with newly diagnosed advanced ovarian cancer with a "	( Olaparib plus Bevacizumab as First-Line Maintenance in Ovarian Cancer. Berger, R; Buderath, P; Burges, A; Canzler, U; Colombo, N; Combe, P; de Gregorio, N; Dubot, C; Fujiwara, K; González-Martín, A; Guerra Alía, EM; Harter, P; Lefeuvre-Plesse, C; Lortholary, A; Lorusso, D; Mäenpää, J; Marmé, F; Nagao, S; Pautier, P; Pérol, D; Pignata, S; Pujade-Lauraine, E; Ray-Coquard, I; Reinthaller, A; Rodrigues, M; Scambia, G; Sehouli, J; Selle, F; Vergote, I; You, B, 2019)	3.4
"Olaparib has been approved as an active and maintenance therapy for patients with platinum-sensitive, BRCA-mutated high-grade serous ovarian cancer (SOC). "	( Real-world clinical outcomes of olaparib therapy in Chinese patients with advanced serous ovarian cancer treated in Macau. Cao, Y; Chen, H; Hu, H; Huang, Y, 2019)	2.24
"Olaparib has been approved as a PARP inhibitor."	( Design, Synthesis and Activity Evaluation of New Phthalazinone PARP Inhibitors. Cai, J; Chen, X; Huang, M; Ji, M; Li, X; Ren, J; Tang, T; Wang, Y; Yang, J; Yang, Z, 2021)	1.34
"Olaparib has been authorised in the EU for continuous single-agent therapy after the end of platinum-based chemotherapy in patients with "plati- num-sensitive" BRCA-positive ovarian cancer who have already received at least two lines of platinum-based che- motherapy and entered complete or partial remission after the last course of treatment."	( Olaparib (LYNPARZAO) Ovarian cancer: spare patients who are in remission. , 2017)	2.62

Excerpt	Reference	Relevance
"Olaparib was able to enhance the effect of radiation by inhibiting PARP1, inducing DNA lesions and apoptosis."	( PARP inhibitor olaparib sensitizes cholangiocarcinoma cells to radiation. Chen, J; Duan, F; Huang, X; Li, S; Lin, G; Mao, Y; Shuang, Z; Wang, J, 2018)	1.56
"Olaparib can also cause life-threatening myelo- dysplastic syndrome, acute myeloid leukaemia, and haemorrhage."	( Olaparib (LYNPARZAO) Ovarian cancer: spare patients who are in remission. , 2017)	2.62
"Olaparib was used to inhibit PARP."	( The PARP inhibitor olaparib exerts beneficial effects in mice subjected to cecal ligature and puncture and in cells subjected to oxidative stress without impairing DNA integrity: A potential opportunity for repurposing a clinically used oncological drug f Ahmad, A; Ariga, SK; Barbeiro, DF; Barbeiro, HV; de Lima, TM; de Mello, AH; Druzhyna, N; Kiss, A; Liaudet, L; Marcatti, M; Randi, EB; Salomao, R; Soriano, FG; Szabo, C; Szczesny, B; Toliver-Kinsky, T; Törö, G; Vieira, JC, 2019)	1.56
"Olaparib-alone did not inhibit the cell growth and did not induce apoptosis in either HL-60 cells or HL/GO20 cells at concentrations of up to 10 μM."	( Gemtuzumab ozogamicin and olaparib exert synergistic cytotoxicity in CD33-positive HL-60 myeloid leukemia cells. Nishi, R; Shigemi, H; Ueda, T; Uzui, K; Yamauchi, T, 2014)	1.42

Excerpt	Reference	Relevance
"Olaparib treatment led to different cellular responses depending on EBV infection in gastric cancer cell lines. "	( Olaparib-induced Apoptosis Through EBNA1-ATR-p38 MAPK Signaling Pathway in Epstein-Barr Virus-positive Gastric Cancer Cells. Cheong, SH; Hur, DY; Kim, YS; Moon, SH; Noh, MH; Park, NS, 2022)	3.61
"Olaparib-treated patients were interviewed by phone. "	( Olaparib for ovarian cancer: a single-institution, multi-site qualitative study. Asiedu, G; Ehret, C; Hanna, M; Jatoi, A; Martin, NA, 2022)	3.61
"Olaparib treatment markedly reduced their proliferation, migration, invasion, and adhesion."	( Possible Action of Olaparib for Preventing Invasion of Oral Squamous Cell Carcinoma In Vitro and In Vivo. Fujihara, H; Hamada, Y; Kawaguchi, K; Kishi, Y; Masutani, M; Nakamura, N; Nakayama, R; Yamada, H; Yasukawa, M, 2022)	1.77
"Olaparib treatment led to an improvement in progression-free survival compared with placebo (hazard ratio = 0.44, 95% confidence interval: 0.17-1.19; median = 13.8 vs."	( Olaparib maintenance monotherapy in Chinese patients with platinum-sensitive relapsed ovarian cancer: China cohort from the phase III SOLO2 trial. Chen, Y; Cheng, Y; Gao, Y; Hsu, K; Kong, B; Li, W; Liu, J; Lou, G; Lu, W; Lu, X; Ma, X; Wang, J; Wang, Y; Wu, L; Wu, X; Yin, R; Zhou, Q; Zhu, J, 2022)	2.89
"Olaparib treatment resulted in significant improvement in objective response rates (ORRs) and progression-free survival (PFS) over non‑platinum chemotherapy in patients with BRCA1/BRCA2-mutated (BRCAm) platinum-sensitive relapsed ovarian cancer (PSROC) and ≥2 prior lines of platinum-based chemotherapy in the phase III SOLO3 study. "	( Olaparib treatment for platinum-sensitive relapsed ovarian cancer by BRCA mutation and homologous recombination deficiency status: Phase II LIGHT study primary analysis. Aghajanian, C; Altman, AD; Bennett, J; Black, D; Cadoo, K; ElNaggar, AC; Gilbert, L; Kabil, N; Liu, YL; Mathews, C; McCormick, C; Munley, J; Provencher, D; Simpkins, F, 2022)	3.61
"Olaparib treatment demonstrated activity across all cohorts. "	( Olaparib treatment for platinum-sensitive relapsed ovarian cancer by BRCA mutation and homologous recombination deficiency status: Phase II LIGHT study primary analysis. Aghajanian, C; Altman, AD; Bennett, J; Black, D; Cadoo, K; ElNaggar, AC; Gilbert, L; Kabil, N; Liu, YL; Mathews, C; McCormick, C; Munley, J; Provencher, D; Simpkins, F, 2022)	3.61
"Olaparib treatment increased the number of grade ≥3 adverse events (AEs) in patients with advanced ovarian cancer compared with that in the control group."	( Efficacy and safety of olaparib in advanced ovarian cancer: a meta-analysis. Li, H; Tong, X; Yang, X; Yang, Y; Zhu, X, 2023)	1.94
"Olaparib-based treatment modulates the tumor microenvironment leading to upregulation of PD-L1 and induction of protumor features of macrophages."	( Phase II Window Study of Olaparib Alone or with Cisplatin or Durvalumab in Operable Head and Neck Cancer. Anastasiou, M; Aung, TN; Delides, A; Economopoulou, P; Fernandez, AI; Foukas, PG; Fountzilas, G; Gagari, E; Gavrielatou, N; Giotakis, E; Gkolfinopoulos, S; Gkotzamanidou, M; Koliou, GA; Kotsantis, I; Kougioumtzopoulou, A; Kouloulias, V; Kyrodimos, E; Lianidou, E; Moutafi, M; Palialexis, K; Panayiotides, IG; Papadimitriou, NG; Papaxoinis, G; Pectasides, D; Perisanidis, C; Poulios, C; Psyrri, A; Rimm, DL; Shafi, S; Strati, A; Xirou, V; Yaghoobi, V, 2023)	1.93
"Olaparib treatment starts two days before radiotherapy and continues during weekends until two days after radiotherapy."	( Study protocols of three parallel phase 1 trials combining radical radiotherapy with the PARP inhibitor olaparib. de Haan, R; Elkhuizen, P; Peulen, HMU; Schellens, JHM; Sonke, GS; Tesselaar, MET; van den Brekel, MWM; van den Heuvel, MM; van Triest, B; van Werkhoven, E; Vens, C; Verheij, M, 2019)	1.45
"Olaparib cotreatment significantly increased phosphorylated H2A histone family member X (γH2AX) foci as well as 53BP1/γH2AX co-localisation in anticancer drug-treated cells."	( Olaparib Potentiates Anticancer Drug Cytotoxicity Hayashi, I; Hirano, S; Minegaki, T; Miyamoto, K; Nishiguchi, K; Tsujimoto, M, 2020)	2.72
"Olaparib treatment or PARP1/2 deletion promotes osteoclast differentiation and bone loss."	( Differential regulation of breast cancer bone metastasis by PARP1 and PARP2. Fu, YX; Tang, H; Wan, Y; Yang, D; Yang, Q; Zuo, H, 2020)	1.28
"Olaparib treatment reduced cell viability and cell migration in a dose-dependent manner in vitro."	( Olaparib and temozolomide in desmoplastic small round cell tumors: a promising combination in vitro and in vivo. Desar, IME; Fleuren, EDG; Flucke, UE; Hillebrandt-Roeffen, MHS; Mentzel, T; Shipley, J; van Bree, NFHN; van der Graaf, WTA; van Erp, AEM; van Houdt, L; Versleijen-Jonkers, YMH, 2020)	2.72
"Olaparib treatment, when administered alone, depletes primordial follicle oocytes, but olaparib does not exacerbate chemotherapy-mediated ovarian follicle loss in mice."	( The PARP inhibitor, olaparib, depletes the ovarian reserve in mice: implications for fertility preservation. Griffiths, M; Hutt, KJ; Lliberos Requesens, C; Phillips, KA; Sarma, U; Winship, AL, 2020)	2.32
"Olaparib treatment led to more severe autophagy and apoptosis in FLCN deficient ACHN-2 and UOK257 cells compared to the FLCN expressing ACHN and UOK257-F cells."	( Folliculin deficient renal cancer cells exhibit BRCA1 A complex expression impairment and sensitivity to PARP1 inhibitor olaparib. Chen, Y; Li, J; Xia, Q; Xu, Y; Zhang, Q; Zhang, Z, 2021)	1.55
"Olaparib treatment, or silencing of PARP1, consequently, increases Fra-1 levels and enhances its transcriptional activity."	( Blocking Fra-1 sensitizes triple-negative breast cancer to PARP inhibitor. Archer, A; Haldosen, LA; Hases, L; He, H; Sinha, I; Song, D; Williams, C; Yan, F; Zhao, C, 2021)	1.34
"Olaparib maintenance treatment in BRCA-mutated recurrent ovarian cancer is effective and safe in clinical practice. "	( Real-world experience of olaparib as maintenance therapy in BRCA-mutated recurrent ovarian cancer. Cho, A; Kim, DY; Kim, JH; Kim, YM; Kim, YT; Lee, SW; Park, JY; Suh, DS, 2021)	2.37
"Olaparib pretreatment significantly improved the survival of septic mice ("	( Olaparib attenuates sepsis-induced acute multiple organ injury via ERK-mediated CD14 expression. Chen, Y; Chen, Z; Jin, X; Li, Q; Liu, Y; Shao, Z, 2021)	2.79
"Olaparib is a new treatment option for patients with a gBRCAm who have metastatic HER2-negative breast cancer."	( Olaparib tablets for the treatment of germ line BRCA-mutated metastatic breast cancer. Gelmon, KA; Le, D, 2018)	2.64
"Olaparib treatment significantly increased cell death in BRCA2 mutated tumors slices as compared to slices from BRCA2 wild type tumors."	( Ex vivo treatment of prostate tumor tissue recapitulates in vivo therapy response. de Ridder, CMA; Erkens-Schulze, S; Kanaar, R; Meijer, TG; Nonnekens, J; Schönfeld, E; van Gent, DC; van Weerden, WM; Zhang, W, 2019)	1.24
"Olaparib maintenance treatment could be effective for Japanese patients with PPC and multiple BMs."	( Durable response by olaparib for a Japanese patient with primary peritoneal cancer with multiple brain metastases: A case report. Hirotsu, Y; Ikegami, A; Nakagomi, H; Omata, M; Sakamoto, I; Teramoto, K, 2019)	1.56
"Olaparib treatment reduced the degree of bacterial CFUs."	( The PARP inhibitor olaparib exerts beneficial effects in mice subjected to cecal ligature and puncture and in cells subjected to oxidative stress without impairing DNA integrity: A potential opportunity for repurposing a clinically used oncological drug f Ahmad, A; Ariga, SK; Barbeiro, DF; Barbeiro, HV; de Lima, TM; de Mello, AH; Druzhyna, N; Kiss, A; Liaudet, L; Marcatti, M; Randi, EB; Salomao, R; Soriano, FG; Szabo, C; Szczesny, B; Toliver-Kinsky, T; Törö, G; Vieira, JC, 2019)	1.56
"Olaparib treatment achieved a significant reduction in tumor size in a low estrogenic milieu."	( Low levels of circulating estrogen sensitize PTEN-null endometrial tumors to PARP inhibition in vivo. Cheng, D; Faull, K; Janzen, DM; Jung, ME; Kayadibi, H; Memarzadeh, S; Paik, DY; Rosales, MA; Ryan, CM; Witte, ON; Yep, B, 2013)	1.11
"Olaparib-treated U2OS(DR-GFP) cells showed a dramatic decrease in DNA damage repair versus veliparib irrespective of inhibitory potency."	( New insights into PARP inhibitors' effect on cell cycle and homology-directed DNA damage repair. Jelinic, P; Levine, DA, 2014)	1.12
"Olaparib treatment increased unrepaired DNA DSB (P<.001) and apoptosis (P<.001) in hypoxic cells of Calu-6 tumors following radiation, whereas it had no significant effect on radiation-induced DNA damage response in nonhypoxic cells of Calu-6 tumors or in the tumor cells of well-oxygenated Calu-3 tumors."	( Hypoxia Potentiates the Radiation-Sensitizing Effect of Olaparib in Human Non-Small Cell Lung Cancer Xenografts by Contextual Synthetic Lethality. Bokobza, SM; Devery, AM; Hammond, EM; Jiang, Y; Leszczynska, KB; Ryan, AJ; Verbiest, T; Weber, AM, 2016)	1.4
"Treatment with olaparib in combination with radiation delayed tumour cell proliferation in vitro through the reduction of PAR. "	( Radiosensitisation by olaparib through focused ultrasound delivery in a diffuse midline glioma model. 't Hart, E; Berkhout, K; Besse, HC; Bianco, J; Bruin, MAC; Chin Joe Kie, LA; Derieppe, M; Hoving, EW; Huitema, ADR; Ries, MG; Su, Y; van Vuurden, DG, 2023)	1.58
"Treatment was olaparib 300 mg twice a day continuously and celarasertib 160 mg on days 1-7 on a 28-day cycle until disease progression."	( Olaparib and Ceralasertib (AZD6738) in Patients with Triple-Negative Advanced Breast Cancer: Results from Cohort E of the plasmaMATCH Trial (CRUK/15/010). Afshari-Mehr, A; Baird, RD; Bliss, JM; Burcombe, R; Copson, E; Dunne, K; Ferreira, A; Gurel, B; Hickish, T; Johnson, H; Kilburn, LS; Llop-Guevara, A; Macpherson, IR; Martin, S; Moretti, L; Pearson, A; Randle, K; Riisnaes, R; Ring, A; Roylance, R; Serra, V; Turner, NC; Wardley, AM; Winter, MC, 2023)	2.7
"Treatment with olaparib increased phosphorylation of ATM and PTEN while decreasing the phosphorylation of AKT and mTOR and inducing autophagy."	( Poly(adenosine diphosphate ribose) polymerase inhibitors induce autophagy-mediated drug resistance in ovarian cancer cells, xenografts, and patient-derived xenograft models. Amaravadi, RK; Bast, RC; Becker, SE; Heinzen, EP; Hou, X; Llombart-Cussac, A; Lu, Z; Matias-Guiu, X; Maurer, MJ; Oberg, AL; Pang, L; Poveda, A; Rask, P; Romero, I; Rubio, MJ; Santacana, M; Santiago-O'Farrill, JM; Weroha, SJ, 2020)	0.9
"Treatment with olaparib alone was not cytotoxic, but highly radiosensitized cell lines, particularly at high dose per fraction A non-cytotoxic concentration of gemcitabine radiosensitized cells, but less than olaparib."	( Gemcitabine-Based Chemoradiotherapy Enhanced by a PARP Inhibitor in Pancreatic Cancer Cell Lines. Amé, JC; Burckel, H; Mura, C; Noël, G; Waissi, W, 2021)	0.96
"Treatment with olaparib requires patients to take eight capsules twice a day, between meals."	( Olaparib (LYNPARZAO) Ovarian cancer: spare patients who are in remission. , 2017)	2.24

Excerpt	Reference	Relevance
" The most common adverse events (AEs) included fatigue and gastrointestinal events."	( Safety and tolerability of the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib (AZD2281) in combination with topotecan for the treatment of patients with advanced solid tumors: a phase I study. Carmichael, J; Cassidy, J; Macpherson, E; Ranson, M; Samol, J; Scott, E; Thomas, A, 2012)	0.61
" The most common adverse events (AEs) related to olaparib were grade 1/2 nausea and fatigue."	( Phase I study to assess the safety and tolerability of olaparib in combination with bevacizumab in patients with advanced solid tumours. Carmichael, J; Dean, E; Goodege-Kunwar, P; Middleton, MR; Pwint, T; Ranson, M; Swaisland, H, 2012)	0.88
" They continued with olaparib monotherapy in their best interest if they failed to tolerate the combination due to the treatment-related adverse events (TRAEs)."	( Long-term safety and anti-tumour activity of olaparib monotherapy after combination with carboplatin and paclitaxel in patients with advanced breast, ovarian or fallopian tube cancer. Beijnen, JH; Harms, E; Marchetti, S; Mergui-Roelvink, MW; Rehorst, H; Schellens, JH; Sonke, GS; Steeghs, N; van der Noll, R, 2015)	1
"Continued long-term daily olaparib was found to be safe and tolerable."	( Long-term safety and anti-tumour activity of olaparib monotherapy after combination with carboplatin and paclitaxel in patients with advanced breast, ovarian or fallopian tube cancer. Beijnen, JH; Harms, E; Marchetti, S; Mergui-Roelvink, MW; Rehorst, H; Schellens, JH; Sonke, GS; Steeghs, N; van der Noll, R, 2015)	0.98
" Safety and tolerability were assessed for all patients by adverse event (AE) incidence and changes in laboratory parameters."	( Efficacy and safety of olaparib monotherapy in germline BRCA1/2 mutation carriers with advanced ovarian cancer and three or more lines of prior therapy. Aghajanian, C; Audeh, MW; Balmaña, J; Domchek, SM; Fried, G; Friedlander, M; Hubert, A; Kaufman, B; Loman, N; Mann, H; Mitchell, G; Robertson, JD; Rosengarten, O; Schmutzler, RK; Shapira-Frommer, R; Stemmer, SM, 2016)	0.74
" The safety profile of olaparib was similar in patients who had received ≥3 lines of prior chemotherapy compared with the pooled population; grade ≥3 adverse events were reported in 54% and 50% of patients, respectively."	( Olaparib monotherapy in patients with advanced relapsed ovarian cancer and a germline BRCA1/2 mutation: a multistudy analysis of response rates and safety. Audeh, MW; Coleman, RL; Domchek, SM; Gelmon, KA; Ho, TW; Kaufman, B; Kaye, S; Mann, H; Matulonis, UA; Molife, LR; Penson, RT; Robertson, JD; Shapira-Frommer, R, 2016)	2.19
" The most frequent adverse events were nausea (43."	( Safety and tolerability of the olaparib tablet formulation in Japanese patients with advanced solid tumours. Esaki, T; Fujikawa, K; Hatano, B; Hirai, F; Kawata, T; Kodaira, M; Sagawa, T; Shirakawa, T; Takahashi, Y; Tamura, K; Yokoi, Y; Yonemori, K, 2016)	0.72
" The cediranib intermittent schedule (n = 6) was examined because of recurrent grade 2 and non-dose-limiting toxicity grade 3 and 4 adverse events (AEs) on the daily schedule (n = 8)."	( Safety and Clinical Activity of the Programmed Death-Ligand 1 Inhibitor Durvalumab in Combination With Poly (ADP-Ribose) Polymerase Inhibitor Olaparib or Vascular Endothelial Growth Factor Receptor 1-3 Inhibitor Cediranib in Women's Cancers: A Dose-Escala Annunziata, CM; Botesteanu, DA; Cao, L; Cimino-Mathews, A; Figg, WD; Harrell, MI; Ho, TW; Houston, N; Kohn, EC; Lee, JM; Lipkowitz, S; Nguyen, J; Ogurtsova, A; Peer, CJ; Swisher, EM; Taube, JM; Thompson, E; Xu, H; Zimmer, A, 2017)	0.66
" Discontinuation due to adverse events (AEs) was rare and haematological AEs were more common in patients receiving combination treatment."	( Pharmacokinetics and safety of olaparib tablets as monotherapy and in combination with paclitaxel: results of a Phase I study in Chinese patients with advanced solid tumours. Burke, W; Hsu, K; Learoyd, M; Shentu, J; Xu, B; Xu, J; Yuan, P; Zhu, M, 2019)	0.8
" The drug associated Adverse Events (AEs) were collected and short-term efficacy were analyzed by modified Response Evaluation Criteria in Solid Tumors (mRECIST) ."	( Olaparib in the therapy of advanced ovarian cancer: first real world experiences in safety and efficacy from China. Chen, X; Cheng, X; Guo, W; Ni, J; Xu, X; Zhou, R, 2019)	1.96
" Serious Adverse Events(SAEs) were usually managed by dose interruption or dose reduction, rather than discontinuation."	( Olaparib in the therapy of advanced ovarian cancer: first real world experiences in safety and efficacy from China. Chen, X; Cheng, X; Guo, W; Ni, J; Xu, X; Zhou, R, 2019)	1.96
" Safety profile from each selected study was investigated for all-grade and G3-G4 haematological and non-haematological adverse drug events (ADEs)."	( Specific Toxicity of Maintenance Olaparib Abbati, F; Brandi, G; DE Lorenzo, S; DI Marco, M; Mollica, V; Novelli, M; Palloni, A; Ricci, AD; Rizzo, A; Tavolari, S; Tober, N; Turchetti, D, 2020)	0.84
"Despite an increased risk and incidence of several haematological and non-haematological toxicities, olaparib is a relatively safe agent for the treatment of advanced solid tumors."	( Specific Toxicity of Maintenance Olaparib Abbati, F; Brandi, G; DE Lorenzo, S; DI Marco, M; Mollica, V; Novelli, M; Palloni, A; Ricci, AD; Rizzo, A; Tavolari, S; Tober, N; Turchetti, D, 2020)	1.06
" Seven patients came off treatment before the first restaging scan: six because of clinical progression and one because of an adverse event."	( Clinical Activity and Safety of Cediranib and Olaparib Combination in Patients with Metastatic Pancreatic Ductal Adenocarcinoma without BRCA Mutation. Cardin, DB; Glazer, PM; Grossman, SR; Ivy, SP; Kato, S; Kim, JW; LoRusso, PM; Shyr, Y; Vaishampayan, UN, 2021)	0.88
"Few real-world studies have reported detailed management and dose adjustment strategies of adverse events (AEs) of ovarian cancer (OC) patients treated with the poly(adenosine diphosphate-ribose) polymerase inhibitor olaparib."	( Olaparib dose re-escalation in ovarian cancer patients who experienced severe and/or uncommon adverse events: A case series. Chan, KKL; Chu, MMY; Ngan, HYS; Ngu, SF; Tse, KY, 2021)	2.25
"2%) had persistent grade 2 adverse events (breast pain, fibrosis and deformity)."	( Combination of Olaparib with radiotherapy for triple-negative breast cancers: One-year toxicity report of the RADIOPARP Phase I trial. Berger, F; Cao, K; Fourquet, A; Jochem, A; Kirova, Y; Loap, P; Loirat, D; Mosseri, V; Raizonville, L; Ricci, F, 2021)	0.97
" Outcomes of interest included: serious adverse event (SAE), discontinuation due to adverse event (AE), interruption of treatment due to AE, dose reduction due to AE, and specific grade 1-5 AEs."	( Comparative safety and tolerability of approved PARP inhibitors in cancer: A systematic review and network meta-analysis. Cai, Z; Cao, D; Chang, C; Jiang, Z; Liu, C; Mu, M; Shen, C; Yin, X; Yin, Y; Zhang, B; Zhang, L; Zhao, Z, 2021)	0.62
" Grade 3 treatment-related adverse events occurred in 8 patients (16%), predominantly anemia."	( Efficacy and safety of durvalumab with olaparib in metastatic or recurrent endometrial cancer (phase II DOMEC trial). Boere, IA; Bosse, T; Braak, JPBM; Creutzberg, CL; Kroep, JR; Lalisang, RI; Meershoek-Klein Kranenbarg, E; Ottevanger, PB; Post, CCB; Putter, H; Sonke, GS; Westermann, AM; Witteveen, PO, 2022)	0.99
" Although PARP inhibitors have been shown to be well tolerated, adverse side effects can affect the quality of life of patients and lead to the discontinuation of therapy."	( Olaparib-induced cutaneous side effects in a patient with recurrent ovarian cancer. Gou, R; Horikawa, N; Kosaka, K, 2022)	2.16
" Information about treatment efficacy and adverse effects was collected retrospectively from medical records."	( Efficacy and safety of olaparib maintenance monotherapy for Japanese patients with platinum-sensitive relapsed ovarian, fallopian tube, and primary peritoneal cancer. Aoki, D; Chiyoda, T; Kobayashi, Y; Kuroda, Y; Nanki, Y; Sakai, K; Saotome, K; Takahashi, M; Yamagami, W; Yoshihama, T; Yoshimura, T, 2022)	1.03
"Olaparib maintenance therapy for platinum-sensitive recurrent ovarian cancer in the Japanese population is sufficiently safe and no less effective than reports from previous studies."	( Efficacy and safety of olaparib maintenance monotherapy for Japanese patients with platinum-sensitive relapsed ovarian, fallopian tube, and primary peritoneal cancer. Aoki, D; Chiyoda, T; Kobayashi, Y; Kuroda, Y; Nanki, Y; Sakai, K; Saotome, K; Takahashi, M; Yamagami, W; Yoshihama, T; Yoshimura, T, 2022)	2.47
" Olaparib treatment increased the number of grade ≥3 adverse events (AEs) in patients with advanced ovarian cancer compared with that in the control group."	( Efficacy and safety of olaparib in advanced ovarian cancer: a meta-analysis. Li, H; Tong, X; Yang, X; Yang, Y; Zhu, X, 2023)	2.13
" Henceforth, we aimed to seek a strategy to reduce the toxic effects of this combination by taking advantage of the mesoporous polydopamine (MPDA) nanoparticles with good biocompatibility and high drug loading capacity."	( Codelivery of adavosertib and olaparib by tumor-targeting nanoparticles for augmented efficacy and reduced toxicity. Chen, G; Fan, J; Fu, Y; Guo, E; Hu, D; Hu, X; Li, Z; Liu, C; Lu, F; Qin, T; Qin, X; Sun, C; Wang, W; Xiao, R; Xiong, Y; Yang, B; Zhang, L, 2023)	1.2
" Incidence of olaparib-related grade ≥3 adverse events in older patients was comparable with that of younger patients (36."	( Efficacy and safety of maintenance olaparib and bevacizumab in ovarian cancer patients aged ≥65 years from the PAOLA-1/ENGOT-ov25 trial. Canzler, U; Cinieri, S; Colombo, N; Cropet, C; Favier, L; Frindte, J; Gratet, A; Guerra Alía, EM; Hietanen, S; Joly, F; Largillier, R; Marmé, F; Montégut, C; Polterauer, S; Pujade-Lauraine, E; Ray-Coquard, I; Rousseau, F; Sabatier, R; Vergote, I; Yoshida, H, 2023)	1.55
"The metabolic activation of small-molecule drugs into electrophilic reactive metabolites is widely recognized as an indicator of idiosyncratic adverse drug reactions (IADRs)."	( Piperazine ring toxicity in three novel anti-breast cancer drugs: an in silico and in vitro metabolic bioactivation approach using olaparib as a case study. Abuelizz, HA; Alsubi, TA; Attwa, MW; Darwish, HW; Kadi, AA, 2023)	1.11
" No new serious adverse events related to olaparib were observed."	( OlympiAD extended follow-up for overall survival and safety: Olaparib versus chemotherapy treatment of physician's choice in patients with a germline BRCA mutation and HER2-negative metastatic breast cancer. Allen, A; Armstrong, A; Conte, P; Delaloge, S; Domchek, SM; Dymond, M; Fielding, A; Im, SA; Masuda, N; Robson, ME; Senkus, E; Tung, N; Xu, B, 2023)	1.42
" This study aimed to analyze adverse events (AEs) of patients taking Olaparib and the quality of life (QoL) with Olaparib in 1 center of China."	( Analysis of adverse events and quality of life in high-grade serous ovarian cancer patients with Olaparib maintenance therapy: A single-center study in China. Cheng, W; Jiang, Y; Meng, H; Ruan, X; Wu, S; Xu, T; Yuan, L; Zhang, L, 2023)	1.36

Excerpt	Reference	Relevance
" In this work, we take advantage of the synthesis of fluorescent drug conjugates that retain their target binding but are designed with different physiochemical and thus pharmacokinetic properties."	( Effect of small-molecule modification on single-cell pharmacokinetics of PARP inhibitors. Kohler, RH; Reiner, T; Thurber, GM; Weissleder, R; Yang, KS, 2014)	0.4
" Blood samples for pharmacokinetic (PK) assessments were taken pre-dose and up to 72 h post-dose."	( Effect of Food on the Pharmacokinetics of Olaparib after Oral Dosing of the Capsule Formulation in Patients with Advanced Solid Tumors. Bannister, W; Dean, E; Fielding, A; Leunen, K; Rolfo, C; Rutten, A; Slater, S; So, K; Soetekouw, P; Swaisland, H; Verheul, HM, 2015)	0.68
"To further explore this drug interaction, a population pharmacokinetic (PK) model was designed that included a lag time parameter, a second absorption compartment from tablet formulation, a single distribution/elimination compartment, and covariance among the clearance and volume parameters."	( Population pharmacokinetic analyses of the effect of carboplatin pretreatment on olaparib in recurrent or refractory women's cancers. Annunziata, CM; Figg, WD; Kohn, EC; Lee, JM; Minasian, L; Nguyen, J; Peer, CJ; Rodgers, L; Roth, J, 2017)	0.68
" As sensitizers, PARP inhibitors are active at very low concentrations therefore requiring highly sensitive pharmacodynamic (PD) assays."	( Improved pharmacodynamic (PD) assessment of low dose PARP inhibitor PD activity for radiotherapy and chemotherapy combination trials. de Haan, R; George, J; Peulen, H; Pluim, D; Schellens, JHM; van Berlo, D; van den Heuvel, M; van Triest, B; Vens, C; Verheij, M, 2018)	0.48
" This phase I study assessed the safety and pharmacokinetic (PK) profiles of olaparib combined with tamoxifen, anastrozole or letrozole in patients with advanced solid tumours."	( Pharmacokinetic Effects and Safety of Olaparib Administered with Endocrine Therapy: A Phase I Study in Patients with Advanced Solid Tumours. Bailey, C; Birkett, J; De Grève, J; De Vos, FYFL; Dean, E; Dirix, L; Goessl, C; Grundtvig-Sørensen, P; Italiano, A; Jerusalem, G; Learoyd, M; Leunen, K; Molife, LR; Plummer, R; Rolfo, C; Rottey, S; Spencer, S; Spicer, J; Verheul, HM, 2018)	0.98
"We used multiplexed targeted-mass-spectrometry to select pRAD50(Ser635) as a pharmacodynamic biomarker for AZD0156-mediated ATM inhibition from a panel of 45 peptides, then developed and tested a clinically applicable immunohistochemistry assay for pRAD50(Ser635) detection in FFPE tissue."	( pRAD50: a novel and clinically applicable pharmacodynamic biomarker of both ATM and ATR inhibition identified using mass spectrometry and immunohistochemistry. Barrett, JC; Cadogan, EB; Garcia-Trinidad, A; Griffin, N; Harrington, EA; Howat, WJ; Hughes, GD; Ivey, RG; Jones, GN; Lau, A; Odedra, R; Paulovich, AG; Pierce, AJ; Ramos-Montoya, A; Rooney, C; Roudier, M; Whiteaker, JR; Wilson, Z; Young, LA; Zhao, L, 2018)	0.48
"Overall, 44 patients received one or more doses of olaparib and 38 were included in the pharmacokinetic assessment."	( Pharmacokinetics and Safety of Olaparib in Patients with Advanced Solid Tumours and Renal Impairment. Bannister, W; De Grève, J; de Vos-Geelen, J; Dirix, L; Fielding, A; Grundtvig-Sørensen, P; Isambert, N; Jerusalem, G; Learoyd, M; Leunen, K; Mau-Sørensen, M; Molife, LR; Plummer, R; Ravaud, A; Rolfo, C; Schellens, JHM, 2019)	1.05
"Chinese patients have been enrolled in multiple Phase III trials of the poly(ADP-ribose) polymerase (PARP) inhibitor olaparib (Lynparza); however, the pharmacokinetic (PK) profile of olaparib has not been investigated in this population."	( Pharmacokinetics and safety of olaparib tablets as monotherapy and in combination with paclitaxel: results of a Phase I study in Chinese patients with advanced solid tumours. Burke, W; Hsu, K; Learoyd, M; Shentu, J; Xu, B; Xu, J; Yuan, P; Zhu, M, 2019)	1.01
"Preclinical pharmacokinetic studies evaluated olaparib tissue distribution in rats and tumor-bearing mice."	( Pharmacokinetics, safety, and tolerability of olaparib and temozolomide for recurrent glioblastoma: results of the phase I OPARATIC trial. Carruthers, R; Chalmers, AJ; Cruickshank, G; Dunn, L; Erridge, S; Godfrey, L; Halford, S; Hanna, C; Jackson, A; Jefferies, S; Kurian, KM; McBain, C; McCormick, A; Pittman, M; Sleigh, R; Strathdee, K; Watts, C; Williams, K, 2020)	1.07
" Herein, pharmaceutical cocrystallization strategy was employed to optimize the physicochemical and pharmacokinetic properties."	( Improving the physicochemical and pharmacokinetic properties of olaparib through cocrystallization strategy. Chen, JM; Dai, XL; Gao, L; Li, CW; Lu, TB; Lv, WT; Pang, BW; Xiong, J; Zhen, JF, 2023)	1.15

Excerpt	Reference	Relevance
" As such, we conditionally deleted Brca2 and p53 within murine mammary epithelium and treated the resulting tumors in situ with a highly potent PARP-1 inhibitor (AZD2281) alone or in combination with carboplatin."	( Poly(ADP-ribose) polymerase-1 inhibitor treatment regresses autochthonous Brca2/p53-mutant mammary tumors in vivo and delays tumor relapse in combination with carboplatin. Clarke, AR; Cranston, A; Douglas-Jones, A; Hay, T; Lau, A; Martin, NM; Matthews, JR; Nygren, AO; O'Connor, M; Pietzka, L; Smith, GC, 2009)	0.35
"The aim of this phase I study was to determine the safety and tolerability and to establish the maximum tolerated dose (MTD) of orally administered olaparib (AZD2281) in combination with topotecan in patients with advanced solid tumors."	( Safety and tolerability of the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib (AZD2281) in combination with topotecan for the treatment of patients with advanced solid tumors: a phase I study. Carmichael, J; Cassidy, J; Macpherson, E; Ranson, M; Samol, J; Scott, E; Thomas, A, 2012)	0.81
"0 mg/m(2)/day × 3 days) intravenously in combination with oral olaparib 50, 100 or 200 mg bid for six cycles."	( Safety and tolerability of the poly(ADP-ribose) polymerase (PARP) inhibitor, olaparib (AZD2281) in combination with topotecan for the treatment of patients with advanced solid tumors: a phase I study. Carmichael, J; Cassidy, J; Macpherson, E; Ranson, M; Samol, J; Scott, E; Thomas, A, 2012)	0.85
"A bioanalytical assay for the new poly(ADP-ribose) polymerase-1 inhibitor olaparib in combination with melphalan was developed and validated."	( Liquid chromatography-tandem mass spectrometric assay for the PARP-1 inhibitor olaparib in combination with the nitrogen mustard melphalan in human plasma. Beijnen, JH; den Hartigh, J; Martens, I; Schellens, JH; Sparidans, RW; Valkenburg-van Iersel, LB, 2011)	0.83
"To assess the possible radiosensitizing capabilities of two different poly(ADP-ribose) polymerase (PARP) inhibitors in combination with external beam and I-tositumomab in a non-Hodgkin's lymphoma cell line."	( Poly(ADP-ribose) polymerase inhibitors combined with external beam and radioimmunotherapy to treat aggressive lymphoma. James, E; Schaefer, NG; Wahl, RL, 2011)	0.37
" This phase I study established the safety, tolerability and clinical pharmacokinetics of olaparib alone and in combination with bevacizumab."	( Phase I study to assess the safety and tolerability of olaparib in combination with bevacizumab in patients with advanced solid tumours. Carmichael, J; Dean, E; Goodege-Kunwar, P; Middleton, MR; Pwint, T; Ranson, M; Swaisland, H, 2012)	0.85
" capsule formulation) in combination with bevacizumab (10 mg kg(-1) intravenous q2w)."	( Phase I study to assess the safety and tolerability of olaparib in combination with bevacizumab in patients with advanced solid tumours. Carmichael, J; Dean, E; Goodege-Kunwar, P; Middleton, MR; Pwint, T; Ranson, M; Swaisland, H, 2012)	0.63
" PARP inhibitors are being evaluated in cancers with defective DNA repair mechanisms or in combination with cytotoxic therapy or radiation."	( Preclinical evaluation of the PARP inhibitor, olaparib, in combination with cytotoxic chemotherapy in pediatric solid tumors. Adamson, PC; Fox, E; Nguyen, VT; Norris, RE, 2014)	0.66
"The IC50 of olaparib alone and in combination with cytotoxic agents was determined in 10 pediatric solid tumor cell lines."	( Preclinical evaluation of the PARP inhibitor, olaparib, in combination with cytotoxic chemotherapy in pediatric solid tumors. Adamson, PC; Fox, E; Nguyen, VT; Norris, RE, 2014)	1.04
" In RD-ES and NGP xenografts, olaparib inhibited PAR activity by 88-100% as a single agent and 100% when administered with cyclophosphamide/topotecan."	( Preclinical evaluation of the PARP inhibitor, olaparib, in combination with cytotoxic chemotherapy in pediatric solid tumors. Adamson, PC; Fox, E; Nguyen, VT; Norris, RE, 2014)	0.95
"This Phase I study evaluated the safety, tolerability and efficacy of olaparib, a potent oral poly(ADPribose) polymerase (PARP) inhibitor, in combination with paclitaxel in patients with metastatic triple-negative breast cancer (mTNBC)."	( Phase I trial of the oral PARP inhibitor olaparib in combination with paclitaxel for first- or second-line treatment of patients with metastatic triple-negative breast cancer. Carmichael, J; Chan, A; Clemons, M; Dent, RA; Lindeman, GJ; Lowe, ES; McCarthy, NJ; Singer, CF; Watkins, CL; Wildiers, H, 2013)	0.89
"To establish the maximum tolerated dose, determine safety/tolerability and evaluate the pharmacokinetics and preliminary efficacy of olaparib in combination with cisplatin in patients with advanced solid tumors."	( Phase I trial of olaparib in combination with cisplatin for the treatment of patients with advanced breast, ovarian and other solid tumors. Balmaña, J; Baselga, J; Frewer, P; Garber, JE; Graña, B; Isakoff, SJ; Lowe, ES; Ryan, PD; Saura, C; Tung, NM; Winer, E, 2014)	0.95
"Patients aged ≥ 18 years with advanced solid tumors, who had progressed on standard treatment, were assigned to a treatment cohort and received oral olaparib [50-200 mg twice daily (bid); 21-day cycle] continuously or intermittently (days 1-5 or 1-10) in combination with cisplatin (60-75 mg/m(2) intravenously) on day 1 of each cycle."	( Phase I trial of olaparib in combination with cisplatin for the treatment of patients with advanced breast, ovarian and other solid tumors. Balmaña, J; Baselga, J; Frewer, P; Garber, JE; Graña, B; Isakoff, SJ; Lowe, ES; Ryan, PD; Saura, C; Tung, NM; Winer, E, 2014)	0.94
"Olaparib in combination with cisplatin 75 mg/m(2) was not considered tolerable; intermittent olaparib (50 mg bid, days 1-5) with cisplatin 60 mg/m(2) improved tolerability."	( Phase I trial of olaparib in combination with cisplatin for the treatment of patients with advanced breast, ovarian and other solid tumors. Balmaña, J; Baselga, J; Frewer, P; Garber, JE; Graña, B; Isakoff, SJ; Lowe, ES; Ryan, PD; Saura, C; Tung, NM; Winer, E, 2014)	2.18
" This study evaluated olaparib capsules in combination with liposomal doxorubicin (PLD) in patients with advanced solid tumours (NCT00819221)."	( Phase I study of olaparib in combination with liposomal doxorubicin in patients with advanced solid tumours. Cathomas, R; Del Conte, G; Digena, T; Fasolo, A; Gallerani, E; Gianni, L; Locatelli, A; Sessa, C; Tessari, A; Viganò, L; von Moos, R, 2014)	1.06
"Continuous/intermittent olaparib (up to 400 mg bid) combined with PLD (40 mg m(-2)) was generally tolerated and showed evidence of antitumour activity in ovarian cancer."	( Phase I study of olaparib in combination with liposomal doxorubicin in patients with advanced solid tumours. Cathomas, R; Del Conte, G; Digena, T; Fasolo, A; Gallerani, E; Gianni, L; Locatelli, A; Sessa, C; Tessari, A; Viganò, L; von Moos, R, 2014)	1.05
" The aim of this study was to assess the efficacy and tolerability of olaparib in combination with chemotherapy, followed by olaparib maintenance monotherapy, versus chemotherapy alone in patients with platinum-sensitive, recurrent, high-grade serous ovarian cancer."	( Olaparib combined with chemotherapy for recurrent platinum-sensitive ovarian cancer: a randomised phase 2 trial. Barrett, JC; Benzaquen, AO; Cibula, D; Colombo, N; Dougherty, B; Friedlander, M; Hirte, H; Lowe, ES; Mackay, H; Mahner, S; Mathijssen, RH; Oza, AM; Plante, M; Poole, C; Rowbottom, J; Schmalfeldt, B; Sonke, GS; Špaček, J; Vuylsteke, P, 2015)	2.09
"Patients had first participated in a phase I study of olaparib combined with carboplatin and/or paclitaxel."	( Long-term safety and anti-tumour activity of olaparib monotherapy after combination with carboplatin and paclitaxel in patients with advanced breast, ovarian or fallopian tube cancer. Beijnen, JH; Harms, E; Marchetti, S; Mergui-Roelvink, MW; Rehorst, H; Schellens, JH; Sonke, GS; Steeghs, N; van der Noll, R, 2015)	0.93
" However, it is uncertain as to whether PARPi lead to clonogenic kill when combined with radiotherapy (RT)."	( In vivo studies of the PARP inhibitor, AZD-2281, in combination with fractionated radiotherapy: An exploration of the therapeutic ratio. Bristow, RG; Coackley, C; Gani, C; Krause, M; Kumareswaran, R; Schütze, C; Zafarana, G, 2015)	0.42
"Various cytotoxic agents were evaluated in combination with (131) I-MIP-1095 for their capacity to delay the growth of LNCaP cells cultured as multicellular tumour spheroids."	( Preliminary evaluation of prostate-targeted radiotherapy using (131) I-MIP-1095 in combination with radiosensitising chemotherapeutic drugs. Babich, JW; Mairs, RJ; Nixon, C; Rae, C; Tesson, M, 2016)	0.43
"In this phase 1 dose-escalation trial in patients with unresectable PDAC, we determined the maximum tolerated dose (MTD) of olaparib (tablet formulation) in combination with irinotecan 70 mg/m2 on days 1 and 8 and cisplatin 25 mg/m2 on days 1 and 8 of a 28-day cycle (olaparib plus IC)."	( Olaparib in combination with irinotecan, cisplatin, and mitomycin C in patients with advanced pancreatic cancer. Azad, NS; De Jesus-Acosta, A; Donehower, RC; Fine, RL; Goggins, M; Jaffee, EM; Johnson, BA; Laheru, DA; Le, DT; Myzak, MC; Oberstein, PE; Yarchoan, M; Zheng, L, 2017)	2.1
"Olaparib had substantial toxicity when combined with IC or ICM in patients with PDAC, and this treatment combination did not have an acceptable risk/benefit profile for further study."	( Olaparib in combination with irinotecan, cisplatin, and mitomycin C in patients with advanced pancreatic cancer. Azad, NS; De Jesus-Acosta, A; Donehower, RC; Fine, RL; Goggins, M; Jaffee, EM; Johnson, BA; Laheru, DA; Le, DT; Myzak, MC; Oberstein, PE; Yarchoan, M; Zheng, L, 2017)	3.34
"Olaparib combined with paclitaxel has previously shown a significant improvement in overall survival versus placebo plus paclitaxel as second-line therapy in a phase 2 study in Asian patients with advanced gastric cancer, especially in those with ataxia-telangiectasia mutated protein (ATM)-negative tumours."	( Olaparib in combination with paclitaxel in patients with advanced gastric cancer who have progressed following first-line therapy (GOLD): a double-blind, randomised, placebo-controlled, phase 3 trial. Bang, YJ; Boku, N; Chin, K; Hodgson, D; Im, SA; Lee, KW; Liu, YZ; Locker, G; Park, SH; Qin, S; Rha, SY; Rowe, P; Shen, L; Shi, X; Xu, N; Xu, RH, 2017)	3.34
" The study generated informative efficacy and safety data regarding the use of olaparib in combination with a chemotherapeutic agent and provides a foundation for future studies in this difficult-to-treat patient population."	( Olaparib in combination with paclitaxel in patients with advanced gastric cancer who have progressed following first-line therapy (GOLD): a double-blind, randomised, placebo-controlled, phase 3 trial. Bang, YJ; Boku, N; Chin, K; Hodgson, D; Im, SA; Lee, KW; Liu, YZ; Locker, G; Park, SH; Qin, S; Rha, SY; Rowe, P; Shen, L; Shi, X; Xu, N; Xu, RH, 2017)	2.13
" In this study, we examined the normal tissue response in mice treated with PARP inhibitors (BMN673 or AZD2281) in combination with thoracic irradiation."	( PARP Inhibition Combined With Thoracic Irradiation Exacerbates Esophageal and Skin Toxicity in C57BL6 Mice. Cahill, F; Drobnitzky, N; Green, M; Jiang, Y; Lourenco, LM; Moore, J; Patel, A; Ryan, AJ; Shanneik, Y, 2018)	0.48
"The antitumor effects of fractionated irradiation (5 Gy × 4) in combination with BMN673 were evaluated in nude mice bearing established Calu-6 human lung cancer xenografts."	( PARP Inhibition Combined With Thoracic Irradiation Exacerbates Esophageal and Skin Toxicity in C57BL6 Mice. Cahill, F; Drobnitzky, N; Green, M; Jiang, Y; Lourenco, LM; Moore, J; Patel, A; Ryan, AJ; Shanneik, Y, 2018)	0.48
" Using 2D and 3D cell culture models mimicking the different treatment and progression stages of PCa, we evaluated a potential use for olaparib in combination with first-line endocrine treatments, androgen deprivation, and complete androgen blockade, and as a maintenance therapy following on from endocrine therapy."	( Olaparib is effective in combination with, and as maintenance therapy after, first-line endocrine therapy in prostate cancer cells. Bouchal, J; Culig, Z; Feiersinger, GE; Guggenberger, F; Hermann, M; Leitner, PD; Oberhuber, A; Peer, S; Santer, FR; Skvortsova, I; Trattnig, K; Vrbkova, J, 2018)	2.13
"We report physiologically based pharmacokinetic-modeling analyses to determine olaparib (tablet or capsule) drug-drug interactions (DDIs)."	( Physiologically Based Pharmacokinetic Modeling for Olaparib Dosing Recommendations: Bridging Formulations, Drug Interactions, and Patient Populations. Bui, K; Learoyd, M; Pilla Reddy, V; Scarfe, G; Zhou, D, 2019)	0.99
"Olaparib in combination with abiraterone provided clinical efficacy benefit for patients with metastatic castration-resistant prostate cancer compared with abiraterone alone."	( Olaparib combined with abiraterone in patients with metastatic castration-resistant prostate cancer: a randomised, double-blind, placebo-controlled, phase 2 trial. Alekseev, B; Burgents, J; Chiuri, VE; Clarke, N; Fléchon, A; Goessl, C; Hodgson, D; Jassem, J; Jones, R; Kocak, I; Kozarski, R; Learoyd, M; Redfern, C; Saad, F; Sala, N; Wiechno, P, 2018)	3.37
" The drug combination was cytotoxic to TNBC cells, both with regards to short‑term and long‑term sensitivity, as determined using colony forming assays, and they exerted strong synergistic effects on MDA‑MB‑231 and CAL51 cell lines."	( Antitumor effects and mechanisms of olaparib in combination with carboplatin and BKM120 on human triple‑negative breast cancer cells. Hu, Y; Yang, Q; Zhang, J; Zhao, H, 2018)	0.76
"The PARP inhibitor olaparib is efficacious as monotherapy and has potential application in combination with endocrine therapy for the treatment of breast cancer."	( Pharmacokinetic Effects and Safety of Olaparib Administered with Endocrine Therapy: A Phase I Study in Patients with Advanced Solid Tumours. Bailey, C; Birkett, J; De Grève, J; De Vos, FYFL; Dean, E; Dirix, L; Goessl, C; Grundtvig-Sørensen, P; Italiano, A; Jerusalem, G; Learoyd, M; Leunen, K; Molife, LR; Plummer, R; Rolfo, C; Rottey, S; Spencer, S; Spicer, J; Verheul, HM, 2018)	1.08
"Twelve of the tested drug combinations addressed a synthetic lethal interaction with the anti-VEGF inhibitor bevacizumab in combination with paclitaxel being the most studied drug combination addressing the synthetic lethal pair between VEGFA and BCL2."	( Synthetic lethality guiding selection of drug combinations in ovarian cancer. Heinzel, A; Krainer, M; Lukas, A; Marhold, M; Mayer, P; Perco, P; Schwarz, M; Tomasich, E, 2019)	0.51
" This two-part, open-label Phase I study was, therefore, carried out to determine the PK and safety profile of olaparib (tablet formulation) in Chinese patients with advanced solid tumours as monotherapy and in combination with paclitaxel (NCT02430311)."	( Pharmacokinetics and safety of olaparib tablets as monotherapy and in combination with paclitaxel: results of a Phase I study in Chinese patients with advanced solid tumours. Burke, W; Hsu, K; Learoyd, M; Shentu, J; Xu, B; Xu, J; Yuan, P; Zhu, M, 2019)	1.01
" A statistically significant decrease in olaparib exposure was seen when given in combination with paclitaxel."	( Pharmacokinetics and safety of olaparib tablets as monotherapy and in combination with paclitaxel: results of a Phase I study in Chinese patients with advanced solid tumours. Burke, W; Hsu, K; Learoyd, M; Shentu, J; Xu, B; Xu, J; Yuan, P; Zhu, M, 2019)	1.07
" This Phase I trial (NCT00516724) evaluated the safety, pharmacokinetics (PK) and preliminary efficacy of olaparib combined with carboplatin and/or paclitaxel."	( Phase I study of continuous olaparib capsule dosing in combination with carboplatin and/or paclitaxel (Part 1). Ang, JE; Arkenau, HT; Beijnen, JH; Brunetto, AT; de Bono, JS; de Jonge, MJA; Jager, A; Lolkema, MP; Marchetti, S; Mergui-Roelvink, MWJ; Schellens, JHM; Tchakov, I; van der Biessen, DA; van der Noll, R, 2020)	1.07
" Against the background of increasing acquired resistance to FGFR1 inhibitors and our previous work, which partially demonstrated the caspase-3/PARP-mediated antitumor and antimetastatic efficacy of PD173074, a selective FGFR1 inhibitor, against ALDH-high/FGFR1-rich pancreatic ductal adenocarcinoma (PDAC) cells, we investigated the probable synthetic lethality and therapeutic efficacy of targeted PARP inhibition combined with FGFR1 blockade in patients with PDAC."	( Targeted PARP Inhibition Combined with FGFR1 Blockade is Synthetically Lethal to Malignant Cells in Patients with Pancreatic Cancer. Bamodu, OA; Chao, TY; Chen, JH; Lai, SW; Lee, WH; Wu, AT; Yeh, CT, 2020)	0.56
" The role of PADI2 combined with Olaparib treatment in vivo was studied in nude mouse model bearing ovarian cancer tumor."	( Down-regulation of PADI2 prevents proliferation and epithelial-mesenchymal transition in ovarian cancer through inhibiting JAK2/STAT3 pathway in vitro and in vivo, alone or in combination with Olaparib. Guo, W; Liu, L; Ma, Y; Wang, T; Zhang, G; Zhang, Z, 2020)	1.03
" Food and Drug Administration (FDA) granted approval to olaparib monotherapy for first-line maintenance treatment of BRCA-mutated (BRCAm) advanced ovarian cancer and, on May 8, 2020, expanded the indication of olaparib to include its use in combination with bevacizumab for first-line maintenance treatment of homologous recombination deficient (HRD)-positive advanced ovarian cancer."	( FDA Approval Summary: Olaparib Monotherapy or in Combination with Bevacizumab for the Maintenance Treatment of Patients with Advanced Ovarian Cancer. Amiri-Kordestani, L; Arora, S; Balasubramaniam, S; Beaver, JA; Berman, T; Bloomquist, E; Chatterjee, D; Gao, JJ; Ghosh, S; Gong, Y; Narayan, P; Pathak, A; Pazdur, R; Philip, R; Saritas-Yildirim, B; Sridhara, R; Suzman, D; Tang, S; Turcu, FR; Zhang, H, 2021)	1.18
"To identify an MTD of olaparib, a PARP inhibitor, in combination with loco-regional radiotherapy with/without cisplatin for the treatment of non-small cell lung cancer (NSCLC)."	( Phase I and Pharmacologic Study of Olaparib in Combination with High-dose Radiotherapy with and without Concurrent Cisplatin for Non-Small Cell Lung Cancer. de Haan, R; de Langen, AJ; Lalezari, F; Peulen, HMU; Pluim, D; Schellens, JHM; Steeghs, N; van den Heuvel, MM; van Diessen, J; van Triest, B; van Werkhoven, E; Vens, C; Verheij, M; Verwijs-Janssen, M, 2021)	1.21
"In this study, we developed folate-conjugated active targeting olaparib nanoparticles (ATO) and investigated the anti-tumor effect of ATO combined with radiotherapy (RT) in nude mice using cervical cancer xenograft models."	( Enhanced Anti-Cancer Effect of Folate-Conjugated Olaparib Nanoparticles Combined with Radiotherapy in Cervical Carcinoma. Chen, Y; Fu, SZ; Hu, C; Li, D; Liao, Y; Wu, JB; Yang, J, 2020)	1.05
"The results confirmed that ATO in combination with RT significantly inhibited tumor growth and prolonged survival time of tumor-bearing mice."	( Enhanced Anti-Cancer Effect of Folate-Conjugated Olaparib Nanoparticles Combined with Radiotherapy in Cervical Carcinoma. Chen, Y; Fu, SZ; Hu, C; Li, D; Liao, Y; Wu, JB; Yang, J, 2020)	0.81
" The rationale for using these therapies in combination with poly (ADP-ribose) polymerase inhibitors (PARP-Is) has been described, and their in vivo application will benefit from ex vivo platforms that aid in the prediction of patient response or resistance to therapy."	( PD-1/PD-L1 checkpoint inhibitors in combination with olaparib display antitumor activity in ovarian cancer patient-derived three-dimensional spheroid cultures. Appleton, KM; DesRochers, TM; Elrod, AK; Holmes, LM; Lassahn, KA; Shuford, S, 2021)	0.87
" Herein, we firstly reported that an adult DMG patient benefited from olaparib combined with bevacizumab and achieved complete remission."	( Successful treatment of an adult patient with diffuse midline glioma employing olaparib combined with bevacizumab. Luo, N; Qi, C; Tao, R; Wang, Y; Xu, J, 2021)	1.08
"To determine whether the ATR inhibitor, ceralasertib, has clinical activity as a single agent and in combination with the PARP inhibitor, olaparib, in patients with ARID1A 'loss' and 'no loss' clear cell carcinomas and other relapsed gynecological cancers."	( ATARI trial: ATR inhibitor in combination with olaparib in gynecological cancers with ARID1A loss or no loss (ENGOT/GYN1/NCRI). Attygalle, A; Banerjee, S; Bliss, J; Khalique, S; Leary, A; Lheureux, S; Lord, CJ; Natrajan, R; Porta, N; Stewart, J; Tai, J; Toms, C; Vroobel, K, 2021)	1.08
"ATARI (ENGOT/GYN1/NCRI) is a multicenter, international, proof-of-concept, phase II, parallel cohort trial assessing ceralasertib activity as a single agent and in combination with olaparib in ARID1A stratified gynecological cancers."	( ATARI trial: ATR inhibitor in combination with olaparib in gynecological cancers with ARID1A loss or no loss (ENGOT/GYN1/NCRI). Attygalle, A; Banerjee, S; Bliss, J; Khalique, S; Leary, A; Lheureux, S; Lord, CJ; Natrajan, R; Porta, N; Stewart, J; Tai, J; Toms, C; Vroobel, K, 2021)	1.07
"On the basis of strong preclinical rationale, we sought to confirm recommended phase II dose (RP2D) for olaparib, a PARP inhibitor, combined with the AKT inhibitor capivasertib and assess molecular markers of response and resistance."	( Phase Ib Dose Expansion and Translational Analyses of Olaparib in Combination with Capivasertib in Recurrent Endometrial, Triple-Negative Breast, and Ovarian Cancer. Blucher, A; Chelariu-Raicu, A; Chen, TH; Coleman, RL; Creason, A; Fang, Y; Fellman, B; Feng, N; Frumovitz, M; Jazaeri, A; Kabil, N; Kim, TB; Labrie, M; Lee, S; Litton, JK; Liu, J; Lu, KH; Ma, X; Marszalek, JR; Meyer, LA; Mills, GB; Murthy, R; Schmeler, KM; Soliman, PT; Sood, AK; Sun, CC; Vellano, CP; Westin, SN; Yuan, Y, 2021)	1.08
" The Olaparib Combinations basket trial explored olaparib alone and in combination with other homologous recombination-directed targeted therapies."	( Ceralasertib-Mediated ATR Inhibition Combined With Olaparib in Advanced Cancers Harboring DNA Damage Response and Repair Alterations (Olaparib Combinations). Avedissian, M; Dean, E; Do, KT; Doroshow, D; Eder, JP; Felicetti, B; Glover, C; Hafez, N; Jürgensmeier, J; Keedy, V; LoRusso, P; Mahdi, H; Mortimer, P; Shapiro, GI; Sklar, J; Sohal, D, 2021)	1.39
"This detailed preclinical investigation, including pharmacokinetics/pharmacodynamics and dose-schedule optimizations, of AZD6738/ceralasertib alone and in combination with chemotherapy or PARP inhibitors can inform ongoing clinical efforts to treat cancer with ATR inhibitors."	( ATR Inhibitor AZD6738 (Ceralasertib) Exerts Antitumor Activity as a Monotherapy and in Combination with Chemotherapy and the PARP Inhibitor Olaparib. Bargh-Dawson, H; Brown, E; Gerrard, J; Hughes, AM; Jones, GN; Lau, A; O'Connor, MJ; Odedra, R; Wallez, Y; Wijnhoven, PWG; Wilson, Z; Young, LA, 2022)	0.92
" We demonstrated the synergism of [Bis + ABT199/venetoclax] in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells."	( Enhanced cytotoxicity of bisantrene when combined with venetoclax, panobinostat, decitabine and olaparib in acute myeloid leukemia cells. Andersson, BS; Murray, D; Nieto, Y; Popat, U; Valdez, BC; Yuan, B, 2022)	1.15
" The aim of this study is identifying its possible therapeutic targets and to evaluate the effects of AM in combination with a PARP inhibitor (olaparib) in the treatment of BRCA wild-type ovarian cancer."	( Anticancer Effect of Active Component of Astragalus Membranaceus Combined with Olaparib on Ovarian Cancer Predicted by Network-Based Pharmacology. Guo, Z; Jiang, J; Lang, F; Li, J; Liu, Y, 2023)	1.34
" The Tdp1 inhibitor OL7-43 was used in combination with olaparib to increase the antitumor effect of the latter."	( [Effect of Usnic Acid-Derived Tyrosyl-DNA Phosphodiesterase 1 Inhibitor Used as Monotherapy or in Combination with Olaparib on Transplanted Tumors In Vivo]. Chepanova, AA; Dyrkheeva, NS; Filimonov, AS; Ilina, ES; Kornienko, TE; Lavrik, OI; Luzina, OA; Nikolin, VP; Popova, NA; Salakhutdinov, NF; Zakharenko, AL; Zakharova, OD, )	0.59
"PARP inhibitors combined with antiangiogenic drugs have been reported to improve outcomes in BRCA wild-type ovarian cancer patients, the mechanism of the combination is unclear."	( Apatinib combined with olaparib induces ferroptosis via a p53-dependent manner in ovarian cancer. Jun, C; Kui, J; Yue, W; Yupeng, G, 2023)	1.22
"Apatinib combined with olaparib-induced ferroptosis in p53 wild-type cells, and p53 mutant cells developed drug resistance."	( Apatinib combined with olaparib induces ferroptosis via a p53-dependent manner in ovarian cancer. Jun, C; Kui, J; Yue, W; Yupeng, G, 2023)	1.53
"This discovery revealed the specific mechanism of ferroptosis induced by apatinib combined with olaparib in p53 wild-type ovarian cancer cells and provided a theoretical basis for the clinical combined use of apatinib and olaparib in p53 wild-type ovarian cancer patients."	( Apatinib combined with olaparib induces ferroptosis via a p53-dependent manner in ovarian cancer. Jun, C; Kui, J; Yue, W; Yupeng, G, 2023)	1.44
"Maintenance therapy with durvalumab in combination with olaparib was not associated with a statistically significant improvement in PFS versus durvalumab alone, although numerical improvement was observed."	( Durvalumab in Combination With Olaparib Versus Durvalumab Alone as Maintenance Therapy in Metastatic NSCLC: The Phase 2 ORION Study. Ahn, MJ; Bondarenko, I; Cho, BC; Demedts, I; Gálffy, G; Gans, SJM; Hussein, M; Kalinka, E; Kislov, N; Lai, Z; Mann, H; Mendoza Oliva, D; Nagarkar, R; Shi, X; Shim, BY; Stewart, R; Sugawara, S, 2023)	1.44
" As patients develop resistance to NAA therapy, the poly(ADP-ribose) polymerase inhibitor (PARPi) olaparib in combination with NAA may become a promising therapy."	( Comparative efficacy of olaparib in combination with or without novel antiandrogens for treating metastatic castration-resistant prostate cancer. Chen, X; Hao, X; Li, M; Liu, X; Pan, Y; Ren, C; Wang, Q; Xie, L, 2023)	1.43

Excerpt	Reference	Relevance
" Olaparib is an orally bioavailable inhibitor of PARP-1 and PARP-2 that has been tested in multiple clinical trials."	( The combination of olaparib and camptothecin for effective radiosensitization. Hareyama, M; Matsumoto, H; Matsumoto, Y; Miura, K; Sakata, K; Someya, M; Takahashi, A, 2012)	1.62
"Dovitinib (TKI258; formerly CHIR-258) is an orally bioavailable inhibitor of multiple receptor tyrosine kinases."	( Dovitinib induces mitotic defects and activates the G2 DNA damage checkpoint. Mak, JP; Man, WY; Poon, RY, 2014)	0.4
"Olaparib (AZD-2281, Ku-0059436) is an orally bioavailable and well-tolerated poly(ADP-ribose) polymerase (PARP) inhibitor currently under investigation in patients with solid tumors."	( BRCA1, PARP1 and γH2AX in acute myeloid leukemia: Role as biomarkers of response to the PARP inhibitor olaparib. Angelini, DF; Cencioni, MT; Compagnone, M; Dolci, S; Faraoni, I; Graziani, G; Lavorgna, S; Lo-Coco, F; Ottone, T; Panetta, P; Piras, E; Venditti, A, 2015)	2.07
" The presence of food slowed the rate of absorption (time to maximal plasma concentration [t max] was delayed by ~2 h)."	( Effect of Food on the Pharmacokinetics of Olaparib after Oral Dosing of the Capsule Formulation in Patients with Advanced Solid Tumors. Bannister, W; Dean, E; Fielding, A; Leunen, K; Rolfo, C; Rutten, A; Slater, S; So, K; Soetekouw, P; Swaisland, H; Verheul, HM, 2015)	0.68
"Results of this study showed that a high-fat meal decreases the rate of absorption and peak exposure to olaparib 300 mg tablets, although in the absence of an effect on the extent of olaparib absorption."	( Olaparib tablet formulation: effect of food on the pharmacokinetics after oral dosing in patients with advanced solid tumours. Bannister, W; De Grève, J; Fielding, A; Jerusalem, G; Leunen, K; Lolkema, MP; Mau-Sørensen, M; Molife, LR; Nielsen, D; Plummer, R; So, K; Soetekouw, P; Spicer, J; Swaisland, H; van Herpen, CM, 2015)	2.07
" Further optimization of these initial hits for improved declustering potency, solubility, permeability, and oral bioavailability resulted in AZ0108, a PARP1, 2, 6 inhibitor that potently inhibits centrosome clustering and is suitable for in vivo efficacy and tolerability studies."	( Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering. Almeida, L; Daly, K; Ferguson, AD; Grosskurth, SE; Guan, H; Howard, T; Ioannidis, S; Johannes, JW; Kazmirski, S; Lamb, ML; Larsen, NA; Lyne, PD; Mikule, K; Ogoe, C; Peng, B; Petteruti, P; Read, JA; Scott, DA; Su, N; Sylvester, M; Throner, S; Wang, W; Wang, X; Wu, J; Ye, Q; Yu, Y; Zheng, X, 2015)	0.42
" However, clinical outcome is controversial and no benefits have been demonstrated in wild type BRCA cancers, possibly due to poor drug bioavailability and low nuclear delivery."	( H-Ferritin-nanocaged olaparib: a promising choice for both BRCA-mutated and sporadic triple negative breast cancer. Baccarini, F; Bellini, M; Beretta, M; Ciuffreda, P; Corsi, F; Mazzucchelli, S; Ottria, R; Prosperi, D; Ravelli, A; Rizzuto, MA; Sorrentino, L; Truffi, M, 2017)	0.77
"Olaparib is a potent orally bioavailable poly(ADP-ribose) polymerase inhibitor (PARPi), approved for BRCA-mutated ovarian and breast cancers."	( The poly(ADP-ribose) polymerase inhibitor olaparib induces up-regulation of death receptors in primary acute myeloid leukemia blasts by NF-κB activation. Aloisio, F; Consalvo, MI; De Gabrieli, A; Faraoni, I; Graziani, G; Lavorgna, S; Lo-Coco, F; Voso, MT, 2018)	2.19
" Unfortunately, Olaparib is poorly soluble with low bioavailability and tumor accumulation; nano-delivery could be a good choice to overcome these disadvantages."	( Quantitative Characterization of Olaparib in Nanodelivery System and Target Cell Compartments by LC-MS/MS. Casati, S; Ciuffreda, P; Miceli, M; Orioli, M; Ottria, R; Ravelli, A, 2019)	1.14
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51
" Compound 34 is orally bioavailable and displayed favorable pharmacokinetic (PK) properties."	( Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization. Ahirrao, P; Bakhle, D; Bernstein, PR; Bhat, T; Bhonde, M; Bommakanti, A; Bora, P; Francis, A; George, KS; Gole, G; Goyal, H; Gundu, J; Gupta, NR; Gupta, R; Hajare, AK; Jadhav, GR; Jagdale, AR; Jana, G; Kale, R; Kamalakannan, P; Kamble, N; Kamboj, RK; Karche, NP; Khanwalkar, H; Khedkar, N; Kukreja, G; Kumar, P; Kumar, R; Kurhade, SP; Limaye, R; Mallurwar, S; Modi, D; Naidu, S; Naik, KR; Narasimham, L; Nemmani, K; Nigade, PB; Pagdala, V; Palle, VP; Patil, V; Pawar, S; Pawar, Y; Phukan, S; Powar, RG; Praveen Kumar, VR; Rao Irlapati, N; Shaikh, JS; Shankar, RB; Sharma, S; Singh, M; Sinha, N; Thube, BR; Tilekar, AR; Volam, H; Wahid, S, 2020)	0.56
"AZD6738 (ceralasertib) is a potent and selective orally bioavailable inhibitor of ataxia telangiectasia and Rad3-related (ATR) kinase."	( ATR Inhibitor AZD6738 (Ceralasertib) Exerts Antitumor Activity as a Monotherapy and in Combination with Chemotherapy and the PARP Inhibitor Olaparib. Bargh-Dawson, H; Brown, E; Gerrard, J; Hughes, AM; Jones, GN; Lau, A; O'Connor, MJ; Odedra, R; Wallez, Y; Wijnhoven, PWG; Wilson, Z; Young, LA, 2022)	0.92
" The components of AM were analyzed using the Traditional Chinese Medicine System Pharmacology (TCMSP) database to screen the active ingredients of AM based on their oral bioavailability and drug similarity index."	( Anticancer Effect of Active Component of Astragalus Membranaceus Combined with Olaparib on Ovarian Cancer Predicted by Network-Based Pharmacology. Guo, Z; Jiang, J; Lang, F; Li, J; Liu, Y, 2023)	1.14
" The imipridone ONC206 is an orally bioavailable dopamine receptor D2 antagonist and mitochondrial protease ClpP agonist that has anti-tumorigenic effects in endometrial cancer via induction of apoptosis, activation of the integrated stress response and modulation of PI3K/AKT signaling."	( A novel dopamine receptor D2 antagonist (ONC206) potentiates the effects of olaparib in endometrial cancer. Allen, JE; Bae-Jump, V; Fan, Y; Hao, T; Hawkins, GM; Paraghamian, SE; Prabhu, VV; Qiu, J; Sun, W; Suo, H; Zhang, X; Zhao, Z; Zhou, C, 2023)	1.14

Excerpt	Relevance	Reference
" Olaparib was administered as a single-dose on day 1, followed by twice-daily dosing for 28 days from 48 h after a single dose."	( A Phase I, dose-finding and pharmacokinetic study of olaparib (AZD2281) in Japanese patients with advanced solid tumors. Asahina, H; Goto, Y; Kawata, T; Nokihara, H; Shi, X; Shibata, T; Tamura, T; Tanioka, M; Yamada, K; Yamada, Y; Yamamoto, N, 2012)	1.54
" More in general, additional preclinical studies are needed to further improve clinical results in order to define the optimal regimen of combination with PARP1 inhibitor and cytotoxics or molecular targeted agents (sequence of administration, interval between dosing of the agents, duration of treatment)."	( Update on PARP1 inhibitors in ovarian cancer. Sessa, C, 2011)	0.37
" We investigated the toxicities and recommended phase 2 dosing (RP2D) of the combination of cediranib, a multitargeted inhibitor of vascular endothelial growth factor receptor (VEGFR)-1/2/3 and olaparib, a PARP-inhibitor (NCT01116648)."	( A Phase 1 trial of the poly(ADP-ribose) polymerase inhibitor olaparib (AZD2281) in combination with the anti-angiogenic cediranib (AZD2171) in recurrent epithelial ovarian or triple-negative breast cancer. Birrer, M; Buss, MK; Dahlberg, SE; Fleming, GF; Ivy, P; Lee, H; Liu, JF; Matulonis, UA; Tolaney, SM; Tyburski, K; Whalen, C; Winer, E, 2013)	0.82
" Given the encouraging response rate, alternative scheduling and dosing strategies should be considered (funded by AstraZeneca; ClinicalTrials."	( Phase I trial of the oral PARP inhibitor olaparib in combination with paclitaxel for first- or second-line treatment of patients with metastatic triple-negative breast cancer. Carmichael, J; Chan, A; Clemons, M; Dent, RA; Lindeman, GJ; Lowe, ES; McCarthy, NJ; Singer, CF; Watkins, CL; Wildiers, H, 2013)	0.66
" For intermittent dosing studies, mice cycled through olaparib (200 mg/kg diet) for 2 weeks followed by a 4-week rest period on control diet."	( The PARP inhibitors, veliparib and olaparib, are effective chemopreventive agents for delaying mammary tumor development in BRCA1-deficient mice. Collins, RM; Kim, EH; Liby, KT; Risingsong, R; Royce, DB; Sporn, MB; To, C; Williams, CR, 2014)	0.93
" Continuous dosing of olaparib or combination with gemcitabine at doses >600 mg/m(2) was not considered to have an acceptable tolerability profile for further study."	( Phase I study of olaparib plus gemcitabine in patients with advanced solid tumours and comparison with gemcitabine alone in patients with locally advanced/metastatic pancreatic cancer. Bendell, J; Burke, W; Burris, H; Chau, I; Fielding, A; Hochster, H; Middleton, MR; O'Reilly, EM, 2015)	1.07
"The presence of food decreased the rate and increased the extent of absorption of olaparib following oral dosing of the capsule formulation."	( Effect of Food on the Pharmacokinetics of Olaparib after Oral Dosing of the Capsule Formulation in Patients with Advanced Solid Tumors. Bannister, W; Dean, E; Fielding, A; Leunen, K; Rolfo, C; Rutten, A; Slater, S; So, K; Soetekouw, P; Swaisland, H; Verheul, HM, 2015)	0.91
"The pharmacology, clinical efficacy, safety, dosage and administration, and role in therapy of olaparib, a first-in-class treatment for advanced treatment-refractory ovarian cancer, are reviewed."	( Olaparib for the treatment of BRCA-mutated advanced ovarian cancer. Kolesar, J; Munroe, M, 2016)	2.1
"In this open-label, multicentre study (D081BC00001; NCT01813474), a single dose of olaparib (200 or 300 mg, tablets) was administered on day 1, followed 48 h afterwards by multiple dosing (200 or 300 mg twice daily [bid]) for 28-day cycles."	( Safety and tolerability of the olaparib tablet formulation in Japanese patients with advanced solid tumours. Esaki, T; Fujikawa, K; Hatano, B; Hirai, F; Kawata, T; Kodaira, M; Sagawa, T; Shirakawa, T; Takahashi, Y; Tamura, K; Yokoi, Y; Yonemori, K, 2016)	0.95
" We investigated the effect of multiple dosing of the oral poly (ADP-ribose)-polymerase (PARP) inhibitor, olaparib (tablet formulation) on QT/QTc interval."	( Olaparib does not cause clinically relevant QT/QTc interval prolongation in patients with advanced solid tumours: results from two phase I studies. Bannister, W; Dota, C; Fabre, MA; Fielding, A; Garnett, S; Plummer, R; So, K; Swaisland, H, 2016)	2.09
" At pre-dose and up to 12 h post-dose, the upper limits of the 90 % confidence intervals (CIs) for the difference in QTcF least squares means after olaparib multiple dosing versus control (day -1) were <10 ms, suggesting a lack of clinically relevant effect on cardiac repolarization."	( Olaparib does not cause clinically relevant QT/QTc interval prolongation in patients with advanced solid tumours: results from two phase I studies. Bannister, W; Dota, C; Fabre, MA; Fielding, A; Garnett, S; Plummer, R; So, K; Swaisland, H, 2016)	2.08
" Using patient-derived xenografts, we demonstrate that different therapeutics achieve similar integrated inhibition efficiencies under different dosing regimens."	( Target engagement imaging of PARP inhibitors in small-cell lung cancer. Carney, B; Gangangari, KK; Kossatz, S; Lok, BH; Pillarsetty, NVK; Poirier, JT; Reiner, T; Rudin, CM; Schneeberger, V; Weber, WA, 2018)	0.48
" The additive and synergistic inhibition of this combination additionally supports a therapeutic strategy involving lower dosing of each drug to reduce potential side effects."	( Additive and synergistic inhibition of mantle cell lymphoma cell growth by combining olaparib with ibrutinib. Curtis, A; Rajan, S; Rueter, J; Shopland, L; Zhang, R, 2018)	0.7
" The originally approved capsule formulation was dosed as 400 mg twice daily (eight 50 mg capsules)."	( Administration of the Tablet Formulation of Olaparib in Patients with Ovarian Cancer: Practical Guidance and Expectations. Birrer, MJ; Moore, KN, 2018)	0.74
" Finally, this model was used to simulate exposure in scenarios where clinical data of olaparib are lacking, such as severe renal or hepatic impairment populations, and provided initial dosing recommendations in pediatric patients."	( Physiologically Based Pharmacokinetic Modeling for Olaparib Dosing Recommendations: Bridging Formulations, Drug Interactions, and Patient Populations. Bui, K; Learoyd, M; Pilla Reddy, V; Scarfe, G; Zhou, D, 2019)	0.99
" By concurrent administration of carboplatin and olaparib at various molar ratios of drugs, the aim of this study was to explore the optimal dosing ratio of carboplatin-olaparib combinations in a comprehensive panel of eight BRCA-proficient and -deficient high-grade serous ovarian cancer (HGSOC) cell lines."	( BRCA Status Does Not Predict Synergism of a Carboplatin and Olaparib Combination in High-Grade Serous Ovarian Cancer Cell Lines. Allen, C; Evans, JC; Piquette-Miller, M; Shen, YT; Zafarana, G, 2018)	0.98
" Relative to an earlier capsule formulation, the tablet formulation of olaparib has improved bioavailability, thereby reducing pill burden and offering a more convenient dosage regimen."	( Olaparib Tablet: A Review in Ovarian Cancer Maintenance Therapy. Dhillon, S; Heo, YA, 2018)	2.16
" Educating patients when transitioning from capsules to tablets is critical to avoid dosing errors and maintain both safety and efficacy of olaparib maintenance therapy."	( Practical considerations for clinicians for transitioning patients on maintenance therapy with olaparib capsules to the tablet formulation of olaparib. Friedlander, M; Goh, J; Mileshkin, L; Scott, C; Shannon, C, 2018)	0.9
" The original dosage form of olaparib was a 50 mg capsule, requiring 16 capsules per day for patients at full dose therapy which prompted development of a tablet dosage form with improved bioavailability."	( Olaparib: A tale of two dosage forms. Christ, TN, 2019)	2.25
"Continuous low dosage administration of olaparib induced senescence under P16 or P53 dependent manner in ovarian cancer."	( Olaparib induced senescence under P16 or P53 dependent manner in ovarian cancer. Gao, J; Liu, H; Wang, Z; Xu, C; Zhou, J, 2019)	2.22
" We investigated the pharmacokinetics and safety of olaparib in patients with mild or moderate renal impairment to provide dosing recommendations."	( Pharmacokinetics and Safety of Olaparib in Patients with Advanced Solid Tumours and Renal Impairment. Bannister, W; De Grève, J; de Vos-Geelen, J; Dirix, L; Fielding, A; Grundtvig-Sørensen, P; Isambert, N; Jerusalem, G; Learoyd, M; Leunen, K; Mau-Sørensen, M; Molife, LR; Plummer, R; Ravaud, A; Rolfo, C; Schellens, JHM, 2019)	1.05
" Conclusions Olaparib in combination with carboplatin and/or paclitaxel resulted in increased hematologic toxicities, making it challenging to establish a dosing regimen that could be tolerated for multiple cycles without dose modifications."	( Phase I study of continuous olaparib capsule dosing in combination with carboplatin and/or paclitaxel (Part 1). Ang, JE; Arkenau, HT; Beijnen, JH; Brunetto, AT; de Bono, JS; de Jonge, MJA; Jager, A; Lolkema, MP; Marchetti, S; Mergui-Roelvink, MWJ; Schellens, JHM; Tchakov, I; van der Biessen, DA; van der Noll, R, 2020)	1.22
" The tablet formulation has improved bioavailability, reducing pill burden and offering a more convenient dosage regimen."	( Pharmacological issues concerning olaparib capsule and tablet formulations in treating ovarian cancer: Are they really the same drug? Cabiddu, M; Castelli, EA; Nozza, R; Oggionni, E; Omati, E; Perego, G; Petrelli, F; Scolari, C, 2020)	0.84
" We investigated the pharmacokinetics (PK) and safety of olaparib in patients with mild or moderate hepatic impairment to provide dosing recommendations."	( Pharmacokinetics and safety of olaparib in patients with advanced solid tumours and mild or moderate hepatic impairment. Bannister, W; Blay, JY; de Vos-Geelen, J; Decaens, T; Demlova, R; Isambert, N; Italiano, A; Kopeckova, K; Kristeleit, R; Learoyd, M; Lee, MA; Locker, G; Molife, LR; Ravaud, A; Rolfo, C; Rosmorduc, O; Schellens, JHM, 2020)	1.09
" In determining which patients should be offered front-line maintenance PARP inhibitors, and which agent to use, there are multiple factors to consider, including FDA indication, dosing preference, toxicity, risks versus benefits for each patient population, and cost."	( Movement of Poly-ADP Ribose (PARP) Inhibition into Frontline Treatment of Ovarian Cancer. Coleman, RL; Onstad, M; Westin, SN, 2020)	0.56
" Further evaluation of this combination should include alternate dosing strategies in genomically-selected populations."	( Combination ATR and PARP Inhibitor (CAPRI): A phase 2 study of ceralasertib plus olaparib in patients with recurrent, platinum-resistant epithelial ovarian cancer. Armstrong, D; Burger, RA; Dean, E; Domchek, S; Drapkin, R; Gaillard, S; Giuntoli, R; Haggerty, A; Hwang, WT; Latif, N; Martin, LP; Morgan, M; Pagan, C; Rodriguez, D; Shah, PD; Shih, IM; Simpkins, F; Smith, SA; Tanyi, J; Torigian, DA; Wethington, SL; Zarrin, H, 2021)	0.85
" This translated to in vivo antitumor activity, with tumor control requiring continuous dosing and free plasma exposures, which correlated with induction of pCHK1, pRAD50, and γH2AX."	( ATR Inhibitor AZD6738 (Ceralasertib) Exerts Antitumor Activity as a Monotherapy and in Combination with Chemotherapy and the PARP Inhibitor Olaparib. Bargh-Dawson, H; Brown, E; Gerrard, J; Hughes, AM; Jones, GN; Lau, A; O'Connor, MJ; Odedra, R; Wallez, Y; Wijnhoven, PWG; Wilson, Z; Young, LA, 2022)	0.92
" This work suggests that AZD7648, an inhibitor of DNA-PK, dosed in combination with PLD or olaparib is an exciting therapeutic option that could benefit patients with ovarian cancer and should be explored in clinical trials."	( The DNA-PK Inhibitor AZD7648 Sensitizes Patient-Derived Ovarian Cancer Xenografts to Pegylated Liposomal Doxorubicin and Olaparib Preventing Abdominal Metastases. Anastasia, A; Baakza, H; Bani, MR; Cadogan, EB; Chiorino, G; Dellavedova, G; Ghilardi, C; Giavazzi, R; James, N; Ramos-Montoya, A; Russo, M; Wilson, J, 2022)	1.15
" We have used this developed model further to investigate other doses of olaparib and ceralasertib in combination, which can be potentially helpful in exploring optimized dosage and delivery."	( A Mathematical Model to Investigate the Effects of Ceralasertib and Olaparib in Targeting the Cellular DNA Damage Response Pathway. Davies, M; Powathil, G; Pugh, K, 2023)	1.38
" The current study detected the cardioprotective effect of olaparib at a dosage of 10 mg/kg/day."	( Poly (ADP-ribose) polymerase pathway inhibitor (Olaparib) upregulates SERCA2a expression and attenuates doxorubicin-induced cardiomyopathy in mice. Abdo, VB; Ashour, RH; El Beltagy, HM; El Fatah, DSA; El-Karef, A; Elkatary, RG, 2023)	1.41

Role	Description
antineoplastic agent	A substance that inhibits or prevents the proliferation of neoplasms.
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor	An EC 2.4.2.* (pentosyltransferase) inhibitor that interferes with the action of a NAD(+) ADP-ribosyltransferase (EC 2.4.2.30).
apoptosis inducer	Any substance that induces the process of apoptosis (programmed cell death) in multi-celled organisms.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Class	Description
N-acylpiperazine
cyclopropanes	Cyclopropane and its derivatives formed by substitution.
monofluorobenzenes	Any member of the class of fluorobenzenes containing a mono- or poly-substituted benzene ring carrying a single fluorine substitutent.
phthalazines
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Pathway	Proteins	Compounds
NAD metabolism, sirtuins and aging	0	3

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
PPM1D protein	Homo sapiens (human)	Potency	18.5569	0.0052	9.4661	32.9993	AID1347411
EWS/FLI fusion protein	Homo sapiens (human)	Potency	10.3000	0.0013	10.1577	42.8575	AID1259252; AID1259253; AID1259255; AID1259256
Interferon beta	Homo sapiens (human)	Potency	18.5569	0.0033	9.1582	39.8107	AID1347411
Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus	Potency	22.3872	0.0096	10.5250	35.4813	AID1479145
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)	IC50 (µMol)	10.2785	0.0019	0.6293	5.0000	AID1265292; AID1265312; AID1350590; AID1428392; AID1868337; AID1895769; AID386695
Cytochrome P450 1A2	Homo sapiens (human)	IC50 (µMol)	0.0200	0.0001	1.7740	10.0000	AID1500669
Cholinesterase	Homo sapiens (human)	IC50 (µMol)	0.0035	0.0000	1.5599	10.0000	AID386694; AID386709
Poly [ADP-ribose] polymerase 1	Homo sapiens (human)	IC50 (µMol)	0.1741	0.0002	0.8123	9.8100	AID1064455; AID1064607; AID1128175; AID1152976; AID1155630; AID1186400; AID1205269; AID1261692; AID1261693; AID1261694; AID1265289; AID1276413; AID1350577; AID1403931; AID1428384; AID1428385; AID1428386; AID1474432; AID1486291; AID1486467; AID1499315; AID1500669; AID1508852; AID1557937; AID1557954; AID1557957; AID1565230; AID1581911; AID1591450; AID1631788; AID1667252; AID1682011; AID1683489; AID1683890; AID1697311; AID1734012; AID1736000; AID1758275; AID1764044; AID1784222; AID1798813; AID1802336; AID1830902; AID1831146; AID1849629; AID1849656; AID1861250; AID1862285; AID1862317; AID1868336; AID1868381; AID1868630; AID1872299; AID1878578; AID1882326; AID1895766; AID1896630; AID1896632; AID1908536; AID1909228; AID386691; AID386709; AID728422; AID728437; AID762672
Poly [ADP-ribose] polymerase 1	Homo sapiens (human)	Ki	0.0008	0.0006	0.6595	5.0000	AID1515647
Cytochrome P450 2D6	Homo sapiens (human)	IC50 (µMol)	0.0200	0.0000	2.0151	10.0000	AID1500669
Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)	IC50 (µMol)	1.8000	1.8000	1.8000	1.8000	AID1265317
Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)	IC50 (µMol)	12.6565	2.4000	6.4097	9.0000	AID1428398; AID1734010
Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)	IC50 (µMol)	5.2854	0.5623	4.1053	9.7724	AID1428394; AID1428395
Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)	IC50 (µMol)	5.1143	0.4270	3.5519	5.1286	AID1428399
Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)	IC50 (µMol)	10.1414	0.0790	2.4307	6.6500	AID1428396
Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)	IC50 (µMol)	2.4458	0.0021	0.6750	5.1300	AID1265293; AID1265312; AID1350591; AID1428393; AID1868338
Histamine H3 receptor	Cavia porcellus (domestic guinea pig)	IC50 (µMol)	0.0010	0.0010	2.9070	8.6900	AID386694
Poly [ADP-ribose] polymerase 2	Homo sapiens (human)	IC50 (µMol)	0.1866	0.0001	0.2188	6.6000	AID1265290; AID1403932; AID1428387; AID1428388; AID1486292; AID1486468; AID1508854; AID1557953; AID1581971; AID1682012; AID1683490; AID1683889; AID1736001; AID1784223; AID1830903; AID1872300; AID1895767; AID1896631; AID1896633; AID1908537; AID386694; AID728422
Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)	IC50 (µMol)	0.4087	0.3300	1.6827	4.3900	AID1428390
Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)	IC50 (µMol)	0.1315	0.0035	1.1218	6.3000	AID1265291; AID1428389; AID728422
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Poly [ADP-ribose] polymerase 1	Homo sapiens (human)	EC50 (µMol)	2.6804	0.0004	0.1809	3.0000	AID1064614; AID1276416; AID1683865; AID1683888; AID762670; AID762671
Poly [ADP-ribose] polymerase 1	Homo sapiens (human)	Kd	1.3278	0.0002	0.4356	5.3100	AID1240632; AID1784247; AID1817373; AID1895777
Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)	Kd	9.7000	3.1000	6.0600	9.7000	AID1895786
Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)	Kd	10.0000	1.1000	1.1000	1.1000	AID1895784
Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)	Kd	10.0000	1.0000	1.9500	2.9000	AID1895790
Poly [ADP-ribose] polymerase 2	Homo sapiens (human)	EC50 (µMol)	0.0036	0.0025	0.0084	0.0240	AID1276416
Poly [ADP-ribose] polymerase 2	Homo sapiens (human)	Kd	0.0004	0.0003	0.2914	1.4000	AID1240634; AID1784248; AID1895778
Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)	Kd	0.1410	0.0007	0.2043	0.5030	AID1895780
Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)	EC50 (µMol)	0.0036	0.0025	0.0084	0.0240	AID1276416
Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)	Kd	0.0058	0.0058	0.2456	0.7000	AID1895779
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
peptidyl-serine phosphorylation	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
peptidyl-threonine phosphorylation	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
protein polyubiquitination	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
mitotic spindle organization	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
protein transport	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
Wnt signaling pathway	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
regulation of telomere maintenance via telomerase	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
positive regulation of telomere maintenance via telomerase	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
mRNA transport	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
spindle assembly	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
cell division	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
positive regulation of telomerase activity	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
protein localization to chromosome, telomeric region	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
protein poly-ADP-ribosylation	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
protein auto-ADP-ribosylation	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
positive regulation of canonical Wnt signaling pathway	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
positive regulation of telomere capping	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengthening	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
negative regulation of telomeric DNA binding	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
negative regulation of maintenance of mitotic sister chromatid cohesion, telomeric	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell activation involved in immune response	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway	Interferon beta	Homo sapiens (human)
cell surface receptor signaling pathway via JAK-STAT	Interferon beta	Homo sapiens (human)
response to virus	Interferon beta	Homo sapiens (human)
positive regulation of autophagy	Interferon beta	Homo sapiens (human)
cytokine-mediated signaling pathway	Interferon beta	Homo sapiens (human)
natural killer cell activation	Interferon beta	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT protein	Interferon beta	Homo sapiens (human)
cellular response to interferon-beta	Interferon beta	Homo sapiens (human)
B cell proliferation	Interferon beta	Homo sapiens (human)
negative regulation of viral genome replication	Interferon beta	Homo sapiens (human)
innate immune response	Interferon beta	Homo sapiens (human)
positive regulation of innate immune response	Interferon beta	Homo sapiens (human)
regulation of MHC class I biosynthetic process	Interferon beta	Homo sapiens (human)
negative regulation of T cell differentiation	Interferon beta	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Interferon beta	Homo sapiens (human)
defense response to virus	Interferon beta	Homo sapiens (human)
type I interferon-mediated signaling pathway	Interferon beta	Homo sapiens (human)
neuron cellular homeostasis	Interferon beta	Homo sapiens (human)
cellular response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
cellular response to virus	Interferon beta	Homo sapiens (human)
negative regulation of Lewy body formation	Interferon beta	Homo sapiens (human)
negative regulation of T-helper 2 cell cytokine production	Interferon beta	Homo sapiens (human)
positive regulation of apoptotic signaling pathway	Interferon beta	Homo sapiens (human)
response to exogenous dsRNA	Interferon beta	Homo sapiens (human)
B cell differentiation	Interferon beta	Homo sapiens (human)
natural killer cell activation involved in immune response	Interferon beta	Homo sapiens (human)
adaptive immune response	Interferon beta	Homo sapiens (human)
T cell activation involved in immune response	Interferon beta	Homo sapiens (human)
humoral immune response	Interferon beta	Homo sapiens (human)
steroid catabolic process	Cytochrome P450 1A2	Homo sapiens (human)
porphyrin-containing compound metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
xenobiotic metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
cholesterol metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
estrogen metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
toxin biosynthetic process	Cytochrome P450 1A2	Homo sapiens (human)
post-embryonic development	Cytochrome P450 1A2	Homo sapiens (human)
alkaloid metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
regulation of gene expression	Cytochrome P450 1A2	Homo sapiens (human)
monoterpenoid metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
dibenzo-p-dioxin metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
epoxygenase P450 pathway	Cytochrome P450 1A2	Homo sapiens (human)
lung development	Cytochrome P450 1A2	Homo sapiens (human)
methylation	Cytochrome P450 1A2	Homo sapiens (human)
monocarboxylic acid metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
xenobiotic catabolic process	Cytochrome P450 1A2	Homo sapiens (human)
retinol metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
long-chain fatty acid biosynthetic process	Cytochrome P450 1A2	Homo sapiens (human)
cellular respiration	Cytochrome P450 1A2	Homo sapiens (human)
aflatoxin metabolic process	Cytochrome P450 1A2	Homo sapiens (human)
hydrogen peroxide biosynthetic process	Cytochrome P450 1A2	Homo sapiens (human)
oxidative demethylation	Cytochrome P450 1A2	Homo sapiens (human)
cellular response to cadmium ion	Cytochrome P450 1A2	Homo sapiens (human)
omega-hydroxylase P450 pathway	Cytochrome P450 1A2	Homo sapiens (human)
xenobiotic metabolic process	Cholinesterase	Homo sapiens (human)
learning	Cholinesterase	Homo sapiens (human)
negative regulation of cell population proliferation	Cholinesterase	Homo sapiens (human)
neuroblast differentiation	Cholinesterase	Homo sapiens (human)
peptide hormone processing	Cholinesterase	Homo sapiens (human)
response to alkaloid	Cholinesterase	Homo sapiens (human)
cocaine metabolic process	Cholinesterase	Homo sapiens (human)
negative regulation of synaptic transmission	Cholinesterase	Homo sapiens (human)
response to glucocorticoid	Cholinesterase	Homo sapiens (human)
response to folic acid	Cholinesterase	Homo sapiens (human)
choline metabolic process	Cholinesterase	Homo sapiens (human)
acetylcholine catabolic process	Cholinesterase	Homo sapiens (human)
DNA damage response	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
mitochondrion organization	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
mitochondrial DNA metabolic process	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
regulation of protein localization	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cellular response to oxidative stress	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein modification process	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
mitochondrial DNA repair	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
telomere maintenance	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
DNA repair	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
double-strand break repair	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
transcription by RNA polymerase II	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
apoptotic process	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
DNA damage response	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
transforming growth factor beta receptor signaling pathway	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
response to gamma radiation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of cardiac muscle hypertrophy	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
carbohydrate biosynthetic process	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein autoprocessing	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
signal transduction involved in regulation of gene expression	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
macrophage differentiation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
DNA ADP-ribosylation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of DNA-templated transcription, elongation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cellular response to insulin stimulus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of intracellular estrogen receptor signaling pathway	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of transcription elongation by RNA polymerase II	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cellular response to UV	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transduction	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
innate immune response	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
regulation of circadian sleep/wake cycle, non-REM sleep	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of innate immune response	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of DNA-templated transcription	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
decidualization	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
regulation of catalytic activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of mitochondrial depolarization	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of SMAD protein signal transduction	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of necroptotic process	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein poly-ADP-ribosylation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein auto-ADP-ribosylation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein localization to chromatin	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cellular response to zinc ion	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
replication fork reversal	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of cGAS/STING signaling pathway	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of protein localization to nucleus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
regulation of oxidative stress-induced neuron intrinsic apoptotic signaling pathway	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of single strand break repair	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
response to aldosterone	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of adipose tissue development	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengthening	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cellular response to amyloid-beta	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of myofibroblast differentiation	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
regulation of base-excision repair	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
positive regulation of double-strand break repair via homologous recombination	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cellular response to nerve growth factor stimulus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
ATP generation from poly-ADP-D-ribose	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
negative regulation of ATP biosynthetic process	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
xenobiotic metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
steroid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
cholesterol metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
estrogen metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
coumarin metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
alkaloid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
alkaloid catabolic process	Cytochrome P450 2D6	Homo sapiens (human)
monoterpenoid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
isoquinoline alkaloid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
xenobiotic catabolic process	Cytochrome P450 2D6	Homo sapiens (human)
retinol metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
long-chain fatty acid biosynthetic process	Cytochrome P450 2D6	Homo sapiens (human)
negative regulation of binding	Cytochrome P450 2D6	Homo sapiens (human)
oxidative demethylation	Cytochrome P450 2D6	Homo sapiens (human)
negative regulation of cellular organofluorine metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
arachidonic acid metabolic process	Cytochrome P450 2D6	Homo sapiens (human)
positive regulation of dendrite morphogenesis	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
protein auto-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
endoplasmic reticulum unfolded protein response	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
protein poly-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
negative regulation of gene expression	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
chromatin organization	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
negative regulation of gene expression	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
viral protein processing	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
translesion synthesis	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
negative regulation of NF-kappaB transcription factor activity	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
NAD biosynthesis via nicotinamide riboside salvage pathway	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
negative regulation of DNA-templated transcription	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
negative regulation of fibroblast proliferation	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
protein poly-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
protein auto-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
negative regulation of protein K63-linked ubiquitination	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
protein auto-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
endoplasmic reticulum unfolded protein response	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
viral protein processing	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
endoplasmic reticulum unfolded protein response	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
NAD biosynthesis via nicotinamide riboside salvage pathway	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
IRE1-mediated unfolded protein response	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
protein auto-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
cellular response to leukemia inhibitory factor	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
negative regulation of cytoplasmic translation	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
protein auto-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
protein polyubiquitination	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
Wnt signaling pathway	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
positive regulation of telomere maintenance via telomerase	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
protein localization to chromosome, telomeric region	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
protein poly-ADP-ribosylation	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
protein auto-ADP-ribosylation	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
positive regulation of canonical Wnt signaling pathway	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
positive regulation of telomere capping	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengthening	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
DNA repair	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
base-excision repair	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
DNA damage response	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
DNA ADP-ribosylation	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
decidualization	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
positive regulation of cell growth involved in cardiac muscle cell development	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
protein poly-ADP-ribosylation	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
protein auto-ADP-ribosylation	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
response to oxygen-glucose deprivation	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
extrinsic apoptotic signaling pathway	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
hippocampal neuron apoptotic process	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
DNA repair-dependent chromatin remodeling	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
double-strand break repair	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
DNA repair	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
inflammatory response	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
DNA damage response	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
response to xenobiotic stimulus	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
protein modification process	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
regulation of telomerase activity	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
protein poly-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
telomere maintenance	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
double-strand break repair	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
positive regulation of DNA ligation	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
regulation of mitotic spindle organization	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
protein localization to site of double-strand break	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
DNA ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
negative regulation of isotype switching	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
protein auto-ADP-ribosylation	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
negative regulation of telomerase RNA reverse transcriptase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
positive regulation of double-strand break repair via nonhomologous end joining	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
double-strand break repair	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
NAD+ ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
protein binding	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
zinc ion binding	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
nucleotidyltransferase activity	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
histone binding	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
cytokine activity	Interferon beta	Homo sapiens (human)
cytokine receptor binding	Interferon beta	Homo sapiens (human)
type I interferon receptor binding	Interferon beta	Homo sapiens (human)
protein binding	Interferon beta	Homo sapiens (human)
chloramphenicol O-acetyltransferase activity	Interferon beta	Homo sapiens (human)
monooxygenase activity	Cytochrome P450 1A2	Homo sapiens (human)
iron ion binding	Cytochrome P450 1A2	Homo sapiens (human)
protein binding	Cytochrome P450 1A2	Homo sapiens (human)
electron transfer activity	Cytochrome P450 1A2	Homo sapiens (human)
oxidoreductase activity	Cytochrome P450 1A2	Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen	Cytochrome P450 1A2	Homo sapiens (human)
enzyme binding	Cytochrome P450 1A2	Homo sapiens (human)
heme binding	Cytochrome P450 1A2	Homo sapiens (human)
demethylase activity	Cytochrome P450 1A2	Homo sapiens (human)
caffeine oxidase activity	Cytochrome P450 1A2	Homo sapiens (human)
aromatase activity	Cytochrome P450 1A2	Homo sapiens (human)
estrogen 16-alpha-hydroxylase activity	Cytochrome P450 1A2	Homo sapiens (human)
estrogen 2-hydroxylase activity	Cytochrome P450 1A2	Homo sapiens (human)
hydroperoxy icosatetraenoate dehydratase activity	Cytochrome P450 1A2	Homo sapiens (human)
amyloid-beta binding	Cholinesterase	Homo sapiens (human)
catalytic activity	Cholinesterase	Homo sapiens (human)
acetylcholinesterase activity	Cholinesterase	Homo sapiens (human)
cholinesterase activity	Cholinesterase	Homo sapiens (human)
protein binding	Cholinesterase	Homo sapiens (human)
hydrolase activity, acting on ester bonds	Cholinesterase	Homo sapiens (human)
enzyme binding	Cholinesterase	Homo sapiens (human)
choline binding	Cholinesterase	Homo sapiens (human)
identical protein binding	Cholinesterase	Homo sapiens (human)
DNA binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
chromatin binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
damaged DNA binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
RNA binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
zinc ion binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nucleotidyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
enzyme binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein kinase binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nuclear estrogen receptor binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nucleosome binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
ubiquitin protein ligase binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
identical protein binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein homodimerization activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
histone deacetylase binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
R-SMAD binding	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
transcription regulator activator activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-protein-serine ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-protein-tyrosine ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-protein-histidine ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-histone H2BS6 serine ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-histone H3S10 serine ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-histone H2BE35 glutamate ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
monooxygenase activity	Cytochrome P450 2D6	Homo sapiens (human)
iron ion binding	Cytochrome P450 2D6	Homo sapiens (human)
oxidoreductase activity	Cytochrome P450 2D6	Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygen	Cytochrome P450 2D6	Homo sapiens (human)
heme binding	Cytochrome P450 2D6	Homo sapiens (human)
anandamide 8,9 epoxidase activity	Cytochrome P450 2D6	Homo sapiens (human)
anandamide 11,12 epoxidase activity	Cytochrome P450 2D6	Homo sapiens (human)
anandamide 14,15 epoxidase activity	Cytochrome P450 2D6	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
NAD+- protein-cysteine ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
protein serine/threonine kinase activator activity	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
kinase binding	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
transcription corepressor activity	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
protein binding	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
NAD+ binding	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
protein binding	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
K63-linked polyubiquitin modification-dependent protein binding	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
DNA-binding transcription factor binding	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
transcription corepressor activity	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
NAD+- protein-cysteine ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
protein serine/threonine kinase activator activity	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
kinase binding	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
protein binding	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
kinase binding	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
protein serine/threonine kinase activator activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
RNA binding	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
metal ion binding	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
NAD+- protein-cysteine ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
protein binding	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
nucleotidyltransferase activity	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
enzyme binding	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
metal ion binding	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
chromatin binding	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
damaged DNA binding	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
protein binding	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleotidyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleosome binding	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
poly-ADP-D-ribose binding	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
NAD+-protein-serine ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
poly-ADP-D-ribose modification-dependent protein binding	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
DNA binding	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
protein binding	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
enzyme binding	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
catalytic activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
NAD+ ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
protein binding	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
nucleotidyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activity	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
Golgi membrane	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
pericentriolar material	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
chromosome, telomeric region	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
nucleoplasm	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
Golgi apparatus	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
cytosol	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
nuclear body	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
nuclear membrane	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
mitotic spindle pole	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
nuclear pore	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
nucleus	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
cytoplasm	Poly [ADP-ribose] polymerase tankyrase-1	Homo sapiens (human)
extracellular space	Interferon beta	Homo sapiens (human)
extracellular region	Interferon beta	Homo sapiens (human)
endoplasmic reticulum membrane	Cytochrome P450 1A2	Homo sapiens (human)
intracellular membrane-bounded organelle	Cytochrome P450 1A2	Homo sapiens (human)
intracellular membrane-bounded organelle	Cytochrome P450 1A2	Homo sapiens (human)
extracellular region	Cholinesterase	Homo sapiens (human)
nuclear envelope lumen	Cholinesterase	Homo sapiens (human)
endoplasmic reticulum lumen	Cholinesterase	Homo sapiens (human)
blood microparticle	Cholinesterase	Homo sapiens (human)
plasma membrane	Cholinesterase	Homo sapiens (human)
extracellular space	Cholinesterase	Homo sapiens (human)
nucleus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
cytosol	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
site of double-strand break	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nuclear replication fork	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
site of DNA damage	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
chromosome, telomeric region	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nucleus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nuclear envelope	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nucleoplasm	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nucleolus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
mitochondrion	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
membrane	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nuclear body	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
site of double-strand break	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
site of DNA damage	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
chromatin	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
transcription regulator complex	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein-containing complex	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
protein-DNA complex	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
nucleolus	Poly [ADP-ribose] polymerase 1	Homo sapiens (human)
mitochondrion	Cytochrome P450 2D6	Homo sapiens (human)
endoplasmic reticulum	Cytochrome P450 2D6	Homo sapiens (human)
endoplasmic reticulum membrane	Cytochrome P450 2D6	Homo sapiens (human)
cytoplasm	Cytochrome P450 2D6	Homo sapiens (human)
intracellular membrane-bounded organelle	Cytochrome P450 2D6	Homo sapiens (human)
virion membrane	Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus
nuclear envelope	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
endoplasmic reticulum tubular network	Protein mono-ADP-ribosyltransferase PARP6	Homo sapiens (human)
nucleus	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
cytoplasm	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
nucleus	Protein mono-ADP-ribosyltransferase PARP15	Homo sapiens (human)
nucleus	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
nucleolus	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
cytoplasm	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
Golgi apparatus	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
cytosol	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
cytoplasm	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
nucleus	Protein mono-ADP-ribosyltransferase PARP10	Homo sapiens (human)
endoplasmic reticulum tubular network	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
nuclear envelope	Protein mono-ADP-ribosyltransferase PARP8	Homo sapiens (human)
nuclear envelope	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
endoplasmic reticulum	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
endoplasmic reticulum membrane	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
cytosol	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
membrane	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
endoplasmic reticulum tubular network	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
nuclear envelope	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
endoplasmic reticulum tubular network	Protein mono-ADP-ribosyltransferase PARP16	Homo sapiens (human)
nucleus	Protein mono-ADP-ribosyltransferase PARP12	Homo sapiens (human)
Golgi membrane	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
pericentriolar material	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
chromosome, telomeric region	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
nucleus	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
nuclear envelope	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
cytoplasm	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
cytosol	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
perinuclear region of cytoplasm	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
cytoplasm	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
nucleus	Poly [ADP-ribose] polymerase tankyrase-2	Homo sapiens (human)
site of DNA damage	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleus	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleoplasm	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleolus	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
site of DNA damage	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleolus	Poly [ADP-ribose] polymerase 2	Homo sapiens (human)
nucleus	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
nucleoplasm	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
cytoplasm	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
cytosol	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
spindle microtubule	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
membrane	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
extracellular exosome	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
ribonucleoprotein complex	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
cytoplasm	Protein mono-ADP-ribosyltransferase PARP4	Homo sapiens (human)
nucleoplasm	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
cytoplasm	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
centrosome	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
centriole	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
nuclear body	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
site of double-strand break	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
intercellular bridge	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
nucleolus	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
site of double-strand break	Protein mono-ADP-ribosyltransferase PARP3	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (731)

Assay ID	Title	Year	Journal	Article
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347159	Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347160	Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID686947	qHTS for small molecule inhibitors of Yes1 kinase: Primary Screen	2013	Bioorganic & medicinal chemistry letters, Aug-01, Volume: 23, Issue:15	Identification of potent Yes1 kinase inhibitors using a library screening approach.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID1347110	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347115	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347122	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347124	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347129	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347116	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347121	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347113	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1591452	Antiproliferative activity against human MDA-MB-231 cells incubated for 2 to 5 days by MTT assay	2019	Bioorganic & medicinal chemistry letters, 08-01, Volume: 29, Issue:15	Discovery of naphthacemycins as a novel class of PARP1 inhibitors.
AID1878581	Antiproliferative activity against human THP-1 cells expressing BRD4 assessed as inhibition of cell growth measured after 3 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1276421	Cytotoxicity against BRCA1-deficient human MX1 cells	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1896634	Antiproliferative activity against human DLD-1 cells harbouring BRCA-2 mutant assessed as inhibition of cell growth	2022	Bioorganic & medicinal chemistry letters, 12-15, Volume: 78	Synthesis and in vitro biological evaluation of 3-ethyl-1,5-naphthyridin-2(1H)-one derivatives as potent PARP-1 selective inhibitors and PARP-1 DNA trappers.
AID1862295	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G2/M phase at 0.312 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 27.14 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1499362	Cmax in Sprague-Dawley rat at 10 mg/kg, iv by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1868337	Inhibition of TNKS1 (unknown origin) using biotin-NAD+ as substrate incubated for 1 hr in the presence of deoxy-oligonucleotide by ELISA analysis relative to control	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1486307	Antiproliferative activity against human HCC1937 cells after 3 days by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1758293	Antitumor activity against human MDA-MB-468 cells xenografted in BALB/c mouse assessed as tumor growth inhibition at 50 mg/kg, ip administered for 32 days along with GDC-0980 relative to control	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1861252	Antiproliferative activity against human MDA-MB-231 cells assessed as reduction in cell viability measured after 7 days	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1862303	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 2.5 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 32.62 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1276416	Inhibition of PARP in human LoVo cells assessed as inhibition of poly(ADP)-ribose polymerization for 30 mins by fluorescence assay	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1486302	Antiproliferative activity against human MDA-MB-231 cells after 5 days by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1428399	Inhibition of full length recombinant human His6-tagged PARP16 expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1508854	Inhibition of human N-terminal GST-tagged PARP2 (2 to 583 residues) expressed in baculovirus infected Sf9 insect cells using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay
AID1878661	Upregulation of E2F2 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1428394	Inhibition of full length recombinant human His6-tagged PARP10 expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1831246	Effect on cell cycle progression in human SW1990 cells assessed as reduction in PLK1 expression at 6 uM after 4 days by Western blot analysis
AID1735999	Inhibition of human recombinant GST-tagged PARP-1 expressed in Escherichia coli at 100 nM incubated for 30 mins in presence and NAD by resazurin dye based fluorescence analysis relative to control	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1515648	Antiproliferative activity against human DLD1 cells by Celltiter-Glo assay	2019	MedChemComm, Jun-01, Volume: 10, Issue:6	Controlling cellular distribution of drugs with permeability modifying moieties.
AID1862304	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G2/M phase at 2.5 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 27.14 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1741671	Induction of endoplasmic reticulum stress in human MDA-MB-231 cells assessed as upregulation of CHOP protein expression at 5 uM incubated for 48 to 72 hrs by western blot analysis	2020	European journal of medicinal chemistry, Oct-15, Volume: 204	Augmentation of the antitumor effects of PARP inhibitors in triple-negative breast cancer via degradation by hydrophobic tagging modulation.
AID1882326	Inhibition of PARP1 (unknown origin)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Dual-target inhibitors of poly (ADP-ribose) polymerase-1 for cancer therapy: Advances, challenges, and opportunities.
AID1895791	Binding affinity to PARP1 (unknown origin) assessed as residence time	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1403976	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured on day 10 (Rvb = 21.1 +/- 1.8 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1697256	Antiproliferative activity against human CAPAN-1 cells assessed as cell growth inhibition incubated for 13 days by by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1581928	Antiproliferative activity against human Ramos cells measured after 7 days by Celltiter-glo assay
AID1683890	Inhibition of human PARP-1 catalytic domain (662 to 1011 residues) expressed in Escherichia coli BL21(DE3) cells pre-incubated for 30 mins before addition of activated DNA and NAD by fluorescence based assay	2020	Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24	Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1878666	Upregulation of CCND1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1741672	Induction of endoplasmic reticulum stress in human MDA-MB-231 cells assessed as upregulation of XBP-1s protein expression at 5 uM incubated for 48 to 72 hrs by western blot analysis	2020	European journal of medicinal chemistry, Oct-15, Volume: 204	Augmentation of the antitumor effects of PARP inhibitors in triple-negative breast cancer via degradation by hydrophobic tagging modulation.
AID1878629	Induction of apoptosis in human SW1990 cells assessed as necrotic cells at 6 uM measured after 4 days by Annexin V-FITC and propidium iodide staining based flow cytometry (Rvb = 2.45%)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1303569	Potentiation of 2.5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1878587	Antiproliferative activity against human SW1990 cells assessed as inhibition of cell growth measured after 7 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1508861	Inhibition of human N-terminal His/GST-tagged PARP14 (1470 to 1801 residues) expressed in baculovirus infected Sf9 insect cells at 500 nM using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay relative to
AID386696	Plasma concentration in mouse at 10 mg/kg, po after 30 mins	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1499340	Induction of apoptosis in human MDA-MB-436 cells assessed as late apoptotic cells at 0.1 uM after 96 hrs by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 5.61%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878667	Upregulation of E2F2 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1486299	Antiproliferative activity against human HeLa cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1064615	Resistant factor, ratio of IC50 for human A2780/DX cells to IC50 for human A2780 cells	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1831253	Effect on cell cycle progression in human SW1990 cells xenografted in BALB/c mouse assessed as reduction in PLK1 expression at 45 mg/kg, ip after 4 days by Q-PCR analysis
AID1303565	Potentiation of 0.0025 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID386712	Cytotoxicity against BRCA1-deficient human HCC1937 cells upto 4 uM after 7 to 14 days by clonogenic assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1868343	Inhibition of PARP in human HCT-116 cells assessed as decrease in pADPr levels at 10 uM by Western blot analysis	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1499329	Cell cycle arrest in human Capan1 cells assessed as accumulation at G2/M phase at 1 uM after 72 hrs by propidium iodide-staining based flow cytometry (Rvb = 15.26%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1831206	Invivo inhibition of BRD4 expression in human SW1900 cells xenografted in BALB/c mouse at 45 mg/kg, ip administered for 28 consecutive days by Western blot analysis
AID1878643	Induction of cell cycle arrest in human SW1990 cells assessed as accumulation of cells at S phase at 6 uM incubated for 4 days by propidium iodide staining based flow cytometry (Rvb = 29.32%)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1403955	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured on day 10 (Rvb = 786 +/- 229 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1878572	Toxicity in nude mouse xenografted with human SW1990 cells assessed as kidney damage at 45 mg/kg, ip administered for 28 days by H and E staining based fluorescence microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1667257	Antiproliferative activity against human MDA-MB-231 cells assessed as cell growth inhibition by MTT assay
AID1831205	Invivo inhibition of PARP1 expression in human SW1900 cells xenografted in BALB/c mouse at 45 mg/kg, ip administered for 28 consecutive days by Western blot analysis
AID1265317	Inhibition of full length human PARP6 expressed in a Baculovirus infected Sf9 insect cells using activated DNA as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1128188	In vitro antiproliferative activity against human A549 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1831215	Induction of apoptosis in human SW1990 cells assessed as early apoptotic cells at 6 uM after 4 days by Annexin V-FITC and propidium iodide staining based flow cytometry (Rvb = 1.91%)
AID1697264	Protac activity at CRBN/PARP1 in human MDA-MB-436 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 1000 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1508880	Inhibition of human N-terminal GST-tagged TNKS1 (1001 to 1327 residues) expressed in baculovirus infected Sf9 insect cells using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay
AID1128216	Systemic toxicity in NCr nu/nu athymic mouse xenografted with human A549 cells assessed as body weight at 92 umol/kg, iv administered two times a week for 4 weeks (Rvb = 25.0 +/-0.78 gms)	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1697315	Antiproliferation activity against human LNCAP assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1064614	Inhibition of PARP-1 in human HeLa cells assessed as decrease of H2O2-induced PARylation after 3 hrs by fluorescence assay	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1878723	Effect on CDK6 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1697275	Protac activity at VHL/PARP2 in human CAPAN-1 cells assessed as induction of PARP2 protein degradation up to 1 uM incubated for 24 hrs by Western blot analysis	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1186400	Inhibition of human PARP1	2014	Bioorganic & medicinal chemistry letters, Aug-15, Volume: 24, Issue:16	Synthesis and biological evaluation of substituted 4-(thiophen-2-ylmethyl)-2H-phthalazin-1-ones as potent PARP-1 inhibitors.
AID1867210	Cytotoxicity against human MX1 cells harbouring BRCA1 mutant assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1729547	Induction of apoptosis in human MDA-MB-468 cells assessed as necrotic cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 0.13%)	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1896631	Inhibition of PARP-2 (unknown origin)	2022	Bioorganic & medicinal chemistry letters, 12-15, Volume: 78	Synthesis and in vitro biological evaluation of 3-ethyl-1,5-naphthyridin-2(1H)-one derivatives as potent PARP-1 selective inhibitors and PARP-1 DNA trappers.
AID1878675	Upregulation of CDK6 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1683000	Cytotoxicity against human MDA-MB-468 cells measured after 72 hrs by Celltiter-Glo assay	2020	Journal of medicinal chemistry, 12-10, Volume: 63, Issue:23	Design, Synthesis, and Characterization of an Orally Active Dual-Specific ULK1/2 Autophagy Inhibitor that Synergizes with the PARP Inhibitor Olaparib for the Treatment of Triple-Negative Breast Cancer.
AID386709	Ex vivo inhibition of PARP1 in human SW620 cells assessed as amount of poly(ADP-ribose) by whole cell assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1499361	Volume of distribution in Sprague-Dawley rat at 10 mg/kg, iv by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1350588	Cytotoxicity against human BRCA1-restored UWB1.289 cells assessed as reduction in cell viability after 4 to 7 days by cell-titer glo assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1668085	Antiproliferative activity against BRCA1-deficient human MX1 cells after 48 hrs by MTT assay	2020	Bioorganic & medicinal chemistry, 05-01, Volume: 28, Issue:9	Synthesis of novel dual target inhibitors of PARP and HSP90 and their antitumor activities.
AID1155630	Inhibition of PARP-1 (unknown origin) using biotinylated NAD+ as substrate after 60 mins by spectrophotometry	2014	Journal of medicinal chemistry, Jul-10, Volume: 57, Issue:13	Discovery and structure-activity relationship of novel 2,3-dihydrobenzofuran-7-carboxamide and 2,3-dihydrobenzofuran-3(2H)-one-7-carboxamide derivatives as poly(ADP-ribose)polymerase-1 inhibitors.
AID1831247	Effect on cell cycle progression in human SW1990 cells assessed as reduction in PLK1 expression at 6 uM after 4 days by Q-PCR analysis
AID1878731	Effect on FOXM1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID386695	Inhibition of histidine-tagged recombinant tankyrase-1 by flashplate scintillation proximity assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1683865	Inhibition of human PARP-1 catalytic domain (662 to 1011 residues) expressed in Escherichia coli BL21(DE3) cells incubated for 0.5 hrs by fluorescence polarization assay based DNA trapping activity assay	2020	Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24	Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1861255	Antiproliferative activity against human A549 cells assessed as reduction in cell viability	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1741641	Cytotoxicity against human MDA-MB-231 cells assessed as reduction in cell viability measured after 96 hrs by CCK8 assay	2020	European journal of medicinal chemistry, Oct-15, Volume: 204	Augmentation of the antitumor effects of PARP inhibitors in triple-negative breast cancer via degradation by hydrophobic tagging modulation.
AID386694	Inhibition of recombinant PARP2 by flashplate scintillation proximity assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1878734	Effect on MDC1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1729545	Induction of apoptosis in human MDA-MB-468 cells assessed as early apoptotic cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 3.88%)	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1697325	Induction of DNA damage in human MDA-MB-436 cells assessed as increase in gammaH2AX foci formation incubated for 24 hrs by Western blot analysis	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1403979	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured on day 21 (Rvb = 23.4 +/- 1.7 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1499316	Antiproliferative activity against human MDA-MB-436 cells after 7 days by CCK8 or SRB assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1735994	Antiproliferative activity against human SK-OV-3 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1862285	Binding affinity to PARP1 (unknown origin)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1591451	Antiproliferative activity against human MDA-MB-436 cells harboring BRCA1 mutation incubated for 2 to 5 days by MTT assay	2019	Bioorganic & medicinal chemistry letters, 08-01, Volume: 29, Issue:15	Discovery of naphthacemycins as a novel class of PARP1 inhibitors.
AID1861997	Inhibition of human PARP1 using chemiluminescent HRP substrate at 20 uM measured after 3 hrs by highly sensitive fluorescence assay relative to control
AID1758280	Antiproliferative activity against human BRCA proficient MDA-MB-231 cells assessed as reduction in cell growth incubated for 7 days by cell titer-glo assay	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1403933	Cytotoxicity against Chinese hamster VC8 cells harboring BRCA2 deficient after 3 days by CCK8 assay	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1499343	Induction of apoptosis in human MDA-MB-436 cells assessed as early apoptotic cells at 0.1 uM after 96 hrs in presence of pancaspase inhibitor Z-VAD-FMK by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 2.32%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1500674	Antiproliferative activity against human HCT116 cells expressing topoisomerase-1 after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Design, synthesis and biological evaluation of 4-amidobenzimidazole acridine derivatives as dual PARP and Topo inhibitors for cancer therapy.
AID1831252	Effect on cell cycle progression in human SW1990 cells xenografted in BALB/c mouse assessed as reduction in PLK1 expression at 45 mg/kg, ip after 4 days by Western blot analysis
AID1862317	Inhibition of human recombinant PARP1 in presence of NAD+ by ELISA	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1831136	Induction of autophagy in human SW1990 cells assessed as reduction in p62 expression at 6 uM incubated for 4 days by immunofluorescence assay
AID1878594	Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 5 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID386708	Potentiation of methyl methanesulfonate-induced growth inhibition of human SW620 cells after 4 days by sulforhodamine B assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1508881	Inhibition of human N-terminal GST-tagged TNKS2 (667 to 1166 residues) expressed in baculovirus infected Sf9 insect cells using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay
AID1862326	Induction of DNA double strand breaks in human CAPAN-1 cells assessed as increase in gamma-H2AX level incubated for 48 hrs by western blot analysis	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1878588	Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 3 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1261696	Intrinisc clerarance in human liver microsomes assessed as residual compound level at 60 uM preincubated for 10 mins followed by NADPH addition in KH2PO4 at pH 7.4 by LC-MS method	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Synthesis and Evaluation of a Radioiodinated Tracer with Specificity for Poly(ADP-ribose) Polymerase-1 (PARP-1) in Vivo.
AID1631788	Inhibition of PARP1 (unknown origin)	2016	Bioorganic & medicinal chemistry letters, 08-15, Volume: 26, Issue:16	Design, synthesis and biological evaluation of novel 5-fluoro-1H-benzimidazole-4-carboxamide derivatives as potent PARP-1 inhibitors.
AID1697336	Antitumor activity against CAPAN-1 cells xenografted in Balb/c mouse assessed as tumor growth inhibition at 100 mg/kg, po qd administered for 21 days	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1831251	Effect on cell cycle progression in human SW1990 cells xenografted in BALB/c mouse assessed as reduction in CCND1 expression at 45 mg/kg, ip after 4 days by Q-PCR analysis
AID1128306	Inhibition of recombinant human PARP-10 at 10 uM relative to control	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Design, synthesis, crystallographic studies, and preliminary biological appraisal of new substituted triazolo[4,3-b]pyridazin-8-amine derivatives as tankyrase inhibitors.
AID1591453	Antiproliferative activity against human MCF7 cells incubated for 2 to 5 days by MTT assay	2019	Bioorganic & medicinal chemistry letters, 08-01, Volume: 29, Issue:15	Discovery of naphthacemycins as a novel class of PARP1 inhibitors.
AID1878721	Effect on CDK1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862336	Induction of apoptosis in human CAPAN-1 cells assessed as late apoptotic cells at 5 uM incubated for 96 hrs by AnnexinV-FITC/PI staining based flow cytometry (Rvb = 8.99%)	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1878722	Effect on CCNB1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1758275	Inhibition of PARP1 (unknown origin) using biotin-NAD+ as substrate incubated for 1 hr by ELISA	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1128308	Inhibition of recombinant human PARP-12 at 10 uM relative to control	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Design, synthesis, crystallographic studies, and preliminary biological appraisal of new substituted triazolo[4,3-b]pyridazin-8-amine derivatives as tankyrase inhibitors.
AID1428396	Inhibition of recombinant human His6-tagged PARP12 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1649880	Growth inhibition of human DU145 cells after 5 days by SRB assay	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Design and Synthesis of a Trifunctional Molecular System "Programmed" to Block Epidermal Growth Factor Receptor Tyrosine Kinase, Induce High Levels of DNA Damage, and Inhibit the DNA Repair Enzyme (Poly(ADP-ribose) Polymerase) in Prostate Cancer Cells.
AID748125	Inhibition of PARP7 (unknown origin) at 10 uM relative to control	2013	Journal of medicinal chemistry, Jun-13, Volume: 56, Issue:11	Fragment-based ligand design of novel potent inhibitors of tankyrases.
AID1499351	Antitumor activity against human MDA-MB-436 cells harboring BRCA1 mutant xenografted in nude BALB/cA mouse assessed as tumor growth inhibition at 100 mg/kg, po administered once daily for 21 consecutive days measured twice per week	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1515645	Permeability of compound in 5% DMSO after 7 hrs by PAMPA	2019	MedChemComm, Jun-01, Volume: 10, Issue:6	Controlling cellular distribution of drugs with permeability modifying moieties.
AID1862275	Antiproliferative activity against human MDA-MB-231 cells assessed as cell growth inhibition incubated for 5 days by MTT assay	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1758289	Antitumor activity against human MDA-MB-468 cells xenografted in BALB/c mouse assessed as tumor growth inhibition at 50 mg/kg, ip once daily administered for 32 days relative to control	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1276437	Decrease in PAR level in athymic nu/nu mouse xenografted with human MX1 cells at 100 mg/kg, po measured after 2 and 8 hrs by ELISA	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1741668	Cytotoxicity against human MDA-MB-468 cells assessed as reduction in cell viability measured after 96 hrs by CCK8 assay	2020	European journal of medicinal chemistry, Oct-15, Volume: 204	Augmentation of the antitumor effects of PARP inhibitors in triple-negative breast cancer via degradation by hydrophobic tagging modulation.
AID1428395	Inhibition of recombinant human His6-tagged PARP10 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID762669	Chemopotentiation factor, ratio of EC50 for PARP1 in human Jurkat cells to EC50 for PARP1 in human Jurkat cells in presence of 100 uM of temozolomide	2013	Bioorganic & medicinal chemistry letters, Aug-15, Volume: 23, Issue:16	Discovery of novel benzo[b][1,4]oxazin-3(4H)-ones as poly(ADP-ribose)polymerase inhibitors.
AID1591450	Inhibition of recombinant human full length C-terminal His-tagged PARP1 expressed in Sf9 insect cells preincubated for 15 mins followed by NAD+ addition and measured after 40 mins by fluorescence based assay	2019	Bioorganic & medicinal chemistry letters, 08-01, Volume: 29, Issue:15	Discovery of naphthacemycins as a novel class of PARP1 inhibitors.
AID1683798	Antitumor activity against human MDA-MB-436 cells xenografted in BALB/c nude mouse assessed as inhibition of tumor growth at 25 to 50 mg/kg, po BID for 28 days followed by treatment was interruption and monitored for additional 2 months	2020	Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24	Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1831171	Inhibition of BRD4 expression in human SW1990 cells at 6 uM after 4 days by Western blot analysis
AID1878788	Upregulation of FOXM1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878571	Toxicity in nude mouse xenografted with human SW1990 cells assessed as lung damage at 45 mg/kg, ip administered for 28 days by H and E staining based fluorescence microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862338	Induction of apoptosis in human CAPAN-1 cells assessed as late apoptotic cells at 10 uM incubated for 96 hrs by AnnexinV-FITC/PI staining based flow cytometry (Rvb = 8.99%)	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1403954	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured on day 7 (Rvb = 644 +/- 199 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1499342	Induction of apoptosis in human MDA-MB-436 cells assessed as late apoptotic cells at 1 uM after 96 hrs by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 5.61%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878676	Upregulation of CCNB1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1895766	Inhibition of human recombinant N-terminal 6His-6Lys-TEV tagged PARP1 full length expressed in pFastBac expression system incubated for 4 hrs by fluorescence anisotropy binding assay	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1736029	Antitumor activity against human SKOV3 cells xenografted in Balb/c nude mouse assessed as tumor growth inhibition at 25 mg/kg, po for 21 days and measured every third day	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1064455	Inhibition of GST-tagged recombinant human PARP-1 expressed in Escherichia coli after 30 mins by fluorescence-based assay	2014	Bioorganic & medicinal chemistry letters, Jan-15, Volume: 24, Issue:2	Novel PARP-1 inhibitors based on a 2-propanoyl-3H-quinazolin-4-one scaffold.
AID1878730	Effect on FOXO1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862319	Antiproliferative activity against BRCA1-deficient human UWB1289 cells assessed as inhibition of cell proliferation incubated for 7 days by SRB assay	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1908551	In vivo antitumor activity against human MDA-MB-231 cells xenografted BALB/c mouse assessed as tumor growth inhibition at 100 mg/kg, IG measured after 21 days	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1064608	Toxicity in human MX1 cells harboring BRCA1 deletion and BRCA2 mutant xenografted SCID mouse assessed as mortality at 167 mg/kg, ip administered every 2 days for 2 weeks measured on day 38 relative to control	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1403958	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured on day 21 (Rvb = 1948 +/- 538 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1862273	Antiproliferative activity against human CAPAN-1 cells assessed as cell growth inhibition incubated for 5 days by MTT assay	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1499363	Cmax in Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1649878	Growth inhibition of human 22Rv1 cells after 5 days by SRB assay	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Design and Synthesis of a Trifunctional Molecular System "Programmed" to Block Epidermal Growth Factor Receptor Tyrosine Kinase, Induce High Levels of DNA Damage, and Inhibit the DNA Repair Enzyme (Poly(ADP-ribose) Polymerase) in Prostate Cancer Cells.
AID1697286	Antiproliferation activity against human PC-3 assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1758279	Antiproliferative activity against human BRCA-1 deficient HCC1937 cells assessed as reduction in cell growth incubated for 7 days by cell titer-glo assay	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1831232	Induction of cell cycle arrest in human SW1990 cells assessed as accumulation of cells at G2/M phase at 6 uM incubated for 4 days by propidium iodide staining based flow cytometry (Rvb = 5.89%)
AID1276394	Volume of distribution at steady state in Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1682012	Inhibition of N-terminal GST-tagged human PARP2 (2 to 583 residues) expressed in baculovirus infected Sf9 cells using histone mixture (H2A and H2B) and biotinylated NAD+ as substrate in presence of activated DNA incubated for 60 mins by chemiluminescence	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1895788	Binding affinity to PARP12 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1831142	Antiproliferative activity against human CAPAN-1 cells assessed as reduction in cell viability after 4 days by MTT assay
AID1784223	Inhibition of recombinant human full-length PARP-2 using biotinylated substrate
AID1862301	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G2/M phase at 1.25 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 27.14 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1581914	Antiproliferative activity against human HCT116 cells measured after 7 days by Celltiter-glo assay
AID1868333	Inhibition of PARP-1 (unknown origin) using biotinylated NAD+ as substrate at 10 nM incubated for 45 mins in the presence of deoxy-oligonucleotide by microplate reader method relative to control	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1697342	Acute toxicity in Balb/c mouse xenografted with SW-620 cells assessed as mean weight loss at 10 mg/kg, po qd administered for 5 days in presence of TMZ measured on day 9 relative to control	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1882343	Antiproliferative activity against BRCA proficient human MCF7 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Dual-target inhibitors of poly (ADP-ribose) polymerase-1 for cancer therapy: Advances, challenges, and opportunities.
AID1862294	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 0.312 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 32.62 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1276393	Cmax in Sprague-Dawley rat at 10 mg/kg, po by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1831279	Inhibition of homologous recombinant repair in human SW1990 cells assessed as reduction in FOXM1 expression at 6 uM after 4 days by Western blot analysis
AID1878729	Effect on Rad51 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1683882	Oral bioavailability in Sprague-Dawley rat at 5 mg/kg by LC-MS/MS analysis	2020	Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24	Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1729544	Induction of apoptosis in human MDA-MB-468 cells assessed as viable cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 95.2%)	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID386703	Half life in dog at 2.5 mg/kg, iv and 10 mg/kg, po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1240635	Binding affinity to recombinant human HisGST-tagged PARP-2 catalytic domain assessed as dissociation half life by surface plasmon resonance analysis	2015	Journal of medicinal chemistry, Sep-10, Volume: 58, Issue:17	Discovery of 2-[1-(4,4-Difluorocyclohexyl)piperidin-4-yl]-6-fluoro-3-oxo-2,3-dihydro-1H-isoindole-4-carboxamide (NMS-P118): A Potent, Orally Available, and Highly Selective PARP-1 Inhibitor for Cancer Therapy.
AID1303580	Potentiation of 5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID748126	Inhibition of PARP11 (unknown origin) at 10 uM relative to control	2013	Journal of medicinal chemistry, Jun-13, Volume: 56, Issue:11	Fragment-based ligand design of novel potent inhibitors of tankyrases.
AID1868342	Inhibition of Wnt/beta-Catenin signaling in human HCT-116 cells assessed as decrease in cyclin D1 levels at 10 uM by Western blot analysis	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1303584	Potentiation of 0.0050 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1868630	Inhibition of PARP1 (unknown origin)	2022	Journal of medicinal chemistry, 05-26, Volume: 65, Issue:10	Targeting Enhancer of Zeste Homolog 2 for the Treatment of Hematological Malignancies and Solid Tumors: Candidate Structure-Activity Relationships Insights and Evolution Prospects.
AID1667254	Inhibition of HDAC1 (unknown origin)
AID1128189	In vitro antiproliferative activity against human NCI-H2023 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1179159	Terminal half life in advanced breast cancer patient with BRCA1/2 mutations at 400 mg dosed twice daily	2014	Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19	Development of synthetic lethality anticancer therapeutics.
AID1682063	Potentiation of anticancer activity against human SK-ES-1 cells harboring EWSF1 translocation xenografted in SCID/nude mouse assessed as tumor growth inhibition at 3 mg/kg, po bid for 12 days co-administered with TMZ measured up to 9 weeks post drug admin	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1499403	Inhibition of PARP1 in BRCA1 deficient human MDA-MB-436 cells assessed as increase in DNA double stranded breaks by measuring gammaH2AX levels at 1 and 3 uM after 48 to 72 hrs by Western blot analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1152976	Inhibition of human recombinant PARP-1 after 1 hr by ELISA	2014	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 24, Issue:12	Synthesis of isoquinolinone-based tricycles as novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors.
AID1261694	Inhibition of PARP1 in human T98G cells incubated for 60 mins by immunofluorescence assay	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Synthesis and Evaluation of a Radioiodinated Tracer with Specificity for Poly(ADP-ribose) Polymerase-1 (PARP-1) in Vivo.
AID1784263	Antitumor activity against human SK-OV-3 cells xenografted in BALB/c nude mouse assessed as decrease in tumor volume at 50 mg/kg, po administered once daily measured for 28 days
AID1831204	Invivo inhibition of BRD4 expression in human SW1900 cells xenografted in BALB/c mouse at 45 mg/kg, ip administered for 28 consecutive days by Q-PCR analysis
AID1908524	Antiproliferative activity against human PTEN -/- MDA-MB-468 cells assessed as reduction in cell viability incubated for 5 to 10 days by MTT assay	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1303576	Potentiation of 5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1867211	Cytotoxicity against human SK-BR-3 cells harbouring wild type BRCA1/2 assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1128175	Inhibition of PARP-1 (unknown origin) assessed as incorporation of biotinylated poly ADP-ribose onto histone proteins by colorimetric analysis in presence of GSH and GSTP1	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1868628	Antiproliferative activity against human MDA-MB-468 cells	2022	Journal of medicinal chemistry, 05-26, Volume: 65, Issue:10	Targeting Enhancer of Zeste Homolog 2 for the Treatment of Hematological Malignancies and Solid Tumors: Candidate Structure-Activity Relationships Insights and Evolution Prospects.
AID1303572	Potentiation of 0.0050 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1862335	Induction of apoptosis in human CAPAN-1 cells assessed as early apoptotic cells at 5 uM incubated for 96 hrs by AnnexinV-FITC/PI staining based flow cytometry (Rvb = 5.08%)	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1909228	Inhibition of PARP1 (unknown origin)	2022	Journal of medicinal chemistry, 05-12, Volume: 65, Issue:9	Discovery of 4-Hydroxyquinazoline Derivatives as Small Molecular BET/PARP1 Inhibitors That Induce Defective Homologous Recombination and Lead to Synthetic Lethality for Triple-Negative Breast Cancer Therapy.
AID1240633	Binding affinity to recombinant human HisGST-tagged PARP-1 catalytic domain assessed as dissociation half life by surface plasmon resonance analysis	2015	Journal of medicinal chemistry, Sep-10, Volume: 58, Issue:17	Discovery of 2-[1-(4,4-Difluorocyclohexyl)piperidin-4-yl]-6-fluoro-3-oxo-2,3-dihydro-1H-isoindole-4-carboxamide (NMS-P118): A Potent, Orally Available, and Highly Selective PARP-1 Inhibitor for Cancer Therapy.
AID1499365	AUC in Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878789	Upregulation of ALDH1A1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1303582	Potentiation of 5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID386706	Volume of distribution in dog at 2.5 mg/kg, iv and 10 mg/kg, po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1303575	Potentiation of 2.5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1515649	Antiproliferative activity against BRCA deficient human DLD1 cells by Celltiter-Glo assay	2019	MedChemComm, Jun-01, Volume: 10, Issue:6	Controlling cellular distribution of drugs with permeability modifying moieties.
AID1817362	Protac activity at VHL/PARP-1 in human NCI-H1299 cells assessed as induction of PARP degradation at up to 15 uM incubated for 36 hrs by Western blot analysis	2021	Journal of medicinal chemistry, 06-10, Volume: 64, Issue:11	Rational Design and Synthesis of Novel Dual PROTACs for Simultaneous Degradation of EGFR and PARP.
AID1831278	Inhibition of homologous recombinant repair in human SW1990 cells assessed as reduction in FOXM1 expression at 6 uM after 4 days by Q-PCR analysis
AID1697314	Antiproliferation activity against human MDA-MB-468 assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1867209	Cytotoxicity against human MCF7 cells harbouring wild type BRCA1/2 assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1350586	Cytotoxicity against mouse PARP2 deficient MEF cells expressing PARP1 assessed as reduction in cell viability after 4 to 7 days by cell-titer glo assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1697352	Acute toxicity in Balb/c mouse xenografted with Capan1 cells assessed as lethality at 100 mg/kg, po qd administered for 5 days in presence of cisplatin	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1064607	Inhibition of recombinant human GST-fused PARP-1 expressed in Escherichia coli after 30 mins by fluorescence assay	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1486297	Antiproliferative activity against human MDA-MB-231 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1878664	Upregulation of CDK1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1697267	Protac activity at CRBN/PARP1 in human CAPAN-1 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 100 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1428384	Inhibition of full length recombinant human His6-tagged PARP1 expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1499358	Half life in Sprague-Dawley rat at 10 mg/kg, iv by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1868357	Induction of cell cycle arrest in human HCT-116 cells assessed as G2/M phase cells at 5 uM incubated for 3 days by propidium iodide staining based flow cytometry (Rvb = 68.35 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1499325	Cell cycle arrest in human Capan1 cells assessed as accumulation at S phase at 0.1 uM after 72 hrs by propidium iodide-staining based flow cytometry (Rvb = 21.42%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878622	Upregulation of PARP1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878777	Upregulation of CCNB1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1428393	Inhibition of recombinant human TNKS2 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1508857	Inhibition of human N-terminal GST-tagged TNKS1 (1001 to 1327 residues) expressed in baculovirus infected Sf9 insect cells at 500 nM using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay relative to contr
AID1499350	Induction of apoptosis in human MDA-MB-436 cells assessed as caspase-3/7 activation at 0.1 to 1 uM after 72 hrs by Caspase-Glo 3/7 assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1908537	Inhibition of PARP2 (unknown origin)	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1729535	Antiproliferative activity against human MDA-MB-468 cells measured after 7 days by Celltiter-glo assay	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1868332	Cytotoxicity against mouse AML12 cells assessed as reduction in cell viability incubated for 7 days by MTT assay	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1581936	Inhibition of PI3K in human MDA-MB-468 cells assessed as reduction in BRCA1 mRNA level at 2 uM by Trizol reagent-based RT-PCR analysis
AID1878642	Induction of cell cycle arrest in human SW1990 cells assessed as accumulation of cells at G0/G1 phase at 6 uM incubated for 4 days by propidium iodide staining based flow cytometry (Rvb = 64.79%)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878794	Induction of BRCA2 accumulation in nucleus of human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1729539	Inhibition of PARP1/PI3Kalpha in human MDA-MB-231 cells assessed as down regulation of BRCA1 mRNA expression at 2 uM by RT-PCR analysis	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1831183	Toxicity in BALB/c mouse xenografted with human SW1990 cells assessed as effect on body weight at 45 mg/kg, ip administered for 28 consecutive days
AID1895786	Binding affinity to PARP10 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1868340	Inhibition of Wnt/beta-Catenin signaling in human HCT-116 cells assessed as decrease in active beta-catenin levels at 10 uM by Western blot analysis	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1303574	Potentiation of 5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1428390	Inhibition of recombinant human His6-tagged PARP4 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1862321	Antiproliferative activity against BRCA1-deficient human MDA-MB-436 cells assessed as inhibition of cell proliferation incubated for 7 days by CCK-8 assay	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1878796	Upregulation of PAPR1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 28 days by DAPI staining based laser confocal microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1683493	Selectivity index, ratio of IC50 for PARP-2 (unknown origin) to IC50 for PARP-1 (unknown origin)	2021	Bioorganic & medicinal chemistry letters, 01-01, Volume: 31	Identification of 2-substituted pyrrolo[1,2-b]pyridazine derivatives as new PARP-1 inhibitors.
AID1179157	In vivo inhibition of PARP activity in peripheral blood mononuclear cells of advanced breast cancer patient with BRCA1/2 mutations at 400 mg dosed twice daily	2014	Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19	Development of synthetic lethality anticancer therapeutics.
AID1486298	Antiproliferative activity against human HCC827 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1862302	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at S phase at 1.25 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 37.88 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1303578	Potentiation of 0.0050 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1831203	Invivo inhibition of PARP1 expression in human SW1900 cells xenografted in BALB/c mouse at 45 mg/kg, ip administered for 28 consecutive days by Q-PCR analysis
AID1276441	Antitumor activity against BRCA1 deficient human MX1 cells xenografted in athymic nu/nu mouse at 100 mg/kg, po qd	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1682058	Potentiation of anticancer activity against human MDA-MB-436 cells harboring BRCA mutant xenografted in SCID/nude mouse assessed as tumor growth inhibition at 3 mg/kg, po bid for 12 days co-administered with TMZ measured up to 9 weeks post-drug administra	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID728418	Potentiation of temozolomide-induced cytotoxicity in human SKOV3 cells assessed as reduction in temozolomide IC50 at 0.5 uM after 7 days by sulforhodamine B assay	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1499404	Inhibition of PARP1 in BRCA2 deficient human Capan1 cells assessed as increase in DNA double stranded breaks by measuring gammaH2AX levels at 1 and 3 uM after 48 to 72 hrs by Western blot analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1784224	Selectivity index, ratio of IC50 for inhibition of recombinant human full-length PARP-2 to IC50 for inhibition of recombinant human full-length PARP-1
AID1895782	Binding affinity to PARP5b (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1895798	Antitumor activity against patient derived explant HBCx-17 cells xenografted in mouse assessed as tumor regression administered daily at 100 mg/kg, po for 25 days relative to control	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1862274	Antiproliferative activity against human MDA-MB-468 cells assessed as cell growth inhibition incubated for 5 days by MTT assay	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1403977	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured on day 14 (Rvb = 22.2 +/- 2.0 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID728415	Cytotoxicity against human SKOV3 cells after 7 days by sulforhodamine B assay	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1064618	Antiproliferative activity against BRCA2 gene mutated human Capan1 cells after 72 hrs by SRB assay	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1649876	Inhibition of PARP in human 22Rv1 cells assessed as reduction in auto-PARylation at 10 uM measured after 48 hrs by Western blot analysis	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Design and Synthesis of a Trifunctional Molecular System "Programmed" to Block Epidermal Growth Factor Receptor Tyrosine Kinase, Induce High Levels of DNA Damage, and Inhibit the DNA Repair Enzyme (Poly(ADP-ribose) Polymerase) in Prostate Cancer Cells.
AID1649875	Inhibition of PARP in human PC3 cells assessed as reduction in auto-PARylation at 10 uM measured after 48 hrs by Western blot analysis	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Design and Synthesis of a Trifunctional Molecular System "Programmed" to Block Epidermal Growth Factor Receptor Tyrosine Kinase, Induce High Levels of DNA Damage, and Inhibit the DNA Repair Enzyme (Poly(ADP-ribose) Polymerase) in Prostate Cancer Cells.
AID1303568	Potentiation of 5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1862334	Induction of apoptosis in human CAPAN-1 cells assessed as late apoptotic cells at 1 uM incubated for 96 hrs by AnnexinV-FITC/PI staining based flow cytometry (Rvb = 8.99%)	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1741646	Induction of PARP1 degradation in human MDA-MB-231 cells at 5 uM incubated for 48 to 72 hrs by western blot analysis	2020	European journal of medicinal chemistry, Oct-15, Volume: 204	Augmentation of the antitumor effects of PARP inhibitors in triple-negative breast cancer via degradation by hydrophobic tagging modulation.
AID1303561	Potentiation of 2.5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1350579	Inhibition of PARP1 in human OVCAR8 cells assessed as reduction in PAR expression at 1 to 10000 nM after 6 hrs by Western blot analysis	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1486291	Inhibition of recombinant full length human N-terminal GST-tagged PARP1 expressed in baculovirus infected Sf9 cells using biotinylated substrate after 1 hr by UV/Vis spectrophotometric analysis	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1265312	Inhibition of TNSK1/2-activated Wnt pathway in human DLD-1 TOPFlash/EF1a Renilla reporter cells after 24 hrs by Steady-Glo Luciferase assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1152979	Cytotoxicity against BRCA2-deficient Chinese hamster VC8 cells by sulforhodamine B assay	2014	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 24, Issue:12	Synthesis of isoquinolinone-based tricycles as novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors.
AID1862296	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at S phase at 0.312 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 37.88 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1895785	Binding affinity to PARP9 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1486468	Inhibition of recombinant human PARP-2 expressed in Escherichia coli BL21 (DE3) using sheared DNA as substrate in presence of biotinylated NAD after 1 hr by ELISA	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Discovery of novel quinazoline-2,4(1H,3H)-dione derivatives as potent PARP-2 selective inhibitors.
AID1486306	Antiproliferative activity against human Raji cells after 3 days by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1499327	Cell cycle arrest in human Capan1 cells assessed as accumulation at G0/G1 phase at 1 uM after 72 hrs by propidium iodide-staining based flow cytometry (Rvb = 63.33%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1895779	Binding affinity to PARP3 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1895767	Inhibition of human recombinant N-terminal Avi-6His-TEV tagged PARP2 full length expressed in pFastBac expression system incubated for 4 hrs by fluorescence anisotropy binding assay	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1508852	Inhibition of human full-length N-terminal GST-tagged PARP1 expressed in baculovirus infected Sf9 insect cells using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay
AID1303571	Potentiation of 0.0025 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1895781	Binding affinity to PARP5a (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1261691	Protein binding to human serum albumin at 0.5 to 1.5 mg/ml by HPLC method	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Synthesis and Evaluation of a Radioiodinated Tracer with Specificity for Poly(ADP-ribose) Polymerase-1 (PARP-1) in Vivo.
AID1499326	Cell cycle arrest in human Capan1 cells assessed as accumulation at G2/M phase at 0.1 uM after 72 hrs by propidium iodide-staining based flow cytometry (Rvb = 15.26%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878569	Toxicity in nude mouse xenografted with human SW1990 cells assessed as liver damage at 45 mg/kg, ip administered for 28 days by H and E staining based fluorescence microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1152980	Cytotoxicity against BRCA1-deficient human MDA-MB-436 cells by sulforhodamine B assay	2014	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 24, Issue:12	Synthesis of isoquinolinone-based tricycles as novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors.
AID1240632	Binding affinity to recombinant human HisGST-tagged PARP-1 catalytic domain by surface plasmon resonance analysis	2015	Journal of medicinal chemistry, Sep-10, Volume: 58, Issue:17	Discovery of 2-[1-(4,4-Difluorocyclohexyl)piperidin-4-yl]-6-fluoro-3-oxo-2,3-dihydro-1H-isoindole-4-carboxamide (NMS-P118): A Potent, Orally Available, and Highly Selective PARP-1 Inhibitor for Cancer Therapy.
AID1872301	Selectivity ratio of IC50 for PARP2 (unknown origin) to IC50 for PARP1 (unknown origin)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Recent advances in DDR (DNA damage response) inhibitors for cancer therapy.
AID1581916	Antiproliferative activity against human MDA-MB-231 cells measured after 7 days by Celltiter-glo assay
AID1868629	Antiproliferative activity against human MCF7 cells	2022	Journal of medicinal chemistry, 05-26, Volume: 65, Issue:10	Targeting Enhancer of Zeste Homolog 2 for the Treatment of Hematological Malignancies and Solid Tumors: Candidate Structure-Activity Relationships Insights and Evolution Prospects.
AID1403957	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured on day 17 (Rvb = 1488 +/- 417 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1908536	Inhibition of PARP1 (unknown origin)	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1276417	Potentiation of temozolomide-induced cytotoxicity in human LoVo cells assessed as temozolomide GI50 at 0.4 uM after 5 days by Celltiter-Glo assay	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1878732	Effect on TOPBP1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1581923	Antiproliferative activity against human A2780 cells measured after 7 days by Celltiter-glo assay
AID1895787	Binding affinity to PARP11 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1403973	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured immediately after first dose (Rvb = 19.7 +/- 1.3 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1668090	Antiproliferative activity against BRCA-proficient human MDA-MB-231 cells after 48 hrs by MTT assay	2020	Bioorganic & medicinal chemistry, 05-01, Volume: 28, Issue:9	Synthesis of novel dual target inhibitors of PARP and HSP90 and their antitumor activities.
AID1831230	Induction of cell cycle arrest in human SW1990 cells assessed as accumulation of cells at G0/G1 phase at 6 uM incubated for 4 days by propidium iodide staining based flow cytometry (Rvb = 64.79%)
AID1861251	Inhibition of HDAC derived from human HeLa cell nucleus	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1605288	Induction of DNA damage in BRCA2 defective human Capan1 cells assessed as increase in gamma-H2AX labelling at 10 uM after 48 hrs by immunofluorescence microscopic analysis	2020	Journal of medicinal chemistry, 03-12, Volume: 63, Issue:5	Synthetic Lethality in Pancreatic Cancer: Discovery of a New RAD51-BRCA2 Small Molecule Disruptor That Inhibits Homologous Recombination and Synergizes with Olaparib.
AID1064606	Antiproliferative activity against BRCA1 gene mutated human HCC1937 cells after 72 hrs by SRB assay	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1878728	Effect on BRCA2 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1831249	Effect on cell cycle progression in human SW1990 cells xenografted in BALB/c mouse assessed as reduction in CDK6 expression at 45 mg/kg, ip after 4 days by Q-PCR analysis
AID1831245	Effect on cell cycle progression in human SW1990 cells assessed as reduction in CCND1 expression at 6 uM after 4 days by Q-PCR analysis
AID386700	AUC (0 to infinity) in rat at 15 mg/kg, iv and po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1878655	Upregulation of CDC25B expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1831231	Induction of cell cycle arrest in human SW1990 cells assessed as accumulation of cells at S phase at 6 uM incubated for 4 days by propidium iodide staining based flow cytometry (Rvb = 29.32%)
AID1428388	Inhibition of recombinant human His6-tagged PARP2 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1697263	Protac activity at CRBN/PARP1 in human MDA-MB-436 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 100 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1820832	Antiproliferative activity against human MDA-MB-231 cells at 3 uM for 10 days by SRB staining based clone formation assay relative to control	2022	European journal of medicinal chemistry, Jan-15, Volume: 228	Noncovalent CDK12/13 dual inhibitors-based PROTACs degrade CDK12-Cyclin K complex and induce synthetic lethality with PARP inhibitor.
AID1581926	Antiproliferative activity against human A549 cells measured after 7 days by Celltiter-glo assay
AID1428389	Inhibition of full length recombinant human His6-tagged PARP3 expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1736001	Inhibition of human recombinant N-terminal GST-tagged PARP-2 expressed in Baculovirus infected Sf9 cells assessed as reduction in NAD+-dependent ADP ribosylation using histone mixture (H2A and H2B) as substrate in presence of activated DNA incubated for 3	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1895780	Binding affinity to PARP4 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1878682	Induction of DNA damage in human SW1990 cells assessed as increase in tail DNA at 6 uM incubated for 4 days by comet assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862333	Induction of apoptosis in human CAPAN-1 cells assessed as early apoptotic cells at 1 uM incubated for 96 hrs by AnnexinV-FITC/PI staining based flow cytometry (Rvb = 5.08%)	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1668086	Antiproliferative activity against BRCA1-deficient human HCC1937 cells after 48 hrs by MTT assay	2020	Bioorganic & medicinal chemistry, 05-01, Volume: 28, Issue:9	Synthesis of novel dual target inhibitors of PARP and HSP90 and their antitumor activities.
AID1581937	Inhibition of PI3K in human MDA-MB-468 cells assessed as reduction in BRCA2 mRNA level at 2 uM by Trizol reagent-based RT-PCR analysis
AID1735997	Antiproliferative activity against human Caco-2 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1186401	Inhibition of human PARP1 at 1 umol	2014	Bioorganic & medicinal chemistry letters, Aug-15, Volume: 24, Issue:16	Synthesis and biological evaluation of substituted 4-(thiophen-2-ylmethyl)-2H-phthalazin-1-ones as potent PARP-1 inhibitors.
AID1831281	Inhibition of homologous recombinant repair in human SW1990 cells assessed as reduction in BRCA1 expression at 6 uM after 4 days by Western blot analysis
AID1861250	Inhibition of PARP-1 derived from human HeLa cell nucleus	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1878720	Effect on CDC25A gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1128190	In vitro antiproliferative activity against human H460 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1831271	Induction of DNA damage in human SW1990 cells assessed as tail DNA at 6 uM incubated for 4 days by comet assay
AID748129	Inhibition of PARP3 (unknown origin) at 10 uM relative to control	2013	Journal of medicinal chemistry, Jun-13, Volume: 56, Issue:11	Fragment-based ligand design of novel potent inhibitors of tankyrases.
AID1683889	Inhibition of PARP-2 (unknown origin) pre-incubated for 30 mins before addition of activated DNA and NAD by chemiluminescent assay	2020	Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24	Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1736000	Inhibition of human recombinant GST-tagged PARP-1 expressed in Escherichia coli assessed as reduction in NAD+-dependent ADP ribosylation incubated for 30 mins in presence and NAD by resazurin dye based fluorescence analysis	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID728422	Inhibition of PARP1/PARP2 in human SKOV3 cells assessed as reduction in H2O2-induced PARylation incubated for 4 hrs prior to H2O2 treatment	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1758281	Antiproliferative activity against human BRCA proficient MDA-MB-468 cells assessed as reduction in cell growth incubated for 7 days by cell titer-glo assay	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1668089	Antiproliferative activity against BRCA-proficient human SKBR3 cells after 48 hrs by MTT assay	2020	Bioorganic & medicinal chemistry, 05-01, Volume: 28, Issue:9	Synthesis of novel dual target inhibitors of PARP and HSP90 and their antitumor activities.
AID1428386	Inhibition of recombinant human His6-tagged PARP1 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1682056	Toxicity in SCID/nude mouse xenografted with human MDA-MB-436 cells harboring BRCA mutant assessed as body weight loss at 50 mg/kg, po bid	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1683492	Antiproliferative activity against BRCA1 deficient human MDA-MB-436 cells	2021	Bioorganic & medicinal chemistry letters, 01-01, Volume: 31	Identification of 2-substituted pyrrolo[1,2-b]pyridazine derivatives as new PARP-1 inhibitors.
AID1697274	Protac activity at VHL/PARP2 in human MDA-MB-436 cells assessed as induction of PARP2 protein degradation up to 1 uM incubated for 24 hrs by Western blot analysis	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1428397	Inhibition of recombinant human His6-tagged PARP14 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1303563	Potentiation of 2.5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1831148	Inhibition of recombinant BRD4 (unknown origin) incubated for 120 mins by TR-FRET assay
AID762671	Inhibition of PARP1 in human Jurkat cells assessed as reduction of cell viability after 96 hrs by MTS assay	2013	Bioorganic & medicinal chemistry letters, Aug-15, Volume: 23, Issue:16	Discovery of novel benzo[b][1,4]oxazin-3(4H)-ones as poly(ADP-ribose)polymerase inhibitors.
AID1499345	Induction of apoptosis in human MDA-MB-436 cells assessed as early apoptotic cells at 1 uM after 96 hrs in presence of pancaspase inhibitor Z-VAD-FMK by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 2.32%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1261693	Inhibition of PARP1 in human G7 cells incubated for 60 mins by immunofluorescence assay	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Synthesis and Evaluation of a Radioiodinated Tracer with Specificity for Poly(ADP-ribose) Polymerase-1 (PARP-1) in Vivo.
AID1895784	Binding affinity to PARP8 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1403932	Inhibition of recombinant human PARP2 using histone as substrate after 1.5 hr in presence of NAD+ by ELISA	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1265292	Inhibition of human TNKS1 (1001 to 1327 residues) expressed in Baculovirus infected Sf9 insect cells using activated DNA as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1276391	Oral bioavailability in Sprague-Dawley rat at 10 mg/kg by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1868356	Induction of cell cycle arrest in human HCT-116 cells assessed as S phase cells at 5 uM incubated for 3 days by propidium iodide staining based flow cytometry (Rvb = 11.26 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1128183	In vitro antiproliferative activity against human NCI-H1355 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1729529	Inhibition of PARP1 (unknown origin) at 10 nM relative to control	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1667252	Inhibition of PARP1 (unknown origin)
AID1303581	Potentiation of 2.5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1276392	AUC in Sprague-Dawley rat at 10 mg/kg, po by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1128185	In vitro antiproliferative activity against human NCI-H2030 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1261692	Inhibition of PARP1 (unknown origin) incubated for 10 mins using biotinylated NAD+ and activated DNA by colorimetric assay	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Synthesis and Evaluation of a Radioiodinated Tracer with Specificity for Poly(ADP-ribose) Polymerase-1 (PARP-1) in Vivo.
AID748128	Inhibition of PARP2 (unknown origin) at 10 uM relative to control	2013	Journal of medicinal chemistry, Jun-13, Volume: 56, Issue:11	Fragment-based ligand design of novel potent inhibitors of tankyrases.
AID1895768	Selectivity ratio of IC50 for PARP1 (unknown origin) to IC50 for PARP2 (unknown origin )	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1499328	Cell cycle arrest in human Capan1 cells assessed as accumulation at S phase at 1 uM after 72 hrs by propidium iodide-staining based flow cytometry (Rvb = 21.42%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878590	Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 5 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862297	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 0.625 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 32.62 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1867207	Cytotoxicity against human MDA-MB-468 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1878644	Induction of cell cycle arrest in human SW1990 cells assessed as accumulation of cells at G2/M phase at 6 uM incubated for 4 days by propidium iodide staining based flow cytometry (Rvb = 5.89%)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1565232	Cytotoxicity against human MCF7 cells at 2.5 to 5 uM incubated for 30 hrs by MTT assay	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Discovery of novel functionalized 1,2,4-triazoles as PARP-1 inhibitors in breast cancer: Design, synthesis and antitumor activity evaluation.
AID1878724	Effect on CCND1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1831170	Inhibition of PARP1 expression in human SW1990 cells at 6 uM after 4 days by Western blot analysis
AID1683490	Inhibition of PARP-2 (unknown origin)	2021	Bioorganic & medicinal chemistry letters, 01-01, Volume: 31	Identification of 2-substituted pyrrolo[1,2-b]pyridazine derivatives as new PARP-1 inhibitors.
AID1428398	Inhibition of recombinant human His6-tagged PARP15 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1909177	Induction of DNA damage in human MDA-MB-468 cells assessed as up-regulation of gammaH2AX expression level at 3 uM by DAPI staining based immunofluorescence assay	2022	Journal of medicinal chemistry, 05-12, Volume: 65, Issue:9	Discovery of 4-Hydroxyquinazoline Derivatives as Small Molecular BET/PARP1 Inhibitors That Induce Defective Homologous Recombination and Lead to Synthetic Lethality for Triple-Negative Breast Cancer Therapy.
AID1128186	In vitro antiproliferative activity against human NCI-H1944 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1508858	Inhibition of human N-terminal GST-tagged TNKS2 (667 to 1166 residues) expressed in baculovirus infected Sf9 insect cells at 500 nM using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay relative to contro
AID1908523	Antiproliferative activity against human BRCA2 -/- CAPAN-1 cells assessed as reduction in cell viability incubated for 5 to 10 days by MTT assay	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1831192	Toxicity in BALB/c mouse xenografted with human SW1990 cells assessed as spleen damage at 45 mg/kg, ip administered for 28 consecutive days by H and E staining based fluorescence microscopic analysis
AID1486296	Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1667255	Antiproliferative activity against human K562 cells assessed as cell growth inhibition by MTT assay
AID1878776	Upregulation of CDK1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862322	Antiproliferative activity against BRCA2-deficient human CAPAN-1 cells assessed as inhibition of cell proliferation incubated for 7 days by CellTiter-Glo assay	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1581927	Antiproliferative activity against human CAKI-1 cells measured after 7 days by Celltiter-glo assay
AID1581929	Antiproliferative activity against human SW620 cells measured after 7 days by Celltiter-glo assay
AID1878727	Effect on BRCA1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1861254	Antiproliferative activity against human DU-145 cells assessed as reduction in cell viability	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID762672	Inhibition of human PARP1 catalytic activity after 10 mins by ELISA	2013	Bioorganic & medicinal chemistry letters, Aug-15, Volume: 23, Issue:16	Discovery of novel benzo[b][1,4]oxazin-3(4H)-ones as poly(ADP-ribose)polymerase inhibitors.
AID1830902	Inhibition of recombinant human PARP1 using NAD+ as substrate incubated for 1 hr by ELISA
AID1499318	Cytotoxicity against BRCA2 expressing Chinese hamster V79 cells after 3 days by CCK8 or SRB assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1152978	Cytotoxicity against Chinese hamster V79 cells by sulforhodamine B assay	2014	Bioorganic & medicinal chemistry letters, Jun-15, Volume: 24, Issue:12	Synthesis of isoquinolinone-based tricycles as novel poly(ADP-ribose) polymerase-1 (PARP-1) inhibitors.
AID1878726	Effect on HEXIM1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1831217	Induction of apoptosis in human SW1990 cells assessed as necrotic cells at 6 uM after 4 days by Annexin V-FITC and propidium iodide staining based flow cytometry (Rvb = 1.89%)
AID1878592	Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 3 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1557954	Inhibition of PARP1 (unknown origin) by colorimetric assay	2019	Bioorganic & medicinal chemistry, 09-15, Volume: 27, Issue:18	Synthesis and biological activity of structurally diverse phthalazine derivatives: A systematic review.
AID762670	Inhibition of PARP1 in human Jurkat cells assessed as reduction of cell viability after 96 hrs by MTS assay in presence of 100 uM of temozolomide	2013	Bioorganic & medicinal chemistry letters, Aug-15, Volume: 23, Issue:16	Discovery of novel benzo[b][1,4]oxazin-3(4H)-ones as poly(ADP-ribose)polymerase inhibitors.
AID1697354	Acute toxicity in Balb/c mouse xenografted with SW-620 cells assessed as lethality at 10 mg/kg, po qd administered for 5 days in presence of TMZ	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1878630	Induction of apoptosis in human SW1990 cells assessed as late apoptotic cells at 6 uM measured after 4 days by Annexin V-FITC and propidium iodide staining based flow cytometry (Rvb = 7.23%)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1128305	Inhibition of recombinant human PARP-8 at 10 uM relative to control	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Design, synthesis, crystallographic studies, and preliminary biological appraisal of new substituted triazolo[4,3-b]pyridazin-8-amine derivatives as tankyrase inhibitors.
AID728420	Inhibition of PARP1 in Chinese hamster V79 cells expressing wild type BRCA2 assessed as increase in gamma-H2AX level after 24 hrs by Western blotting analysis	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1868350	Induction of apoptosis in human HCT-116 cells assessed as necrotic cells at 5 uM incubated for 3 days by annexinV-FITC/propidium iodide staining based flow cytometry (Rvb = 3.65 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1697255	Antiproliferative activity against human MDA-MB-436 cells assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1728101	Antiproliferative activity against human MDA-MB-231 cells assessed as cell viability after 24 hrs	2021	European journal of medicinal chemistry, Jan-15, Volume: 210	Potent antiproliferative activity of bradykinin B2 receptor selective agonist FR-190997 and analogue structures thereof: A paradox resolved?
AID1878665	Upregulation of CDC25B expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID386701	Volume of distribution in rat at 15 mg/kg, iv and po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1697350	Acute toxicity in Balb/c mouse xenografted with Capan1 cells assessed as mean weight loss at 100 mg/kg, po qd administered for 5 days in presence of cisplatin measured on day 10 relative to control	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1868336	Inhibition of PARP-1 (unknown origin) using biotinylated NAD+ as substrate incubated for 45 mins in the presence of deoxy-oligonucleotide by microplate reader method relative to control	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1179156	Cmax in advanced breast cancer patient with BRCA1/2 mutations at 400 mg dosed twice daily	2014	Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19	Development of synthetic lethality anticancer therapeutics.
AID1403974	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured on day 3 (Rvb = 20.2 +/- 1.3 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1862309	PROTAC activity at CRBN/PARP1 in human MDA-MB-231 cells assessed as induction of PARP1 degradation at 1 uM incubated for 24 hrs by DAPI and Rhodamine staining based immunofluorescence assay	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1868348	Induction of apoptosis in human HCT-116 cells assessed as early apoptotic cells at 5 uM incubated for 3 days by annexinV-FITC/propidium iodide staining based flow cytometry (Rvb = 7.67 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1895789	Binding affinity to PARP14 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1831194	Toxicity in BALB/c mouse xenografted with human SW1990 cells assessed as heart damage at 45 mg/kg, ip administered for 28 consecutive days by H and E staining based fluorescence microscopic analysis
AID1831244	Effect on cell cycle progression in human SW1990 cells assessed as reduction in CCND1 expression at 6 uM after 4 days by Western blot analysis
AID1831282	Inhibition of homologous recombinant repair in human SW1990 cells assessed as reduction in Rad51 expression at 6 uM after 4 days by Q-PCR analysis
AID1667256	Antiproliferative activity against human MCF7 cells assessed as cell growth inhibition by MTT assay
AID1403931	Inhibition of recombinant human PARP1 using histone as substrate after 1 hr in presence of NAD+ by ELISA	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1830903	Inhibition of recombinant human PARP2 using NAD+ as substrate incubated for 1 hr by ELISA
AID1831250	Effect on cell cycle progression in human SW1990 cells xenografted in BALB/c mouse assessed as reduction in CCND1 expression at 45 mg/kg, ip after 4 days by Western blot analysis
AID1128187	In vitro antiproliferative activity against human NCI-H1792 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1265291	Inhibition of PARP3 (unknown origin) using activated DNA as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1878791	Upregulation of BRCA2 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1697265	Protac activity at CRBN/PARP1 in human CAPAN-1 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 1 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1668088	Antiproliferative activity against BRCA-proficient human MCF7 cells after 48 hrs by MTT assay	2020	Bioorganic & medicinal chemistry, 05-01, Volume: 28, Issue:9	Synthesis of novel dual target inhibitors of PARP and HSP90 and their antitumor activities.
AID1697313	Antiproliferation activity against human 22Rv1 assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1895777	Binding affinity to PARP1 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1403934	Cytotoxicity against Chinese hamster V79 cells at 10 uM after 3 days by CCK8 assay	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1697311	Inhibition of recombinant human C-terminal His-tagged PARP1 expressed in Sf9 insect cells preincubated for 20 mins in presence of activated DNA followed by 32P-NAD+ addition and further incubated for 2 hrs by chemiluminescence assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1908525	Antiproliferative activity against wild type human MDA-MB-231 cells assessed as reduction in cell viability incubated for 5 to 10 days by MTT assay	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1499346	Induction of apoptosis in human MDA-MB-436 cells assessed as late apoptotic cells at 1 uM after 96 hrs in presence of pancaspase inhibitor Z-VAD-FMK by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 5.11%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID386711	Cytotoxicity against BRCA1-deficient human MDA-MB-463 cells upto 4 uM after 7 to 14 days by clonogenic assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1265289	Inhibition of full length human PARP1 expressed in Baculovirus infected Sf9 insect cells using activated DNA as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1403978	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured on day 17 (Rvb = 22.7 +/- 1.8 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1499359	Half life in Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878595	Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 7 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1697262	Protac activity at CRBN/PARP1 in human MDA-MB-436 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 10 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1276413	Inhibition of human PARP1 using [3H]NAD as substrate after 1 min by microplate scintillation counting analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1872300	Inhibition of PARP2 (unknown origin)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Recent advances in DDR (DNA damage response) inhibitors for cancer therapy.
AID1581917	Antiproliferative activity against human MDA-MB-468 cells measured after 7 days by Celltiter-glo assay
AID1428401	Selectivity ratio of IC50 for recombinant human His6-tagged PARP2 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) to IC50 for full length recombinant human His6-tagged PARP2 expressed in Escherichia coli BL21(DE3)	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1128194	Induction of apoptosis in human NCI-H1703 cells assessed as cleaved caspase-7 level at 5 to 25 uM by immunoblot analysis	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1849629	Inhibition of human full length PARP1 expressed in Escherichia coli rosetta (DE3) incubated for 20 mins by fluorescence analysis	2021	European journal of medicinal chemistry, Jan-01, Volume: 209	Pyridazine as a privileged structure: An updated review on anticancer activity of pyridazine containing bioactive molecules.
AID748130	Inhibition of PARP1 (unknown origin) at 10 uM relative to control	2013	Journal of medicinal chemistry, Jun-13, Volume: 56, Issue:11	Fragment-based ligand design of novel potent inhibitors of tankyrases.
AID1878795	Induction of Rad51 accumulation in nucleus of human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1486467	Inhibition of recombinant human PARP-1 expressed in Escherichia coli BL21 (DE3) using sheared DNA as substrate in presence of biotinylated NAD after 1 hr by ELISA	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Discovery of novel quinazoline-2,4(1H,3H)-dione derivatives as potent PARP-2 selective inhibitors.
AID1868329	Antiproliferative activity against human MDA-MB-231 cells assessed as inhibition of cell growth incubated for 7 days by MTT assay	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1831310	Induction of autophagy in human SW1990 cells assessed as increase in LC3B expression at 6 uM incubated for 4 days by immunofluorescence assay
AID728435	Cytotoxicity against Chinese hamster BRCA2-deficient VC8 cells assessed as growth inhibition	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1557937	Inhibition of N-terminal GST-tagged human PARP1 expressed in a Baculovirus infected Sf9 insect cells using biotinylated substrate incubated for 1 hr by colorimetric method	2019	Bioorganic & medicinal chemistry, 09-15, Volume: 27, Issue:18	Synthesis and biological activity of structurally diverse phthalazine derivatives: A systematic review.
AID1265293	Inhibition of human TNKS2 (667 to 1166 residues) expressed in Baculovirus infected Sf9 insect cells using activated DNA as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1878674	Upregulation of E2F2 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1867208	Cytotoxicity against human MDA-MB-231 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1878677	Upregulation of CDK1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878578	Inhibition of PARP1 (unknown origin) using biotinylated NAD+ as substrate by microplate reader method	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1581953	Induction of apoptosis in human MDA-MB-468 cells assessed as necrotic cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 0.13%)
AID1581922	Antiproliferative activity against human BxPC3 cells measured after 7 days by Celltiter-glo assay
AID1557953	Inhibition of PARP2 (unknown origin)	2019	Bioorganic & medicinal chemistry, 09-15, Volume: 27, Issue:18	Synthesis and biological activity of structurally diverse phthalazine derivatives: A systematic review.
AID1683491	Antiproliferative activity against BRCA2 deficient chinese hamster V-C8 cells	2021	Bioorganic & medicinal chemistry letters, 01-01, Volume: 31	Identification of 2-substituted pyrrolo[1,2-b]pyridazine derivatives as new PARP-1 inhibitors.
AID1508859	Inhibition of PARP8 (unknown origin) at 500 nM using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay relative to control
AID1831202	Invivo inhibition of BRD4 expression in human SW1900 cells xenografted in BALB/c mouse at 45 mg/kg, ip administered for 28 consecutive days by immunohistochemical analysis
AID1867222	Synergistic cytotoxicity against human MCF7 cells harbouring wild type BRCA1/2 assessed as combination index at 25 uM incubated for 48 hrs in presence of 0.8 uM adriamycin by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1064610	Toxicity in human MX1 cells harboring BRCA1 deletion and BRCA2 mutant xenografted SCID mouse assessed as reduction of body weight at 167 mg/kg, ip administered every 2 days for 2 weeks measured on day 38 relative to control	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID728434	Cytotoxicity against Chinese hamster V79 cells expressing wild type BRCA2 assessed as growth inhibition	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1403956	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured on day 14 (Rvb = 1216 +/- 310 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1303577	Potentiation of 0.0025 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1736031	Toxicity in Balb/c nude mouse xenografted with human SKOV3 cells assessed as change in body weight at 25 mg/kg, po for 21 days and measured every third day	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1735998	Cytotoxicity against human HL7702 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1830958	Antitumor activity against human MX1 cells xenografted in athymic nu/nu mouse assessed as tumor growth inhibition at 25 mg/kg, po administered once daily for 5 days and measured on day 17 in presence of 50 mg/kg TMZ
AID1250343	Induction of DNA damage in human BRCA2-deficient Capan1 cells assessed as increase in gammaH2AX levels at 8 uM after 24 hrs by flow cytometry analysis	2015	European journal of medicinal chemistry, Sep-18, Volume: 102	Quinazolinedione SIRT6 inhibitors sensitize cancer cells to chemotherapeutics.
AID1878778	Upregulation of CDK6 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1909181	Induction of DNA damage in human MDA-MB-231 cells assessed as increase in tail DNA measured at 3 uM after 3 days by comet assay	2022	Journal of medicinal chemistry, 05-12, Volume: 65, Issue:9	Discovery of 4-Hydroxyquinazoline Derivatives as Small Molecular BET/PARP1 Inhibitors That Induce Defective Homologous Recombination and Lead to Synthetic Lethality for Triple-Negative Breast Cancer Therapy.
AID1831201	Invivo inhibition of PARP1 expression in human SW1900 cells xenografted in BALB/c mouse at 45 mg/kg, ip administered for 28 consecutive days by immunohistochemical analysis
AID1581925	Antiproliferative activity against human DU145 cells measured after 7 days by Celltiter-glo assay
AID1878662	Upregulation of CDK6 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1784265	Antitumor activity against human SK-OV-3 cells xenografted in BALB/c nude mouse assessed as relative tumor volume at 50 mg/kg, po administered once daily for 12 days
AID1128181	In vitro antiproliferative activity against human NCI-H2122 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1831193	Toxicity in BALB/c mouse xenografted with human SW1990 cells assessed as liver damage at 45 mg/kg, ip administered for 28 consecutive days by H and E staining based fluorescence microscopic analysis
AID1499324	Cell cycle arrest in human Capan1 cells assessed as accumulation at G0/G1 phase at 0.1 uM after 72 hrs by propidium iodide-staining based flow cytometry (Rvb = 63.33%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1581911	Inhibition of recombinant human PARP1 using histone as substrate after 1 hr in presence of biotinylated NAD+ by ELISA
AID1403975	Toxicity in mouse xenografted with human MDA-MB-436 cells assessed as body weight at 30 mg/kg, po qd for 21 days measured on day 7 (Rvb = 20.7 +/- 1.7 g)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1499315	Inhibition of PARP1 (unknown origin) by ELISA	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1403952	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured immediately after first dose (Rvb = 237 +/- 82 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1499317	Cytotoxicity against BRCA2 deficient Chinese hamster VC8 cells after 3 days by CCK8 or SRB assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1350590	Inhibition of human N-terminal GST-tagged TNKS1 (1001 to 1327 residues) expressed in baculovirus infected sf9 cells using histone as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1682077	Selectivity index, ratio of IC50 for inhibition of N-terminal GST-tagged human PARP2 (2 to 583 residues) expressed in baculovirus infected Sf9 cells to IC50 for inhibition of N-terminal GST-tagged human full length PARP1 (2 to 1041 residues) expressed in	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1868378	Antitumor activity against human HCT-116 cells xenografted in BALB/c nude mouse assessed as tumor growth inhibition at 50 mg/kg, ip administered once daily for 28 days	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1878793	Induction of BRCA1 accumulation in nucleus of human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1303687	Cytotoxicity against human K562 cells assessed as decrease in cell viability up to 2.5 to 10 uM after 24 to 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1878593	Antiproliferative activity against human CFPAC-1 cells assessed as inhibition of cell growth measured after 4 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID386692	Potentiation factor, ratio of IC50 for methyl methanesulfonate to IC50 for methyl methanesulfonate with 200 uM drug for inhibition of human HeLa B cells	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1784248	Binding affinity to recombinant human PARP-2 by SPR analysis
AID1831248	Effect on cell cycle progression in human SW1990 cells xenografted in BALB/c mouse assessed as reduction in CDK6 expression at 45 mg/kg, ip after 4 days by Western blot analysis
AID1862307	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G2/M phase at 5 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 27.14 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID386707	Oral bioavailability in dog at 10 mg/kg, po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1878582	Antiproliferative activity against human SW1990 cells assessed as inhibition of cell growth after 3 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID386698	Half life in rat at 15 mg/kg, iv and po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1179155	Toxicity in advanced breast cancer patient with BRCA1/2 mutations assessed as maximum tolerated dose for twice daily dosing	2014	Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19	Development of synthetic lethality anticancer therapeutics.
AID1581971	Inhibition of recombinant human PARP2 using histone as substrate after 1 hr in presence of biotinylated NAD+ by ELISA
AID1872299	Inhibition of PARP1 (unknown origin)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Recent advances in DDR (DNA damage response) inhibitors for cancer therapy.
AID1868381	Inhibition of PARP-1 (unknown origin)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID728421	Inhibition of PARP1 in Chinese hamster BRCA2-deficient VC8 cells assessed as increase in gamma-H2AX level after 24 hrs by Western blotting analysis	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1867206	Cytotoxicity against human HCC1937 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1668087	Antiproliferative activity against BRCA2-deficient human Capan1 cells after 48 hrs by MTT assay	2020	Bioorganic & medicinal chemistry, 05-01, Volume: 28, Issue:9	Synthesis of novel dual target inhibitors of PARP and HSP90 and their antitumor activities.
AID1276419	Cytotoxicity against BRCA2-deficient human Capan1 cells	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1861257	Antiproliferative activity against human CAPAN-1 cells assessed as reduction in cell viability	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1862327	Induction of DNA double strand breaks in human CAPAN-1 cells assessed as increase in gamma-H2AX level at 10 uM incubated for 48 hrs by immunofluorescence-based laser confocal microscopy	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID748127	Inhibition of PARP6 (unknown origin) at 10 uM relative to control	2013	Journal of medicinal chemistry, Jun-13, Volume: 56, Issue:11	Fragment-based ligand design of novel potent inhibitors of tankyrases.
AID1486300	Antiproliferative activity against human K562 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1557957	Inhibition of human PARP1 expressed in Escherichia coli incubated for 10 mins by colorimetric assay	2019	Bioorganic & medicinal chemistry, 09-15, Volume: 27, Issue:18	Synthesis and biological activity of structurally diverse phthalazine derivatives: A systematic review.
AID1878591	Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 7 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1683888	Inhibition of PARP-1 in human HeLa cells incubated for 18 hrs in presence of H2O2	2020	Journal of medicinal chemistry, 12-24, Volume: 63, Issue:24	Discovery of Pamiparib (BGB-290), a Potent and Selective Poly (ADP-ribose) Polymerase (PARP) Inhibitor in Clinical Development.
AID1831191	Toxicity in BALB/c mouse xenografted with human SW1990 cells assessed as lung damage at 45 mg/kg, ip administered for 28 consecutive days by H and E staining based fluorescence microscopic analysis
AID1896632	Inhibition of PARP-1 (unknown origin) binding to DNA assessed as DNA trapping activity	2022	Bioorganic & medicinal chemistry letters, 12-15, Volume: 78	Synthesis and in vitro biological evaluation of 3-ethyl-1,5-naphthyridin-2(1H)-one derivatives as potent PARP-1 selective inhibitors and PARP-1 DNA trappers.
AID1861253	Antiproliferative activity against human ES2 cells assessed as reduction in cell viability measured after 7 days	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1908549	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G2/M phase measured after 24 hrs by flow cytometry analysis	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1861256	Antiproliferative activity against human HCC1937 cells assessed as reduction in cell viability	2022	Bioorganic & medicinal chemistry letters, 09-01, Volume: 71	Design, synthesis and antitumor activity study of PARP-1/HDAC dual targeting inhibitors.
AID1261690	Octanol-water partition coefficient, log P of the compound at 0.5 to 1.5 mg/ml by HPLC method	2015	Journal of medicinal chemistry, Nov-12, Volume: 58, Issue:21	Synthesis and Evaluation of a Radioiodinated Tracer with Specificity for Poly(ADP-ribose) Polymerase-1 (PARP-1) in Vivo.
AID1862325	Induction of DNA double strand breaks in human MDA-MB-436 cells assessed as increase in gamma-H2AX level incubated for 48 hrs by western blot analysis	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1508856	Inhibition of human full-length N-terminal GST-tagged PARP3 expressed in baculovirus infected Sf9 insect cells at 500 nM using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescence assay relative to control
AID1878576	Antiproliferative activity against BRCA-proficient human MDA-MB-231 cells assessed as inhibition of cell growth measured after 7 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1683489	Inhibition of PARP-1 (unknown origin)	2021	Bioorganic & medicinal chemistry letters, 01-01, Volume: 31	Identification of 2-substituted pyrrolo[1,2-b]pyridazine derivatives as new PARP-1 inhibitors.
AID1499360	Clearance in Sprague-Dawley rat at 10 mg/kg, iv by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1758276	Inhibition of PI3Kalpha (unknown origin) using PIP2 as substrate measured after 40 mins by ADP-glo plus luminescence assay	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1581951	Induction of apoptosis in human MDA-MB-468 cells assessed as early apoptotic cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 3.88%)
AID1831143	Antiproliferative activity against human SW1990 cells assessed as reduction in cell viability after 4 days by MTT assay
AID1882345	Antiproliferative activity against BRCA deficient human HCC1937 cells assessed as inhibition of cell growth incubated for 48 hrs by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Dual-target inhibitors of poly (ADP-ribose) polymerase-1 for cancer therapy: Advances, challenges, and opportunities.
AID1878719	Effect on CDC25B gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1303566	Potentiation of 0.0050 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1896633	Inhibition of PARP-2 (unknown origin) binding to DNA assessed as DNA trapping activity	2022	Bioorganic & medicinal chemistry letters, 12-15, Volume: 78	Synthesis and in vitro biological evaluation of 3-ethyl-1,5-naphthyridin-2(1H)-one derivatives as potent PARP-1 selective inhibitors and PARP-1 DNA trappers.
AID1303573	Potentiation of 2.5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1128180	In vitro antiproliferative activity against human NCI-H1693 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID386699	Clearance in rat at 15 mg/kg, iv and po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1486292	Inhibition of recombinant human N-terminal GST-tagged PARP2 (2 to 583 residues) expressed in baculovirus infected Sf9 cells using biotinylated substrate after 1 hr by UV/Vis spectrophotometric analysis	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1697343	Potentiation of TMZ induced antitumor activity against SW-620 cells xenografted in Balb/c mouse assessed as tumor growth suppression at 10 mg/kg, po qd administered for 5 days	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1878663	Upregulation of CCNB1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862272	Antiproliferative activity against human MDA-MB-436 cells assessed as cell growth inhibition incubated for 5 days by MTT assay	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1508884	Cytotoxicity against BRCA1-proficient human SUM149 cells measured after 6 days by microscopic analysis
AID1895778	Binding affinity to PARP2 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1500670	Antiproliferative activity against human MCF7 cells after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Design, synthesis and biological evaluation of 4-amidobenzimidazole acridine derivatives as dual PARP and Topo inhibitors for cancer therapy.
AID1697268	Protac activity at CRBN/PARP1 in human CAPAN-1 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 1000 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1565230	Inhibition of recombinant human full length N-terminal GST- tagged PARP1 expressed in baculovirus infected sf9 cells using Colorimetric HRP as substrate incubated for 30 mins by UV/Vis spectrophotometer analysis	2019	European journal of medicinal chemistry, Nov-15, Volume: 182	Discovery of novel functionalized 1,2,4-triazoles as PARP-1 inhibitors in breast cancer: Design, synthesis and antitumor activity evaluation.
AID1878798	Upregulation of BRD4 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1697316	Antiproliferation activity against human SW620 assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1878575	Antiproliferative activity against BRCA-proficient human MDA-MB-468 cells assessed as inhibition of cell growth measured after 7 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1682061	Potentiation of anticancer activity against human CAPAN-1 cells harboring BRCA mutant xenografted in SCID/nude mouse assessed as tumor growth inhibition at 3 mg/kg, po bid for 12 days co-administered with TMZ measured up to 9 weeks post-drug administratio	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1896635	Antiproliferative activity against human DLD-1 cells harbouring wild type BRCA assessed as inhibition of cell growth	2022	Bioorganic & medicinal chemistry letters, 12-15, Volume: 78	Synthesis and in vitro biological evaluation of 3-ethyl-1,5-naphthyridin-2(1H)-one derivatives as potent PARP-1 selective inhibitors and PARP-1 DNA trappers.
AID1908548	Induction of cell cycle arrest in human (BRAC1-/-) MDA-MB-436 cells assessed as accumulation at G2/M phase measured after 48 hrs by flow cytometry analysis	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1735996	Antiproliferative activity against human HepG2 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1831280	Inhibition of homologous recombinant repair in human SW1990 cells assessed as reduction in BRCA1 expression at 6 uM after 4 days by Q-PCR analysis
AID1428392	Inhibition of recombinant human TNKS1 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1729546	Induction of apoptosis in human MDA-MB-468 cells assessed as late apoptotic cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 0.78%)	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1064612	Antitumor activity against human MX1 cells harboring BRCA1 deletion and BRCA2 mutant xenografted in SCID mouse assessed as reduction of tumor volume at 167 mg/kg, ip administered every 2 days for 2 weeks measured on day 38 relative to control	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1064616	Antiproliferative activity against human A2780/DX cells after 72 hrs by SRB assay	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1128178	In vitro antiproliferative activity against human NCI-H1703 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1817373	Binding affinity to human GST-tagged PARP-1 ART domain (788 to 1014 residues) expressed in Escherichia coli BL21 (DE3) assessed as dissociation constant incubated for 30 mins by microscale thermophoresis analysis	2021	Journal of medicinal chemistry, 06-10, Volume: 64, Issue:11	Rational Design and Synthesis of Novel Dual PROTACs for Simultaneous Degradation of EGFR and PARP.
AID1878792	Upregulation of Rad51 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878631	Induction of apoptosis in human SW1990 cells assessed as early apoptotic cells at 6 uM measured after 4 days by Annexin V-FITC and propidium iodide staining based flow cytometry (Rvb = 1.62%)	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1303583	Potentiation of 0.0025 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID386697	Plasma concentration in mouse at 10 mg/kg, po after 60 mins	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1868347	Induction of apoptosis in human HCT-116 cells assessed as viable cells at 5 uM incubated for 3 days by annexinV-FITC/propidium iodide staining based flow cytometry (Rvb = 60.0 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1403953	Antitumor activity against human MDA-MB-436 cells xenografted in mouse assessed as tumor volume at 30 mg/kg, po qd for 21 days measured on day 3 (Rvb = 337 +/- 832 mm3)	2018	European journal of medicinal chemistry, Feb-10, Volume: 145	Design and synthesis of 2-(4,5,6,7-tetrahydrothienopyridin-2-yl)-benzoimidazole carboxamides as novel orally efficacious Poly(ADP-ribose)polymerase (PARP) inhibitors.
AID1508860	Inhibition of human N-terminal FLAG-tagged/C-terminal Strep-tagged PARP10 (805 to 1025 residues) expressed in baculovirus infected Sf9 insect cells at 500 nM using histone as substrate measured after 1 hr by horseradish peroxidase-coupled chemiluminescenc
AID1878570	Toxicity in nude mouse xenografted with human SW1990 cells assessed as spleen damage at 45 mg/kg, ip administered for 28 days by H and E staining based fluorescence microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1500673	Antiproliferative activity against human HCC1937 cells harboring BRCA1 mutant after 72 hrs by MTT assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Design, synthesis and biological evaluation of 4-amidobenzimidazole acridine derivatives as dual PARP and Topo inhibitors for cancer therapy.
AID1250341	Induction of DNA damage in human BRCA2-deficient Capan1 cells assessed as increase in gammaH2AX levels at 8 uM after 24 hrs by confocal microscopy	2015	European journal of medicinal chemistry, Sep-18, Volume: 102	Quinazolinedione SIRT6 inhibitors sensitize cancer cells to chemotherapeutics.
AID1276396	Terminal eliminational half life in Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1764047	Antiproliferative activity against BRCA1-deficient human HCC1937 cells assessed as cell growth inhibition	2021	Bioorganic & medicinal chemistry letters, 09-01, Volume: 47	Design, synthesis and biological evaluation of novel molecules as potent PARP-1 inhibitors.
AID1764044	Inhibition of PARP1 (unknown origin)	2021	Bioorganic & medicinal chemistry letters, 09-01, Volume: 47	Design, synthesis and biological evaluation of novel molecules as potent PARP-1 inhibitors.
AID1350583	Cytotoxicity against mouse wild type MEF cells assessed as reduction in cell viability after 4 to 7 days by cell-titer glo assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1878790	Upregulation of BRCA1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1868355	Induction of cell cycle arrest in human HCT-116 cells assessed as G0/G1 phase cells at 5 uM incubated for 3 days by propidium iodide staining based flow cytometry (Rvb = 68.35 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1697317	Antiproliferation activity against human MDA-MB-231 assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1350589	Cytotoxicity against human BRCA1-deficient UWB1.289 cells assessed as reduction in cell viability after 4 to 7 days by cell-titer glo assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1350577	Binding affinity to PARP1 in human OVCAR8 cells assessed as reduction in [125I]-KX1 binding by gamma counting analysis	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1878718	Effect on c-Myc gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1682011	Inhibition of N-terminal GST-tagged human full length PARP1 (2 to 1041 residues) expressed in baculovirus infected Sf9 cells using histone mixture (H2A and H2B) and biotinylated NAD+ as substrate in presence of activated DNA incubated for 60 mins by chemi	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1240634	Binding affinity to recombinant human HisGST-tagged PARP-2 catalytic domain by surface plasmon resonance analysis	2015	Journal of medicinal chemistry, Sep-10, Volume: 58, Issue:17	Discovery of 2-[1-(4,4-Difluorocyclohexyl)piperidin-4-yl]-6-fluoro-3-oxo-2,3-dihydro-1H-isoindole-4-carboxamide (NMS-P118): A Potent, Orally Available, and Highly Selective PARP-1 Inhibitor for Cancer Therapy.
AID1508886	Cytotoxicity against BRCA1-deficient human SUM149 cells measured after 6 days by microscopic analysis
AID1867219	Potentiation of adriamycin-induced cytotoxicity in human MCF7 cells harbouring wild type BRCA1/2 assessed as inhibition of cell growth at 25 uM incubated for 48 hrs in presence of 0.8 uM adriamycin by MTT assay relative to control	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1499341	Induction of apoptosis in human MDA-MB-436 cells assessed as early apoptotic cells at 1 uM after 96 hrs by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 1.90%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1867216	Cytotoxicity against human MCF7 cells harbouring wild type BRCA1/2 assessed as inhibition of cell growth at 25 uM incubated for 48 hrs by MTT assay relative to control	2022	Bioorganic & medicinal chemistry, 05-01, Volume: 61	Synthesis of novel dual target inhibitors of PARP and EGFR and their antitumor activities in triple negative breast cancers.
AID1831243	Effect on cell cycle progression in human SW1990 cells assessed as reduction in CDK6 expression at 6 uM after 4 days by Q-PCR analysis
AID1736002	Selectivity index, ratio of IC50 for inhibition of human recombinant N-terminal GST-tagged PARP-2 to IC50 for inhibition of human recombinant GST-tagged PARP-1	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1303562	Potentiation of 5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1868341	Inhibition of Wnt/beta-Catenin signaling in human HCT-116 cells assessed as decrease in total beta-catenin levels at 10 uM by Western blot analysis	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1764052	Octanol-water partition coefficient, logP of the compound	2021	Bioorganic & medicinal chemistry letters, 09-01, Volume: 47	Design, synthesis and biological evaluation of novel molecules as potent PARP-1 inhibitors.
AID1303564	Potentiation of 5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as fraction ratio affected at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1831175	Inhibition of PARP1 expression in human SW1990 cells at 6 uM after 4 days by Q-PCR analysis
AID1862306	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 5 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 32.62 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1697266	Protac activity at CRBN/PARP1 in human CAPAN-1 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 10 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1581952	Induction of apoptosis in human MDA-MB-468 cells assessed as late apoptotic cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 0.78%)
AID1831283	Inhibition of homologous recombinant repair in human SW1990 cells assessed as reduction in Rad51 expression at 6 uM after 4 days by Western blot analysis
AID386705	AUC (0 to infinity) in dog at 2.5 mg/kg, iv and 10 mg/kg, po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1515647	Binding affinity to full length His-tagged PARP1 (unknown origin) after 11 mins in presence of NAD+ by TR-FRET assay	2019	MedChemComm, Jun-01, Volume: 10, Issue:6	Controlling cellular distribution of drugs with permeability modifying moieties.
AID1817355	Protac activity at VHL/EGFR in human NCI-H1299 cells assessed as induction of EGFR degradation at up to 15 uM incubated for 36 hrs by Western blot analysis	2021	Journal of medicinal chemistry, 06-10, Volume: 64, Issue:11	Rational Design and Synthesis of Novel Dual PROTACs for Simultaneous Degradation of EGFR and PARP.
AID1735995	Antiproliferative activity against human Bel-7402 cells assessed as cell growth inhibition incubated for 48 hrs by MTT assay	2019	Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6	Discovery of Novel Bromophenol-Thiosemicarbazone Hybrids as Potent Selective Inhibitors of Poly(ADP-ribose) Polymerase-1 (PARP-1) for Use in Cancer.
AID1908522	Antiproliferative activity against human BRCA1 -/- MDA-MB-436 cells assessed as reduction in cell viability incubated for 5 to 10 days by MTT assay	2022	European journal of medicinal chemistry, Jun-05, Volume: 236	Selective degradation of PARP2 by PROTACs via recruiting DCAF16 for triple-negative breast cancer.
AID1831242	Effect on cell cycle progression in human SW1990 cells assessed as reduction in CDK6 expression at 6 uM after 4 days by Western blot analysis
AID1276422	Cytotoxicity against human MRC5 cells	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1868338	Inhibition of TNKS2 (unknown origin) using biotin-NAD+ as substrate incubated for 1 hr in the presence of deoxy-oligonucleotide by ELISA analysis relative to control	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1831141	Antiproliferative activity against human CFPAC-1 cells assessed as reduction in cell viability after 4 days by MTT assay
AID1784222	Inhibition of recombinant human full-length PARP-1 using biotinylated substrate
AID1486295	Antiproliferative activity against human T47D cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1831190	Toxicity in BALB/c mouse xenografted with human SW1990 cells assessed as kidney damage at 45 mg/kg, ip administered for 28 consecutive days by H and E staining based fluorescence microscopic analysis
AID386704	Clearance in dog at 2.5 mg/kg, iv and 10 mg/kg, po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1831216	Induction of apoptosis in human SW1990 cells assessed as late apoptotic cells at 6 uM after 4 days by Annexin V-FITC and propidium iodide staining based flow cytometry (Rvb = 6.22%)
AID1784247	Binding affinity to recombinant human PARP-1 by SPR analysis
AID1817371	Antiproliferative activity against human NCI-H1299 cells assessed as inhibition of cell growth incubated for 72 hrs by CCK8 assay	2021	Journal of medicinal chemistry, 06-10, Volume: 64, Issue:11	Rational Design and Synthesis of Novel Dual PROTACs for Simultaneous Degradation of EGFR and PARP.
AID1868331	Antiproliferative activity against human MDA-MB-468 cells assessed as inhibition of cell growth incubated for 7 days by MTT assay	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1697326	Induction of DNA damage in human Capan1 cells assessed as increase in gammaH2AX foci formation incubated for 24 hrs by Western blot analysis	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1878725	Effect on E2F2 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862320	Antiproliferative activity against human UWB1289 cells with restoration of BRCA1 expression assessed as inhibition of cell proliferation incubated for 7 days by SRB assay	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1878686	Induction of DNA damage in human SW1990 cells assessed as increase in gammaH2AX expression at 6 uM incubated for 4 days by DAPI staining based laser confocal microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1895783	Binding affinity to PARP7 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1862298	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G2/M phase at 0.625 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 27.14 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1831275	Induction of DNA damage in human SW1990 cells assessed as increase in gammaH2AX at 6 uM incubated for 4 days by immunofluorescence assay
AID1499319	Solubility of the compound in water after 24 hrs by HPLC analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1868330	Antiproliferative activity against human HCT-116 cells assessed as inhibition of cell growth incubated for 7 days by MTT assay	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1895769	Inhibition of human recombinant PARP5a (E1023 to T1327 amino acids) incubated for 4 hrs by fluorescence anisotropy binding assay	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID386691	Inhibition of PARP1 by flashplate scintillation proximity assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1878599	Toxicity in nude mouse xenografted with human SW1990 cells assessed as heart damage at 45 mg/kg, ip administered for 28 days by H and E staining based fluorescence microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1499366	Oral bioavailability in Sprague-Dawley rat at 20 mg/kg by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1581940	Inhibition of PI3K in human MDA-MB-468 cells assessed as reduction in RAD51 foci formation at 2 uM measured after 72 hrs by DAPI staining based immunofluorescence microscopic analysis
AID1499344	Induction of apoptosis in human MDA-MB-436 cells assessed as late apoptotic cells at 0.1 uM after 96 hrs in presence of pancaspase inhibitor Z-VAD-FMK by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 5.11%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1896630	Inhibition of PARP-1 (unknown origin)	2022	Bioorganic & medicinal chemistry letters, 12-15, Volume: 78	Synthesis and in vitro biological evaluation of 3-ethyl-1,5-naphthyridin-2(1H)-one derivatives as potent PARP-1 selective inhibitors and PARP-1 DNA trappers.
AID1729576	Antitumor activity against human MDA-MB-231 cells xenografted in BALB/c mouse assessed as tumor growth inhibition at 50 mg/kg, ip administered every two days for 34 days relative to control	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1868349	Induction of apoptosis in human HCT-116 cells assessed as late apoptotic cells at 5 uM incubated for 3 days by annexinV-FITC/propidium iodide staining based flow cytometry (Rvb = 8.71 %)	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID1862300	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at G0/G1 phase at 1.25 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 32.62 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1265313	Cytotoxicity against human OCI-LY19 assessed as growth inhibition after 3 days by Alamar Blue assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1428400	Selectivity ratio of IC50 for recombinant human His6-tagged PARP1 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) to IC50 for full length recombinant human His6-tagged PARP1 expressed in Escherichia coli BL21(DE3)	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1474432	Inhibition of recombinant human PARP1 expressed in Escherichia coli BL21(DE3) using histone as substrate measured after 1 hr in presence of biotinylated NAD+ by ELISA	2017	European journal of medicinal chemistry, May-26, Volume: 132	Discovery of 2-substituted 1H-benzo[d]immidazole-4-carboxamide derivatives as novel poly(ADP-ribose)polymerase-1 inhibitors with in vivo anti-tumor activity.
AID1581924	Antiproliferative activity against human Jurkat cells measured after 7 days by Celltiter-glo assay
AID1878584	Antiproliferative activity against human SW1990 cells assessed as inhibition of cell growth measured after 5 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862299	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at S phase at 0.625 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 37.88 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID728437	Inhibition of human recombinant PARP1 after 1 hr by ELISA	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1499339	Induction of apoptosis in human MDA-MB-436 cells assessed as early apoptotic cells at 0.1 uM after 96 hrs by Annexin V-FITC/propidium iodide double-staining based flow cytometery (Rvb = 1.90%)	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1831176	Inhibition of BRD4 expression in human SW1990 cells at 6 uM after 4 days by Q-PCR analysis
AID664855	Inhibition of PARP1 in MEF cells assessed as potentiation of MMC-induced cytotoxicity at 0.01 uM incubated for 1 hr by clonogenic survival assay relative to untreated control	2012	Journal of medicinal chemistry, Apr-12, Volume: 55, Issue:7	Inhibition of homologous recombination in human cells by targeting RAD51 recombinase.
AID1265290	Inhibition of human PARP2 (2 to 583 residues) expressed in Baculovirus infected Sf9 insect cells using activated DNA as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2015	Bioorganic & medicinal chemistry letters, Dec-15, Volume: 25, Issue:24	Discovery of AZ0108, an orally bioavailable phthalazinone PARP inhibitor that blocks centrosome clustering.
AID1878797	Upregulation of BRD4 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 28 days by DAPI staining based laser confocal microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1428385	Inhibition of recombinant human His6-tagged PARP1 C-3-zinc finger domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1849656	Inhibition of PARP1 (unknown origin) by colorimetric assay	2021	European journal of medicinal chemistry, Jan-01, Volume: 209	Pyridazine as a privileged structure: An updated review on anticancer activity of pyridazine containing bioactive molecules.
AID1499320	Inhibition of PARP1 in BRCA1 deficient human MDA-MB-436 cells assessed as increase in PARP1-DNA trapping at 1 uM after 4 hrs by Western blot analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1581944	Induction of DNA damage in human MDA-MB-468 cells at 2 uM measured after 72 hrs by comet assay
AID1179158	In vivo inhibition of PARP activity in tumor tissue of advanced breast cancer patient with BRCA1/2 mutations at 400 mg dosed twice daily	2014	Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19	Development of synthetic lethality anticancer therapeutics.
AID1500669	Inhibition of PARP1 (unknown origin) assessed as reduction in biotinylated poly(ADP-ribose) incorporation on to histone protein by ELISA based colorimetric assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Design, synthesis and biological evaluation of 4-amidobenzimidazole acridine derivatives as dual PARP and Topo inhibitors for cancer therapy.
AID1895790	Binding affinity to PARP16 (unknown origin) assessed as apparent dissociation constant	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1303579	Potentiation of 2.5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 48 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1486303	Antiproliferative activity against human MCF10A cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1303570	Potentiation of 5x10'-4 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1128179	In vitro antiproliferative activity against human H441 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1350591	Inhibition of human N-terminal GST-tagged TNKS2 (667 to 1166 residues) expressed in baculovirus infected sf9 cells using histone as substrate after 1 hr by streptavidin-horseradish peroxidase-based luminescence assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1878583	Antiproliferative activity against human SW1990 cells assessed as inhibition of cell growth measured after 4 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1499347	Antiproliferative activity against human Capan1 cells after 7 days by CCK8 or SRB assay	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1128184	In vitro antiproliferative activity against human H23 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1581915	Antiproliferative activity against human HCC1937 cells measured after 7 days by Celltiter-glo assay
AID1758278	Antiproliferative activity against human BRCA-2 proficient SW-620 cells assessed as reduction in cell growth incubated for 7 days by cell titer-glo assay	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1895770	Antiproliferative activity against human DLD-1 deficient in BRCA-2 cells measured after 7 days	2021	Journal of medicinal chemistry, 10-14, Volume: 64, Issue:19	Discovery of 5-{4-[(7-Ethyl-6-oxo-5,6-dihydro-1,5-naphthyridin-3-yl)methyl]piperazin-1-yl}-
AID1499321	Inhibition of PARP1 in BRCA2 deficient human Capan1 cells assessed as increase in PARP1-DNA trapping at 0.1 uM after 4 hrs by Western blot analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1878773	Downregulation of Ki67 expression in human SW1990 cells at 45 mg/kg, ip measured after 28 days by immuno histochemical staining based fluorescence microscopic analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862337	Induction of apoptosis in human CAPAN-1 cells assessed as early apoptotic cells at 10 uM incubated for 96 hrs by AnnexinV-FITC/PI staining based flow cytometry (Rvb = 5.08%)	2022	European journal of medicinal chemistry, Oct-05, Volume: 240	Design, synthesis and pharmacological evaluation of new PARP1 inhibitors by merging pharmacophores of olaparib and the natural product alantolactone.
AID1697312	Antiproliferation activity against human HCC1937 assessed as cell growth inhibition incubated for 7 days by CCK-8 assay	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1764046	Antiproliferative activity against BRCA2-deficient human HCT116 cells assessed as cell growth inhibition	2021	Bioorganic & medicinal chemistry letters, 09-01, Volume: 47	Design, synthesis and biological evaluation of novel molecules as potent PARP-1 inhibitors.
AID1741673	Induction of autophagy in human MDA-MB-231 cells assessed as upregulation of LC3B protein expression at 5 uM incubated for 48 to 72 hrs by western blot analysis	2020	European journal of medicinal chemistry, Oct-15, Volume: 204	Augmentation of the antitumor effects of PARP inhibitors in triple-negative breast cancer via degradation by hydrophobic tagging modulation.
AID1499364	AUC in Sprague-Dawley rat at 10 mg/kg, iv by LC-MS/MS analysis	2017	European journal of medicinal chemistry, Sep-29, Volume: 138	Discovery, mechanism and metabolism studies of 2,3-difluorophenyl-linker-containing PARP1 inhibitors with enhanced in vivo efficacy for cancer therapy.
AID1820831	Antiproliferative activity against human MDA-MB-231 cells at 1 uM for 10 days by SRB staining based clone formation assay relative to control	2022	European journal of medicinal chemistry, Jan-15, Volume: 228	Noncovalent CDK12/13 dual inhibitors-based PROTACs degrade CDK12-Cyclin K complex and induce synthetic lethality with PARP inhibitor.
AID728432	Cytotoxicity against human BRCA1-deficient MDA-MB-436 cells assessed as growth inhibition	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1581950	Induction of apoptosis in human MDA-MB-468 cells assessed as viable cells at 2 uM measured after 72 hrs by Annexin V-FITC/propidium iodide staining based flow cytometry (Rvb = 95.2%)
AID1831146	Inhibition of PARP1 (unknown origin) incubated for 45 mins in presence of biotinylated-NAD+ by microplate reader analysis
AID1697254	Protac activity at CRBN/PARP1 in human MDA-MB-436 cells assessed as induction of PARP1 degradation by measuring ratio of PARP1 to beta tubulin protein level at 1 nM incubated for 24 hrs by Western blot analysis (Rvb = 100 No_unit)	2020	Journal of medicinal chemistry, 10-08, Volume: 63, Issue:19	Discovery of SK-575 as a Highly Potent and Efficacious Proteolysis-Targeting Chimera Degrader of PARP1 for Treating Cancers.
AID1878735	Effect on Rad52 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID386702	Oral bioavailability in rat at 15 mg/kg, po	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1878589	Antiproliferative activity against human CAPAN-1 cells assessed as inhibition of cell growth measured after 4 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862305	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at S phase at 2.5 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 37.88 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID1878679	Upregulation of CCND1 expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878733	Effect on ALDH1A1 gene expression in human SW1990 cells at 6 uM by Q-PCR analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1682054	Anticancer activity against human MDA-MB-436 cells harboring BRCA mutant xenografted in SCID/nude mouse assessed as tumor growth regression at 50 mg/kg, po bid and measured up to 5 weeks post-drug administration	2020	Bioorganic & medicinal chemistry, 12-15, Volume: 28, Issue:24	Discovery of isoquinolinone and naphthyridinone-based inhibitors of poly(ADP-ribose) polymerase-1 (PARP1) as anticancer agents: Structure activity relationship and preclinical characterization.
AID1758277	Antiproliferative activity against human BRCA-2 deficient HCT-116 cells assessed as reduction in cell growth incubated for 7 days by cell titer-glo assay	2021	European journal of medicinal chemistry, May-05, Volume: 217	Discovery of novel and potent PARP/PI3K dual inhibitors for the treatment of cancer.
AID1128177	In vitro antiproliferative activity against human NCI-H1568 cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1878580	Antiproliferative activity against BRCA2-mutated human HCT-116 cells assessed as inhibition of cell growth measured after 7 days by MTT assay	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1878678	Upregulation of CDC25B expression in nude mouse xenografted with human SW1990 cells at 45 mg/kg, ip measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1862308	Induction of cell cycle arrest in human MDA-MB-231 cells assessed as accumulation at S phase at 5 uM incubated for 24 hrs by propidium iodide staining based flow cytometry analysis (Rvb = 37.88 %)	2022	Bioorganic & medicinal chemistry, 09-01, Volume: 69	Synthesis and biological evaluation of a tumor-selective degrader of PARP1.
AID386710	Ex vivo inhibition of PARP1 in human SW620 cells assessed as amount of poly(ADP-ribose) at 30 to 100 nM by whole cell assay	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1868339	Inhibition of Wnt/beta-Catenin signaling in human HCT-116 cells assessed as increase in axin2 levels at 10 uM by Western blot analysis	2022	European journal of medicinal chemistry, Jul-05, Volume: 237	Rational design, synthesis and biological evaluation of dual PARP-1/2 and TNKS1/2 inhibitors for cancer therapy.
AID728416	Potentiation of temozolomide-induced cytotoxicity in human SKOV3 cells assessed as reduction in temozolomide IC50 at 1 uM after 7 days by sulforhodamine B assay	2013	Journal of medicinal chemistry, Apr-11, Volume: 56, Issue:7	Design, synthesis, and biological evaluation of a series of benzo[de][1,7]naphthyridin-7(8H)-ones bearing a functionalized longer chain appendage as novel PARP1 inhibitors.
AID1064617	Antiproliferative activity against human A2780 cells after 72 hrs by SRB assay	2014	Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3	7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID1428387	Inhibition of full length recombinant human His6-tagged PARP2 expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay	2017	Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4	Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1303567	Potentiation of 2.5x10'-5 uM (-)-lomaiviticin A-induced cytotoxicity against human K562 cells assessed as combination index at 5 uM after 24 hrs by cell titer-glo luminescence assay	2016	Bioorganic & medicinal chemistry letters, 07-01, Volume: 26, Issue:13	Synergistic potentiation of (-)-lomaiviticin A cytotoxicity by the ATR inhibitor VE-821.
AID1276395	Clearance in Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis	2016	Journal of medicinal chemistry, Jan-14, Volume: 59, Issue:1	Discovery and Characterization of (8S,9R)-5-Fluoro-8-(4-fluorophenyl)-9-(1-methyl-1H-1,2,4-triazol-5-yl)-2,7,8,9-tetrahydro-3H-pyrido[4,3,2-de]phthalazin-3-one (BMN 673, Talazoparib), a Novel, Highly Potent, and Orally Efficacious Poly(ADP-ribose) Polymer
AID1486301	Antiproliferative activity against human U937 cells after 72 hrs by MTT assay	2017	Bioorganic & medicinal chemistry, 08-01, Volume: 25, Issue:15	Olaparib hydroxamic acid derivatives as dual PARP and HDAC inhibitors for cancer therapy.
AID1729530	Inhibition of PI3Kalpha (unknown origin) at 100 nM relative to control	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1831152	Antiproliferative activity against human MDA-MB-231 cells assessed as reduction in cell viability after 7 days
AID1878779	Upregulation of CCND1 expression in human SW1990 cells at 6 uM measured after 4 days by Western blot analysis	2022	European journal of medicinal chemistry, Feb-15, Volume: 230	Design, synthesis and mechanism studies of novel dual PARP1/BRD4 inhibitors against pancreatic cancer.
AID1350584	Cytotoxicity against mouse PARP1 deficient MEF cells assessed as reduction in cell viability after 4 to 7 days by cell-titer glo assay	2018	Journal of medicinal chemistry, 06-28, Volume: 61, Issue:12	Examination of Diazaspiro Cores as Piperazine Bioisosteres in the Olaparib Framework Shows Reduced DNA Damage and Cytotoxicity.
AID1128182	In vitro antiproliferative activity against human NCI-H322M cells assessed as inhibition of cell proliferation after 72 hrs by MTT assay	2014	Journal of medicinal chemistry, Mar-27, Volume: 57, Issue:6	Nitric oxide (NO) releasing poly ADP-ribose polymerase 1 (PARP-1) inhibitors targeted to glutathione S-transferase P1-overexpressing cancer cells.
AID1729540	Inhibition of PARP1/PI3Kalpha in human MDA-MB-231 cells assessed as down regulation of BRCA2 mRNA expression at 2 uM by RT-PCR analysis	2021	European journal of medicinal chemistry, Mar-05, Volume: 213	Discovery of novel PARP/PI3K dual inhibitors with high efficiency against BRCA-proficient triple negative breast cancer.
AID1205269	Inhibition of PARP1 (unknown origin)	2015	Journal of medicinal chemistry, Apr-23, Volume: 58, Issue:8	Niraparib: A Poly(ADP-ribose) Polymerase (PARP) Inhibitor for the Treatment of Tumors with Defective Homologous Recombination.
AID1868627	Antiproliferative activity against human MDA-MB-23 cells	2022	Journal of medicinal chemistry, 05-26, Volume: 65, Issue:10	Targeting Enhancer of Zeste Homolog 2 for the Treatment of Hematological Malignancies and Solid Tumors: Candidate Structure-Activity Relationships Insights and Evolution Prospects.
AID1649879	Growth inhibition of human PC3 cells after 5 days by SRB assay	2020	Journal of medicinal chemistry, 06-11, Volume: 63, Issue:11	Design and Synthesis of a Trifunctional Molecular System "Programmed" to Block Epidermal Growth Factor Receptor Tyrosine Kinase, Induce High Levels of DNA Damage, and Inhibit the DNA Repair Enzyme (Poly(ADP-ribose) Polymerase) in Prostate Cancer Cells.
AID1798813	PARP-1 Enzyme Assay from Article 10.1021/jm8001263: \\4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.\\	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1802336	In Vitro PARP1 Activity Assay from Article 10.1016/j.chembiol.2016.10.011: \\Proteome-wide Profiling of Clinical PARP Inhibitors Reveals Compound-Specific Secondary Targets.\\	2016	Cell chemical biology, Dec-22, Volume: 23, Issue:12	Proteome-wide Profiling of Clinical PARP Inhibitors Reveals Compound-Specific Secondary Targets.
AID1346183	Human poly(ADP-ribose) polymerase 1 (2.4.2.30 poly(ADP-ribose)polymerases)	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1346183	Human poly(ADP-ribose) polymerase 1 (2.4.2.30 poly(ADP-ribose)polymerases)	2003	Journal of biomolecular screening, Jun, Volume: 8, Issue:3	A FlashPlate assay for the identification of PARP-1 inhibitors.
AID1346152	Human poly(ADP-ribose) polymerase 2 (2.4.2.30 poly(ADP-ribose)polymerases)	2003	Journal of biomolecular screening, Jun, Volume: 8, Issue:3	A FlashPlate assay for the identification of PARP-1 inhibitors.
AID1346152	Human poly(ADP-ribose) polymerase 2 (2.4.2.30 poly(ADP-ribose)polymerases)	2008	Journal of medicinal chemistry, Oct-23, Volume: 51, Issue:20	4-[3-(4-cyclopropanecarbonylpiperazine-1-carbonyl)-4-fluorobenzyl]-2H-phthalazin-1-one: a novel bioavailable inhibitor of poly(ADP-ribose) polymerase-1.
AID1745854	NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS	2023	Disease models & mechanisms, 03-01, Volume: 16, Issue:3	In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1745855	NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay	2023	Disease models & mechanisms, 03-01, Volume: 16, Issue:3	In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	0 (0.00)	18.7374
1990's	0 (0.00)	18.2507
2000's	14 (1.08)	29.6817
2010's	728 (56.09)	24.3611
2020's	556 (42.84)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	172 (13.10%)	5.53%
Reviews	143 (10.89%)	6.00%
Case Studies	71 (5.41%)	4.05%
Observational	5 (0.38%)	0.25%
Other	922 (70.22%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (385)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
Olaparib Dose Escalation in Combination With High Dose Radiotherapy to the Breast Andregional Lymph Nodes in Patients With Breast Cancer [NCT02227082]	Phase 1	7 participants (Actual)	Interventional	2013-10-21	Completed
A Phase I/Ib Study of Anti-CD47 Hu5F9-G4 (Magrolimab) in Combination With Olaparib in Patients With BRCA1/2-Mutant Tumors [NCT05807126]	Phase 1	33 participants (Anticipated)	Interventional	2024-03-05	Recruiting
A Randomized Phase II Trial of Triplet Therapy (A PD-L1 Inhibitor Durvalumab (MEDI4736) in Combination With Olaparib and Cediranib) Compared to Olaparib and Cediranib or Durvalumab (MEDI4736) and Cediranib or Standard of Care Chemotherapy in Women With Pl [NCT04739800]	Phase 2	164 participants (Anticipated)	Interventional	2021-06-10	Active, not recruiting
A Phase 1/1b Dose Escalation Study of Abemaciclib and Olaparib for Recurrent Platinum-Resistant Ovarian Cancer [NCT04633239]	Phase 1	42 participants (Anticipated)	Interventional	2021-07-02	Recruiting
The PRIME Trial: PARP Inhibition in IDH Mutant Effectiveness Trial. A Phase II Study of Olaparib in Isocitrate Dehydrogenase (IDH) Mutant Relapsed/Refractory Acute Myeloid Leukemia and Myelodysplastic Syndrome [NCT03953898]	Phase 2	94 participants (Anticipated)	Interventional	2020-08-04	Active, not recruiting
A Phase II Study of Olaparib and AZD6738 in Isocitrate Dehydrogenase (IDH) Mutant Solid Tumors [NCT03878095]	Phase 2	50 participants (Anticipated)	Interventional	2020-01-30	Suspended(stopped due to Other - Pending Data Analysis)
A Randomised, Double-blind, Placebo-controlled, Multicentre Phase III Study of Olaparib Plus Abiraterone Relative to Placebo Plus Abiraterone as First-line Therapy in Men With Metastatic Castration-resistant Prostate Cancer (PROpel Study) [NCT03732820]	Phase 3	796 participants (Actual)	Interventional	2018-10-31	Active, not recruiting
A Randomized Phase II Study Comparing Single-Agent Olaparib, Single Agent Cediranib, and the Combinations of Cediranib/Olaparib, Olaparib/Durvalumab (MEDI4736), Cediranib/Durvalumab (MEDI4736), Olaparib/AZD5363 (Capivasertib) in Women With Recurrent, Pers [NCT03660826]	Phase 2	288 participants (Anticipated)	Interventional	2018-09-27	Active, not recruiting
A Phase 1/2 Study of Combination Olaparib and Radium-223 in Men With Metastatic Castration-Resistant Prostate Cancer With Bone Metastases (COMRADE) [NCT03317392]	Phase 1/Phase 2	133 participants (Anticipated)	Interventional	2019-02-04	Recruiting
A Phase 2 Study of the PARP Inhibitor Olaparib (AZD2281) in IDH1 and IDH2 Mutant Advanced Solid Tumors [NCT03212274]	Phase 2	145 participants (Anticipated)	Interventional	2019-01-30	Recruiting
A Phase II Open-Label, Randomized Study of PARP Inhibition (Olaparib) Either Alone or in Combination With Anti-PD-L1 Therapy (Atezolizumab; MPDL3280A) in Homologous DNA Repair (HDR) Deficient, Locally Advanced or Metastatic Non-HER2-Positive Breast Cancer [NCT02849496]	Phase 2	81 participants (Anticipated)	Interventional	2017-03-30	Active, not recruiting
A Randomized Phase II/III Study of the Combination of Cediranib and Olaparib Compared to Cediranib or Olaparib Alone, or Standard of Care Chemotherapy in Women With Recurrent Platinum-Resistant or -Refractory Ovarian, Fallopian Tube, or Primary Peritoneal [NCT02502266]	Phase 2/Phase 3	562 participants (Anticipated)	Interventional	2016-05-03	Active, not recruiting
A Randomized, Double-blinded, Placebo Controlled, Multicentre Phase III Study to Assess the Efficacy and Safety of Olaparib (AZD2281) in Combination With Paclitaxel, Compared to Placebo in Combination With Paclitaxel, in Asian Patients With Advanced Gastr [NCT01924533]	Phase 3	525 participants (Actual)	Interventional	2013-09-03	Completed
Phase II, Open Label, Non-Randomized Study of AZD2281 in the Treatment of Patients With Known BRCA or Recurrent High Grade Serous/ Undifferentiated Tubo-Ovarian Carcinoma and in Known BRCA or Triple Negative Breast Cancer to Determine Response Rate and Co [NCT00679783]	Phase 2	99 participants (Actual)	Interventional	2008-07-08	Completed
Phase II Trial of Olaparib in Homologous Recombination Deficient (HRD) Malignant Mesothelioma [NCT04515836]	Phase 2	56 participants (Anticipated)	Interventional	2021-02-19	Recruiting
Bipolar Androgen Therapy Plus Olaparib in Patient With Castration-Resistant Prostate Cancer [NCT03516812]	Phase 2	36 participants (Actual)	Interventional	2018-08-29	Active, not recruiting
Olaparib Dose Escalating Trial in Patients Treated With Radiotherapy With or Without Daily Dose Cisplatin for Locally Advanced Non-small Cell Lung Carcinoma [NCT01562210]	Phase 1	28 participants (Actual)	Interventional	2012-04-30	Completed
Sensitivity Detection and Drug Resistance Mechanism of Breast Cancer Therapeutic Drugs Based on Organ-like Culture [NCT03925233]		300 participants (Anticipated)	Observational	2019-01-02	Enrolling by invitation
A Randomized Clinical Trial Investigating Olaparib, Durvalumab (MEDI4736) and UV1 as Maintenance Therapy in BRCAwt Patients With Recurrent Ovarian Cancer [NCT04742075]	Phase 2	184 participants (Anticipated)	Interventional	2021-12-15	Recruiting
A Phase 3 Study of Pembrolizumab in Combination With Pemetrexed/Platinum (Carboplatin or Cisplatin) Followed by Pembrolizumab and Maintenance Olaparib vs Maintenance Pemetrexed in the First-Line Treatment of Participants With Metastatic Nonsquamous Non-Sm [NCT03976323]	Phase 3	1,005 participants (Actual)	Interventional	2019-06-28	Active, not recruiting
A Randomized Phase 3, Double-Blind Study of Chemotherapy With or Without Pembrolizumab Followed by Maintenance With Olaparib or Placebo for the First-Line Treatment of BRCA Non-mutated Advanced Epithelial Ovarian Cancer (EOC) (KEYLYNK-001 / ENGOT-ov43 / G [NCT03740165]	Phase 3	1,367 participants (Actual)	Interventional	2018-12-18	Active, not recruiting
Olaparib for Pulmonary Arterial Hypertension: a Pilot Clinical Study [NCT03251872]	Early Phase 1	6 participants (Actual)	Interventional	2018-10-25	Terminated(stopped due to OPTION pilot trial merged with the new NCT03782818 - OPTION multicenter trial)
Single Arm Feasibility of Multi-maintenance Olaparib After Disease Recurrence in Participants With Platinum Sensitive BRCAm High Grade Serous Ovarian Cancer [NCT02855697]	Early Phase 1	28 participants (Actual)	Interventional	2017-05-26	Completed
Olaparib in Prostate Cancer Patients With Evidence of Homologous Recombination Deficiency as Assessed Using an Integrated Genomic Signature [NCT04951492]	Phase 2	2 participants (Actual)	Interventional	2022-11-09	Terminated(stopped due to Withdrawal of funding)
Phase IIA Trial of Short-term Chemotherapy and Pembrolizumab, Followed by Pembrolizumab and Olaparib as Firstline Therapy in Her-2 Negative Gastric/Gastroesophageal-junction (GEJ) Adenocarcinoma [NCT05268510]	Phase 2	31 participants (Actual)	Interventional	2022-09-15	Active, not recruiting
Olaparib Beyond Progression Compared to Platinum Chemotherapy After Secondary Cytoreductive Surgery in Recurrent Ovarian Cancer Patients. The Phase III Randomized, Open Label MITO 35b Study: a Project of the MITO-MANGO Groups. [NCT05255471]	Phase 3	200 participants (Anticipated)	Interventional	2022-01-21	Recruiting
A Phase IIIb, Randomised, Double-blind, Placebo-controlled, Multicentre Study of Olaparib Maintenance Retreatment in Patients With Epithelial Ovarian Cancer Previously Treated With a PARPi and Responding to Repeat Platinum Chemotherapy [NCT03106987]	Phase 3	220 participants (Actual)	Interventional	2017-06-08	Completed
A Phase 1, Randomised, Open-label, 4-Period Crossover Study to Develop an In Vitro-In Vivo Correlation for Olaparib Tablets in Subjects With Solid Tumors [NCT03553108]	Phase 1	18 participants (Actual)	Interventional	2018-05-16	Completed
A Phase I of Olaparib With Radiation Therapy in Patients With Inflammatory, Loco-regionally Advanced or Metastatic TNBC (Triple Negative Breast Cancer) or Patient With Operated TNBC With Residual Disease [NCT03109080]	Phase 1	24 participants (Actual)	Interventional	2017-07-24	Completed
A Phase III, Randomised, Double Blind, Placebo Controlled, Multicentre Study of Olaparib Maintenance Monotherapy in Patients With BRCA Mutated Advanced (FIGO Stage III-IV) Ovarian Cancer Following First Line Platinum Based Chemotherapy. [NCT01844986]	Phase 3	450 participants (Actual)	Interventional	2013-08-26	Active, not recruiting
PHASE 1 DOSE ESCALATION TRIAL OF β-LAPACHONE (ARQ761) IN COMBINATION WITH PARP INHIBITOR, OLAPARIB, FOR REFRACTORY, ADVANCED SOLID TUMORS [NCT03575078]	Phase 1	0 participants (Actual)	Interventional	2018-06-25	Withdrawn(stopped due to Project Never Initiated - no human subjects were enrolled and no data regarding humans was collected or studied)
A Phase I Trial of the Combination of Olaparib and Navitoclax in Women With High Grade Serous Epithelial Ovarian Cancer and Triple Negative Breast Cancer [NCT05358639]	Phase 1	36 participants (Anticipated)	Interventional	2022-11-09	Recruiting
A Proof of Concept, Multi-centre, Clinical Trial of the Combination Cediranib-Olaparib at the Time of Disease Progression on PARP Inhibitor in Ovarian Cancer [NCT02681237]		34 participants (Actual)	Interventional	2016-04-29	Completed
Olaparib for Pulmonary Arterial Hypertension: a Multicenter Clinical Trial [NCT03782818]	Phase 1/Phase 2	20 participants (Anticipated)	Interventional	2019-11-20	Recruiting
A Randomized Phase 2 Trial of Cediranib and Olaparib Compared to Bevacizumab in Patients With Recurrent Glioblastoma Who Have Not Received Prior VEGF Therapy [NCT02974621]	Phase 2	70 participants (Actual)	Interventional	2017-12-07	Active, not recruiting
A Phase II Study of Olaparib in Patients With Advanced Biliary Tract Cancer With Aberrant DNA Repair Gene Mutations [NCT04042831]	Phase 2	36 participants (Anticipated)	Interventional	2020-06-24	Recruiting
Efficacy of Olaparib in Advanced Cancers Occurring in Patients With Germline Mutations or Somatic Tumor Mutations in Homologous Recombination Genes [NCT03967938]	Phase 2	540 participants (Anticipated)	Interventional	2019-02-07	Recruiting
Genomics Guided Targeted Post-neoadjuvant Therapy in Patients With Early Breast Cancer - a Multicenter, Open-label, Umbrella Phase-II Study - COGNITION-GUIDE [NCT05332561]	Phase 2	240 participants (Anticipated)	Interventional	2023-06-29	Recruiting
A Pilot Study to Evaluate the Efficacy and Safety of Preoperative Olaparib Monotherapy and Preoperative Olaparib Plus Pembrolizumab Combination Therapy in Patients With HRD-Positive Stage III or IV Advanced Epithelial Ovarian/Fallopian Tube/Primary Perito [NCT04417192]	Phase 2	30 participants (Actual)	Interventional	2020-12-01	Completed
Phase I/IIa Study of Concomitant Radiotherapy With Olaparib and Temozolomide in Unresectable High Grade Gliomas Patients [NCT03212742]	Phase 1/Phase 2	91 participants (Anticipated)	Interventional	2017-09-04	Recruiting
A Phase I, Randomised, 2 Period Cross Over Study to Determine the Comparative Bioavailability of Two Different Oral Formulations of AZD2281 in Cancer Patients With Advanced Solid Tumours [NCT00777582]	Phase 1	197 participants (Actual)	Interventional	2008-10-27	Active, not recruiting
Phase 2 Trial of Olaparib in Patients With Metastatic Urothelial Cancer Harboring DNA Damage Response Gene Alterations [NCT03448718]	Phase 2	19 participants (Actual)	Interventional	2018-04-17	Completed
Targeted Agent and Profiling Utilization Registry (TAPUR) Study [NCT02693535]	Phase 2	3,791 participants (Anticipated)	Interventional	2016-03-14	Recruiting
MITO 35a: A Multicenter, Prospective, Single Arm Trial of Olaparib Maintenance Therapy in Newly Diagnosed BRCA Wildtype Advanced Ovarian, Fallopian Tube and Primitive Peritoneal Cancer [NCT05233982]	Phase 2	200 participants (Anticipated)	Interventional	2021-12-09	Recruiting
A Phase II Trial of Olaparib in Patients With Recurrent Ovarian Cancer Wild Type for Germline and Somatic BRCA 1 and 2 Genes: The MITO 31 Translational Study [NCT04091204]	Phase 2	200 participants (Anticipated)	Interventional	2019-07-04	Recruiting
Neoadjuvant Olaparib and Durvalumab for Patients With BRCA-associated Triple Negative Breast Cancer [NCT05209529]	Phase 2	152 participants (Anticipated)	Interventional	2022-09-01	Not yet recruiting
A Phase III, Randomised, Double Blind, Placebo Controlled, Multicentre Study of Olaparib Maintenance Monotherapy in Patients With Platinum Sensitive Relapsed Ovarian Cancer Who Are in Complete or Partial Response Following Platinum Based Chemotherapy and [NCT02392676]	Phase 3	0 participants (Actual)	Interventional	2016-07-31	Withdrawn(stopped due to Study is unlikely to be feasible given the evolving ovarian cancer landscape and alternative studies have the potential to meet future clinical demand.)
A Phase Ib Study on the Combination of Trabectedin and Olaparib in Unresectable Advanced/Metastatic Sarcomas After Failure of Standard Therapies [NCT02398058]	Phase 1	50 participants (Actual)	Interventional	2014-07-20	Completed
Durvalumab (MEDI4736) and Olaparib (AZD2281) for Treatment of Biochemically Recurrent Prostate Cancer in Men Predicted to Have a High Neoantigen Load: A Multicenter Pilot Study [NCT04336943]	Phase 2	30 participants (Anticipated)	Interventional	2021-04-13	Recruiting
An uMbrella Study of BIomarker-driven Targeted Therapy In Patients With Platinum-resistant Recurrent OvariaN Cancer(AMBITION) [NCT03699449]	Phase 2	104 participants (Anticipated)	Interventional	2018-11-26	Recruiting
"A Preoperative Window-opportunity, Multicenter, Pharmacokinetic-pharmacodynamic Study to Evaluate the Inhibitory Effects of Single Agent AZD2281 (Olaparib), in Patients With Early-stage Endometrial Carcinoma" [NCT02506816]		36 participants (Actual)	Observational	2016-02-29	Completed
Non-Randomized, Open-Label Phase II Study to Assess Olaparib Tablets as a Treatment for Subjects With Different HRD Tumor Status and With Platinum-Sensitive, Relapsed, High-Grade Serous or High-Grade Endometrioid Epithelial Ovarian, Fallopian Tube, or Pri [NCT02983799]	Phase 2	272 participants (Actual)	Interventional	2016-12-22	Completed
Phase II, Single-arm Study of AZD6738 and Olaparib Combination Therapy in Relapsed Small Cell Lung Cancer Patients [SUKSES-N2] [NCT03428607]	Phase 2	26 participants (Actual)	Interventional	2018-10-17	Completed
A Phase I Multi-centre Trial of the Combination of Olaparib (PARP Inhibitor) and AZD5363 (AKT Inhibitor) in Patients With Advanced Solid Tumours [NCT02338622]	Phase 1	60 participants (Actual)	Interventional	2014-03-31	Completed
A Pilot Trial of Hyperthermia in Combination With Olaparib in Breast Cancer Patients With Chest Wall Recurrences [NCT03955640]	Phase 1	3 participants (Anticipated)	Interventional	2019-05-20	Active, not recruiting
Multicenter Phase I/Ib Trial of Olaparib in Combination With Vorinostat in Patients With Relapsed/Refractory and/or Metastatic Breast Cancer [NCT03742245]	Phase 1	28 participants (Anticipated)	Interventional	2019-06-11	Recruiting
A Phase II Study of Olaparib in Recurrent IDH-mutant High Grade Gliomas OLAGLI [NCT03561870]	Phase 2	35 participants (Actual)	Interventional	2019-03-20	Completed
A Phase IIIb, Single-arm, Open-label Multicentre Study of Olaparib Maintenance Monotherapy in Platinum Sensitive Relapsed Non-Germline BRCA Mutated Ovarian Cancer Patients Who Are in Complete or Partial Response Following Platinum Based Chemotherapy [NCT03402841]	Phase 3	279 participants (Actual)	Interventional	2018-01-30	Completed
A Multi-center, Single-arm, Prospective Study to Investigate the Efficacy and Safety of Olaparib Monotherapy in Newly Diagnosed mCRPC Patients Who Progressed on NHA and With HRR Gene Mutation [NCT05262608]	Phase 2	30 participants (Anticipated)	Interventional	2021-12-07	Recruiting
A Phase 3 Randomized, Open-label Study to Evaluate the Efficacy and Safety of Olaparib Alone or in Combination With Bevacizumab Compared to Bevacizumab With a Fluoropyrimidine in Participants With Unresectable or Metastatic Colorectal Cancer Who Have Not [NCT04456699]	Phase 3	335 participants (Actual)	Interventional	2020-08-19	Completed
A Phase I/II Evaluation of Olaparib in Combination With Durvalumab (Medi4736) and Tremelimumab in the Treatment of Recurrent Platinum Sensitive or Resistant or Refractory Epithelial Ovarian, Fallopian Tube, or Primary Peritoneal Cancer in Patients Who Car [NCT02953457]	Phase 2	40 participants (Actual)	Interventional	2017-06-29	Active, not recruiting
Phase 2 Randomized Trial of Trabectedin + Olaparib vs. Trabectedin in Advanced, Metastatic or Unresectable Soft Tissue Sarcoma After Failure of Standard Treatments. [NCT03838744]	Phase 2	126 participants (Anticipated)	Interventional	2020-05-26	Active, not recruiting
A Phase 1 Dose-Escalation Study of Intraperitoneal (IP) Cisplatin, IV/IP Paclitaxel, IV Bevacizumab, and Oral Olaparib for Newly Diagnosed Ovarian, Primary Peritoneal, and Fallopian Tube Cancer [NCT02121990]	Phase 1	17 participants (Actual)	Interventional	2014-04-21	Completed
Bioequivalence Study of Two Olaparib Tablets in Patients With Cancers [NCT05860530]		48 participants (Actual)	Interventional	2021-05-10	Completed
Arterial Hypertension With PARP Inhibitors in Cancer Patients: an Observational and Retrospective Study Using the WHO Pharmacovigilance Database (ArteRIB) [NCT04774406]		2,336 participants (Actual)	Observational	2021-02-24	Completed
Pembrolizumab and Olaparib Treatment for Relapsed or Refractory Peripheral T-Cell Lymphoma [NCT06160843]	Phase 2	24 participants (Anticipated)	Interventional	2024-02-29	Not yet recruiting
A Randomised, Double-blind, Placebo-controlled, Phase III Study of Olaparib Maintenance Monotherapy in Participants With BRCA Wild Type Advanced High Grade Serous or Endometrioid Ovarian Cancer Following Response to Standard First-line Platinum-based Chem [NCT04884360]	Phase 3	420 participants (Anticipated)	Interventional	2021-05-31	Recruiting
A Phase II, Open Label, Randomised, Multi-centre Study to Assess the Safety and Efficacy of Agents Targeting DNA Damage Repair in Combination With Olaparib Versus Olaparib Monotherapy in the Treatment of Metastatic Triple Negative Breast Cancer Patients S [NCT03330847]	Phase 2	273 participants (Actual)	Interventional	2018-03-07	Active, not recruiting
Impact of the Combination of Durvalumab (MEDI4736) Plus Olaparib (AZD2281) Administered Prior to Surgery in the Molecular Profile of Resectable Urothelial Bladder Cancer. [NCT03534492]	Phase 2	29 participants (Actual)	Interventional	2018-11-16	Completed
Biomarker and Tumor Cell Culture-Driven Pilot Trial for Treatment of Recurrent Glioblastoma [NCT05432518]	Early Phase 1	10 participants (Anticipated)	Interventional	2023-06-27	Recruiting
A Randomized Phase II Study of Temozolomide Monotherapy or in Combination With Olaparib in Patients With METHYLATED 06-Methylguanine-DNA Methyltransferase (MGMT) Pre-Treated Triple Negative Breast Cancer (TNBC) [NCT05128734]	Phase 2	40 participants (Anticipated)	Interventional	2023-12-01	Not yet recruiting
A Randomized Phase-2 Study of Trabectedin/Olaparib Compared to Physician's Choice in Subjects With Previously Treated Advanced or Recurrent Solid Tumors Harboring DNA Repair Deficiencies [NCT03127215]	Phase 2	102 participants (Actual)	Interventional	2018-10-25	Active, not recruiting
Optimal Dosing of Oral Anticancer Drugs in Older Adults With Cancer: a Randomized Pilot Study. [NCT05949424]	Phase 4	30 participants (Anticipated)	Interventional	2024-05-31	Not yet recruiting
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: PRIME [NCT03878524]	Phase 1	2 participants (Actual)	Interventional	2020-04-01	Active, not recruiting
Predicting Olaparib Sensitivity in Patients With Unresectable Locally Advanced/Metastatic HER2-negative Breast Cancer With BRCA1, BRCA2, PALB2, RAD51C or RAD51D Mutations or RAD51-foci Low Test: RADIOLA TRIAL [NCT05340413]	Phase 2	63 participants (Anticipated)	Interventional	2022-03-25	Recruiting
Immunotherapy in Combination With PARP Inhibition in Advanced Cervical Cancer Patients Functionally Competent or Deficient for the Fanconi Anemia Repair Pathway [NCT04483544]	Phase 2	48 participants (Anticipated)	Interventional	2020-12-03	Recruiting
A Phase II, Open-Label, Randomized, Multi-Centre Study, of Neoadjuvant Olaparib in Patients With Platinum Sensitive Recurrent High Grade Serous Ovarian/Primary Peritoneal or Fallopian Tube Cancer [NCT02489006]	Phase 2	71 participants (Anticipated)	Interventional	2016-07-19	Active, not recruiting
A Dutch National Study on Behalf of the CPCT to Facilitate Patient Access to Commercially Available, Targeted Anti-cancer Drugs to Determine the Potential Efficacy in Treatment of Advanced Cancers With a Known Molecular Profile [NCT02925234]	Phase 2	1,550 participants (Anticipated)	Interventional	2016-08-31	Recruiting
Substantially Improving the Cure Rate of High-risk BRCA1-like Breast Cancer Patients With Personalized Therapy (SUBITO) - an International Randomized Phase III Trial [NCT02810743]	Phase 3	174 participants (Anticipated)	Interventional	2017-01-25	Active, not recruiting
Basket Combination Study of Inhibitors of DNA Damage Response, Angiogenesis and Programmed Death Ligand 1 in Patients With Advanced Solid Tumors [NCT03851614]	Phase 2	90 participants (Anticipated)	Interventional	2019-04-08	Active, not recruiting
A Pilot Study of Olaparib and Durvalumab in Patients With Metastatic Triple Negative Breast Cancer [NCT03544125]	Phase 1	3 participants (Actual)	Interventional	2018-05-03	Completed
A Phase II Study of the PARP Inhibitor Olaparib (AZD2281) Alone and in Combination With AZD1775, AZD5363, or AZD6738 in Advanced Solid Tumors [NCT02576444]	Phase 2	67 participants (Actual)	Interventional	2015-11-30	Terminated(stopped due to The study was paused during COVID and without the ability to initiate the 4th arm in the study, the decision was to terminate the study in 2022.)
Durvalumab and Olaparib in Metastatic or Recurrent Endometrial Cancer [NCT03951415]	Phase 2	55 participants (Actual)	Interventional	2019-07-08	Active, not recruiting
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: Adaptive Clinical Treatment (ACT) [NCT05238831]	Early Phase 1	25 participants (Anticipated)	Interventional	2023-12-01	Not yet recruiting
Phase III Randomised, Double Blind, Placebo Controlled Study of Olaparib Maintenance Monotherapy in Platinum Sensitive Relapsed BRCA Mutated Ovarian Cancer Patients With a Complete or Partial Response Following Platinum Based Chemotherapy [NCT01874353]	Phase 3	327 participants (Actual)	Interventional	2013-09-03	Active, not recruiting
PHOENIX DDR/Anti-PD-L1 Trial: A Pre-surgical Window of Opportunity and Post-surgical Adjuvant Biomarker Study of DNA Damage Response Inhibition and/or Anti-PD-L1 Immunotherapy in Patients With Neoadjuvant Chemotherapy Resistant Residual Triple Negative Br [NCT03740893]	Phase 2	81 participants (Anticipated)	Interventional	2019-10-15	Recruiting
A Randomised, Double-blind, Placebo-controlled, Multicentre Phase III Study of Olaparib Plus Abiraterone Relative to Placebo Plus Abiraterone as First-line Therapy in Men With Metastatic Castration-resistant Prostate Cancer (PROpel Study) [NCT05171816]	Phase 3	108 participants (Actual)	Interventional	2021-06-24	Active, not recruiting
A Study Into the Pharmacodynamic Biomarker Effects of Olaparib (a PARP Inhibitor) ± Degarelix (a GnRH Antagonist) Given Prior to Radical Prostatectomy [NCT02324998]	Phase 1	20 participants (Actual)	Interventional	2016-12-31	Completed
Phase II Study of Olaparib in Subjects With Malignant Mesothelioma [NCT03531840]	Phase 2	23 participants (Actual)	Interventional	2018-07-11	Completed
EPIK-O: A Phase III, Multi-center, Randomized (1:1), Open-label, Active-controlled, Study to Assess the Efficacy and Safety of Alpelisib (BYL719) in Combination With Olaparib as Compared to Single Agent Cytotoxic Chemotherapy, in Participants With no Germ [NCT04729387]	Phase 3	358 participants (Actual)	Interventional	2021-07-02	Active, not recruiting
Randomized Phase II Study of Olaparib Maintenance Following Cabazitaxel-Carboplatin Induction Chemotherapy in Men With Aggressive Variant Prostate Cancer (AVPC) [NCT03263650]	Phase 2	119 participants (Actual)	Interventional	2017-10-03	Active, not recruiting
A Randomised, Double-blind, Parallel Group, Placebo-controlled Multi-centre Phase III Study to Assess the Efficacy and Safety of Olaparib Versus Placebo as Adjuvant Treatment in Patients With gBRCA1/2 Mutations and High Risk HER2 Negative Primary Breast C [NCT02032823]	Phase 3	1,836 participants (Actual)	Interventional	2014-04-22	Active, not recruiting
A Phase I/II Study of Olaparib With Entinostat in the Treatment of Recurrent, Platinum-Refractory or Resistant, Homologous Recombination Repair Proficient Ovarian, Primary Peritoneal, and Fallopian Tube Cancers [NCT03924245]	Phase 1	3 participants (Actual)	Interventional	2020-10-01	Terminated(stopped due to Change in participant landscape and other treatment availability)
An Investigator Sponsored Phase I Study of the Safety, Tolerability and Pharmacodynamics of Escalating Doses of Combination Treatment of AZD5363 + Olaparib + Durvalumab (MEDI4736) in Patients With Advanced or Metastatic Solid Tumor Malignancies. [NCT03772561]	Phase 1	40 participants (Anticipated)	Interventional	2018-12-03	Recruiting
A Pharmacokinetic/Pharmacodynamic Study With a Phase I Run-In With a PARP Inhibitor (Olaparib) in Combination With Carboplatin for Refractory or Recurrent Women's Cancers [NCT01237067]	Phase 1	77 participants (Actual)	Interventional	2011-02-07	Completed
Phase II Multicenter Study of Durvalumab and Olaparib in Platinum tReated Advanced Triple Negative Breast Cancer [NCT03167619]	Phase 2	45 participants (Actual)	Interventional	2018-10-04	Completed
Phase II Study of Olaparib in Combination With Pembrolizumab in Patients With Advanced Melanoma With Homologous Recombination (HR) Pathway Gene Mutation [NCT04633902]	Phase 2	41 participants (Anticipated)	Interventional	2021-03-03	Recruiting
An Open Label Dose Escalation/Expansion Study of Tremelimumab Alone or Combined With Olaparib for Recurrent or Persistent EOC (Epithelial Ovarian, Fallopian Tube or Primary Peritoneal Carcinoma) [NCT02485990]	Phase 1	24 participants (Actual)	Interventional	2016-01-08	Terminated(stopped due to Withdrawal of sponsor support)
The BAROCCO Study (Best Approach in Recurrent-Ovarian-Cancer-with Cediranib-Olaparib): an Italian Multicenter Randomized Phase II Study of Weekly Paclitaxel vs. Cediranib-Olaparib With Continuous Schedule vs. Cediranib-Olaparib With Intermittent Schedule [NCT03314740]	Phase 2	100 participants (Anticipated)	Interventional	2017-06-01	Active, not recruiting
Effects of PARP Inhibitor on Tumor Microenvironment in High-risk Endometrial Cancer Patients [NCT05320757]	Early Phase 1	20 participants (Anticipated)	Interventional	2022-04-01	Recruiting
A Randomized Phase II Trial Comparing the Combination of PI3K Inhibitor Copanlisib (BAY 80-6946) and PARP Inhibitor Olaparib (AZD2281) to Standard Chemotherapy in Patients With Recurrent Platinum Resistant Ovarian, Fallopian Tube, or Primary Peritoneal Ca [NCT05295589]	Phase 2	0 participants (Actual)	Interventional	2022-06-30	Withdrawn(stopped due to Drug supply issues)
A Phase I, Open Label, Study of the Safety and Tolerability of KU-0059436 and Dacarbazine in the Treatment of Patients With Advanced Solid Tumours [NCT00516802]	Phase 1	40 participants (Actual)	Interventional	2007-01-31	Completed
A Randomized Double-blind Phase II Trial Evaluating Maintenance Olaparib Versus Placebo in Patients With Platinum-sensitive Advanced Non-small Cell Lung Cancer [NCT02679963]	Phase 2	600 participants (Anticipated)	Interventional	2016-01-31	Recruiting
Phase 2 Study to Evaluate the Safety & Efficacy of EP0057 in Combination With Olaparib in Advanced Ovarian Cancer Patients Who Have: Cohort 1 - Platinum Resistant Disease; Cohort 2 - Had at Least 1 Prior Line of Therapy Which Must Include at Least 1 Line [NCT04669002]	Phase 2	34 participants (Actual)	Interventional	2020-12-14	Completed
Window-of-opportunity Proof-of-concept, Non-randomized, Open-label Phase II Trial of Olaparib Given Alone (Cohort A) or in Combination With Durvalumab (Cohort B) Prior to Primary Debulking Surgery in Histologically Proven High-grade Epithelial Ovarian Can [NCT04644289]	Phase 2	60 participants (Anticipated)	Interventional	2022-05-05	Recruiting
DDR-Umbrella Study of DDR (DNA-Damage Response) Targeting Agents in Advanced Biliary Tract Cancer [NCT04298021]	Phase 2	74 participants (Anticipated)	Interventional	2020-06-25	Active, not recruiting
Canadian Profiling and Targeted Agent Utilization Trial (CAPTUR): A Phase II Basket Trial [NCT03297606]	Phase 2	720 participants (Anticipated)	Interventional	2018-03-23	Recruiting
A Phase I Study of AZD2281 in Combination With Irinotecan in Patients With Locally Advanced or Metastatic Incurable Colorectal Cancer [NCT00535353]	Phase 1	26 participants (Actual)	Interventional	2008-01-02	Completed
Neoadjuvant and Adjuvant Olaparib Plus Pembrolizumab Following Platinum Based Chemotherapy Plus Pembrolizumab for Germline BRCA Mutated Triple Negative Breast Cancer (WJOG14020B) [NCT05485766]	Phase 2	23 participants (Anticipated)	Interventional	2022-10-01	Not yet recruiting
A Phase Ib Study of AZD1775 and Olaparib in Patients With Refractory Solid Tumours [NCT02511795]	Phase 1	128 participants (Actual)	Interventional	2015-08-06	Completed
Improving Peptide Receptor Radionuclide Therapy With PARP Inhibitors [NCT05870423]	Phase 1	24 participants (Anticipated)	Interventional	2022-06-01	Recruiting
A Phase II Study of Olaparib and Durvalumab (MEDI 4736) in Patients With IDH-Mutated Solid Tumors [NCT03991832]	Phase 2	58 participants (Anticipated)	Interventional	2019-12-31	Recruiting
A Window of Opportunity (WoO) Study Evaluating Pembrolizumab With or Without Olaparib in Tertiary Lymphoid Structures (TLS)-Positive Selected Resectable Soft Tissue Sarcoma (STS) Followed by Adjuvant Pembrolizumab [NCT06116578]	Phase 2	36 participants (Anticipated)	Interventional	2024-03-31	Not yet recruiting
A Phase I/II Trial of PARP Inhibition, Radiation, and Immunotherapy in Patients With Extensive-Stage Small Cell Lung Cancer (ES-SCLC) - PRIO Trial [NCT04728230]	Phase 1/Phase 2	63 participants (Anticipated)	Interventional	2021-01-05	Recruiting
Phase I Trial With 177Lu-DOTA-TATE and Olaparib in Somatostatin Receptor Positive Tumours [NCT04375267]	Phase 1	18 participants (Actual)	Interventional	2020-04-23	Active, not recruiting
A Phase I/II Trial of EP0057, a Nanoparticle Camptothecin With Olaparib in Patients With Relapsed/Refractory Small Cell Lung, Bladder and Prostate Cancers [NCT02769962]	Phase 1/Phase 2	123 participants (Anticipated)	Interventional	2016-05-09	Recruiting
A Randomised, Double-Blind, Placebo-Controlled, Multicentre Phase II Study to Compare the Efficacy, Safety and Tolerability of Olaparib Versus Placebo When Given in Addition to Abiraterone Treatment in Patients With Metastatic Castrate-Resistant Prostate [NCT01972217]	Phase 2	158 participants (Actual)	Interventional	2014-04-01	Completed
A Randomized, Open Label, Multi-centre, Two-treatment, Two-period, Two-sequence, Two-stage, Multiple Dose, Steady-state, Crossover, Bioequivalence Study of Olaparib Tablets, 150 mg (Lek Pharmaceuticals d.d.) and Lynparza® (Olaparib) Tablets 150 mg (AstraZ [NCT05258747]	Phase 1	70 participants (Actual)	Interventional	2022-04-07	Completed
Olaparib for BRCAness Phenotype in Pancreatic Cancer: Phase II Study [NCT02677038]	Phase 2	23 participants (Actual)	Interventional	2016-11-11	Completed
Open Label, Phase Ib Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Clinical Activity of CYH33, an Oral PI3K Inhibitor in Combination With Olaparib, an Oral PARP Inhibitor in Patients With Advanced Solid Tumors. [NCT04586335]	Phase 1	350 participants (Anticipated)	Interventional	2020-09-28	Recruiting
Olaparib Expanded Access Program for BRCA Mutated Platinum Sensitive Relapsed High Grade Epithelial Ovarian Cancer Patients [NCT03063710]		0 participants	Expanded Access		No longer available
Phase 1/2, Multi-Center, Open-Label Study to Evaluate the Safety, Tolerability, and Preliminary Antitumor Activity of TNG348 Single Agent and in Combination With a PARP Inhibitor in Patients With BRCA 1/2 Mutant or Other HRD+ Solid Tumors [NCT06065059]	Phase 1/Phase 2	140 participants (Anticipated)	Interventional	2023-12-08	Recruiting
Phase I/II Study of Stereotactic Radiosurgery With Concurrent Administration of DNA Damage Response (DDR) Inhibitor (OLAparib) Followed by Adjuvant Combination of DuRvalumab (MEDI4736) and Physician's Choice Systemic Therapy in Subjects With BreAst Cancer [NCT04711824]	Phase 1/Phase 2	41 participants (Anticipated)	Interventional	2022-03-09	Recruiting
Phase II Study of PARP Inhibitor Olaparib and IV Ascorbate in Castration Resistant Prostate Cancer [NCT05501548]	Phase 2	15 participants (Anticipated)	Interventional	2023-06-30	Recruiting
A Phase Ib/II Clinical Study Evaluating the Safety, Tolerability, and Efficacy of Selinexor Combined With Olaparib in the Treatment of Recurrent/Refractory Extensive-stage Small Cell Lung Cancer [NCT05975944]	Phase 1/Phase 2	49 participants (Anticipated)	Interventional	2023-09-30	Recruiting
A Phase II Trial of Olaparib in Combination With Pembrolizumab for Advanced Uveal Melanoma [NCT05524935]	Phase 2	37 participants (Anticipated)	Interventional	2022-10-11	Recruiting
ATARI: ATr Inhibitor in Combination With Olaparib in Gynaecological Cancers With ARId1A Loss [NCT04065269]	Phase 2	40 participants (Anticipated)	Interventional	2019-11-27	Recruiting
Phase Ib Trial of the KRAS G12C Inhibitor Adagrasib (MRTX849) in Combination With the PARP Inhibitor Olaparib in Patients With KRAS G12C Mutated Advanced Solid Tumors, With a Focus on Gynecological, Breast, Pancreatic and KEAP1 Mutated Non-small Cell Lung [NCT06130254]	Phase 1	52 participants (Anticipated)	Interventional	2024-05-31	Not yet recruiting
A Phase II Study of Pembrolizumab, Olaparib, and Temozolomide in Patients With Glioma [NCT05188508]	Phase 2	57 participants (Anticipated)	Interventional	2022-01-14	Recruiting
Olaparib in Combination With Pembrolizumab and Carboplatin as First-Line Treatment of Recurrent or Metastatic Head and Neck Squamous-Cell Carcinoma: A Single-Arm, Phase 2 Trial [NCT04643379]	Phase 2	30 participants (Actual)	Interventional	2021-08-07	Active, not recruiting
A Phase II, Randomized, Active-Controlled, Multi-Center Study Comparing the Efficacy and Safety of Targeted Therapy or Cancer Immunotherapy Guided by Genomic Profiling Versus Platinum-Based Chemotherapy in Patients With Cancer of Unknown Primary Site Who [NCT03498521]	Phase 2	790 participants (Anticipated)	Interventional	2018-07-10	Active, not recruiting
A Phase 2 Study of Olaparib and Cediranib for the Treatment of Recurrent Ovarian Cancer [NCT02345265]	Phase 2	72 participants (Actual)	Interventional	2016-05-17	Active, not recruiting
A Phase Ib/II Trial of Combination RP-3500 and Olaparib in DNA Damage Repair Pathway Deficient Relapsed/Refractory Chronic Lymphocytic Leukemia [NCT05405309]	Phase 1/Phase 2	39 participants (Anticipated)	Interventional	2022-09-23	Suspended(stopped due to Enrollment suspended pending IRB approval of protocol amendment; interventions ongoing for enrolled, active participants)
A Multi-Center Phase II Study Testing the Activity of Olaparib and AZD6738 (ATR Inhibitor) in Metastatic Castration-Resistant Prostate Cancer [NCT03787680]	Phase 2	49 participants (Actual)	Interventional	2019-10-31	Active, not recruiting
A Phase 2 Randomized, Multi-Centre Study to Investigate the Efficacy and Tolerability of a Second Maintenance Treatment in Patients With Platinum Sensitive Relapsed Epithelial Ovarian Cancer, Who Have Previously Received PARP Inhibitor Maintenance Treatme [NCT04239014]	Phase 2	0 participants (Actual)	Interventional	2020-08-07	Withdrawn(stopped due to Sponsor made the decision to terminate the DUETTE study based on the interim analysis of the VIOLETTE study (NCT03330847) investigating the combination of ceralasertib and Olaparib, where study closure was recommended due to insufficient efficacy.)
A Phase I, Open Label, Study of the Safety and Tolerability of KU-0059436 in Combination With Gemcitabine in the Treatment of Patients With Advanced Solid Tumours [NCT00515866]	Phase 1	68 participants (Actual)	Interventional	2007-08-31	Completed
Precision Medicine Phase II Study Evaluating the Efficacy of a Double Immunotherapy by Durvalumab and Tremelimumab Combined With Olaparib in Patients With Solid Cancers and Carriers of Homologous Recombination Repair Genes Mutation in Response or Stable A [NCT04169841]	Phase 2	270 participants (Anticipated)	Interventional	2020-02-10	Recruiting
A Phase II, Open-Label, Multicenter Trial to Assess the Efficacy and Safety of the PARP Inhibitor, Olaparib, Alone in Previously-Treated Patients With Stage IV, Measurable Colorectal Cancer, Stratified by MSI Status [NCT00912743]	Phase 2	33 participants (Actual)	Interventional	2009-05-31	Completed
A Pilot Pharmacodynamic Study to Assess the Anti-proliferative Activity a of the Poly ADP Ribose Polymerase (PARP) Inhibitor Olaparib in Patients With Human Papilloma Virus (HPV) Positive and Human Papilloma Virus (HPV) Negative Head and Neck Squamous Cel [NCT02686008]	Phase 1	0 participants (Actual)	Interventional	2018-01-31	Withdrawn(stopped due to The study was stopped due to lack of funding.)
"A Phase II, Open Label, Controlled Study of Olaparib in Locally Advanced ER, PgR and HER2 Negative (Triple Negative) and in Locally Advanced Germline BRCA Mutation-positive Breast Cancer Patients: Biological Evaluation From a Window of Opportunity Trial" [NCT02681562]	Phase 2	45 participants (Actual)	Interventional	2016-01-31	Active, not recruiting
Open, Non-Randomized, Single Centre Phase I Study to Assess the Metabolism, Excretion and Pharmacokinetics of a Single Oral 100 mg Dose of [14C]-AZD2281 (KU-0059436) in Patients With Advanced or Metastatic Solid Tumours Refractory to Standard Treatments [NCT00633269]	Phase 1	6 participants (Anticipated)	Interventional	2008-04-30	Completed
Phase 1/2 Safety and Efficacy Study of NUV-868 as Monotherapy and in Combination With Olaparib or Enzalutamide in Adult Patients With Advanced Solid Tumors [NCT05252390]	Phase 1/Phase 2	657 participants (Anticipated)	Interventional	2022-03-29	Recruiting
Phase Ib/II Study to Evaluate the Efficacy and Tolerability of PM01183 in Combination With Olaparib in Patients With Advanced Solid Tumors [NCT02684318]	Phase 1/Phase 2	100 participants (Anticipated)	Interventional	2015-07-31	Recruiting
PErsonalized TREatment of High-risk MAmmary Cancer - the PETREMAC Trial [NCT02624973]	Phase 2	200 participants (Actual)	Interventional	2016-04-15	Active, not recruiting
A Phase I Combination Study of AZD2281 and Cisplatin Plus Gemcitabine in Adults With Solid Tumors [NCT00678132]	Phase 1	23 participants (Actual)	Interventional	2008-04-24	Completed
European Proof-of-Concept Therapeutic Stratification Trial of Molecular Anomalies in Relapsed or Refractory Tumors [NCT02813135]	Phase 1/Phase 2	460 participants (Anticipated)	Interventional	2016-08-03	Recruiting
A Phase II, Open-Label, Multicenter, Platform Study Evaluating the Efficacy and Safety of Biomarker-Driven Therapies in Patients With Persistent or Recurrent Rare Epithelial Ovarian Tumors [NCT04931342]	Phase 2	550 participants (Anticipated)	Interventional	2021-10-07	Recruiting
A Phase 1b Biomarker-Driven Combination Trial of Copanlisib, Olaparib, and Durvalumab (MEDI4736) in Patients With Advanced Solid Tumors [NCT03842228]	Phase 1	108 participants (Anticipated)	Interventional	2019-11-21	Active, not recruiting
A Phase II Randomized Trial of Olaparib (NSC-747856) Administered Concurrently With Radiotherapy Versus Radiotherapy Alone for Inflammatory Breast Cancer [NCT03598257]	Phase 2	300 participants (Anticipated)	Interventional	2019-01-18	Recruiting
A Phase II, Open-Label, Multi-Arm Study to Determine the Preliminary Efficacy of Novel Combinations of Treatment in Patients With Platinum Refractory Extensive-Stage Small-Cell Lung Cancer [NCT02937818]	Phase 2	72 participants (Actual)	Interventional	2016-11-28	Completed
A Phase I/II Study of MEDI4736 (Anti-PD-L1 Antibody) in Combination With Olaparib (PARP Inhibitor) in Patients With Advanced Solid Tumors [NCT02734004]	Phase 1/Phase 2	264 participants (Actual)	Interventional	2016-03-17	Active, not recruiting
A Phase II Open-label, Non-comparative, International, Multicentre Study to Assess the Efficacy and Safety of KU 0059436 Given Orally Twice Daily in Patients With Advanced BRCA1 or BRCA2 Associated Ovarian Cancer [NCT00494442]	Phase 2	58 participants (Actual)	Interventional	2007-06-11	Completed
A Randomised, Multicentre, Double-blind, Placebo-controlled, Phase III Study of First-line Carboplatin and Paclitaxel in Combination With Durvalumab, Followed by Maintenance Durvalumab With or Without Olaparib in Patients With Newly Diagnosed Advanced or [NCT04269200]	Phase 3	805 participants (Actual)	Interventional	2020-05-05	Active, not recruiting
Combination ATR and PARP Inhibitor (CAPRI) Trial With AZD 6738 and Olaparib in Recurrent Ovarian Cancer [NCT03462342]	Phase 2	86 participants (Anticipated)	Interventional	2018-03-09	Recruiting
An Open-Label, Multi-Drug, Biomarker-Directed, Multi-Centre Phase II Umbrella Study in Patients With Non-Small Cell Lung Cancer, Who Progressed on an Anti-PD-1/PD-L1 Containing Therapy (HUDSON). [NCT03334617]	Phase 2	531 participants (Actual)	Interventional	2017-12-18	Active, not recruiting
A Phase II Clinical Trial to Analyse Olaparib Response in Patients With BRCA1 and/or 2 Promoter Methylation Diagnosed of Advanced Breast Cancer (COMETA-Breast Study) [NCT03205761]	Phase 2	11 participants (Actual)	Interventional	2017-09-13	Completed
A Phase Ib/II Study of Olaparib With Sapacitabine in BRCA Mutant Breast Cancer [NCT03641755]	Phase 1	10 participants (Actual)	Interventional	2018-10-01	Active, not recruiting
A Phase Ib Study of Olaparib With Concomitant Radiotherapy in Locally Advanced/Unresectable Soft-tissue Sarcoma [NCT02787642]	Phase 1	41 participants (Actual)	Interventional	2016-01-31	Completed
Olaparib Maintenance Therapy in Patients With Metastatic Breast Cancer Following DNA-damaging Based Chemotherapy [NCT05629429]	Phase 2	300 participants (Anticipated)	Interventional	2022-12-12	Recruiting
Phase IIA Trial of Delayed Initiation of Olaparib Maintenance Therapy in Platinum Sensitive Recurrent Ovarian Cancer [NCT04377087]	Phase 2	3 participants (Actual)	Interventional	2020-06-29	Terminated(stopped due to Slow enrollment)
A Phase I, Open Label, Dual Centre Study To Assess The Safety And Tolerability Of AZD2281 In Combination With Bevacizumab (Avastin®) In Patients With Advanced Solid Tumours [NCT00710268]	Phase 1	18 participants (Actual)	Interventional	2008-06-30	Completed
Biomarker-oriented Study of Durvalumab (MEDI4736) in Combination With Olaparib and Paclitaxel in Gastric Cancer [NCT03579784]	Phase 2	40 participants (Anticipated)	Interventional	2018-11-26	Active, not recruiting
Randomised Phase II Trial of Olaparib, Chemotherapy or Olaparib and Cediranib in Patients With Platinum-resistant Ovarian Cancer [NCT03117933]	Phase 2	139 participants (Actual)	Interventional	2017-03-09	Active, not recruiting
A Phase I, Open-label, Parallel Group Study to Investigate Olaparib Safety and Tolerability, Efficacy and Pharmacokinetics in Paediatric Patients With Solid Tumours [NCT04236414]	Phase 1	30 participants (Anticipated)	Interventional	2020-01-14	Recruiting
A Phase I/II Study of the Fluorescent PARP1 Binding Imaging Agent PARPi-FL in Patients With Oral Squamous Cell Carcinomas [NCT03085147]	Phase 1/Phase 2	23 participants (Actual)	Interventional	2017-03-15	Active, not recruiting
A Phase III Study Comparing Single-Agent Olaparib or the Combination of Cediranib and Olaparib to Standard Platinum-Based Chemotherapy in Women With Recurrent Platinum-Sensitive Ovarian, Fallopian Tube, or Primary Peritoneal Cancer [NCT02446600]	Phase 3	579 participants (Actual)	Interventional	2016-03-28	Active, not recruiting
A Phase I, Open-Label, Study of the Safety and Tolerability of KU-0059436 and Topotecan in the Treatment of Patients With Advanced Solid Tumours [NCT00516438]	Phase 1	48 participants (Anticipated)	Interventional	2007-07-31	Completed
A Randomized Phase II Trial to Assess the Efficacy of Paclitaxel and Olaparib in Comparison to Paclitaxel / Carboplatin Followed by Epirubicin/Cyclophosphamide as Neoadjuvant Chemotherapy in Patients With HER2-negative Early Breast Cancer and Homologous R [NCT02789332]	Phase 2	107 participants (Actual)	Interventional	2016-09-30	Completed
A Phase II, Open-Label, Randomised, Comparative, International Multicentre Study to Assess the Safety and Efficacy of Different Doses of AZD2281 Given Orally Twice Daily Versus Intravenous Liposomal Doxorubicin Given Monthly in Patients With Advanced BRCA [NCT00628251]	Phase 2	97 participants (Actual)	Interventional	2008-07-30	Completed
A Phase II, Open Label, Non Randomised, Non Comparative, Multicentre Study to Assess the Efficacy and Safety of Olaparib Given Orally Twice Daily in Patients With Advanced Cancers Who Have a Confirmed Genetic BRCA 1 and/or BRCA2 Mutation [NCT01078662]	Phase 2	298 participants (Actual)	Interventional	2010-02-21	Active, not recruiting
A Cancer Research UK Phase I Trial of Olaparib (AZD2281), an Oral PARP Inhibitor, in Combination With Extended Low-Dose Oral Temozolomide in Patients With Relapsed Glioblastoma [NCT01390571]	Phase 1	34 participants (Anticipated)	Interventional	2011-07-31	Completed
A Single Arm, Open-label, Phase IIb Study to Assess the Efficacy and Safety of the Combination of Cediranib and Olaparib Tablets in Women With Recurrent Platinum Resistant Epithelial Ovarian Cancer, Including Fallopian Tube and/or Primary Peritoneal Cance [NCT02889900]	Phase 2	62 participants (Actual)	Interventional	2017-01-17	Completed
A Randomised, Double Blinded, Multicentre Phase II Study to Assess the Efficacy of Olaparib (AZD2281, KU-0059436) in Combination With Paclitaxel Versus Paclitaxel in Patients With Recurrent or Metastatic Gastric Cancer Who Progress Following First-line Th [NCT01063517]	Phase 2	124 participants (Actual)	Interventional	2010-02-02	Completed
Olaparib as Salvage Treatment for Cisplatin-resistant Germ Cell Tumor [NCT02533765]	Phase 2	18 participants (Actual)	Interventional	2015-09-11	Active, not recruiting
Circulating Tumor DNA Guiding (Olaparib) Lynparza® Treatment in Ovarian [NCT02822157]	Phase 2	160 participants (Actual)	Interventional	2016-08-31	Active, not recruiting
A Phase III, Open Label, Randomised, Controlled, Multi-centre Study to Assess the Efficacy and Safety of Olaparib Monotherapy Versus Physicians Choice Chemotherapy in the Treatment of Metastatic Breast Cancer Patients With Germline BRCA1/2 Mutations. [NCT02000622]	Phase 3	302 participants (Actual)	Interventional	2014-03-27	Active, not recruiting
A Phase I Open Label, Multi Centre Study of AZD2281 Administered Orally in Combination With Cisplatin, to Assess the Safety and Tolerability in Patients With Advanced Solid Tumours [NCT00782574]	Phase 1	57 participants (Actual)	Interventional	2008-11-12	Completed
Olaparib and Durvalumab (MEDI4736) in Patients With Metastatic Pancreatic Cancer and DNA Damage Repair Genes Alterations [NCT05659914]	Phase 2	40 participants (Anticipated)	Interventional	2022-11-28	Recruiting
A Phase 1-2 Study of the Combination of Olaparib and Tremelimumab, in BRCA1 and BRCA2 Mutation Carriers With Recurrent Ovarian Cancer [NCT02571725]	Phase 1/Phase 2	50 participants (Anticipated)	Interventional	2016-02-23	Active, not recruiting
APOLLO: A Randomized Phase II Double-Blind Study of Olaparib Versus Placebo Following Curative Intent Therapy in Patients With Resected Pancreatic Cancer and a Pathogenic BRCA1, BRCA2 or PALB2 Mutation [NCT04858334]	Phase 2	152 participants (Anticipated)	Interventional	2021-06-22	Recruiting
A Phase III, Open-label, Randomised Study of Neoadjuvant Datopotamab Deruxtecan (Dato-DXd) Plus Durvalumab Followed by Adjuvant Durvalumab With or Without Chemotherapy Versus Neoadjuvant Pembrolizumab Plus Chemotherapy Followed by Adjuvant Pembrolizumab W [NCT06112379]	Phase 3	1,728 participants (Anticipated)	Interventional	2023-11-14	Recruiting
Phase II Trial of Ceralasertib (AZD6738) Alone and in Combination With Olaparib or Durvalumab in Patients With Selected Solid Tumor Malignancies [NCT03682289]	Phase 2	89 participants (Anticipated)	Interventional	2019-01-17	Recruiting
A Phase I Trial of Olaparib in Addition to Cisplatin-based Concurrent Chemoradiotherapy for Patients With High Risk Locally Advanced Squamous Cell Carcinoma of the Head and Neck (NHSCC) [NCT02308072]	Phase 1	70 participants (Anticipated)	Interventional	2015-09-30	Active, not recruiting
A Non-randomised, Open-label, Sequential, Three-part, Phase I Study to Assess the Effect of Itraconazole (a CYP3A4 Inhibitor) on the Pharmacokinetics of Olaparib Following Oral Dosing of a Tablet Formulation, and to Provide Data on the Effect of Olaparib [NCT01900028]	Phase 1	85 participants (Actual)	Interventional	2013-10-31	Completed
Harnessing Olaparib, Palbociclib and Endocrine Therapy: A Phase I/II Trial of Olaparib, Palbociclib and Fulvestrant in Patients With BRCA Mutation-associated, Hormone Receptor-positive, Human Epidermal Growth Factor Receptor 2 (HER2)-Negative Metastatic B [NCT03685331]	Phase 1	54 participants (Anticipated)	Interventional	2020-10-15	Active, not recruiting
A Prospective, Single-arm, Single-center, Exploratory Phase II Study to Evaluate the Efficacy and Safety of Anlotinib Combined With Dose-reduced Olaparib in Patients With Platinum-Sensitive Recurrent Ovarian Cancer [NCT04566952]	Phase 2	68 participants (Anticipated)	Interventional	2020-10-28	Recruiting
A Phase II, Open-Label, Study of Olaparib in Combination With Either Durvalumab (MEDI4736), Selumetinib or Capivasertib, or Ceralasertib Monotherapy in Patients With Metastatic Triple-Negative Breast Cancer [NCT03801369]	Phase 2	132 participants (Anticipated)	Interventional	2018-12-12	Recruiting
A Phase I/Ib Study of Olaparib and ASTX727 in BRCA1/2- and HRD-mutated Tumors [NCT06177171]	Phase 1	18 participants (Anticipated)	Interventional	2024-04-01	Not yet recruiting
A Phase II Evaluation of Maintenance Therapy Combination Mirvetuximab Soravtansine and Olaparib in Recurrent Platinum Sensitive Ovarian, Peritoneal, and Fallopian Tube Cancer [NCT05887609]	Phase 2	53 participants (Anticipated)	Interventional	2023-10-03	Recruiting
A Phase I Study of Olaparib and Low Dose Thoracic Radiotherapy for Extensive Stage Small Cell Lung Cancer [NCT03532880]	Phase 1	26 participants (Actual)	Interventional	2018-07-12	Active, not recruiting
A Phase II Study of Olaparib and Durvalumab in Men With Castration Sensitive Biochemically Recurrent Non-Metastatic Prostate Cancer Harboring Mutations in DNA Damage Repair [NCT03810105]	Phase 2	5 participants (Actual)	Interventional	2019-03-07	Completed
Randomized Phase II Clinical Trial of Olaparib + Pembrolizumab vs. Olaparib Alone as Maintenance Therapy in Metastatic Pancreatic Cancer Patients With Germline BRCA1 or BRCA2 Mutations [NCT04548752]	Phase 2	88 participants (Anticipated)	Interventional	2021-02-22	Recruiting
BrUOG 337: Olaparib Prior to Radical Prostatectomy For Patients With Locally Advanced Prostate Cancer and Defects in DNA Repair Genes [NCT03432897]	Phase 2	1 participants (Actual)	Interventional	2018-05-25	Terminated(stopped due to Lack of enrollment secondary to eligibility criteria)
A Phase I, Open-label, Dose Escalation Study to Assess the Safety and Tolerability of AZD2281 Following Single and Multiple Oral Doses in Patients in Japan With Advanced Solid Malignancies [NCT00572364]	Phase 1	18 participants (Anticipated)	Interventional	2007-11-30	Completed
An Open Label, Single-Arm, Multi-center Phase Ib/II Study to Evaluate the Efficacy of Paclitaxel in Combination With Pembrolizumab and Olaparib as a Second Line Treatment in Recurrent/Advanced Gastric and Gastro-esophageal Junction(GEJ) Cancer With Homolo [NCT04592211]	Phase 1/Phase 2	71 participants (Anticipated)	Interventional	2021-10-01	Not yet recruiting
177Lu-PSMA-617 Therapy and Olaparib in Patients With Metastatic Castration Resistant Prostate Cancer [NCT03874884]	Phase 1	52 participants (Anticipated)	Interventional	2019-07-09	Recruiting
Phase II(Window) Preoperative Study of Olaparib With Cisplatin or With Durvalumab (MEDI4736) or Alone or no Treatment in Patients With Histologically Proven Squamous Cell Carcinoma of the Head and Neck Who Are Candidates for Surgery. [NCT02882308]	Phase 2	41 participants (Actual)	Interventional	2016-10-20	Completed
Phase II Randomized Study of Neoadjuvant Durvalumab (MEDI4736) Alone Versus Durvalumab (MEDI4736) With Olaparib (AZD2281) in Patients Ineligible for Cisplatin With Muscle-Invasive Urothelial Carcinoma of the Bladder Followed by Radical Cystectomy [NCT04579133]	Phase 2	140 participants (Actual)	Interventional	2021-03-01	Terminated(stopped due to Not approved)
A Phase II Trial of Olaparib in Patients With Advanced Castration Resistant Prostate Cancer (TOPARP) [NCT01682772]	Phase 2	148 participants (Actual)	Interventional	2012-07-31	Active, not recruiting
A Phase I/II Trial to Assess the Safety and Efficacy of Metronomic Cyclophosphamide, Metformin and Olaparib in Recurrent Advanced/Metastatic Endometrial Cancer Patients [NCT02755844]	Phase 1/Phase 2	35 participants (Actual)	Interventional	2016-09-23	Completed
A Phase 0/2 Clinical Trial of Pamiparib in Newly-Diagnosed and Recurrent Glioblastoma Patients [NCT04614909]	Early Phase 1	30 participants (Anticipated)	Interventional	2021-01-11	Recruiting
Phase II Trial of Olaparib in Combination With Ceralasertib in Patients With Recurrent Osteosarcoma [NCT04417062]	Phase 2	63 participants (Anticipated)	Interventional	2020-11-24	Recruiting
A Phase II Multicentric Study of Olaparib in PALB2-related Advanced Pancreatic Cancer (PALBOLA) [NCT06078787]	Phase 2	16 participants (Anticipated)	Interventional	2023-08-01	Recruiting
An Open Label, Single Arm, Multicentre Study to Assess the Clinical Efficacy and Safety of Lynparza (Olaparib) Tablets Maintenance Monotherapy in Platinum Sensitive Relapsed Ovarian Cancer Patients Who Are in Complete or Partial Response Following Platinu [NCT03534453]	Phase 3	229 participants (Actual)	Interventional	2018-05-29	Active, not recruiting
MAZEPPA: Phase II PRODIGE-GERCOR Study to Evaluate MAintenance Therapy With Olaparib or Selumetinib Plus Durvalumab According to BRCAness and KRAS Somatic Status Personalized in Metastatic Pancreatic Adenocarcinoma Patients [NCT04348045]	Phase 2	307 participants (Anticipated)	Interventional	2020-12-07	Recruiting
A Phase II, Multicentre, Open-Label Study to Assess the Efficacy and Safety of Olaparib Monotherapy and Olaparib Plus Durvalumab Combination as Neoadjuvant Therapy in Patients With BRCA Mutations and Early Stage HER2-Negative Breast Cancer [NCT05498155]	Phase 2	50 participants (Anticipated)	Interventional	2022-11-07	Recruiting
Phase IB Study to Evaluate the Safety of Selinexor (KPT-330) in Combination With Multiple Standard Chemotherapy or Immunotherapy Agents in Patients With Advanced Malignancies [NCT02419495]	Phase 1	221 participants (Actual)	Interventional	2015-06-26	Active, not recruiting
A 3-Arm Randomised Phase II Evaluation of Cediranib in Combination With Weekly Paclitaxel or Olaparib Versus Weekly Paclitaxel Chemotherapy for Advanced Endometrial Carcinoma or for Disease Relapse Within 18 Months of Adjuvant Carboplatin-paclitaxel Chemo [NCT03570437]	Phase 2	124 participants (Actual)	Interventional	2018-05-17	Active, not recruiting
A Phase 2 Study of Neoadjuvant PARP Inhibition Followed by Radical Prostatectomy in Patients With Unfavorable Intermediate-Risk or High-Risk Prostate Cancer With BRCA1/2 Gene Alterations (NePtune) [NCT05498272]	Phase 2	32 participants (Anticipated)	Interventional	2023-02-01	Recruiting
Phase I/II Randomised, Double- Blind, Multi-centre Study to Assess the Efficacy of AZD2281 When Given in Combination With Paclitaxel in the 1st or 2nd Line Treatment of Patients With Metastatic Triple Negative Breast Cancer. [NCT00707707]	Phase 1	19 participants (Actual)	Interventional	2008-09-15	Completed
Phase II Randomised, Double Blind, Multicentre Study to Assess the Efficacy of AZD2281 in the Treatment of Patients With Platinum Sensitive Relapsed Serous Ovarian Cancer Following Treatment With Two or More Platinum Containing Regimens [NCT00753545]	Phase 2	265 participants (Actual)	Interventional	2008-08-28	Active, not recruiting
A Multicenter, Open-Label, Parallel, Phase 1b/2a Study of PLX2853 in Combination With Abiraterone Acetate and Prednisone and Phase 1b/2a Study of PLX2853 in Combination With Olaparib in Subjects With Metastatic Castration-Resistant Prostate Cancer (mCRPC) [NCT04556617]	Phase 1/Phase 2	19 participants (Actual)	Interventional	2020-09-21	Terminated(stopped due to study terminated due to business realignment)
Phase II Study of Olaparib in Subjects With Advanced Pancreatic Acinar Cell Carcinoma [NCT05286827]	Phase 2	20 participants (Anticipated)	Interventional	2023-12-14	Recruiting
Phase Ib/II Trial of Pembrolizumab (MK-3475) Combination Therapies in Metastatic Castration-Resistant Prostate Cancer (mCRPC) (KEYNOTE-365) [NCT02861573]	Phase 1/Phase 2	1,200 participants (Anticipated)	Interventional	2016-11-17	Recruiting
Phase II of Neoadjuvant Olaparib in Combination With Pembrolizumab in Patients With Triple Negative Breast Cancer (TNBC) or Hormone Receptor-positive HER2-negative Breast Cancer and Germline Mutations in DNA Damage Repair Genes [NCT05203445]	Phase 2	23 participants (Anticipated)	Interventional	2022-01-31	Recruiting
A Randomized, Double-blind, Placebo-controlled Phase 3 Study of Pembrolizumab (MK-3475) in Combination With Concurrent Chemoradiation Therapy Followed by Pembrolizumab With or Without Olaparib (MK-7339), Compared to Concurrent Chemoradiation Therapy Alone [NCT04624204]	Phase 3	672 participants (Anticipated)	Interventional	2020-12-08	Recruiting
A Phase 2 Study of Olaparib Monotherapy in Participants With Previously Treated, Homologous Recombination Repair Mutation (HRRm) or Homologous Recombination Deficiency (HRD) Positive Advanced Cancer [NCT03742895]	Phase 2	390 participants (Anticipated)	Interventional	2018-12-12	Recruiting
A Two-part, Randomised, Open-label, Multicentre, Phase I Study to Determine the Effect of Food on the Pharmacokinetics of Olaparib Following Single 400 mg Doses of the Capsule Formulation in Patients With Advanced Solid Tumours. [NCT01851265]	Phase 1	32 participants (Actual)	Interventional	2013-07-04	Completed
Phase I Study of Olaparib and Temozolomide in Adult Patients With Recurrent/Metastatic Ewing's Sarcoma or Rhabdomyosarcoma Following Failure of Prior Chemotherapy [NCT01858168]	Phase 1	93 participants (Anticipated)	Interventional	2013-07-31	Recruiting
A GINECO Phase II Trialo Assessing the Safety and the Efficacy of the Bevacizumab, Olaparib and Durvalumab (MEDI 4736) Combination in Patients With Advanced Epithelial Ovarian Cancer in Relapse [NCT04015739]	Phase 2	74 participants (Actual)	Interventional	2019-03-01	Active, not recruiting
Outcomes of First-line Olaparib Combined With Bevacizumab Maintenance Therapy in Newly Diagnosed Ovarian Cancer Patients With tBRCA Wild-type Tumors: a Real-world Study [NCT05440578]		50 participants (Anticipated)	Observational	2022-06-30	Not yet recruiting
An Open-label, Multicentric, Phase Ib/II Study to Assess the Safety and Efficacy of AsiDNATM, a DNA Repair Inhibitor, Administered Intravenously in Addition to Niraparib in Patients With Relapsed Platinum Sensitive Ovarian Cancer Already Treated With Nira [NCT04826198]	Phase 1/Phase 2	26 participants (Anticipated)	Interventional	2020-10-05	Recruiting
A Phase I/II Study of Olaparib in Addition to Cisplatin Based Concurrent Chemoradiotherapy for Patients With High Risk Locally Advanced Squamous Cell Carcinoma of the Head and Neck (HNSCC) [NCT01491139]	Phase 1	0 participants (Actual)	Interventional		Withdrawn(stopped due to Study stopped due to issues surrounding development and formulation of olaparib)
Multi-agent Low Dose Chemotherapy (Gemcitabine, Nab-paclitaxel, Capecitabine, Cisplatin, Irinotecan) Followed by Maintenance Olaparib and Pembrolizumab in Untreated Metastatic Pancreatic Ductal Adenocarcinoma. [NCT04753879]	Phase 2	38 participants (Anticipated)	Interventional	2021-09-29	Recruiting
Phase 2 Study of Paclitaxel, Pembrolizumab and Olaparib in Previously Treated Advanced Gastric Adenocarcinoma [NCT04209686]	Phase 2	36 participants (Anticipated)	Interventional	2020-07-31	Recruiting
Temozolomide and Olaparib for O6-Methylguanine DNA Methyltransferase Promoter Hypermethylated Colorectal Cancer [NCT04166435]	Phase 2	11 participants (Actual)	Interventional	2020-06-17	Completed
Observational Retrospective Cohort Study in Patients With Relapsed Epithelial Ovarian, Fallopian Tube, or Peritoneal Cancer Treated With Olaparib Following Response to Platinium-based Chemotherapy [NCT04152941]		130 participants (Actual)	Observational	2018-10-11	Completed
A Phase II Randomized, Multi-Center, Double-Blind, Global Study to Determine the Efficacy and Safety of Durvalumab Plus Olaparib Combination Therapy Compared With Durvalumab Monotherapy as Maintenance Therapy in Patients Whose Disease Has Not Progressed F [NCT03775486]	Phase 2	401 participants (Actual)	Interventional	2018-12-21	Active, not recruiting
A Phase II Study of Olaparib Plus Cediranib in Combination With Standard Therapy for Small Cell Lung Cancer [NCT02899728]	Phase 2	9 participants (Actual)	Interventional	2018-03-30	Terminated(stopped due to Inadequate accrual rate)
A Clinical Trial to Investigate Biomarker Effects of Pre-Surgical Treatment With DDR Agents in Patients With Head and Neck Squamous Cell Carcinoma (HNSCC) Who Are Planned to Undergo Surgery That is Likely to be Followed by Radiotherapy and/or Chemotherapy [NCT03022409]	Phase 1	21 participants (Actual)	Interventional	2017-09-18	Completed
Phase II, Single-arm Study of Olaparib Monotherapy in Relapsed Small Cell Lung Cancer Patients With HR Pathway Gene Mutations Not Limited to BRCA 1/2 Mutations, ATM Deficiency or MRE11A Mutations(SUKSES-B) [NCT03009682]	Phase 2	15 participants (Actual)	Interventional	2016-08-31	Completed
Phase II, Single-arm Study of Olaparib and Bevacizumab Combination Therapy in Relapsed Small Cell Lung Cancer Subjects With DNA Damage Response and the Repair Pathway Alteration, ATM Deficiency, SLFN11 Positive, or POU2F3 Positive [NCT04939662]	Phase 2	28 participants (Anticipated)	Interventional	2021-06-11	Recruiting
A Phase I, Open-Label Study to Assess the Safety and Tolerability of KU-0059436 in Combination With Carboplatin, KU-0059436 in Combination With a Paclitaxel/Carboplatin T/C Doublet and KU-0059436 in Combination With Paclitaxel in the Treatment of Patients [NCT00516724]	Phase 1	189 participants (Actual)	Interventional	2007-06-22	Active, not recruiting
Phase II, Two-cohorts, Randomized Trial Comparing Standard of Care Versus Immune- Based Combination in Relapsed Stage III Non-small-cell Lung Cancer (NSCLC) Pretreated With Chemoradiotherapy and Durvalumab (MEDI4736) [NCT05568212]	Phase 2	176 participants (Anticipated)	Interventional	2022-05-02	Recruiting
A Phase 1 Study of PARP Inhibitor Olaparib and HSP90 Inhibitor AT13387 for Treatment of Advanced Solid Tumors With Expansion in Patients With Recurrent Epithelial Ovarian, Fallopian Tube, Peritoneal Cancer or Recurrent Triple-Negative Breast Cancer [NCT02898207]	Phase 1	28 participants (Actual)	Interventional	2017-05-19	Completed
A Phase 1/2 Study of Olaparib in Combination With Ramucirumab in Metastatic Gastric and Gastroesophageal Junction Adenocarcinoma (10017760) [NCT03008278]	Phase 1/Phase 2	49 participants (Anticipated)	Interventional	2018-02-06	Active, not recruiting
Randomized Open-labeled Phase 2 Study of Maintenance Olaparib With or Without Durvalumab for DDR Gene Mutated Advanced Biliary Tract Cancer Following Platinum-based Chemotherapy [NCT05222971]	Phase 2	62 participants (Anticipated)	Interventional	2022-04-01	Recruiting
A Phase I, Pharmacokinetic and Biological Evaluation of a Small Molecule Inhibitor of Poly ADP-Ribose Polymerase-1 (PARP-1), KU-0059436, in Patients With Advanced Tumours. [NCT00516373]	Phase 1	98 participants (Actual)	Interventional	2005-07-11	Completed
Open Label, Phase II Pilot Study of Immune Checkpoint Inhibition With Pembrolizumab in Combination With PARP Inhibition With Olaparib in Advanced BRCA-mutated or HDR-defect Breast Cancers [NCT03025035]	Phase 2	20 participants (Anticipated)	Interventional	2017-09-10	Recruiting
Molecular Analysis for Combination Therapy Choice (ComboMATCH) [NCT05564377]	Phase 2	2,900 participants (Anticipated)	Interventional	2023-04-07	Recruiting
A Randomized Trial of Selumetinib and Olaparib or Selumetinib Alone in Patients With Recurrent or Persistent RAS Pathway Mutant Ovarian and Endometrial Cancers: A ComboMATCH Treatment Trial [NCT05554328]	Phase 2	165 participants (Anticipated)	Interventional	2023-04-25	Recruiting
A Randomized Phase 2/3 Study of Olaparib Plus Temozolomide Versus Investigator's Choice for the Treatment of Patients With Advanced Uterine Leiomyosarcoma After Progression on Prior Chemotherapy [NCT05432791]	Phase 2/Phase 3	190 participants (Anticipated)	Interventional	2023-03-30	Recruiting
Phase I/II Study of Cediranib and Olaparib in Combination for Treatment of Recurrent Papillary-Serous Ovarian, Fallopian Tube, or Peritoneal Cancer or for Treatment of Recurrent Triple-Negative Breast Cancer [NCT01116648]	Phase 1/Phase 2	155 participants (Actual)	Interventional	2010-04-14	Active, not recruiting
A Phase III, Open Label, Randomized Study to Assess the Efficacy and Safety of Olaparib (Lynparza™) Versus Enzalutamide or Abiraterone Acetate in Men With Metastatic Castration-Resistant Prostate Cancer Who Have Failed Prior Treatment With a New Hormonal [NCT02987543]	Phase 3	387 participants (Actual)	Interventional	2017-02-06	Completed
A Single-arm Phase II Study of Olaparib Maintenance With Pembrolizumab & Bevacizumab in BRCA Non-mutated Patients With Platinum-sensitive Recurrent Ovarian Cancer (OPEB-01) [NCT04361370]	Phase 2	44 participants (Anticipated)	Interventional	2020-10-28	Enrolling by invitation
A Phase 1b/2 Basket Study To Assess The Safety And Efficacy Of AsiDNA™ In Combination With Olaparib In Participants With Recurrent Solid Tumors [NCT05700669]	Phase 1/Phase 2	115 participants (Anticipated)	Interventional	2023-02-20	Recruiting
Multicentric Single Arm Phase II Clinical Trial, to Evaluate Safety and Efficacy of the Combination of Olaparib and PLD for Platinum Resistant Ovarian Primary Peritoneal Carcinoma, and Fallopian Tube Cancer Patients. [NCT03161132]	Phase 2	32 participants (Actual)	Interventional	2017-12-13	Completed
Phase II Trial Evaluating Olaparib Maintenance in Patients With MCRPC After Docetaxel Treatment Reaching Partial or Stable Response. [NCT03434158]	Phase 2	16 participants (Actual)	Interventional	2018-02-06	Completed
The NUVOLA TRIAL: Neoadjuvant Chemotherapy in Unresectable oVarian Cancer With OLAparib and Weekly Carboplatin Plus Paclitaxel: A Phase II Open-label Multicentre Study [NCT04261465]	Phase 2	35 participants (Anticipated)	Interventional	2019-12-01	Recruiting
A Phase II Randomized Trial of Olaparib Versus Olaparib Plus Tremelimumab in Platinum-Sensitive Recurrent Ovarian Cancer [NCT04034927]	Phase 2	61 participants (Actual)	Interventional	2019-12-04	Active, not recruiting
A Phase II Study of the PARP Inhibitor Olaparib in Combination With the DNA Damaging Agent Temozolomide for the Treatment of Advanced Uterine Leiomyosarcoma [NCT03880019]	Phase 2	23 participants (Actual)	Interventional	2019-08-19	Active, not recruiting
Multicenter, Randomized, Phase Ib/IIb Study to Evaluate the Efficacy and Tolerability of Gefitinib in Combination With Olaparib (AZD2281) Versus Gefitinib Alone, in Patients With EGFR Mutation Positive Advanced Non-small-cell Lung Cancer [NCT01513174]	Phase 1/Phase 2	186 participants (Actual)	Interventional	2011-08-31	Completed
An Open-label, Single-arm, Single-center Exploratory Clinical Study of Olaparib in the Treatment of BRCA1/2 Unmutated and BRCA1 Promoter Methylated Recurrent and Metastatic Triple-negative Breast Cancer [NCT05522491]	Phase 2	30 participants (Anticipated)	Interventional	2022-09-01	Not yet recruiting
A Phase I Study of DS-8201a in Combination With Olaparib in HER2-Expressing Malignancies [NCT04585958]	Phase 1	55 participants (Anticipated)	Interventional	2021-05-21	Recruiting
Pancytopenia Related to PARP Inhibitors in Cancer Patients : an Observational and Retrospective Study Using the WHO's Pharmacovigilance Database (PancytoRIB) [NCT04774627]		200 participants (Actual)	Observational	2021-02-07	Completed
Molecular Profiling of Advanced Soft-tissue Sarcomas. A Phase III Study [NCT03784014]	Phase 3	960 participants (Anticipated)	Interventional	2019-10-19	Recruiting
Efficacy and Safety of Precision Therapy in Refractory Tumor (Long March Pathway) [NCT03239015]	Phase 2	300 participants (Anticipated)	Interventional	2017-01-01	Recruiting
Phase II Study of Pembrolizumab and Ablative Radiotherapy With or Without Olaparib in Metastatic Triple-Negative or Hormone-Receptor Positive/Her2 Negative Breast Cancers : Initial Test Cohorts of a Platform Trial to Sequentially Investigate Immunotherapy [NCT04683679]	Phase 2	34 participants (Anticipated)	Interventional	2021-04-21	Recruiting
Effectiveness of Olaparib Plus Trastuzumab in HER2-positive BRCA-mutated Advanced Breast Cancer Patients (The OPHELIA Study) [NCT03931551]	Phase 2	5 participants (Actual)	Interventional	2019-04-30	Terminated(stopped due to Very slow recruitment due to subject profile)
IMPACT: A Phase 0 Randomized Window-of-Opportunity Study of Novel and Repurposed Therapeutic Agents in Women Triaged to Primary Surgery for Advanced Epithelial Ovarian Cancer in Stages IIIa - IV. [NCT03378297]	Early Phase 1	26 participants (Actual)	Interventional	2018-05-04	Completed
A Two-stage Simon Design Phase II Study for NOn-BRCA Metastatic BReast Cancer (MBC) Patients With Homologous Recombination Deficiency Treated With OLAparib Single Agent [NCT03367689]	Phase 2	7 participants (Actual)	Interventional	2018-04-17	Terminated(stopped due to Very slow recruitment due to subject profile)
"A Surgical Window-of-Opportunity and Phase II Trial of Pembrolizumab, Olaparib and Temozolomide in Recurrent Glioblastoma" [NCT05463848]	Phase 2	78 participants (Anticipated)	Interventional	2022-10-21	Recruiting
Phase II Multi-Center Trial of Trabectedin in Combination With Olaparib in Advanced Unresectable or Metastatic Sarcoma [NCT04076579]	Phase 2	29 participants (Actual)	Interventional	2020-03-17	Active, not recruiting
Olaparib Combined With High-Dose Chemotherapy for Refractory Lymphomas [NCT03259503]	Phase 1	50 participants (Actual)	Interventional	2019-09-13	Active, not recruiting
Phase I/II Study of the Anti-Programmed Death Ligand-1 Antibody Durvalumab (MEDI4736) in Combination With Olaparib and/or Cediranib for Advanced Solid Tumors and Advanced or Recurrent Ovarian, Triple Negative Breast, Lung, Prostate and Colorectal Cancers [NCT02484404]	Phase 1/Phase 2	384 participants (Anticipated)	Interventional	2015-06-29	Recruiting
Phase I Study of the Oral PI3kinase Inhibitor BKM120 or BYL719 and the Oral PARP Inhibitor Olaparib in Patients With Recurrent Triple Negative Breast Cancer or High Grade Serous Ovarian Cancer [NCT01623349]	Phase 1	118 participants (Actual)	Interventional	2012-09-30	Completed
Phase Ib With Expansion of Patients at the MTD Study of Olaparib Plus Weekly (Metronomic) Carboplatin and Paclitaxel in Relapsed Ovarian Cancer Patients [NCT01650376]	Phase 1/Phase 2	52 participants (Anticipated)	Interventional	2012-08-31	Active, not recruiting
A Phase II Study Combining Pembrolizumab With Olaparib in Metastatic Pancreatic Adenocarcinoma (PDA) Patients With High Tumour Mutation Burden [NCT05093231]	Phase 2	20 participants (Anticipated)	Interventional	2022-03-03	Not yet recruiting
Phase II Study of Single Agent Olaparib for Patients With Recurrent BRCA Deficient Ovarian Cancer With No Prior PARP Exposure or Prior PARP Inhibitor Exposure [NCT01661868]	Phase 2	0 participants (Actual)	Interventional	2012-08-31	Withdrawn(stopped due to Drug not available.)
An Open Label, Multicenter Phase 2 Study of Durvalumab (MEDI4736) + Olaparib as Maintenance Therapy in Patients With Extensive Stage Small-Cell Lung Cancer [NCT05245994]	Phase 2	60 participants (Anticipated)	Interventional	2021-08-21	Recruiting
Roll Over StudY for Patients Who Have Completed a Previous Oncology Study With Olaparib and Are Judged by the Investigator to Clinically Benefit From Continued Treatment [NCT04421963]	Phase 3	292 participants (Anticipated)	Interventional	2020-08-04	Enrolling by invitation
A Phase 3 Study of Pembrolizumab (MK-3475) in Combination With Concurrent Chemoradiation Therapy Followed by Pembrolizumab With or Without Olaparib vs Concurrent Chemoradiation Therapy Followed by Durvalumab in Participants With Unresectable, Locally Adva [NCT04380636]	Phase 3	870 participants (Anticipated)	Interventional	2020-07-06	Active, not recruiting
A Phase 2 Study of Olaparib in Combination With Pembrolizumab in Participants With Previously Treated, Homologous Recombination Repair Mutation (HRRm) and/or Homologous Recombination Deficiency (HRD)-Positive Advanced Cancer [NCT04123366]	Phase 2	300 participants (Anticipated)	Interventional	2019-11-18	Active, not recruiting
A Phase II Study of Olaparib (AZD2281) in Patients With Metastatic/Advanced Urothelial Carcinoma and Other Genitourinary Tumors With DNA-Repair Defects [NCT03375307]	Phase 2	150 participants (Anticipated)	Interventional	2020-11-03	Recruiting
A Modular Phase I, Open-Label, Multicentre Study to Assess the Safety, Tolerability, Pharmacokinetics and Preliminary Anti-tumour Activity of Ceralasertib in Combination With Cytotoxic Chemotherapy and/or DNA Damage Repair/Novel Anti-cancer Agents in Pati [NCT02264678]	Phase 1/Phase 2	466 participants (Anticipated)	Interventional	2014-10-31	Recruiting
A Randomised Phase II Trial of Olaparib Maintenance Versus Placebo Monotherapy in Patients With Chemosensitive Advanced Non-Small Cell Lung Cancer [NCT01788332]	Phase 2	70 participants (Actual)	Interventional	2014-01-31	Active, not recruiting
A Phase I/IIa, Open-label, Multi-center Study to Assess the Safety, Tolerability, Pharmacokinetics, and Preliminary Efficacy of the DNA Polymerase Theta Inhibitor ART6043 Administered Orally as Monotherapy and in Combination to Patients With Advanced or M [NCT05898399]	Phase 1/Phase 2	250 participants (Anticipated)	Interventional	2023-06-30	Recruiting
A Phase II Open Label Randomised Comparative Multicentre Study to Compare the Efficacy and Tolerability of Olaparib in Combination With Paclitaxel and Carboplatin Versus Paclitaxel and Carboplatin Alone in Patients With Platinum Sensitive Advanced Serous [NCT01081951]	Phase 2	162 participants (Actual)	Interventional	2010-02-04	Active, not recruiting
A Window of Opportunity Strategy for Targeted Pathway Inhibition in Patients With Pancreatic Ductal Adenocarcinoma [NCT04005690]	Early Phase 1	80 participants (Anticipated)	Interventional	2019-08-01	Recruiting
Phase I Trial of Olaparib (AZD2281) in Combination With C225 and Radiation Therapy in Patients With Locally Advanced, Stage IVA-B Squamous Cell Carcinomas of the Head/Neck With Heavy Smoking Histories [NCT01758731]	Phase 1	17 participants (Actual)	Interventional	2012-10-22	Completed
An Open-label, Multicenter Phase II Study to Compare the Efficacy of Carboplatin as First-line Followed by Second-line Olaparib Versus Olaparib as First-line Followed by Second-line Carboplatin in the Treatment of Patients With Castration Resistant Prosta [NCT04038502]	Phase 2	100 participants (Anticipated)	Interventional	2019-10-01	Recruiting
A Proof of Concept Clinical Trial of the Combination Cediranib-Olaparib at the Time of Disease Progression on Olaparib in Ovarian Cancer [NCT02340611]	Phase 2	4 participants (Actual)	Interventional	2015-06-30	Completed
NCI-COG Pediatric MATCH (Molecular Analysis for Therapy Choice) Screening Protocol [NCT03155620]	Phase 2	2,316 participants (Anticipated)	Interventional	2017-07-31	Recruiting
Olaparib Dose Escalation Trial in Patients Treated With Radiotherapy for Stage II-III Laryngeal and Stage II-III HPV-negative Oropharyngeal Squamous Cell Carcinoma [NCT02229656]	Phase 1	12 participants (Actual)	Interventional	2014-09-24	Active, not recruiting
Window of Opportunity Trial of Olaparib and Durvalumab (MEDI4736) Before Standard Neoadjuvant Chemotherapy for Stage II/III Triple Negative or Low ER+ Breast Cancer [NCT03594396]	Phase 1/Phase 2	54 participants (Actual)	Interventional	2018-06-29	Active, not recruiting
A Phase II Open-Label Study for the Comprehensive Analysis of Predictors of the Treatment With Pembrolizumab and Olaparib in Patients With Unresectable or Metastatic HER2 Negative Breast Cancer and a Deleterious Germline Mutation in BRCA1/2, ATM, BARD1, C [NCT05033756]	Phase 2	89 participants (Anticipated)	Interventional	2022-07-30	Recruiting
A Phase IIIb, Single-arm, Open-label Multicentre Study of Olaparib Monotherapy in the Treatment of HER2-ve Metastatic Breast Cancer Patients With Germline or Somatic BRCA1/2 Mutations. [NCT03286842]	Phase 3	256 participants (Actual)	Interventional	2018-01-17	Completed
Phase II Study of Pembrolizumab in Combination With Radiation With or Without Olaparib in Localized High-risk Prostate Cancer [NCT05568550]	Phase 2	64 participants (Anticipated)	Interventional	2023-07-27	Recruiting
An Open-label Phase I/IIa Study to Evaluate the Safety and Efficacy of CCS1477 as Monotherapy and in Combination, in Patients With Advanced Solid/Metastatic Tumours. [NCT03568656]	Phase 1/Phase 2	350 participants (Anticipated)	Interventional	2018-07-23	Recruiting
A Phase 2 Trial to Evaluate the Safety and Antitumor Activity of Pembrolizumab and OLApaRib (POLAR) Maintenance for Patients With Metastatic Pancreatic Ductal Adenocarcinoma and Homologous Recombination Deficiency and/or Exceptional Treatment Response to [NCT04666740]	Phase 2	63 participants (Anticipated)	Interventional	2020-12-18	Recruiting
I-SPY Trial (Investigation of Serial Studies to Predict Your Therapeutic Response With Imaging And moLecular Analysis 2) [NCT01042379]	Phase 2	5,000 participants (Anticipated)	Interventional	2010-03-01	Recruiting
Radiotherapy & Olaparib in COmbination for Carcinoma of the Oesophagus. A Phase I Trial. [NCT01460888]	Phase 1	36 participants (Anticipated)	Interventional	2013-07-31	Recruiting
A Phase I, Open-Label, 2 Part Multicentre Study to Assess the Safety, Tolerability and Efficacy of Olaparib in Combination With Carboplatin: Part A: Dose Escalation of Olaparib in Combination With Carboplatin in Patients With Advanced HER-2 Negative Breas [NCT02561832]	Phase 1	15 participants (Actual)	Interventional	2015-11-06	Terminated(stopped due to This decision was based upon strategic considerations impacting the clinical development of olaparib in this indication.)
The Effect of Glucose Level and Diabetes Mellitus on the Plasma Minimum Steady-state Concentration Ctrough of Olaparib in Patients With Ovarian Cancer [NCT05081765]		40 participants (Anticipated)	Observational [Patient Registry]	2021-09-20	Recruiting
A Phase III, Open Label, Randomised, Controlled, Multi-centre Study to Assess the Efficacy and Safety of Olaparib Monotherapy Versus Physician's Choice Single Agent Chemotherapy in the Treatment of Platinum Sensitive Relapsed Ovarian Cancer in Patients Ca [NCT02282020]	Phase 3	266 participants (Actual)	Interventional	2015-02-06	Completed
Pilot Trial of Olaparib in Patients With Unresectable or Metastatic Melanoma With Mutations in BRCA1/2 Genes [NCT05482074]	Phase 2	15 participants (Anticipated)	Interventional	2022-10-04	Recruiting
Multicenter Double Blind Randomized Phase II Trial of Olaparib vs Placebo as Maintenance Therapy in Platinum-sensitive Advanced Endometrial Carcinoma [NCT03745950]	Phase 2	147 participants (Actual)	Interventional	2019-02-01	Active, not recruiting
Outcomes of First-line Olaparib Mono-maintenance Therapy in Newly Diagnosed Ovarian Cancer Patients With tBRCA Wild-type Tumors: a Realworld Study [NCT05153603]		50 participants (Anticipated)	Observational	2022-04-30	Not yet recruiting
A Single-center, Single-arm, Prospective Study to Investigate the Efficacy and Safety of Olaparib Combined With Abiraterone and Prednisone in mHSPC Patients With HRR Gene Mutation [NCT05167175]	Phase 2	30 participants (Anticipated)	Interventional	2022-03-01	Recruiting
Phase II Study of Olaparib in Metastatic Renal Cell Carcinoma Patients Harboring a BAP-1 or Other DNA Repair Gene Mutations (ORCHID) [NCT03786796]	Phase 2	20 participants (Anticipated)	Interventional	2019-06-03	Recruiting
Pre-Surgical Window Pilot Investigation of the Effect of PARP Inhibition on the Cellular and Molecular Changes in Primary Ovarian and Breast Cancer [NCT04041128]	Early Phase 1	14 participants (Actual)	Interventional	2019-07-23	Completed
A Randomized Multi-center Phase I/II Trial of ICM (Irinotecan, Cisplatin, Mitomycin C) With or Without AZD2281 (Olaparib) in Patients With Advanced Pancreatic Cancer [NCT01296763]	Phase 1	18 participants (Actual)	Interventional	2011-01-31	Completed
Safety and Oversight of the Individually Tailored Treatment Approach: A Novel Pilot Study [NCT04801966]		3 participants (Actual)	Interventional	2021-09-23	Terminated(stopped due to low recruitment)
International Phase III Randomised Study to Evaluate the Efficacy of Maintenance Therapy With Olaparib and Cediranib or Olaparib Alone in Patients With Relapsed Ovarian Cancer Following a Response to Platinum-based Chemotherapy [NCT03278717]	Phase 3	330 participants (Anticipated)	Interventional	2018-06-15	Recruiting
A Translational Phase II Study of Single Agent Olaparib in the Treatment of Advanced Oesophagogastric Cancer [NCT03829345]	Phase 2	54 participants (Anticipated)	Interventional	2019-07-02	Recruiting
A Phase 2 Study of Olaparib Monotherapy in Metastatic Breast Cancer Patients With Germline or Somatic Mutations in DNA Repair Genes (Olaparib Expanded) [NCT03344965]	Phase 2	114 participants (Anticipated)	Interventional	2018-04-01	Recruiting
Intergroup Trial UNICANCER UC 0105-1305/ IFCT 1301: SAFIR02_Lung - Evaluation of the Efficacy of High Throughput Genome Analysis as a Therapeutic Decision Tool for Patients With Metastatic Non-small Cell Lung Cancer [NCT02117167]	Phase 2	999 participants (Actual)	Interventional	2014-04-23	Active, not recruiting
Correlation Between Homologous Recombination Deficiency and Response to Olaparib in Patients With Recurrent Epithelial Ovarian Cancer (EOC) [NCT04780945]	Phase 2	55 participants (Anticipated)	Interventional	2019-01-21	Recruiting
A Phase I, Open-Label Study to Assess the Safety, Tolerability, Pharmacokinetics and Preliminary Efficacy of Ascending Doses of AZD0156 Monotherapy or in Combination With Either Cytotoxic Chemotherapies or Novel Anti-Cancer Agents in Patients With Advance [NCT02588105]	Phase 1	84 participants (Actual)	Interventional	2015-11-10	Completed
A Phase I, Open Label, Multicenter Study to Assess the Safety, Tolerability and Pharmacology of AZD2281 in Combination With Liposomal Doxorubicin (Caelyx®) in Patients With Advanced Solid Tumors [NCT00819221]	Phase 1	44 participants (Actual)	Interventional	2009-01-05	Terminated
A Phase II Open Label, Umbrella Study Evaluating the Efficacy and Safety of Fulvestrant Plus DNA Damage Repair Inhibitors in Hormone Receptor-positive Advanced Breast Cancer After a CDK4/6 Inhibitor [NCT05536128]	Phase 2	64 participants (Anticipated)	Interventional	2022-12-31	Not yet recruiting
A Multiple Parallel Cohort, Multi-centre Phase IIa Trial Aiming to Provide Proof of Principle Efficacy for Designated Targeted Therapies in Patients With Advanced Breast Cancer Where the Targetable Mutation is Identified Through ctDNA [NCT03182634]	Phase 2	1,150 participants (Anticipated)	Interventional	2016-12-15	Recruiting
A Pan-European Non-interventional, Retrospective Observational Cohort Study of Patients With BRCA Mutated Advanced (FIGO Stage III-IV) Ovarian Cancer Treated With Olaparib Tablets in the First-line Maintenance Setting [NCT04532645]		350 participants (Anticipated)	Observational	2020-12-11	Active, not recruiting
Phase 1 Combination Study of Prexasertib (LY2606368), CHK1 Inhibitor, and Olaparib, PARP Inhibitor, in Patients With Advanced Solid Tumors [NCT03057145]	Phase 1	29 participants (Actual)	Interventional	2017-03-10	Completed
Pharmacokinetic Boosting of Olaparib to Improve Exposure, Tolerance and Cost-effectiveness [NCT05078671]	Phase 4	160 participants (Anticipated)	Interventional	2021-12-15	Recruiting
Study of Induction SBRT and Olaparib Followed by Combination Pembrolizumab/Olaparib in Gastric and Gastroesophageal Junction (GEJ) Cancers [NCT05379972]	Phase 2	26 participants (Anticipated)	Interventional	2023-01-12	Recruiting
Phase-II Study of Olaparib as Maintenance Therapy After Response to Trabectedin-pegylated Liposomal Doxorubicin in Recurrent Ovarian Carcinoma [NCT03470805]	Phase 2	9 participants (Actual)	Interventional	2018-06-21	Completed
An Open Label, Single Arm, Multicentre Study to Assess the Clinical Effectiveness and Safety of Lynparza (Olaparib) Capsules Maintenance Monotherapy in Platinum Sensitive Relapsed Somatic or Germline BRCA Mutated Ovarian Cancer Patients Who Are in Complet [NCT02476968]	Phase 4	181 participants (Actual)	Interventional	2015-09-28	Completed
Phase II Trial of Pembrolizumab and Olaparib in Homologous-recombination Deficient (HRD) Advanced Colorectal Cancer (CRC). [NCT05201612]	Phase 2	40 participants (Anticipated)	Interventional	2022-07-07	Recruiting
Phase II Study of Pembrolizumab and Bevacizumab in Combination With Platinum-based Chemotherapy Followed by Pembrolizumab, Bevacizumab and Olaparib in Patients With Platinum-sensitive Recurrent Ovarian Cancer [NCT05158062]	Phase 2	35 participants (Anticipated)	Interventional	2022-04-20	Recruiting
A Phase 2 Study of Pembrolizumab in Combination With Olaparib in Patients With Recurrent or Metastatic Cervical Cancer Who Had Disease Progression During or After Platinum-based Chemotherapy [NCT04641728]	Phase 2	28 participants (Actual)	Interventional	2021-01-01	Active, not recruiting
An Open-Label, Randomised, Multi-Drug, Biomarker-Directed, Multi-Centre, Multi-arm Phase 1b Study in Patients With Muscle Invasive Bladder Cancer (MIBC) Who Have Progressed on Prior Treatment (BISCAY). [NCT02546661]	Phase 1	156 participants (Actual)	Interventional	2016-10-03	Active, not recruiting
A Phase II, Single-arm Study of Combination Pembrolizumab and Olaparib in the Treatment of Patients With Advanced Cholangiocarcinoma [NCT04306367]	Phase 2	13 participants (Actual)	Interventional	2020-04-01	Active, not recruiting
A Phase I, Open-label Study to Assess the Safety and Tolerability of Doses of Olaparib Tablet in Japanese Patients With Advanced Solid Malignancies [NCT01813474]	Phase 1	23 participants (Actual)	Interventional	2013-03-25	Completed
A Non-randomised, Open-label, Sequential, Multicentre, Two-part, Phase I Study to Assess the Effect of Rifampicin, a CYP Inducer, on the Pharmacokinetics of Olaparib Following Oral Dosing of a Tablet Formulation in Patients With Advanced Solid Tumours [NCT01929603]	Phase 1	32 participants (Actual)	Interventional	2013-12-31	Completed
A Phase II Trial of Induction and Maintenance Pembrolizumab and Olaparib in Locally Advanced Head and Neck Squamous Cell Carcinoma (HNSCC) [NCT05366166]	Phase 2	45 participants (Anticipated)	Interventional	2022-09-02	Recruiting
A Phase II Trial of Pembrolizumab Plus Olaparib for the Treatment of Patients With Persistent/Recurrent Endometrial Cancers [NCT05156268]	Phase 2	25 participants (Anticipated)	Interventional	2022-01-27	Recruiting
Phase 2 Multiple-Dose, Multiple-Arm, Parallel Assignment Study to Evaluate the Safety, Tolerability, and Preliminary Efficacy of XmAb®20717 Alone or in Combination With Chemotherapy or Targeted Therapies in Selected Subjects With Metastatic Castration-Res [NCT05005728]	Phase 2	85 participants (Anticipated)	Interventional	2021-10-22	Recruiting
A Prospective, Multicentre, Phase-IV Clinical Trial of Olaparib in Indian Patients With Platinum Sensitive Relapsed Ovarian Cancer Who Are in Complete or Partial Response Following Platinum Based Chemotherapy and Metastatic Breast Cancer With Germline BRC [NCT04330040]	Phase 4	162 participants (Actual)	Interventional	2020-05-30	Completed
Open-Label, Pilot Study of Olaparib as a Neoadjuvant Therapy for Patients Undergoing Prostatectomy for Localized Prostate Cancer [NCT03570476]	Phase 2	2 participants (Actual)	Interventional	2018-09-11	Terminated(stopped due to Terminated due to slow accrual)
A Phase IV Trial to Confirm the Efficacy of Olaparib in Combination With Bevacizumab as Frontline Treatment of HRD Positive Ovarian Tumors [NCT06121401]	Phase 4	190 participants (Anticipated)	Interventional	2023-09-15	Recruiting
A Non-randomized Prospective Phase II Study of Upfront Maintenance Olaparib in Advanced Ovarian Cancer BRCAwt Patients With Known Homologous Recombination Deficiency [NCT06120972]	Phase 2	80 participants (Anticipated)	Interventional	2023-11-30	Not yet recruiting
Phase 1b/2 Study of ATR InhibiTor RP-3500 and PARP Inhibitor Combinations in Patients With Molecularly Selected Cancers (ATTACC) [NCT04972110]	Phase 1/Phase 2	196 participants (Anticipated)	Interventional	2021-07-21	Recruiting
An International Multicenter Phase II Trial of Durvalumab (MEDI4736) Plus OLAparib Plus Fulvestrant in Metastatic or Locally Advanced ER-positive, HER2-negative Breast Cancer Patients Selected Using Criteria That Predict Sensitivity to Olaparib [NCT04053322]	Phase 2	172 participants (Actual)	Interventional	2019-08-26	Active, not recruiting
A Phase 2 Multi-arm, Open Label Study to Assess the Safety and Efficacy of EP0057 in Combination With Olaparib in Defined Populations of Patients With Relapsed Advanced Gastric Cancer and Small Cell Lung Cancer [NCT05411679]	Phase 2	0 participants (Actual)	Interventional	2023-04-30	Withdrawn(stopped due to Futility analysis decision to terminate EP0057 compound and all Ellipses sponsored studies involving EP0057.)
Neoadjuvant Chemotherapy With Pressurized Intra Peritoneal Aerosol Chemotherapy(PIPAC) Plus SOX Plus Olaparib (PISOXO) for Locally-invaded-gastric Cancer (LIGC) [NCT04410887]	Phase 1/Phase 2	30 participants (Anticipated)	Interventional	2020-12-31	Not yet recruiting
An Open-label, Randomized, Phase 2/3 Study of Olaparib Plus Pembrolizumab Versus Chemotherapy Plus Pembrolizumab After Induction of Clinical Benefit With First-line Chemotherapy Plus Pembrolizumab in Participants With Locally Recurrent Inoperable or Metas [NCT04191135]	Phase 2	462 participants (Actual)	Interventional	2019-12-19	Active, not recruiting
Phase II Study of the PARP Inhibitor, Olaparib, in Adult Patients With Recurrent/Metastatic Ewing's Sarcoma Following Failure of Prior Chemotherapy [NCT01583543]	Phase 2	12 participants (Actual)	Interventional	2012-05-31	Completed
WIndow of Opportunity Clinical Trials Platform for Evaluation of Novel Treatments Strategies in REnal Cell Cancer [NCT03741426]	Phase 2	60 participants (Anticipated)	Interventional	2020-07-27	Recruiting
An Open-label, Non-randomised, Multicentre, Comparative, Phase I Study to Determine the Pharmacokinetics, Safety and Tolerability of Olaparib Following a Single Oral 300 mg Dose to Patients With Advanced Solid Tumours and Normal Hepatic Function or Mild o [NCT01894243]	Phase 1	31 participants (Actual)	Interventional	2014-03-13	Completed
Randomized, Double-Blind, Phase III Trial Olaparib vs. Placebo Patients With Advanced FIGO Stage IIIB-IV High Grade Serious or Endometrioid Ovarian, Fallopian Tube, or Peritoneal Cancer Treated Standard First-Line Treatment [NCT02477644]	Phase 3	806 participants (Actual)	Interventional	2015-05-06	Completed
Phase 1b Study of Olaparib and Estradiol in Advanced ER+ Breast Cancer (PHOEBE) [NCT05900895]	Phase 1	6 participants (Anticipated)	Interventional	2023-12-31	Not yet recruiting
A Phase II, Randomized, Multi-Center, Double-Blind, Comparative Global Study to Determine the Efficacy and Safety of Durvalumab in Combination With Olaparib for First-Line Treatment in Platinum-Ineligible Patients With Unresectable Stage IV Urothelial Can [NCT03459846]	Phase 2	154 participants (Actual)	Interventional	2018-03-16	Active, not recruiting
A Phase Ib Study of the Oral PARP Inhibitor Olaparib With the Oral mTORC1/2 Inhibitor AZD2014 or the Oral AKT Inhibitor AZD5363 for Recurrent Endometrial, Triple Negative Breast, and Ovarian, Primary Peritoneal, or Fallopian Tube Cancer [NCT02208375]	Phase 1/Phase 2	159 participants (Actual)	Interventional	2014-11-11	Active, not recruiting
BRCAAway: A Randomized Phase II Trial of Abiraterone, Olaparib, or Abiraterone + Olaparib in Patients With Metastatic Castration-Resistant Prostate Cancer With DNA Repair Defects [NCT03012321]	Phase 2	70 participants (Anticipated)	Interventional	2017-01-12	Active, not recruiting
Induction of Cisplatin/Nab-paclitaxel/Pembrolizumab Followed by Olaparib/Pembrolizumab Maintenance in Triple-negative Metastatic Breast Cancer Patients [NCT05174832]	Phase 2	136 participants (Anticipated)	Interventional	2022-09-07	Recruiting
Focal Radiation With Pulsed Systemic Therapy of Abiraterone, ADT, Lynparza Towards Castration Sensitive Oligometastatic Prostate Cancer (FAALCON): A Phase II, Single Arm, Single Institution Study [NCT04748042]	Phase 2	29 participants (Anticipated)	Interventional	2021-05-28	Recruiting
Phase II Trial of Olaparib (LYNPARZA) Plus Durvalumab (IMFINZI) in EGFR-Mutated Adenocarcinomas That Transform to Small Cell Lung Cancer (SCLC) and Other Neuroendocrine Tumors [NCT04538378]	Phase 2	14 participants (Anticipated)	Interventional	2021-07-07	Recruiting
Phase I/II Study of Lu-177-DOTATATE (Lutathera) in Combination With Olaparib in Inoperable Gastroenteropancreatico Neuroendocrine Tumors (GEP-NET) [NCT04086485]	Phase 1/Phase 2	37 participants (Anticipated)	Interventional	2022-10-03	Recruiting
A Phase III Randomised, Double-Blind, Placebo-Controlled, Multicentre Study of Durvalumab in Combination With Chemotherapy and Bevacizumab, Followed by Maintenance Durvalumab, Bevacizumab and Olaparib in Newly Diagnosed Advanced Ovarian Cancer Patients (D [NCT03737643]	Phase 3	1,407 participants (Actual)	Interventional	2019-01-04	Active, not recruiting
NCI-COG Pediatric MATCH (Molecular Analysis for Therapy Choice)- A Phase 2 Subprotocol of Olaparib in Patients With Tumors Harboring Defects in DNA Damage Repair Genes [NCT03233204]	Phase 2	6 participants (Actual)	Interventional	2017-09-14	Active, not recruiting
Phase II Study of Olaparib in Men With High-Risk Biochemically-Recurrent Prostate Cancer Following Radical Prostatectomy, With Integrated Biomarker Analysis [NCT03047135]	Phase 2	50 participants (Anticipated)	Interventional	2017-03-01	Active, not recruiting
Randomised, Phase II/III, 3 Stage Trial to Evaluate the Safety and Efficacy of the Addition of Olaparib to Platinum-based Neoadjuvant Chemotherapy in Breast Cancer Patients With TNBC and/or gBRCA. [NCT03150576]	Phase 2/Phase 3	780 participants (Anticipated)	Interventional	2016-05-31	Recruiting
A Multiple Patient Expanded Access Program for Olaparib Tablets for the Maintenance Treatment Following Response (Complete Response or Partial Response) to Platinum-based Chemotherapy in Patients With Platinum-sensitive Relapsed High-grade Epithelial Ovar [NCT03079687]		0 participants	Expanded Access		Approved for marketing
A Randomised, Open-label, Three-part, Phase I Study to Determine the Effect of Food on the Pharmacokinetics of Olaparib and to Provide Data on the Effect of Olaparib on QT Interval Following Oral Dosing of a Tablet Formulation in Patients With Advanced So [NCT01921140]	Phase 1	60 participants (Actual)	Interventional	2013-09-24	Completed
A Prospective, Multi-Institutional Phase II Trial Evaluating Temozolomide vs. Temozolomide and Olaparib for Advanced Pheochromocytoma and Paraganglioma [NCT04394858]	Phase 2	76 participants (Anticipated)	Interventional	2021-03-17	Recruiting
An Open-Label, Non-randomised, Parallel Group, Multicentre, Phase I Study to Assess the Safety and Effect of Olaparib at Steady State on the Pharmacokinetics of the Anti-hormonal Agents Anastrozole, Letrozole and Tamoxifen at Steady State, and the Effect [NCT02093351]	Phase 1	79 participants (Actual)	Interventional	2014-09-01	Completed
An Open-label, Non-randomised, Multicentre, Comparative, Phase I Study of the Pharmacokinetics, Safety and Tolerability of Olaparib Following a Single Oral 300 mg Dose to Patients With Advanced Solid Tumours and Normal Renal Function or Renal Impairment [NCT01894256]	Phase 1	56 participants (Actual)	Interventional	2013-11-30	Completed
A Phase III, Randomised, Double Blind, Placebo Controlled, Multicentre Study of Maintenance Olaparib Monotherapy in Patients With gBRCA Mutated Metastatic Pancreatic Cancer Whose Disease Has Not Progressed on First Line Platinum Based Chemotherapy [NCT02184195]	Phase 3	154 participants (Actual)	Interventional	2014-12-16	Completed
Pembrolizumab and Olaparib in Recurrent/Metastatic, Platinum Resistant Nasopharyngeal Cancer [NCT04825990]	Phase 2	30 participants (Anticipated)	Interventional	2022-03-24	Recruiting
NOW: Neoadjuvant Olaparib Window Trial in Newly Diagnosed BRCA-Mutant Ovarian Cancer [NCT03943173]	Early Phase 1	15 participants (Actual)	Interventional	2019-06-07	Active, not recruiting
A Phase 3 Study of Pembrolizumab in Combination With Carboplatin/Taxane (Paclitaxel or Nab-paclitaxel) Followed by Pembrolizumab With or Without Maintenance Olaparib in the First-line Treatment of Metastatic Squamous Non-small Cell Lung Cancer (NSCLC) [NCT03976362]	Phase 3	857 participants (Anticipated)	Interventional	2019-06-28	Active, not recruiting
A Phase II Open-label, Non-comparative, International, Multicentre Study to Assess the Efficacy and Safety of KU 0059436 (Olaparib) Given Orally Twice Daily in Patients With Advanced BRCA1 or BRCA2 Associated Breast Cancer [NCT00494234]	Phase 2	54 participants (Actual)	Interventional	2007-06-15	Completed
Phase 2 Trial of Translational Approach to First Line cHemoimmunotherapy Followed by Maintenance With pembrOlizumab and Olaparib in Extensive-Stage Small-Cell Lung CanceR. [NCT05623319]	Phase 2	60 participants (Anticipated)	Interventional	2023-03-27	Recruiting
Refining Adjuvant Treatment IN Endometrial Cancer Based On Molecular Features: the p53abn-RED Trial, the MMRd-GREEN Trial, the NSMP-ORANGE Trial and the POLEmut-BLUE Trial [NCT05255653]	Phase 2/Phase 3	1,615 participants (Anticipated)	Interventional	2021-11-11	Recruiting
A Phase 1 Study of Olaparib in Combination With Durvalumab (MEDI4736) and Concurrent Radiation Therapy Following First-Line Chemotherapy in Locally Advanced Unresectable Pancreatic Cancer [NCT05411094]	Phase 1	18 participants (Anticipated)	Interventional	2023-05-22	Recruiting
Phase I Sequential Trial of Agents Against DNA Repair (STAR) [NCT04197713]	Phase 1	16 participants (Actual)	Interventional	2020-06-30	Active, not recruiting
Sequential Maintenance With Thoracic Radiotherapy and Durvalumab (MEDI4736) Monotherapy or Durvalumab (MEDI 4736) Combinations (Tremelimumab or Olaparib) in Patients With Extensive Stage-Small Cell Lung Cancer After First Line Platinum Based Chemotherapy [NCT03923270]	Phase 1	25 participants (Actual)	Interventional	2019-06-06	Active, not recruiting
A Phase 3, Randomized Open-label Study of Pembrolizumab (MK-3475) Plus Olaparib Versus Abiraterone Acetate or Enzalutamide in Participants With Metastatic Castration-resistant Prostate Cancer (mCRPC) Who Are Unselected for Homologous Recombination Repair [NCT03834519]	Phase 3	793 participants (Actual)	Interventional	2019-05-02	Active, not recruiting
EFFORT: Efficacy of AZD1775 in Parp Resistance; A Randomized 2-Arm, Non-Comparative Phase 2 Study of AZD1775 Alone or AZD1775 and Olaparib in Women With Ovarian Cancer Who Have Progressed During PARP Inhibition [NCT03579316]	Phase 2	104 participants (Anticipated)	Interventional	2018-12-07	Recruiting
A Randomized Phase 2 Study of Cediranib in Combination With Olaparib Versus Olaparib Alone in Men With Metastatic Castration Resistant Prostate Cancer [NCT02893917]	Phase 2	90 participants (Anticipated)	Interventional	2017-08-11	Active, not recruiting
A Phase 2 Study of Cediranib in Combination With Olaparib in Advanced Solid Tumors [NCT02498613]	Phase 2	126 participants (Anticipated)	Interventional	2016-08-31	Active, not recruiting
Olaparib Plus Low-Dose Alpelisib for Breast Cancer: A ComboMATCH Treatment Trial [NCT05967286]	Phase 2	0 participants (Actual)	Interventional	2023-10-23	Withdrawn(stopped due to Other - Protocol moved to Withdrawn)
A Randomized, Open-label Study to Assess the Efficacy and Safety of Olaparib Versus Enzalutamide or Abiraterone Acetate in Chinese Men With Metastatic Castration-Resistant Prostate Cancer Who Have Failed Prior Treatment With a New Hormonal Agent and Have [NCT05457257]	Phase 4	42 participants (Anticipated)	Interventional	2022-07-29	Recruiting
Overcoming PARP Inhibitor Resistance in BRCA Germline Mutation Positive Advanced Breast Cancer [NCT04090567]	Phase 2	60 participants (Anticipated)	Interventional	2020-07-28	Recruiting
A Two-period, Multicenter, Randomized, Open-label, Phase II Study Evaluating the Clinical Benefit of a Maintenance Treatment Targeting Tumor Molecular Alterations in Patients With Progressive Locally-advanced or Metastatic Solid Tumors [NCT02029001]	Phase 2	560 participants (Anticipated)	Interventional	2014-03-31	Recruiting
PHASE II Study - EFFICACY AND SAFETY OF (PARPi )Polyadenosine Diphosphoribose [Poly Polymerisation inhibitorTO TREAT PANCREATIC CANCER [NCT02511223]	Phase 2	24 participants (Actual)	Interventional	2016-07-31	Completed
PERSONALIZED MEDICINE GROUP / UCBG UC-0105/1304: SAFIR02_Breast - Evaluation of the Efficacy of High Throughput Genome Analysis as a Therapeutic Decision Tool for Patients With Metastatic Breast Cancer [NCT02299999]	Phase 2	1,460 participants (Actual)	Interventional	2014-04-07	Active, not recruiting
A Randomised Double Blind Placebo Controlled Phase II Clinical Trial of Cediranib and Olaparib Maintenance in Advanced Recurrent Cervical Cancer (COMICE) [NCT04487587]	Phase 2	108 participants (Anticipated)	Interventional	2018-10-09	Recruiting
Evaluation of the Combination of Selumetinib and Olaparib in Endometrial, Ovarian and Other Solid Tumors With Ras Pathway Alterations, and Ovarian Tumors With PARP Resistance [NCT03162627]	Phase 1	90 participants (Anticipated)	Interventional	2017-08-04	Active, not recruiting
A Phase I, Multicenter Dose-Escalation Study to Assess the Tolerability, Pharmacokinetics and Preliminary Anti-tumor Activity of AZD5153 in Patients With Relapsed/Refractory Malignant Solid Tumors, Including Lymphomas [NCT03205176]	Phase 1	49 participants (Actual)	Interventional	2017-06-30	Completed
Phase I/II Study of Olaparib and Temozolomide in Patients With Recurrent Small Cell Lung Cancer Following Failure of Prior Chemotherapy [NCT02446704]	Phase 1/Phase 2	66 participants (Actual)	Interventional	2015-10-13	Active, not recruiting
A Phase I Followed by a Randomized Phase II Trial of Two Cycles Carboplatin-Olaparib Followed by Olaparib Monotherapy Versus Capecitabine in BRCA-1 or -2 Mutated Her2 Negative Advanced Breast Cancer as First Line Treatment [NCT02418624]	Phase 1	25 participants (Actual)	Interventional	2015-05-31	Completed
A Phase I, Open Label, 2 Part Study to Determine the Pharmacokinetics of Olaparib 300 mg bd Administered as Monotherapy and Olaparib 100 mg bd as Monotherapy and in Combination With Paclitaxel in Chinese Patients With Advanced Solid Tumours [NCT02430311]	Phase 1	36 participants (Actual)	Interventional	2015-06-10	Completed
A Platform Study of DNA Damage Response Inhibitors in Combination With Conventional Radiotherapy in Non Small Cell Lung Cancer [NCT04550104]	Phase 1	200 participants (Anticipated)	Interventional	2021-03-17	Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00494234 (6) [back to overview]	Best Percent Change in Tumour Size
NCT00494234 (6) [back to overview]	Change From Baseline in ECOG Performance Status: Improvement Rate
NCT00494234 (6) [back to overview]	Progression-Free Survival (PFS)
NCT00494234 (6) [back to overview]	The Clinical Benefit Rate (CBR)
NCT00494234 (6) [back to overview]	Duration of Response to Olaparib
NCT00494234 (6) [back to overview]	Confirmed Objective Tumour Response (According to RECIST Criteria)
NCT00494442 (5) [back to overview]	Duration of Response
NCT00494442 (5) [back to overview]	Clinical Benefit (CB)
NCT00494442 (5) [back to overview]	Best Percentage Change in Tumour Size
NCT00494442 (5) [back to overview]	Progression-Free Survival (PFS)
NCT00494442 (5) [back to overview]	Confirmed Objective Tumour Response (According to Response Evaluation Criteria In Solid Tumors (RECIST)
NCT00628251 (12) [back to overview]	Objective Response Rate (ORR)
NCT00628251 (12) [back to overview]	Disease Control Rate
NCT00628251 (12) [back to overview]	Progression Free Survival (PFS)
NCT00628251 (12) [back to overview]	Overall Survival (OS)
NCT00628251 (12) [back to overview]	Overall Duration of Response
NCT00628251 (12) [back to overview]	Confirmed RECIST Response and/or CA-125 Response
NCT00628251 (12) [back to overview]	Best Percentage Change in Tumour Size
NCT00628251 (12) [back to overview]	Best Percentage Change From Baseline in CA-125 Levels
NCT00628251 (12) [back to overview]	Progression Free Survival (PFS)
NCT00628251 (12) [back to overview]	Best QoL Response for Total Functional Analysis of Cancer Therapy - Ovarian (FACT-O)
NCT00628251 (12) [back to overview]	Best Quality of Life (QoL) Response for Trial Outcome Index (TOI)
NCT00628251 (12) [back to overview]	Best QoL Response for FACT-O Symptom Index (FOSI)
NCT00679783 (6) [back to overview]	Best Percentage Change From Baseline in Tumour Size
NCT00679783 (6) [back to overview]	Disease Control Rate (DCR)
NCT00679783 (6) [back to overview]	Duration of Response
NCT00679783 (6) [back to overview]	Objective Response Rate (ORR) Evaluated According to Response Evaluation Criteria In Solid Tumors (RECIST) Guidelines
NCT00679783 (6) [back to overview]	Progression Free Survival (PFS)
NCT00679783 (6) [back to overview]	CA-125 Levels (Ovarian Cancer Patients Only)
NCT00753545 (16) [back to overview]	RECIST and CA-125 Response Separately and Combined
NCT00753545 (16) [back to overview]	Objective Response Rate (ORR) (According to RECIST)
NCT00753545 (16) [back to overview]	Improvement Rate for Total Functional Analysis of Cancer Therapy - Ovarian (FACT-O)
NCT00753545 (16) [back to overview]	Improvement Rate for FACT-O Symptom Index (FOSI)
NCT00753545 (16) [back to overview]	Functional Analysis of Cancer Therapy - Ovarian (FACT-O) Time to Worsening
NCT00753545 (16) [back to overview]	FACT-O Symptom Index (FOSI) Time to Worsening
NCT00753545 (16) [back to overview]	Duration of Response
NCT00753545 (16) [back to overview]	Best Percentage Change in Cancer Antigen 125 (CA-125) Levels
NCT00753545 (16) [back to overview]	Improvement Rate for Trial Outcome Index (TOI)
NCT00753545 (16) [back to overview]	Percentage Change From Baseline in Tumour Size at Week 24
NCT00753545 (16) [back to overview]	Time to Earlier of CA-125 or RECIST Progression
NCT00753545 (16) [back to overview]	Progression Free Survival (PFS) (According to Response Evaluation Criteria in Solid Tumours [RECIST])
NCT00753545 (16) [back to overview]	Trial Outcome Index(TOI)Time to Worsening
NCT00753545 (16) [back to overview]	Best Objective Response
NCT00753545 (16) [back to overview]	Overall Survival (OS)
NCT00753545 (16) [back to overview]	Disease Control Rate
NCT00912743 (3) [back to overview]	Tumour Response
NCT00912743 (3) [back to overview]	Overall Survival
NCT00912743 (3) [back to overview]	Progression Free Survival
NCT01063517 (17) [back to overview]	Objective Response Rate (ORR) in the ATM Negative Patients
NCT01063517 (17) [back to overview]	Objective Response Rate (ORR) in the Overall Study Population
NCT01063517 (17) [back to overview]	Overall Survival (OS) in ATM Negative Patients
NCT01063517 (17) [back to overview]	Overall Survival (OS) in the Overall Study Population
NCT01063517 (17) [back to overview]	Percentage Change in Tumour Size at Week 8 in the ATM Negative Patients
NCT01063517 (17) [back to overview]	Percentage Change in Tumour Size at Week 8 in the Overall Study Population
NCT01063517 (17) [back to overview]	Progression Free Survival (PFS) in Patients With Tumours Defined as Homologous Recombination Deficient by Loss of Ataxia-Telangiectasia Mutation (ATM) Protein [ATM Negative Patients]
NCT01063517 (17) [back to overview]	Progression Free Survival (PFS) in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in Global Quality of Life (QoL) Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Anxiety Domain Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Dysphagia Domain Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Fatigue Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Reflux Domain Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Stomach Pain Domain Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Nausea & Vomiting Domain Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Pain Domain Score in the Overall Study Population
NCT01063517 (17) [back to overview]	Time to Deterioration in QoL Eating Restriction Domain Score in the Overall Study Population
NCT01078662 (7) [back to overview]	Disease Control Rate at Week 16
NCT01078662 (7) [back to overview]	Tumour Response Rate
NCT01078662 (7) [back to overview]	Progression Free Survival
NCT01078662 (7) [back to overview]	Overall Survival Rate at 12 Months
NCT01078662 (7) [back to overview]	Overall Survival
NCT01078662 (7) [back to overview]	Objective Response Rate
NCT01078662 (7) [back to overview]	Duration of Response
NCT01081951 (3) [back to overview]	Overall Survival (OS)
NCT01081951 (3) [back to overview]	Percentage Change in Tumour Size
NCT01081951 (3) [back to overview]	Progression Free Survival (PFS)
NCT01116648 (4) [back to overview]	Number of Participants With Dose Limiting Toxicities of Cediranib Maleate in Combination With Olaparib (Phase I)
NCT01116648 (4) [back to overview]	The Maximum Tolerated Dose (MTD) of Cediranib in Combination With Olaparib Tablet Formulation in the Treatment of Recurrent Ovarian, Fallopian Tube, or Peritoneal Cancer (Phase I-T).
NCT01116648 (4) [back to overview]	The Maximum Tolerated Dose (MTD) of Cediranib in Combination With Olaparib in the Treatment of Recurrent Ovarian, Fallopian Tube, or Peritoneal Cancer or Metastatic Triple-negative Breast Cancer (Phase I)
NCT01116648 (4) [back to overview]	Progression-free Survival (PFS) at the Maximum Tolerated Dose/Recommended Phase 2 Dose of Cediranib Maleate With Olaparib Compared to That of Olaparib Alone (Phase II)
NCT01296763 (2) [back to overview]	Number of Participants Who Experienced a Dose Limiting Toxicity to Determine the Maximum Tolerated Dose (MTD)
NCT01296763 (2) [back to overview]	Number of Years From Cycle 1, Day 1 On-Study to Date of Death
NCT01583543 (4) [back to overview]	Number of Participants Experiencing a Grade 3 or 4 Clinically Significant and Related Adverse Event
NCT01583543 (4) [back to overview]	Objective Response Rate of Olaparib
NCT01583543 (4) [back to overview]	Overall Survival
NCT01583543 (4) [back to overview]	Progression-Free Survival
NCT01758731 (1) [back to overview]	Maximum Tolerated Dose (MTD) of Olaparib
NCT01813474 (8) [back to overview]	Number of Participants With Adverse Events
NCT01813474 (8) [back to overview]	AUC Following Single Dosing
NCT01813474 (8) [back to overview]	Cmax Following Multiple Dosing
NCT01813474 (8) [back to overview]	Tmax Following Single Dosing
NCT01813474 (8) [back to overview]	Tmax Following Multiple Dosing
NCT01813474 (8) [back to overview]	Number of Participants With Dose Limiting Toxicities
NCT01813474 (8) [back to overview]	Cmax Following Single Dosing
NCT01813474 (8) [back to overview]	AUC at Steady State Following Multiple Dosing
NCT01844986 (9) [back to overview]	Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time From Randomization to Study Treatment Discontinuation or Death (TDT)
NCT01844986 (9) [back to overview]	Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Overall Survival
NCT01844986 (9) [back to overview]	Change From Baseline in Health-Related Quality of Life (HRQoL) as Assessed by the the Trial Outcome Index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O)
NCT01844986 (9) [back to overview]	Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time to First Subsequent Therapy or Death (TFST)
NCT01844986 (9) [back to overview]	Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time From Randomization to Second Progression
NCT01844986 (9) [back to overview]	Progression Free Survival (PFS) Using Investigator Assessment According to Modified Response Evaluation Criteria in Solid Tumours (RECIST 1.1)
NCT01844986 (9) [back to overview]	Efficacy in Patients With a Deleterious or Suspected Deleterious Variant in Either of the BRCA Genes by Assessment of PFS
NCT01844986 (9) [back to overview]	Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time to Second Subsequent Therapy or Death (TSST)
NCT01844986 (9) [back to overview]	Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time to Earliest Progression by RECIST or Cancer Antigen (CA-125) or Death
NCT01874353 (10) [back to overview]	Efficacy in Patients With a Deleterious or Suspected Deleterious Variant in Either of the BRCA Genes by Assessment of PFS.
NCT01874353 (10) [back to overview]	Efficacy of Olaparib by Time From Randomization to Study Treatment Discontinuation or Death (TDT)
NCT01874353 (10) [back to overview]	Efficacy of Olaparib by Time to First Subsequent Therapy or Death (TFST)
NCT01874353 (10) [back to overview]	Change From Baseline in Health-Related Quality of Life (HRQoL) as Assessed by the the Trial Outcome Index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O)
NCT01874353 (10) [back to overview]	Efficacy of Olaparib by Time to Second Subsequent Therapy or Death (TSST)
NCT01874353 (10) [back to overview]	Progression Free Survival (PFS) Using Investigator Assessment According to Modified Response Evaluation Criteria In Solid Tumours (RECIST 1.1)
NCT01874353 (10) [back to overview]	Efficacy in Patients Following Platinum Based Chemotherapy by Assessment of Time to Earliest Progression by RECIST or Cancer Antigen (CA-125) or Death
NCT01874353 (10) [back to overview]	Efficacy in Patients Following Platinum Based Chemotherapy by Assessment of Time From Randomization to Second Progression
NCT01874353 (10) [back to overview]	Efficacy in Patients Following Platinum Based Chemotherapy by Assessment of Overall Survival
NCT01874353 (10) [back to overview]	To Determine the Exposure to Olaparib by Pharmacokinetic Analysis
NCT01894243 (11) [back to overview]	Apparent Clearance Following Oral Administration (CL/F)
NCT01894243 (11) [back to overview]	Apparent Volume of Distribution (Vz/F)
NCT01894243 (11) [back to overview]	Area Under the Plasma Concentration Time Curve From Zero to Infinity (AUC)
NCT01894243 (11) [back to overview]	Area Under the Plasma Concentration Time Curve From Zero to the Last Measureable Time Point(AUC 0-t)
NCT01894243 (11) [back to overview]	Ratio of Area Under the Plasma Concentration Time Curve From Zero to Infinity (AUC) - Mild vs Normal and Moderate vs Normal
NCT01894243 (11) [back to overview]	Ratio of Apparent Clearance Following Oral Administration (CL/F)
NCT01894243 (11) [back to overview]	Time to Reach Maximum Plasma Concentration (Tmax)
NCT01894243 (11) [back to overview]	Maximum Plasma Concentration (Cmax)
NCT01894243 (11) [back to overview]	Terminal Half-life (t½)
NCT01894243 (11) [back to overview]	Ratio of Maximum Plasma Concentration (Cmax) - Mild vs Normal and Moderate vs Normal
NCT01894243 (11) [back to overview]	Ratio of Area Under the Plasma Concentration Time Curve From Zero to the Last Measureable Time Point(AUC 0-t)
NCT01894256 (12) [back to overview]	AUC0-t of Olaparib
NCT01894256 (12) [back to overview]	CL/F of Olaparib
NCT01894256 (12) [back to overview]	CL/F of Unbound Olaparib
NCT01894256 (12) [back to overview]	CLR of Olaparib
NCT01894256 (12) [back to overview]	Free AUC of Olaparib
NCT01894256 (12) [back to overview]	Free Cmax of Olaparib
NCT01894256 (12) [back to overview]	Protein Binding of Olaparib
NCT01894256 (12) [back to overview]	t1/2 of Olaparib
NCT01894256 (12) [back to overview]	Tmax of Olaparib
NCT01894256 (12) [back to overview]	Vz/F of Olaparib
NCT01894256 (12) [back to overview]	Cmax of Olaparib
NCT01894256 (12) [back to overview]	AUC of Olaparib
NCT01924533 (7) [back to overview]	Number of Patients Objective Response
NCT01924533 (7) [back to overview]	Progression-Free Survival (PFS)
NCT01924533 (7) [back to overview]	Duration of Response
NCT01924533 (7) [back to overview]	Time to Response
NCT01924533 (7) [back to overview]	Number of Patients With Deterioration of Health Related Quality of Life (HRQoL) as Assessed by the European Organisation for Research and Treatment of Cancer (EORTC) Quality of Questionnaire Core 30 Item Module (QLQ-C30) Global HRQoL Scale
NCT01924533 (7) [back to overview]	Number of Patients With Objective Response.
NCT01924533 (7) [back to overview]	Overall Survival
NCT01972217 (28) [back to overview]	Part B: Median Best Percentage Change From Baseline in Prostate Specific Antigen (PSA) Levels
NCT01972217 (28) [back to overview]	Part B: Median Overall Survival (OS)
NCT01972217 (28) [back to overview]	Part B: Median Radiological Progression-Free Survival (rPFS) Time
NCT01972217 (28) [back to overview]	Part B: Median Time to Second Progression or Death (PFS2)
NCT01972217 (28) [back to overview]	Part B: Percentage of Patients With at Least One Objective Response (Objective Response Rate [ORR])
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone Cmax,ss
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone Cmin,ss
NCT01972217 (28) [back to overview]	Part B: Percentage of Patients Experiencing AEs
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone Cmin,ss
NCT01972217 (28) [back to overview]	Part B: Percentage of Patients With PSA Responses
NCT01972217 (28) [back to overview]	Part A PK Analysis: Olaparib Area Under the Plasma Concentration-Time Curve at Steady State (AUCss)
NCT01972217 (28) [back to overview]	Part B: Percentage of Patients With Progression Events or Death (rPFS)
NCT01972217 (28) [back to overview]	Median Time to First Subsequent Therapy (TFST) and Median Time to Second Subsequent Therapy (TSST)
NCT01972217 (28) [back to overview]	Part A Pharmacokinetics (PK): Olaparib Maximum Plasma Concentration at Steady State (Cmax,ss)
NCT01972217 (28) [back to overview]	Part A Pharmacokinetics (PK): Olaparib Maximum Plasma Concentration at Steady State (Cmax,ss)
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone Cmax,ss
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone AUCss
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone AUCss
NCT01972217 (28) [back to overview]	Part A PK Analysis: Olaparib Time to Reach Maximum Plasma Concentration at Steady State (Tmax,ss)
NCT01972217 (28) [back to overview]	Part A PK Analysis: Olaparib Time to Reach Maximum Plasma Concentration at Steady State (Tmax,ss)
NCT01972217 (28) [back to overview]	Part A PK Analysis: Olaparib Minimum Plasma Concentration at Steady State (Cmin,ss)
NCT01972217 (28) [back to overview]	Part A PK Analysis: Olaparib Minimum Plasma Concentration at Steady State (Cmin,ss)
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone Tmax,ss
NCT01972217 (28) [back to overview]	Part A PK: Abiraterone Tmax,ss
NCT01972217 (28) [back to overview]	Part A: Percentage of Patients Experiencing Adverse Events (AEs)
NCT01972217 (28) [back to overview]	Part A PK Analysis: Olaparib Area Under the Plasma Concentration-Time Curve at Steady State (AUCss)
NCT01972217 (28) [back to overview]	Part B: Median Best Percentage Change From Baseline in Circulating Tumour Cell (CTC) Level
NCT01972217 (28) [back to overview]	Part A: Number of Patients With Dose Limiting Toxicities (DLTs)
NCT02000622 (12) [back to overview]	Time to First Subsequent Cancer Therapy or Death (TFST) at Extended OS
NCT02000622 (12) [back to overview]	Overall Survival (OS) at Final OS
NCT02000622 (12) [back to overview]	Adjusted Mean Change in Global Health Status/Quality of Life (QoL) Score From the European Organisation for Research and Treatment of Cancer - Quality of Life Questionnaire (EORTC QLQ-C30)
NCT02000622 (12) [back to overview]	Time to Second Subsequent Cancer Therapy or Death (TSST) at Extended OS
NCT02000622 (12) [back to overview]	Time to Second Subsequent Cancer Therapy or Death (TSST)
NCT02000622 (12) [back to overview]	Time to Second Progression or Death (PFS2)
NCT02000622 (12) [back to overview]	Objective Response Rate (ORR) Using Blinded Independent Central Review (BICR) Data Assessed by Modified Response Evaluation Criteria In Solid Tumours (RECIST v1.1)
NCT02000622 (12) [back to overview]	Progression-free Survival (PFS) Using Blinded Independent Central Review (BICR) According to Modified Response Evaluation Criteria In Solid Tumours (RECIST v1.1) in Patients Confirmed as Myriad CDx gBRCAm
NCT02000622 (12) [back to overview]	Time to First Subsequent Cancer Therapy or Death (TFST)
NCT02000622 (12) [back to overview]	Overall Survival (OS)
NCT02000622 (12) [back to overview]	Overall Survival (OS) at Extended OS
NCT02000622 (12) [back to overview]	Progression-free Survival (PFS) Using Blinded Independent Central Review (BICR) According to Modified Response Evaluation Criteria In Solid Tumours (RECIST v1.1)
NCT02032823 (8) [back to overview]	Change From Baseline for EORTC QLQ-C30 (European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core Questions 30) Scores for Participants Who Completed Neoadjuvant Chemotherapy
NCT02032823 (8) [back to overview]	Change From Baseline for FACIT-Fatigue (Functional Assessment of Chronic Illness Therapy-Fatigue) Score for Participants Who Completed Adjuvant Chemotherapy
NCT02032823 (8) [back to overview]	Change From Baseline for FACIT-Fatigue (Functional Assessment of Chronic Illness Therapy-Fatigue) Score for Participants Who Completed Neoadjuvant Chemotherapy
NCT02032823 (8) [back to overview]	Distant Disease Free Survival (DDFS)
NCT02032823 (8) [back to overview]	Invasive Disease Free Survival (IDFS)
NCT02032823 (8) [back to overview]	Overall Survival (OS)
NCT02032823 (8) [back to overview]	Number of Participants With Contralateral Invasive and Non-invasive Breast Cancer, New Primary Ovarian Cancer, New Primary Fallopian Tube Cancer and New Primary Peritoneal Cancer
NCT02032823 (8) [back to overview]	Change From Baseline for EORTC QLQ-C30 (European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core Questions 30) Scores for Participants Who Completed Adjuvant Chemotherapy
NCT02093351 (12) [back to overview]	Effect of Tamoxifen on Exposure to Olaparib - Cmax ss
NCT02093351 (12) [back to overview]	Effect of Tamoxifen on Exposure to Olaparib - AUC0-τ
NCT02093351 (12) [back to overview]	Effect of Olaparib on Exposure to Letrozole - Cmax ss
NCT02093351 (12) [back to overview]	Effect of Olaparib on Exposure to Tamoxifen - AUC0-τ
NCT02093351 (12) [back to overview]	Effect of Olaparib on Exposure to Tamoxifen - Cmax ss
NCT02093351 (12) [back to overview]	Effect of Olaparib on Exposure to Letrozole - AUC0-τ
NCT02093351 (12) [back to overview]	Effect of Olaparib on Exposure to Anastrozole - Cmax ss
NCT02093351 (12) [back to overview]	Effect of Olaparib on Exposure to Anastrozole - AUC0-τ
NCT02093351 (12) [back to overview]	Effect of Letrozole on Exposure to Olaparib - Cmax ss
NCT02093351 (12) [back to overview]	Effect of Letrozole on Exposure to Olaparib - AUC0-τ
NCT02093351 (12) [back to overview]	Effect of Anastrozole on Exposure to Olaparib - AUC0-τ
NCT02093351 (12) [back to overview]	Effect of Anastrozole on Exposure to Olaparib - Cmax ss
NCT02184195 (10) [back to overview]	Adjusted Mean Change From Baseline up to 6 Months in Global Quality of Life (QoL) Score From the EORTC-QLQ-C30 Questionnaire
NCT02184195 (10) [back to overview]	Number of Participants With Objective Response Rate (ORR) by BICR Using Modified RECIST 1.1
NCT02184195 (10) [back to overview]	Overall Survival (OS)
NCT02184195 (10) [back to overview]	Progression-free Survival (PFS) by Blinded Independent Central Review (BICR) Using Modified Response Evaluation Criteria in Solid Tumours. This Study Used Modified RECIST Version (v) 1.1 (RECIST v1.1)
NCT02184195 (10) [back to overview]	Time From Randomisation to First Subsequent Therapy or Death (TFST)
NCT02184195 (10) [back to overview]	Time From Randomisation to Second Progression (PFS2)
NCT02184195 (10) [back to overview]	Time From Randomisation to Second Subsequent Therapy or Death (TSST)
NCT02184195 (10) [back to overview]	Time From Randomisation to Study Treatment Discontinuation or Death (TDT)
NCT02184195 (10) [back to overview]	Disease Control Rate (DCR) by BICR Using Modified RECIST 1.1
NCT02184195 (10) [back to overview]	Number of Participants With Adverse Events (AEs)
NCT02282020 (21) [back to overview]	Time From Randomization To First Subsequent Therapy Or Death (TFST)
NCT02282020 (21) [back to overview]	Objective Response Rate (ORR)
NCT02282020 (21) [back to overview]	Duration of Response (DoR)
NCT02282020 (21) [back to overview]	Mean Change From Baseline In Trial Outcome Index (TOI) Score
NCT02282020 (21) [back to overview]	Number of Participants Who Discontinued Study Treatment or Died in BRCA Gene Population
NCT02282020 (21) [back to overview]	Number of Participants Who Experience at Least One Adverse Event (AE)
NCT02282020 (21) [back to overview]	Number of Participants Who Experienced Disease Progression or Death in BRCA Gene Population by Blinded Independent Central Review (BICR)
NCT02282020 (21) [back to overview]	Overall Survival (OS)
NCT02282020 (21) [back to overview]	Number of Participants Who Experienced Second Progression or Death (PFS2) in BRCA Gene Population
NCT02282020 (21) [back to overview]	Number of Participants Who Received Subsequent Chemotherapy or Died in BRCA Gene Population
NCT02282020 (21) [back to overview]	Number of Participants Who Show an Improvement in TOI Score
NCT02282020 (21) [back to overview]	Time From Randomization To Study Treatment Discontinuation Or Death (TDT)
NCT02282020 (21) [back to overview]	Geometric Mean Plasma Concentration of Olaparib
NCT02282020 (21) [back to overview]	Time to Response (TTR)
NCT02282020 (21) [back to overview]	Time To Earliest Progression By RECIST 1.1 Or Cancer Antigen (CA) -125 Or Death
NCT02282020 (21) [back to overview]	Number of Participants Who Received Second Subsequent Chemotherapy or Died in BRCA Gene Population
NCT02282020 (21) [back to overview]	Objective Response Rate (ORR) in Breast Cancer Susceptibility (BRCA) Gene Population by Blinded Independent Central Review (BICR)
NCT02282020 (21) [back to overview]	Time From Randomization To Second Subsequent Therapy Or Death (TSST)
NCT02282020 (21) [back to overview]	Overall Survival (OS) in BRCA Gene Population
NCT02282020 (21) [back to overview]	Progression Free Survival (PFS)
NCT02282020 (21) [back to overview]	Time From Randomisation to Second Progression (PFS2)
NCT02345265 (2) [back to overview]	Progression-Free Survival (PFS) by HRR Status in Platinum-Sensitive Ovarian Cancer
NCT02345265 (2) [back to overview]	Objective Response Rate (ORR) in Platinum-Resistant Ovarian Cancer
NCT02430311 (14) [back to overview]	Steady State PK Parameter--tmax, ss at Day 8
NCT02430311 (14) [back to overview]	Steady State PK Parameter--Cmax, ss and Cmin, ss at Day 9
NCT02430311 (14) [back to overview]	Steady State PK Parameter--Cmax, ss and Cmin, ss at Day 8
NCT02430311 (14) [back to overview]	Steady State PK Parameter--RAC and TCP at Day 8
NCT02430311 (14) [back to overview]	Steady State PK Parameter--AUCss at Day 9
NCT02430311 (14) [back to overview]	Steady State PK Parameter--AUCss at Day 8
NCT02430311 (14) [back to overview]	Single Dose PK Parameter--AUC
NCT02430311 (14) [back to overview]	Steady State PK Parameter--tmax, ss at Day 9
NCT02430311 (14) [back to overview]	Steady State PK Parameter--CLss/F at Day 8
NCT02430311 (14) [back to overview]	Single Dose PK Parameter--Vz/F
NCT02430311 (14) [back to overview]	Single Dose PK Parameter--tmax
NCT02430311 (14) [back to overview]	Single Dose PK Parameter--t1/2, λz
NCT02430311 (14) [back to overview]	Single Dose PK Parameter--Cmax
NCT02430311 (14) [back to overview]	Single Dose PK Parameter--CL/F
NCT02446600 (4) [back to overview]	Overall Survival
NCT02446600 (4) [back to overview]	Patient Reported Scores of Disease-related Symptoms as Measured by the National Comprehensive Cancer Network/Functional Assessment of Cancer Therapy Ovarian Symptom Index-18 Disease-Related Symptom-Physical
NCT02446600 (4) [back to overview]	Progression Free Survival Determined Using Response Evaluation Criteria in Solid Tumors Version 1.1 Criteria
NCT02446600 (4) [back to overview]	Frequency and Severity of Adverse Effects
NCT02476968 (13) [back to overview]	Time to Second Progression (PFS2) or Death; Assessed at Primary Analysis
NCT02476968 (13) [back to overview]	TSST; Assessed at Final Analysis
NCT02476968 (13) [back to overview]	Change From Baseline in Functional Living Index-Emesis (FLIE) Questionnaire Total Scores Over Time
NCT02476968 (13) [back to overview]	Time to Second Subsequent Therapy (Treatment) or Death (TSST); Assessed at Primary Analysis
NCT02476968 (13) [back to overview]	Change From Baseline in Functional Assessment of Cancer Therapy - Ovarian (FACT-O) Trial Outcome Index (TOI) Scores Over Time
NCT02476968 (13) [back to overview]	Progression-Free Survival (PFS)
NCT02476968 (13) [back to overview]	OS; Assessed at Final Analysis
NCT02476968 (13) [back to overview]	Overall Survival (OS); Assessed at Primary Analysis
NCT02476968 (13) [back to overview]	PFS2 or Death; Assessed at Final Analysis
NCT02476968 (13) [back to overview]	Change From Baseline in Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) Total Scores Over Time
NCT02476968 (13) [back to overview]	TFST; Assessed at Final Analysis
NCT02476968 (13) [back to overview]	Time to Discontinuation of Treatment or Death (TDT)
NCT02476968 (13) [back to overview]	Time to First Subsequent Therapy (Treatment) or Death (TFST); Assessed at Primary Analysis
NCT02506816 (4) [back to overview]	Protein Expression of Biomarkers Related to PARP-inhibition
NCT02506816 (4) [back to overview]	Plasma Levels of Olaparib
NCT02506816 (4) [back to overview]	Expression of Cell Cycle-related Proteins
NCT02506816 (4) [back to overview]	Number of Participants With Olaparib-Associated Toxicities
NCT02561832 (1) [back to overview]	Part A: Number of Subjects Reporting Adverse Events (AEs)
NCT02734004 (21) [back to overview]	Second Stage Cohort: Serum Concentrations of Bevacizumab
NCT02734004 (21) [back to overview]	Initial Stage Cohorts: Percentage Change From Baseline in Target Tumor Size at Weeks 12 and 28
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Best Percentage Change From Baseline in Target Tumor Size
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: OS
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Duration of Response (DoR)
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: ORR
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Progression-Free Survival (PFS)
NCT02734004 (21) [back to overview]	Second Stage Cohorts: Percentage Change From Baseline in Target Tumor Size at Weeks 24 and 56
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Time to Study Treatment Discontinuation or Death (TDT)
NCT02734004 (21) [back to overview]	Initial Stage Cohorts: DCR at Week 28
NCT02734004 (21) [back to overview]	Initial Stage Cohorts: Disease Control Rate (DCR) at Week 12
NCT02734004 (21) [back to overview]	Second Stage Cohort: Objective Response Rate (ORR)
NCT02734004 (21) [back to overview]	Second Stage Cohorts: DCR at Week 24
NCT02734004 (21) [back to overview]	Second Stage Cohorts: DCR at Week 56
NCT02734004 (21) [back to overview]	Second Stage Expansion Cohort: DCR at Week 24
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Serum Concentrations of Olaparib
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Number of Participants With Anti-Drug Antibody (ADA) Response to MEDI4736
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Serum Concentrations of MEDI4736
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Serum Concentrations of MEDI4736
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Serum Concentrations of Olaparib
NCT02734004 (21) [back to overview]	Initial and Second Stage Cohorts: Serum Concentrations of Olaparib
NCT02889900 (9) [back to overview]	Median Duration of Response (DoR) by ICR and Investigator Assessment Using RECIST 1.1
NCT02889900 (9) [back to overview]	Median PFS by ICR and Investigator Assessment Using RECIST 1.1
NCT02889900 (9) [back to overview]	Mean Objective Response Rate (ORR) by Independent Central Review (ICR) Using Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1)
NCT02889900 (9) [back to overview]	Median Overall Survival (OS)
NCT02889900 (9) [back to overview]	Median Time to Treatment Discontinuation or Death (TDT)
NCT02889900 (9) [back to overview]	ORR by Investigator Assessment Using RECIST 1.1
NCT02889900 (9) [back to overview]	Best Observed Change From Baseline in EORTC QLQ-OV28
NCT02889900 (9) [back to overview]	Best Observed Change From Baseline in European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) C30 Scales
NCT02889900 (9) [back to overview]	Disease Control Rate (DCR) by ICR and Investigator Assessment Using RECIST 1.1
NCT02898207 (6) [back to overview]	Maximum Tolerated Dose (MTD) of Olaparib Administered in Combination With Onalespib
NCT02898207 (6) [back to overview]	Number of Participants Who Experienced Dose-Limiting Toxicities (DLTs)
NCT02898207 (6) [back to overview]	Number of Participants Progression-Free for At Least 24 Weeks by RECIST 1.1
NCT02898207 (6) [back to overview]	Number of Participants With Objective Responses by RECIST 1.1
NCT02898207 (6) [back to overview]	Number of Participants Who Experienced Treatment-Related Toxicities
NCT02898207 (6) [back to overview]	Maximum Tolerated Dose (MTD) of Onalespib Administered in Combination With Olaparib
NCT02937818 (18) [back to overview]	Serum Concentrations of Durvalumab and Tremelimumab
NCT02937818 (18) [back to overview]	Plasma Concentrations of Adavosertib and Carboplatin
NCT02937818 (18) [back to overview]	Partial Area Under the Concentration-time Curve (AUC0-6)
NCT02937818 (18) [back to overview]	Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT02937818 (18) [back to overview]	Area Under the Concentration-time Curve From Time Zero to the Last Measurable Concentration (AUC0-t)
NCT02937818 (18) [back to overview]	Time to Response (TTR)
NCT02937818 (18) [back to overview]	Time to Maximum Concentration at Steady State (Tmax,ss)
NCT02937818 (18) [back to overview]	Time to Maximum Concentration (Tmax)
NCT02937818 (18) [back to overview]	Progression Free Survival (PFS)
NCT02937818 (18) [back to overview]	Percentage of Participants With Disease Control at 12 Weeks
NCT02937818 (18) [back to overview]	Overall Survival (OS)
NCT02937818 (18) [back to overview]	Apparent Clearance of Drug at Steady State at Steady State (CLss/F)
NCT02937818 (18) [back to overview]	Number of Participants With Overall Response
NCT02937818 (18) [back to overview]	Area Under the Concentration-time Curve at Steady State (AUCss)
NCT02937818 (18) [back to overview]	Minimum Concentration at Steady State (Cmin,ss)
NCT02937818 (18) [back to overview]	Maximum Concentration at Steady State (Cmax,ss)
NCT02937818 (18) [back to overview]	Maximum Concentration (Cmax)
NCT02937818 (18) [back to overview]	Duration of Response (DoR)
NCT02953457 (4) [back to overview]	Overall Survival (OS)
NCT02953457 (4) [back to overview]	Incidence of Dose-limiting Toxicities (DLTs) Defined as the Rate of Drug-related Grade 3-5 Adverse Events Assessed Using the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.03 (Phase I)
NCT02953457 (4) [back to overview]	6 Month Progression Free Survival (PFS) in the Platinum Sensitive Group (Phase II)
NCT02953457 (4) [back to overview]	3 Month Progression Free Survival (PFS) in the All Eligible Patients by Group/Arm
NCT02983799 (8) [back to overview]	Progression Free Survival
NCT02983799 (8) [back to overview]	HRD Status as Per HRRm Gene Panel Assessment Will be Correlated With Clinical Outcome (ORR) for Subjects Enrolled in the 2 Cohorts With BRCAwt (Cohorts 3 and 4)
NCT02983799 (8) [back to overview]	Overall Survival
NCT02983799 (8) [back to overview]	Time to Any Progression
NCT02983799 (8) [back to overview]	Objective Response Rate, Defined as the Percentage of Subjects With a Best Overall Response of Confirmed Complete Response (CR) or Partial Response (PR)
NCT02983799 (8) [back to overview]	CA-125 Response Rate, Defined as the Percentage of Subjects With a CA-125 Response According to GCIG Criteria Divided by the Number of Subjects Evaluable for CA-125 Response
NCT02983799 (8) [back to overview]	Disease Control Rate Defined as the Percentage of Subjects Who Have a Best Overall Response of CR or PR or SD at Greater Than or Equal to 8 Weeks Divided by the Number of Subjects in the Efficacy Analysis Set, Prior to Any PD Event
NCT02983799 (8) [back to overview]	Duration of Response, for Those Subjects With a Confirmed Response of CR or PR
NCT02987543 (3) [back to overview]	Radiological Progression Free Survival (rPFS) by Blinded Independent Central Review (BICR) - Cohort A Only
NCT02987543 (3) [back to overview]	Time to Pain Progression - Cohort A Only
NCT02987543 (3) [back to overview]	Radiological Progression Free Survival (rPFS) by Blinded Independent Central Review (BICR) - Cohort A+B
NCT03106987 (9) [back to overview]	Efficacy: Time to Second Subsequent Treatment Commencement (TSST)
NCT03106987 (9) [back to overview]	Efficacy: Change From Baseline in Health-related Quality of Life (HRQoL)
NCT03106987 (9) [back to overview]	Efficacy: Time to Progression by Gynecologic Cancer Intergroup (GCIG) Criteria
NCT03106987 (9) [back to overview]	Efficacy: Overall Survival (OS)
NCT03106987 (9) [back to overview]	Efficacy: Progression-free Survival (PFS)
NCT03106987 (9) [back to overview]	Number of Patients With Adverse Events (AEs), and Serious Adverse Events (SAEs)
NCT03106987 (9) [back to overview]	Number of Patients With Adverse Event of Special Interest (AESI).
NCT03106987 (9) [back to overview]	Efficacy: Time to Study Treatment Discontinuation (TDT)
NCT03106987 (9) [back to overview]	Efficacy: Time to First Subsequent Treatment Commencement (TFST)
NCT03167619 (8) [back to overview]	Clinical Benefit Rate (CBR) as Measured by the Number of Participants Achieving Complete Response (CR), Partial Response (PR) or Stable Disease for ≥ 24 Weeks (SD) as Defined by RECIST 1.1. (Olaparib Alone)
NCT03167619 (8) [back to overview]	Clinical Benefit Rate (CBR) as Measured by the Number of Participants Achieving Complete Response (CR), Partial Response (PR) or Stable Disease for ≥ 24 Weeks (SD) as Defined by RECIST 1.1. (Olaparib in Combination With Durvalumab)
NCT03167619 (8) [back to overview]	Efficacy of Olaparib in Combination With Durvalumab as Assessed by PFS (Progression-free Survival)
NCT03167619 (8) [back to overview]	Overall Response Rate (ORR) as Measured by Number of Participants Achieving Complete Response (CR) or Partial Response (PR) as Defined by RECIST 1.1 (Olaparib Alone)
NCT03167619 (8) [back to overview]	Efficacy of Olaparib Alone as Assessed by PFS (Progression-free Survival) Reported as Events Per Month
NCT03167619 (8) [back to overview]	Overall Survival (Olaparib in Combination With Durvalumab)
NCT03167619 (8) [back to overview]	Overall Survival (Olaparib Alone)
NCT03167619 (8) [back to overview]	Overall Response Rate (ORR) as Measured by Number of Participants Achieving Complete Response (CR) or Partial Response (PR) as Defined by RECIST 1.1 (Olaparib in Combination With Durvalumab)
NCT03286842 (9) [back to overview]	Clinical Response Rate (CRR) in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Duration of Clinical Response (DoCR) in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Overall Survival (OS) in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Progression-free Survival (PFS) in Real-world Setting in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Time to First Subsequent Treatment or Death (TFST) in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT03286842 (9) [back to overview]	Time to Study Treatment Discontinuation or Death (TDT) in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Time to Second Subsequent Treatment or Death (TSST) in Germline BRCA Mutated Participants
NCT03286842 (9) [back to overview]	Time to Second Progression or Death (PFS2) in Germline BRCA Mutated Participants
NCT03330847 (12) [back to overview]	Overall Survival (OS)
NCT03330847 (12) [back to overview]	Objective Response Rate (ORR) (Per BICR and Per Sensitivity Analysis)
NCT03330847 (12) [back to overview]	Number of Patients With Objective Response (Per BICR and Per Sensitivity Analysis)
NCT03330847 (12) [back to overview]	Duration of Response (DoR) [Per BICR and Per Sensitivity Analysis]
NCT03330847 (12) [back to overview]	Duration of Response (DoR) [Per BICR and Per Sensitivity Analysis]
NCT03330847 (12) [back to overview]	Plasma Drug Concentrations of Olaparib
NCT03330847 (12) [back to overview]	Plasma Drug Concentrations of Ceralasertib and Adavosertib
NCT03330847 (12) [back to overview]	Percentage Change From Baseline in Target Lesion Tumour Size [Per BICR and Per Sensitivity Analysis]
NCT03330847 (12) [back to overview]	Number of Patients With Treatment Emergent Adverse Events (TEAEs)
NCT03330847 (12) [back to overview]	Progression-free Survival (Per BICR)
NCT03330847 (12) [back to overview]	Progression-free Survival Per Stratum (BICR)
NCT03330847 (12) [back to overview]	Progression-free Survival Per Stratum (Sensitivity Analysis)
NCT03402841 (8) [back to overview]	Time to First Subsequent Therapy or Death (TFST)
NCT03402841 (8) [back to overview]	Time to Treatment Discontinuation or Death (TDT)
NCT03402841 (8) [back to overview]	Overall Survival (OS)
NCT03402841 (8) [back to overview]	Chemotherapy-free Interval (CT-FI)
NCT03402841 (8) [back to overview]	Percentage of Patients With a 10-Point Deterioration From Baseline in TOI Score at Any Point During the Treatment Period
NCT03402841 (8) [back to overview]	Percentage of Patients With Any Improvement From Baseline in Trial Outcome Index (TOI) Score at Any Point During the Treatment Period
NCT03402841 (8) [back to overview]	PFS by Homologous Recombination Deficiency (HRD)/ Breast Cancer Susceptibility Gene Mutation (Mutated) (BRCAm) Status
NCT03402841 (8) [back to overview]	Progression Free Survival (PFS)
NCT03432897 (2) [back to overview]	PSA Progression-free Survival of Olaparib and Radical Prostatectomy for Patients With Locally Advanced Prostate Cancer and Defects in DNA Repair Genes.
NCT03432897 (2) [back to overview]	Number of Participants With Prostate Specific Antigen (PSA) Response
NCT03448718 (4) [back to overview]	Objective Response Rate (ORR)
NCT03448718 (4) [back to overview]	Overall Survival (OS)
NCT03448718 (4) [back to overview]	Progression-Free Survival (PFS)
NCT03448718 (4) [back to overview]	Adverse Events
NCT03459846 (2) [back to overview]	Progression-free Survival (PFS)
NCT03459846 (2) [back to overview]	Duration of Response (DoR)
NCT03516812 (2) [back to overview]	Radiographic Response Rate
NCT03516812 (2) [back to overview]	Percent of Patients With a Prostate-specific Antigen (PSA) Decline of at Least 50% Below Baseline PSA50 Response Rate
NCT03531840 (6) [back to overview]	Number of Participants With Germline Deoxyribonucleic Acid (DNA) Repair Mutation Who Experienced Partial or Complete Response.
NCT03531840 (6) [back to overview]	Number of Participants With an Objective Response
NCT03531840 (6) [back to overview]	Number of Participants With Serious and Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v5.0)
NCT03531840 (6) [back to overview]	Number of Participants With Dose Limiting-toxicities (DLT's)
NCT03531840 (6) [back to overview]	Percentage of Subjects With Neither Germline Deoxyribonuclecic Acid (DNA) Repair Mutations Nor Somatic Breast Cancer Type 1 Associated Protein-1 (BAP1) Mutations Who Experienced Partial or Complete Response.
NCT03531840 (6) [back to overview]	Percentage of Participants With Breast Cancer Type 1 Associated Protein-1 (BAP1) Somatic Mutations Who Experienced Partial or Complete Response.
NCT03570476 (3) [back to overview]	Pathologic Complete Response (pCR) Rate
NCT03570476 (3) [back to overview]	Number of Participants With Adverse Events
NCT03570476 (3) [back to overview]	Rate of Positive Surgical Margins
NCT03732820 (9) [back to overview]	Number of Participants With Time to Pain Progression (TTPP) Event
NCT03732820 (9) [back to overview]	Number of Participants With First Symptomatic Skeletal Related Event (SSRE)
NCT03732820 (9) [back to overview]	Number of Participants With Time to First Subsequent Anticancer Therapy or Death (TFST) Event
NCT03732820 (9) [back to overview]	Brief Pain Inventory-Short Form (BPI-SF)
NCT03732820 (9) [back to overview]	Functional Assessment of Cancer Therapy- Prostate Cancer (FACT-P)
NCT03732820 (9) [back to overview]	Number of Participants With Second Progression or Death (PFS2) Event
NCT03732820 (9) [back to overview]	Number of Participants With Opiate Use
NCT03732820 (9) [back to overview]	Number of Participants With Overall Survival (OS) Event
NCT03732820 (9) [back to overview]	Number of Participants With Radiological Progression Free Survival (rPFS) Event by Investigator Assessment
NCT03775486 (11) [back to overview]	Number of Participants With Treatment-Related Adverse Events
NCT03775486 (11) [back to overview]	Change From Baseline in EORTC Quality of Life Questionnaire (QLQ) QLQ-C30
NCT03775486 (11) [back to overview]	Change From Baseline in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-Lung Cancer (LC)13
NCT03775486 (11) [back to overview]	Concentration of Durvalumab
NCT03775486 (11) [back to overview]	Overall Survival
NCT03775486 (11) [back to overview]	Presence of Anti-drug Antibodies (ADAs) for Durvalumab
NCT03775486 (11) [back to overview]	Progression-free Survival
NCT03775486 (11) [back to overview]	Progression-free Survival in Homologous Recombination Repair Related Gene Mutation (HRRm) Population
NCT03775486 (11) [back to overview]	Time to Deterioration in EORTC Quality of Life Questionnaire (QLQ) QLQ-C30
NCT03775486 (11) [back to overview]	Time to Deterioration in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-Lung Cancer (LC)13
NCT03775486 (11) [back to overview]	Duration of Response
NCT03834519 (2) [back to overview]	Overall Survival (OS)
NCT03834519 (2) [back to overview]	Radiographic Progression-Free Survival (rPFS)
NCT03880019 (2) [back to overview]	Number of Patients Experiencing Adverse Events
NCT03880019 (2) [back to overview]	Confirmed Objective Response Rate (ORR) (Complete Response + Partial Response)
NCT04034927 (5) [back to overview]	Dose-limiting Toxicity (DLT) (Safety Lead-In)
NCT04034927 (5) [back to overview]	Number of Participants Died
NCT04034927 (5) [back to overview]	Number of Participants With Adverse Event of Grade 3 or Higher
NCT04034927 (5) [back to overview]	Objective Response (RECIST 1.1)
NCT04034927 (5) [back to overview]	Progression Free Survival (PFS)
NCT04166435 (3) [back to overview]	Count of Participants With Adverse Events Greater or Equal to 3
NCT04166435 (3) [back to overview]	Overall Survival
NCT04166435 (3) [back to overview]	Progression Free Survival

Best Percent Change in Tumour Size

The tumour size is defined as the sum of the longest diameters as measured among all target lesions. (NCT00494234)
Timeframe: End of study

Intervention	Percent change in tumour size (Mean)
Olaparib 100 mg bd	1.15
Olaparib 400 mg bd	-36.06

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Change From Baseline in ECOG Performance Status: Improvement Rate

The change in ECOG performance status was defined as improved (meaning the ECOG score is less than the baseline value), no change (ECOG is same as at baseline), worsened (ECOG score is greater than the baseline value) or missing (the ECOG score is missing or was not recorded at baseline). If no measurement was recorded at Cycle 1 Day 1, the change was calculated in relation to the last recorded ECOG value prior to Day 1. (NCT00494234)
Timeframe: At cycle 7 day 1 (ie, after completing 6 cycles of treatment)

Intervention	Participants with an improvement in ECOG (Number)
Olaparib 100 mg bd	1
Olaparib 400 mg bd	6

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Progression-Free Survival (PFS)

PFS is defined as the time from first dose to the earlier date of radiologic progression (as per RECIST criteria) or death by any cause in the absence of objective progression. Those patients who were withdrawn from the study without disease progression were regarded as censored at their last evaluable RECIST assessment. Where patients had not progressed at the termination of the study, they were also regarded as censored at their last evaluable RECIST assessment. (NCT00494234)
Timeframe: End of study

Intervention	Days (Median)
Olaparib 100 mg bd	122
Olaparib 400 mg bd	193

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The Clinical Benefit Rate (CBR)

The Clinical Benefit Rate (CBR) is defined as the percentage of patients with a RECIST tumour response of confirmed CR, PR or stable disease (SD) for ≥8 weeks +/- 1 week visit window. (NCT00494234)
Timeframe: End of study

Intervention	Percentage of Participants (Number)
Olaparib 100 mg bd	62.5
Olaparib 400 mg bd	84.6

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Duration of Response to Olaparib

(NCT00494234)
Timeframe: Time from response (CR or PR) to progression per RECIST criteria

Intervention	Days (Median)
Olaparib 100 mg bd	140.5
Olaparib 400 mg bd	144.0

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Confirmed Objective Tumour Response (According to RECIST Criteria)

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT/MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease from baseline in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00494234)
Timeframe: Baseline, every 8 also at study termination or initiation of confounding anti-cancer therapy. Up to 2 years.

Intervention	Participants (Number)
Olaparib 100 mg bd	6
Olaparib 400 mg bd	11

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Duration of Response

Duration of response to olaparib (NCT00494442)
Timeframe: End of study

Intervention	Days (Median)
Olaparib 100 mg bd	242
Olaparib 400 mg bd	301

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Clinical Benefit (CB)

Clinical Benefit (CB) is defined as the percentage of patients with a RECIST tumour response of confirmed complete response, partial response or stable disease for ≥8 weeks) (NCT00494442)
Timeframe: End of study

Intervention	Percentage of participants (Number)
Olaparib 100 mg bd	45.5
Olaparib 400 mg bd	71.0

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Best Percentage Change in Tumour Size

The best % change (reduction) from baseline in tumour size (defined as the sum of the longest diameters as measured among all target lesions). (NCT00494442)
Timeframe: End of study

Intervention	Percent change (Median)
Olaparib 100 mg bd	-5.1
Olaparib 400 mg bd	-25.8

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Progression-Free Survival (PFS)

Progression-Free Survival (PFS) is defined as the time from first dose to the earlier date of radiologic progression (as per RECIST criteria) or death by any cause in the absence of objective progression. (NCT00494442)
Timeframe: End of study

Intervention	Days (Median)
Olaparib 100 mg bd	62.5
Olaparib 400 mg bd	226

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Confirmed Objective Tumour Response (According to Response Evaluation Criteria In Solid Tumors (RECIST)

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT/MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease from baseline in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00494442)
Timeframe: Baseline, every 8 also at study termination or initiation of confounding anti-cancer therapy.

Intervention	Participants (Number)
	PP Analysis Set	ITT Analysis Set
Olaparib 100 mg bd	3	3
Olaparib 400 mg bd	11	11

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Objective Response Rate (ORR)

ORR was defined according to RECIST. Complete response (CR) or partial response - (PR)- 30% decrease Patients with a best RECIST response of CR or PR had to have a confirmed response at least 28 days later. (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Participants (Count of Participants)
	Complete response	Number of Partial responders
Liposomal Doxorubicin	0	6
Olaparib 200 mg bd	0	8
Olaparib 400 mg bd	0	10

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Disease Control Rate

The number of patients with confirmed CR (disappearance of all target lesions) or PR (30% decrease in the sum of the longest diameter of target lesions ) or SD ( small changes ) >4 months, divided by the number of randomised patients (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Participants (Count of Participants)
Olaparib 200 mg bd	21
Olaparib 400 mg bd	21
Liposomal Doxorubicin	19

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Progression Free Survival (PFS)

PFS was defined as the time to progression from the date of randomisation until the date of radiological assessment of progression per RECIST criteria or death (by any cause in the absence of progression) (NCT00628251)
Timeframe: Tumour assessment was to be assessed at screening, every 8 weeks during the study and at the withdrawal visit, up to 56 weeks. (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Months (Median)
Olaparib 200 mg bd	6.5
Olaparib 400 mg bd	8.8
Liposomal Doxorubicin	7.1

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Overall Survival (OS)

OS was defined as time from randomisation to date of death from any cause. Patients who had not died at time of analysis were censored at last date they were known to be alive. Median OS was not calculable for olaparib groups due to an insufficient number of deaths so the percentage of participants who died are shown along with 95% confidence intervals (NCT00628251)
Timeframe: At the time of the cut-off for the final analysis of overall survival (30 April 2010)

Intervention	Participants (Count of Participants)
Olaparib 200 mg bd	9
Olaparib 400 mg bd	11
Liposomal Doxorubicin	13

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Overall Duration of Response

The duration of response was defined as time (months) from initial assessment of PR/CR until earliest date of objective progression or death. (Values may be underestimated as some patients had not progressed at final analysis so true duration is likely to be greater than that in database.) (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Months (Median)
Olaparib 200 mg bd	5.95
Olaparib 400 mg bd	6.80
Olaparib 200 mg bd + Olaparib 400 mg bd,	6.24
Liposomal Doxorubicin	5.49

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Confirmed RECIST Response and/or CA-125 Response

The percentage of patients reporting a RECIST confirmed response and/or a CA-125 response (in the absence of progression). A CA-125 response was defined as a confirmed greater or equal to 50% reduction in CA-125. (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Percentage of participants (Number)
Olaparib 200 mg bd	37.5
Olaparib 400 mg bd	59.4
Liposomal Doxorubicin	39.4

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Best Percentage Change in Tumour Size

The percentage change (reduction) from baseline in the sum of the lengths of the longest diameter (LD) of the RECIST target lesions were objectively documented, regardless of whether the patient was still taking study medication (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Percent change (Median)
Olaparib 200 mg bd	-15.90
Olaparib 400 mg bd	-24.60
Liposomal Doxorubicin	-14.3

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Best Percentage Change From Baseline in CA-125 Levels

Best percentage change in cancer antigen 125 (CA-125) levels (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Percent change (Median)
Olaparib 200 mg bd	-37.42
Olaparib 400 mg bd	-71.19
Liposomal Doxorubicin	-55.8

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Progression Free Survival (PFS)

Intervention	Participants (Count of Participants)
Olaparib 200 mg bd	19
Olaparib 400 mg bd	20
Liposomal Doxorubicin	20

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Best QoL Response for Total Functional Analysis of Cancer Therapy - Ovarian (FACT-O)

Best HRQoL response using the total FACT-O endpoint. Improvement was defined as a change from baseline of greater than or equal to +9. (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Participants (Count of Participants)
	Improved	No Change	Worsened	Non-evaluable
Liposomal Doxorubicin	1	11	7	8
Olaparib 200 mg bd	3	14	3	5
Olaparib 400 mg bd	6	11	5	7

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Best Quality of Life (QoL) Response for Trial Outcome Index (TOI)

Best HRQoL response using the TOI endpoint. Improvement was defined as a change from baseline of greater than or equal to +7. The TOI score ranges from 0-100. (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Participants (Count of Participants)
	Improved	No change	Worsened	Non-evaluable
Liposomal Doxorubicin	3	11	6	7
Olaparib 200 mg bd	7	10	3	5
Olaparib 400 mg bd	5	10	7	7

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Best QoL Response for FACT-O Symptom Index (FOSI)

Best HRQoL response using the FOSI endpoint. Improvement was defined as a change from baseline of greater than or equal to +3. (NCT00628251)
Timeframe: At the time that 57 PFS events had occurred (Data cut-off for primary analysis of PFS: 15 September 2009)

Intervention	Participants (Count of Participants)
	Improved	No change	Worsened	Non-evaluable
Liposomal Doxorubicin	3	10	7	7
Olaparib 200 mg bd	5	14	1	5
Olaparib 400 mg bd	4	9	9	7

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Best Percentage Change From Baseline in Tumour Size

The best percentage change (reduction) from baseline in tumour size (defined as the sum of the longest diameters as measured among all target lesions). (NCT00679783)
Timeframe: Each patient with measurable disease at baseline was assessed for best percentage change in tumour size from the sequence of RECIST scan data up to data cut-off, 26 March 2010. RECIST scans were performed every 8 weeks (+/- 2 weeks) from randomization.

Intervention	Percentage (Median)
BRCA Positive Non-serous Ovarian	-44.5
BRCA Positive Serous Ovarian	-21.6
BRCA Negative Non-serous Ovarian	33.6
BRCA Negative Serous Ovarian	-14.1
BRCA Positive Non-triple Negative Breast	-35.3
BRCA Positive Triple Negative Breast	-36.4
BRCA Negative Triple Negative Breast	21.3

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Disease Control Rate (DCR)

Percentage of participants with confirmed best Response Evaluation Criteria In Solid Tumours (RECIST) response of complete response (CR), partial response (PR) orStable Disease (SD) (NCT00679783)
Timeframe: 16 Weeks

Intervention	Percentage of participants (Number)
BRCA Positive Non-serous Ovarian	75
BRCA Positive Serous Ovarian	53.85
BRCA Negative Non-serous Ovarian	0
BRCA Negative Serous Ovarian	47.73
BRCA Positive Non-triple Negative Breast	60
BRCA Positive Triple Negative Breast	20
BRCA Negative Triple Negative Breast	0

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Duration of Response

Duration of response is measured from the time the measurement criteria for CR or PR are met (whichever is first recorded) until the patient progresses (per RECIST criteria). If patient did not progress, they are censored at their last objective tumour assessment date. (NCT00679783)
Timeframe: RECIST tumour assessments carried out every 8 weeks from randomization (+/- 2 weeks) until data cut-off on 26 March 2010.

Intervention	Days (Median)
BRCA Positive Non-serous Ovarian	277
BRCA Positive Serous Ovarian	113
BRCA Negative Serous Ovarian	384

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Objective Response Rate (ORR) Evaluated According to Response Evaluation Criteria In Solid Tumors (RECIST) Guidelines

Percentage of participants with confirmed best RECIST response of complete response (CR) or partial response (PR). Patients with a best RECIST response of CR or PR had to have a confirmed response at least 28 days later. (NCT00679783)
Timeframe: Each patient with measurable disease at baseline was assessed for Objective Response from the sequence of RECIST scan data up to data cut-off, 26 March 2010. RECIST scans were performed every 8 weeks (+/- 2 weeks) from randomization.

Intervention	Percentage of participants (Number)
BRCA Positive Non-serous Ovarian	75
BRCA Positive Serous Ovarian	30.77
BRCA Negative Non-serous Ovarian	0
BRCA Negative Serous Ovarian	25.58
BRCA Positive Non-triple Negative Breast	0
BRCA Positive Triple Negative Breast	0
BRCA Negative Triple Negative Breast	0

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Progression Free Survival (PFS)

PFS is defined as the time from first dose to the earlier date of radiologic progression (as per Response Evaluation Criteria In Solid Tumours (RECIST) criteria or death by any cause in the absence of objective progression. (NCT00679783)
Timeframe: RECIST tumour assessments carried out every 8 weeks from randomization (+/- 2 weeks) until data cut-off on 26 March 2010.

Intervention	Days (Median)
BRCA Positive Non-serous Ovarian	346.5
BRCA Positive Serous Ovarian	219
BRCA Negative Non-serous Ovarian	79.5
BRCA Negative Serous Ovarian	192
BRCA Positive Non-triple Negative Breast	165
BRCA Positive Triple Negative Breast	106
BRCA Negative Triple Negative Breast	54

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CA-125 Levels (Ovarian Cancer Patients Only)

A response according to CA-125 has occurred if there is at least a 50% reduction in CA-125 levels from a pre-treatment sample. (NCT00679783)
Timeframe: 24 weeks

Intervention	Percentage of participants (Number)
BRCA Positive Non-serous Ovarian	75
BRCA Positive Serous Ovarian	33.33
BRCA Negative Non-serous Ovarian	0
BRCA Negative Serous Ovarian	28.57

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RECIST and CA-125 Response Separately and Combined

RECIST and CA-125 response separately and combined [Patients evaluable for either CA-125 response or RECIST response] (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1week) for the first 60 weeks, then every 24 weeks (+/- 1 week) thereafter and monthly for CA-125 measurements, assessed maximum up to 14 months.

Intervention	Participants (Number)
	RECIST Response	Confirmed RECIST Response	Unconfirmed RECIST response	CA-125 Response	Confirmed RECIST or CA-125 Response
Olaparib 400 mg bd	16	7	9	1	8
Placebo bd	2	2	0	1	3

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Objective Response Rate (ORR) (According to RECIST)

For each treatment group, the ORR was the number of Complete Response (CR) and Partial Response (PR) divided by the number of patients in the group in the FAS with measurable disease at baseline (displayed as a percentage below). Evaluable for response set (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1 week) for the first 60 weeks, then every 24 weeks (+/-1 week) thereafter, assessed maximum up to 14 months.

Intervention	percentage of participants (Number)
Olaparib 400 mg bd	12.3
Placebo bd	4.2

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Improvement Rate for Total Functional Analysis of Cancer Therapy - Ovarian (FACT-O)

The percentage of patients with an improvement in total FACT-O. Improvement was defined as a change from baseline of greater than or equal to +9. [Evaluable for FACT-O set] (NCT00753545)
Timeframe: Patient reported outcome questionnaire completed at baseline then every 28 days up to disease progression, assessed maximum up to 14 months.

Intervention	percentage of evaluable participants (Number)
Olaparib 400 mg bd	21.1
Placebo bd	18.9

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Improvement Rate for FACT-O Symptom Index (FOSI)

The percentage of patients with an improvement in FOSI. Improvement was defined as a change from baseline of greater than or equal to +3. [Evaluable for FOSI set] (NCT00753545)
Timeframe: Patient reported outcome questionnaire completed at baseline then every 28 days up to disease progression, assessed maximum up to 14 months.

Intervention	percentage of evaluable participants (Number)
Olaparib 400 mg bd	17.1
Placebo bd	14.8

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Functional Analysis of Cancer Therapy - Ovarian (FACT-O) Time to Worsening

The time to worsening was compared between treatments for each of the TOI, FOSI and total FACT-O. [Evaluable for FACT-O set] (NCT00753545)
Timeframe: Patient reported outcome questionnaire completed at baseline then every 28 days up to disease progression, assessed maximum up to 14 months.

Intervention	Months (Median)
Olaparib 400 mg bd	2.8
Placebo bd	4.6

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FACT-O Symptom Index (FOSI) Time to Worsening

The time to worsening was compared between treatments for each of the TOI, FOSI and total FACT-O. [Evaluable for FOSI set] (NCT00753545)
Timeframe: Patient reported outcome questionnaire completed at baseline then every 28 days up to disease progression, assessed maximum up to 14 months.

Intervention	Months (Median)
Olaparib 400 mg bd	2.8
Placebo bd	3.7

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Duration of Response

Duration of response = time from assessment prior to timepoint where PR or CR confirmed (i.e. initial assessment of PR/CR), until earliest date of objective progression or death. [Responding patients only]. There were insufficient responses to enable conclusions to be drawn. (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1 week) for the first 60 weeks, then every 24 weeks (+/-1 week) thereafter, assessed maximum up to 14 months.

Intervention	Months (Median)
Olaparib 400 mg bd	4.2
Placebo bd	2.3

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Best Percentage Change in Cancer Antigen 125 (CA-125) Levels

Best percentage change from baseline in CA-125 level (NCT00753545)
Timeframe: CA-125 was measured at baseline then every 28 days on treatment, assessed maximum up to 14 months.

Intervention	percentage of change (Median)
Olaparib 400 mg bd	-16.67
Placebo bd	0.00

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Improvement Rate for Trial Outcome Index (TOI)

The percentage of patients with an improvement in TOI. Improvement was defined as a change from baseline of greater than or equal to +7. [Evaluable for TOI set] (NCT00753545)
Timeframe: Patient reported outcome questionnaire completed at baseline then every 28 days up to disease progression, assessed maximum up to 14 months.

Intervention	percentage of evaluable participants (Number)
Olaparib 400 mg bd	20.0
Placebo bd	18.0

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Percentage Change From Baseline in Tumour Size at Week 24

Percentage change from baseline to Week 24 in target tumour size. (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1week) for the first 60 weeks, then every 24 weeks (+/-1 week) thereafter, assessed maximum up to 14 months.

Intervention	Percent change in tumour size (Least Squares Mean)
Olaparib 400 mg bd	-0.8
Placebo bd	26.4

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Time to Earlier of CA-125 or RECIST Progression

Time from randomisation to the earlier date of radiological progression (per RECIST criteria) or CA-125 or death by any cause in the absence of objective progression. [FAS] (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1 week) for the first 60 weeks, then every 24 weeks (+/- 1 week) thereafter and monthly for CA-125 measurements, assessed maximum up to 14 months.

Intervention	Months (Median)
Olaparib 400 mg bd	8.3
Placebo bd	3.7

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Progression Free Survival (PFS) (According to Response Evaluation Criteria in Solid Tumours [RECIST])

PFS was defined as the time from randomisation to the earlier date of radiological progression (per RECIST criteria) or death by any cause in the absence of objective progression. [Full analysis set (FAS)] (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1 week) for the first 60 weeks, then every 24 weeks (+/-1 week) thereafter, assessed maximum up to 14 months.

Intervention	Months (Median)
Olaparib 400 mg bd	8.4
Placebo bd	4.8

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Trial Outcome Index(TOI)Time to Worsening

The time to worsening was compared between treatments for each of the TOI, FOSI and total FACT-O. [Evaluable for TOI set] (NCT00753545)
Timeframe: Patient reported outcome questionnaire completed at baseline then every 28 days up to disease progression, assessed maximum up to 14 months.

Intervention	Months (Median)
Olaparib 400 mg bd	3.8
Placebo bd	4.6

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Best Objective Response

Best overall response from radiologic assessments. [FAS] (NCT00753545)
Timeframe: Radiologic scans performed at baseline then every 12 weeks (+/- 1week) for the first 60 weeks, then every 24 weeks (+/- 1 week) thereafter, assessed maximum up to 14 months.

Intervention	Participants (Number)
	Complete Response	Partial Response	No evidence of disease	Stable Disease >= 11 weeks	Disease Progression	Not Evaluable
Olaparib 400 mg bd	0	7	49	46	24	10
Placebo bd	0	2	42	25	55	5

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Overall Survival (OS)

OS = time from randomisation to date of death from any cause. Patients who had not died at time of analysis were censored at last date patient was known to be alive. (NCT00753545)
Timeframe: Follow up every 12 weeks post progression, assessed maximum up to 90 months.

Intervention	Months (Median)
Olaparib 400 mg bd	29.8
Placebo bd	27.8

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Disease Control Rate

Disease control rate was defined as the percentage of patients who have at least 1 confirmed visit response of CR or PR or have demonstrated SD or NED for at least 23 weeks (ie, 24 weeks +/- 1 week) prior to any evidence of progression. [FAS] (NCT00753545)
Timeframe: Assessed at 24 weeks. Radiologic scans performed at baseline, week 12 (+/- 1 week) and week 24 (+/- 1 week).

Intervention	percentage of participants (Number)
Olaparib 400 mg bd	53.7
Placebo bd	25.6

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Tumour Response

Tumour response is the number of patients who experienced complete or partial response at least once during the assessment period, according to the definitions of Response Evaluation Criteria In Solid Tumours (RECIST version 1.1) (NCT00912743)
Timeframe: From baseline, i.e. up to 28 days before first study drug dose, and then every 2 cycles (8 weeks) up to objective disease progression by RECIST, assessed up to 35 months

Intervention	Percentage of Participants (Number)
MSI-H	0
Non-MSI-H	0

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Overall Survival

Overall survival is defined as the duration from first dose till death from any cause. In absence of death, the time is calculated from first dose till the date subject last known to be alive (NCT00912743)
Timeframe: Survival follow-up from first dose till death of the patient or till end of study in absence of death, assessed up to 35 months

Intervention	days (Median)
MSI-H	248
Non-MSI-H	290.5

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Progression Free Survival

Progression free survival is defined as the duration from first dose till objective progression or death. In absence of progression or death, the time is calculated from first dose till last evaluable scanning visit. (NCT00912743)
Timeframe: From baseline, i.e. up to 28 days before first study drug dose, and then every 2 cycles (8 weeks) up to objective disease progression by RECIST, assessed up to 35 months

Intervention	days (Median)
MSI-H	61
Non-MSI-H	55

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Objective Response Rate (ORR) in the ATM Negative Patients

Objective response rate is the proportion of ATM negative patients with at least one measurable lesion at baseline, who experienced complete or partial response at least once during the assessment period, according to the definitions of Response Evaluation Criteria In Solid Tumours (RECIST version 1.1). (NCT01063517)
Timeframe: Tumour assessments carried out at baseline, 28 days before randomisation then every 8 weeks until week 40, after week 40 assessments will be carried out every 16 weeks until objective disease progression, assessed maximum up to 27 months

Intervention	Participants (Number)
Olaparib+Paclitaxel	9
Placebo+Paclitaxel	6

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Objective Response Rate (ORR) in the Overall Study Population

Objective response rate is the proportion of patients with at least one measurable lesion at baseline, who experienced complete or partial response at least once during the assessment period, according to the definitions of Response Evaluation Criteria In Solid Tumours (RECIST version 1.1). (NCT01063517)
Timeframe: Tumour assessments carried out at baseline, 28 days before randomisation then every 8 weeks until week 40, after week 40 assessments will be carried out every 16 weeks until objective disease progression, assessed maximum up to 27 months

Intervention	Participants (Number)
Olaparib+Paclitaxel	14
Placebo+Paclitaxel	9

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Overall Survival (OS) in ATM Negative Patients

Overall survival is defined as the duration from randomisation till death. In absence of death, the time is calculated from randomisation till the date subject last known to be alive. (NCT01063517)
Timeframe: Survival follow up from randomisation till death of the patient or till end of study in absence of death, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	NA
Placebo+Paclitaxel	8.20

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Overall Survival (OS) in the Overall Study Population

Intervention	months (Median)
Olaparib+Paclitaxel	13.1
Placebo+Paclitaxel	8.3

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Percentage Change in Tumour Size at Week 8 in the ATM Negative Patients

Percentage change in tumour size from baseline to Week 8 calculated as 100 X (week 8 tumour size - baseline tumour size) / (baseline tumour size) (NCT01063517)
Timeframe: Tumour scans done at Baseline and week 8

Intervention	Percent change (Mean)
Olaparib+Paclitaxel	-6.9
Placebo+Paclitaxel	-5.9

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Percentage Change in Tumour Size at Week 8 in the Overall Study Population

Intervention	Percent change (Mean)
Olaparib+Paclitaxel	-5.8
Placebo+Paclitaxel	2.2

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Progression Free Survival (PFS) in Patients With Tumours Defined as Homologous Recombination Deficient by Loss of Ataxia-Telangiectasia Mutation (ATM) Protein [ATM Negative Patients]

PFS is defined as the time from randomisation till objective progression or death. In absence of progression or death, the time is calculated from randomisation till last evaluable scanning visit. (NCT01063517)
Timeframe: Tumour assessments are carried out at baseline and then follow up assessments taken every 8 weeks up to Week 40 and then every 16 weeks until objective disease progression as defined by RECIST 1.1, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	5.29
Placebo+Paclitaxel	3.68

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Progression Free Survival (PFS) in the Overall Study Population

PFS is defined as the time from randomisation till objective progression or death. In absence of progression or death, the time is calculated from randomisation till last evaluable scanning visit. (NCT01063517)
Timeframe: Tumour assessments were carried out at baseline and then follow up assessments taken every 8 weeks up to Week 40 and then every 16 weeks until objective disease progression as defined by RECIST 1.1, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	3.91
Placebo+Paclitaxel	3.55

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Time to Deterioration in Global Quality of Life (QoL) Score in the Overall Study Population

Time calculated from randomisation till worsening of Global QoL score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	3.6
Placebo+Paclitaxel	2.8

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Time to Deterioration in QoL Anxiety Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of anxiety domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	2.8
Placebo+Paclitaxel	1.9

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Time to Deterioration in QoL Dysphagia Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of dysphagia domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	3.7
Placebo+Paclitaxel	1.9

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Time to Deterioration in QoL Fatigue Score in the Overall Study Population

Time calculated from randomisation till worsening of fatigue score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	1.9
Placebo+Paclitaxel	1.8

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Time to Deterioration in QoL Reflux Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of reflux domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	4.3
Placebo+Paclitaxel	2.8

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Time to Deterioration in QoL Stomach Pain Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of stomach pain domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	6.9
Placebo+Paclitaxel	5.7

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Time to Deterioration in QoL Nausea & Vomiting Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of nausea & vomiting domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	3.7
Placebo+Paclitaxel	3.7

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Time to Deterioration in QoL Pain Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of pain domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	3.2
Placebo+Paclitaxel	3.1

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Time to Deterioration in QoL Eating Restriction Domain Score in the Overall Study Population

Time calculated from randomisation till worsening of eating restriction domain score based on European Organisation for Research and Treatment of Cancer (EORTC) questionnaire data (NCT01063517)
Timeframe: Questionnaire data collected at Baseline ie on or before date of randomisation, every 4 weeks post baseline, assessed maximum up to 27 months

Intervention	months (Median)
Olaparib+Paclitaxel	4.6
Placebo+Paclitaxel	5.1

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Disease Control Rate at Week 16

Disease control rate is the proportion of patients with best response of complete or partial response or stable disease according to definitions of Response Evaluation Criteria In Solid Tumours (RECIST version 1.1) till week 16. (NCT01078662)
Timeframe: Tumour assessments carried out at baseline ie 28 days before first study drug dose and then at week 8 and week 16

Intervention	Percentage of participants (Number)
Breast Cancer	37.1
Ovarian Cancer	58
Pancreatic Cancer	47.8
Prostate Cancer	62.5
Other Cancers	33.3
All Patients	52

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Tumour Response Rate

Tumour response rate is the proportion of patients who experienced complete or partial response at least once during the assessment period, according to the definitions of Response Evaluation Criteria In Solid Tumours (RECIST version 1.1). (NCT01078662)
Timeframe: Tumour assessments carried out at baseline ie 28 days before first study drug dose and then every 8 weeks up to 6 months after starting study treatment, then every 12 weeks until objective disease progression, assessed maximum up to 29 months

Intervention	Percentage of participants (Number)
Breast Cancer	12.9
Ovarian Cancer	31.1
Pancreatic Cancer	21.7
Prostate Cancer	50
Other Cancers	8.3
All Patients	26.2

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Progression Free Survival

Progression free survival is defined as the duration from first dose till objective progression or death. In absence of progression or death, the time is calculated from first dose till last evaluable scanning visit. (NCT01078662)
Timeframe: Tumour assessments are carried out at baseline ie 28 days before first study drug dose and then every 8 weeks up to 6 months after starting study treatment, then every 12 weeks until objective disease progression, assessed maximum up to 29 months

Intervention	months (Median)
Breast Cancer	3.68
Ovarian Cancer	7.03
Pancreatic Cancer	4.55
Prostate Cancer	7.15

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Overall Survival Rate at 12 Months

Overall survival rate at 12 months is defined as the proportion of patients who are alive 12 months after date of first dose (NCT01078662)
Timeframe: Survival follow-up from first dose till death of the patient or till end of study in absence of death, assessed maximum up to 29 months

Intervention	Percentage of participants (Number)
Breast Cancer	44.7
Ovarian Cancer	64.4
Pancreatic Cancer	40.9
Prostate Cancer	50

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Overall Survival

Overall survival is defined as the duration from first dose till death. In absence of death, the time is calculated from first dose till the date subject last known to be alive. (NCT01078662)
Timeframe: Survival follow-up from first dose till death of the patient or till end of study in absence of death, assessed maximum up to 29 months

Intervention	months (Median)
Breast Cancer	11.01
Ovarian Cancer	16.62
Pancreatic Cancer	9.81
Prostate Cancer	18.38

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Objective Response Rate

Objective response rate is the proportion of patients with at least one measurable lesion at baseline, who experienced complete or partial response at least once during the assessment period, according to the definitions of Response Evaluation Criteria In Solid Tumours (RECIST version 1.1). (NCT01078662)
Timeframe: Tumour assessments carried out at baseline ie 28 days before first study drug dose and then every 8 weeks up to 6 months after starting study treatment, then every 12 weeks until objective disease progression, assessed maximum up to 29 months

Intervention	Percentage of participants (Number)
Breast Cancer	13.8
Ovarian Cancer	35.9
Pancreatic Cancer	21.7
Prostate Cancer	57.1
Other Cancers	9.1
All Patients	29.3

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Duration of Response

Duration of response is calculated from the date of first documented response (complete or partial) until date of documented progression (as defined by RECIST 1.1) or death (by any cause) in the absence of disease progression. (NCT01078662)
Timeframe: From onset of first occurrence of complete or partial response till documented progression or death by any cause in the absence of progression, assessed maximum up to 29 months

Intervention	days (Median)
Breast Cancer	204
Ovarian Cancer	225
Pancreatic Cancer	134
Prostate Cancer	326.5
Other Cancers	165
All Patients	208

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Overall Survival (OS)

OS was defined as the time from randomisation until death by any cause. Patients who had not died at the time of analysis were censored at the last date the patient was known to be alive. (NCT01081951)
Timeframe: Following disease progression, patients will be contacted every 12 weeks to assess survival status until the final analysis (approximately 50 months)

Intervention	Participants (Number of deaths) (Number)
Olaparib/Carboplatin AUC4/Paclitaxel	54
Carboplatin AUC6/Paclitaxel	47

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Percentage Change in Tumour Size

The total tumour size was defined as the sum of the longest diameters of the target lesions. At week 9, the percentage change in tumour size was calculated as [(week 9 sum of target lesions - baseline sum of target lesions)/baseline sum of target lesions]*100 for each patient. Imputations were used for missing data where possible. (NCT01081951)
Timeframe: Week 9 (+/- 1 week)

Intervention	Percentage change (Least Squares Mean)
Olaparib/Carboplatin AUC4/Paclitaxel	-38.4
Carboplatin AUC6/Paclitaxel	-39.1

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Progression Free Survival (PFS)

PFS (based on independent central review) was defined as the time from randomisation until objective disease progression as defined by Response Evaluation Criteria In Solid Tumours (RECIST) v1.1 (≥20% increase in the sum of the diameters of target lesions from minimum, clinically significant progression in non-target lesions or the presence of a new lesion) or death (by any cause in the absence of progression). (NCT01081951)
Timeframe: Radiologic scans performed at weeks 9 and 18 (+/-1 week) and every 12 weeks thereafter relative to the date of randomisation until the primary analysis (approximately 20 months)

Intervention	months (Median)
Olaparib/Carboplatin AUC4/Paclitaxel	12.2
Carboplatin AUC6/Paclitaxel	9.6

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Number of Participants With Dose Limiting Toxicities of Cediranib Maleate in Combination With Olaparib (Phase I)

Was determined using the National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0 (NCT01116648)
Timeframe: At 28 days

Intervention	Participants (Count of Participants)
Level 0	0
Level 1	0
Level 2	0
Level 3	2

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The Maximum Tolerated Dose (MTD) of Cediranib in Combination With Olaparib Tablet Formulation in the Treatment of Recurrent Ovarian, Fallopian Tube, or Peritoneal Cancer (Phase I-T).

The Phase 1-T component of this trial employed a 3+3 design, escalating on 0/3 or 1/6 DLT, and de-escalating if 2 DLTs were encountered. The MTD (maximum tolerated dose) was the dose at which no more than 1 patient developed a DLT when at least 6 patients had been treated. (NCT01116648)
Timeframe: At 28 days

Intervention	mg (Number)
	Cediranib PO daily	Olaparib (tablet) PO BID
All Phase 1-T Participants	30	200

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The Maximum Tolerated Dose (MTD) of Cediranib in Combination With Olaparib in the Treatment of Recurrent Ovarian, Fallopian Tube, or Peritoneal Cancer or Metastatic Triple-negative Breast Cancer (Phase I)

This trial employed a 3+3 design, escalating on 0/3 or 1/6 DLT, and de-escalating if 2 DLTs were encountered. The MTD (maximum tolerated dose) was the dose at which no more than 1 patient developed a dose-limiting toxicity (DLT) when at least 6 patients had been treated. (NCT01116648)
Timeframe: At 28 Days

Intervention	mg (Number)
	Cediranib PO daily	Olaparib PO BID
All Phase 1 Participants (28 Participants)	30	200

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Progression-free Survival (PFS) at the Maximum Tolerated Dose/Recommended Phase 2 Dose of Cediranib Maleate With Olaparib Compared to That of Olaparib Alone (Phase II)

"Evaluated by Kaplan-Meier analysis and log-rank test for between group comparison, and median survival times reported.~PFS is defined as time from randomization to investigator-assessed radiographic progression by RECIST 1.1 criteria or death.~Patients alive without evidence of progression were censored at the last disease assessment." (NCT01116648)
Timeframe: Time from start of treatment to time of objective disease progression, assessed up to 5 years

Intervention	months (Median)
Phase 2 - Olaparib Alone (46 Participants)	8.2
Phase 2 - Cediranib/Olaparib (44 Participants)	16.5

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Number of Participants Who Experienced a Dose Limiting Toxicity to Determine the Maximum Tolerated Dose (MTD)

"1.Phase I - Assess the safety and toxicities of IC with Olaparib escalating to ICM with Olaparib in patients with locally advanced and metastatic pancreatic cancer and determine the phase 2 dose. The number of subjects who experienced a dose limiting toxicity was assessed.Dose-limiting toxicity (DLT) is defined as any of the following study drug-related events experienced during Cycle 1:~Thrombocytopenia with platelets <25,000 x106/l > 7 days. Grade 4 neutropenia lasting ≥7 days. Grade 3 or 4 febrile neutropenia. Grade 3 or greater non-haematological toxicities; excluding grade 3 diarrhoea, nausea or vomiting despite adequate treatment and grade 3 fatigue, lethargy and GGT elevation.~Delay of >2 weeks for next scheduled IC/ICM for reasons of toxicity." (NCT01296763)
Timeframe: 2 years

Intervention	participants (Number)
Dose Level 1	0
Dose Level 2	2
Dose Level 5	2

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Number of Years From Cycle 1, Day 1 On-Study to Date of Death

The overall survival of subjects with locally advanced and/or metastatic pancreatic cancer treated with Irinotecan, Cisplatin, Olaparib, with escalation to the addition of Mitomycin-C. Survival from cycle 1, day 1 on-study to date of death was assessed. (NCT01296763)
Timeframe: 5 years

Intervention	years (survival) from C1D1 to death (Mean)
Dose Level 1	1.43
Dose Level 2	0.44
Dose Level 5	0.60

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Number of Participants Experiencing a Grade 3 or 4 Clinically Significant and Related Adverse Event

Adverse events were graded according to CTCAE v.4 (Common Terminology Criteria for Adverse Events). Events are graded on a scale of 1 = mild, 2 = moderate, 3 = severe, 4 = life-threatening, 5 = fatal. Only events that are clinically significant and which the treating investigator considers to be related to administration of olaparib are counted for this outcome measure. (NCT01583543)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Olaparib	4

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Objective Response Rate of Olaparib

"Number of participants with objective response rate as defined as PR+CR as determined by RECIST vs. 1.1.~Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR." (NCT01583543)
Timeframe: 2 years

Intervention	Participants (Count of Participants)
Olaparib	0

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Overall Survival

Number of patients survived for 2 years after enrolling onto this study. (NCT01583543)
Timeframe: Two years

Intervention	Participants (Count of Participants)
Olaparib	1

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Progression-Free Survival

Number of patients with progression free survival after two years from starting the trial. (NCT01583543)
Timeframe: Two years

Intervention	Participants (Count of Participants)
Olaparib	0

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Maximum Tolerated Dose (MTD) of Olaparib

Maximum tolerated dose (MTD) of Olaparib to be used for Phase II clinical testing. (NCT01758731)
Timeframe: 10 weeks from the start of protocol therapy

Intervention	mg twice daily (Number)
Olaparib With C225 and Radiation Therapy	50

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Number of Participants With Adverse Events

An adverse event is the development of an undesirable medical condition or the deterioration of a pre-existing medical condition following or during exposure to a pharmaceutical product, whether or not considered causally related to the product. This was recorded if it happend from the start dose to 30 days after the last of study drug. (NCT01813474)
Timeframe: From the start dose to 30 days after the last dose of study drug

Intervention	Participants (Number)
	At least 1 Adverse Events (AE)	At least 1 AE of CTCAE Grade 3 or higher	At least 1 Serious Adverse Events (SAE)
200 mg Bid, Dose Escalation Part	4	1	1
300 mg Bid, Dose Escalation Part	7	3	0
300 mg Bid, Expansion Part	10	1	0

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AUC Following Single Dosing

(NCT01813474)
Timeframe: Day 1: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48 hours at post-dose

Intervention	μg*h/mL (Geometric Mean)
200 mg Bid, Dose Escalation Part	61.97
300 mg Bid, Dose Escalation Part	46.21

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Cmax Following Multiple Dosing

(NCT01813474)
Timeframe: Day 15: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12 hours at post-dose

Intervention	μg/mL (Geometric Mean)
200 mg Bid, Dose Escalation Part	7.668
300 mg Bid, Dose Escalation Part	8.434

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Tmax Following Single Dosing

(NCT01813474)
Timeframe: Day 1: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48 hours at post-dose

Intervention	hour (Median)
200 mg Bid, Dose Escalation Part	2.00
300 mg Bid, Dose Escalation Part	1.98

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Tmax Following Multiple Dosing

(NCT01813474)
Timeframe: Day 15: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12 hours at post-dose

Intervention	hour (Median)
200 mg Bid, Dose Escalation Part	1.50
300 mg Bid, Dose Escalation Part	3.00

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Number of Participants With Dose Limiting Toxicities

Dose Limiting Toxicities were defined as study specific events that is determined to be possibly or probably related to olaparib (as determined by the investigator) and occurring during the first cycle of treatment (28 days after the first dose), irrespective of whether the toxicity resolved. (NCT01813474)
Timeframe: From the start dose to 28 days after the first dose of study drug

Intervention	Participants (Number)
200 mg Bid, Dose Escalation Part	0
300 mg Bid, Dose Escalation Part	0

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Cmax Following Single Dosing

(NCT01813474)
Timeframe: Day 1: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48 hours at post-dose

Intervention	μg/mL (Geometric Mean)
200 mg Bid, Dose Escalation Part	6.697
300 mg Bid, Dose Escalation Part	7.743

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AUC at Steady State Following Multiple Dosing

(NCT01813474)
Timeframe: Day 15: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12 hours at post-dose

Intervention	μg*h/mL (Geometric Mean)
200 mg Bid, Dose Escalation Part	36.50
300 mg Bid, Dose Escalation Part	52.34

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Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time From Randomization to Study Treatment Discontinuation or Death (TDT)

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of time from randomisation to study treatment discontinuation or death (TDT). Reports results of a pre-specified interim analysis; final analysis results will later be added at time of final OS analysis (anticipated 2029). (NCT01844986)
Timeframe: Time elapsed from randomization to study treatment discontinuation or death. Analysis performed with DCO: 17May2018. Further analyses will be performed at 7 years (descriptive), after 206 events and after 60% maturity.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	24.6
Placebo Tablets (Global Cohort)	13.8
Olaparib 300mg Tablets (China Cohort)	24.8
Placebo Tablets (China Cohort)	8.6

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Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Overall Survival

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of overall survival (OS). Reports results of a pre-specified interim analysis; results for final OS analysis (235 OS events) anticipated 2029. (NCT01844986)
Timeframe: Assessed every 4 weeks until treatment discontinues (up to a max of 156 weeks), then as per protocol. Analysis performed with DCO: 17May2018. Further analyses will be performed at 7 years (descriptive), after 206 events and after 60% maturity.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	NA
Olaparib 300mg Tablets (China Cohort)	NA
Placebo Tablets (China Cohort)	NA

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Change From Baseline in Health-Related Quality of Life (HRQoL) as Assessed by the the Trial Outcome Index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O)

To compare the effects of olaparib maintenance monotherapy compared to placebo on Health-related Quality of Life (HRQoL) as assessed by the trial outcome index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O) in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy. The TOI ranges from 0-100 and a higher score indicates a higher HRQoL. (NCT01844986)
Timeframe: Questionnaires will be given to the patient at baseline, at Day 29 and then every 12 weeks for 156 weeks, then every 24 weeks or until the data cut off for the PFS analysis, change in TOI over 24 months reported

Intervention	Scores on a scale (Least Squares Mean)
Olaparib 300mg Tablets (Global Cohort)	0.30
Placebo Tablets (Global Cohort)	3.30

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Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time to First Subsequent Therapy or Death (TFST)

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of time from randomisation to first subsequent therapy or death (TFST). Reports results of a pre-specified interim analysis; final analysis results will later be added at time of final OS analysis (anticipated 2029). (NCT01844986)
Timeframe: Assessed every 12 weeks following treatment discontinuation. Analysis performed with DCO: 17May2018. Further analyses will be performed at 7 years (descriptive), after 206 events and after 60% maturity.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	51.8
Placebo Tablets (Global Cohort)	15.1
Olaparib 300mg Tablets (China Cohort)	34.3
Placebo Tablets (China Cohort)	10.3

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Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time From Randomization to Second Progression

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	41.9
Olaparib 300mg Tablets (China Cohort)	NA
Placebo Tablets (China Cohort)	NA

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Progression Free Survival (PFS) Using Investigator Assessment According to Modified Response Evaluation Criteria in Solid Tumours (RECIST 1.1)

To determine the efficacy by progression free survival (PFS) using investigator assessment according to modified Response Evaluation Criteria in Solid Tumours (RECIST 1.1) of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy. (NCT01844986)
Timeframe: Radiologic scans performed at baseline then every 12 weeks up to 156 weeks, then every 24 weeks thereafter until objective radiological disease progression. DCO: 17 May 2018

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	13.8
Olaparib 300mg Tablets (China Cohort)	NA
Placebo Tablets (China Cohort)	9.3

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Efficacy in Patients With a Deleterious or Suspected Deleterious Variant in Either of the BRCA Genes by Assessment of PFS

To assess efficacy of olaparib in patients identified as having a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and potential future BRCA mutation assays (gene sequencing and large rearrangement analysis) (NCT01844986)
Timeframe: Radiologic scans performed at baseline then every 12 weeks for the first 156 weeks, then every 24 weeks thereafter, assessed until disease progression. Analysis of data assessed up to a maximum of 54 months.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	13.8

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Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time to Second Subsequent Therapy or Death (TSST)

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of time from randomisation to second subsequent therapy or death (TSST). Reports results of a pre-specified interim analysis; final analysis results will later be added at time of final OS analysis (anticipated 2029). (NCT01844986)
Timeframe: Assessed every 12 weeks following treatment discontinuation. Analysis performed with DCO: 17May2018. Further analyses will be performed at 7 years (descriptive), after 206 events and after 60% maturity.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	40.7
Olaparib 300mg Tablets (China Cohort)	NA
Placebo Tablets (China Cohort)	27.4

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Efficacy in Patients Following First Line Platinum Based Chemotherapy by Assessment of Time to Earliest Progression by RECIST or Cancer Antigen (CA-125) or Death

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of time to earliest progression by RECIST or Cancer Antigen-125 (CA-125) or death (NCT01844986)
Timeframe: CA-125 performed at baseline + every 4 weeks. Radiologic scans performed at baseline + every 12 weeks up to 156 weeks, then every 24 weeks until objective radiological disease progression. DCO:17May2018

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	12.0
Olaparib 300mg Tablets (China Cohort)	NA
Placebo Tablets (China Cohort)	8.9

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Efficacy in Patients With a Deleterious or Suspected Deleterious Variant in Either of the BRCA Genes by Assessment of PFS.

To assess efficacy of olaparib in patients identified as having a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and future BRCA mutation assays (gene sequencing and large rearrangement analysis). (NCT01874353)
Timeframe: Radiologic scans performed at baseline then every ~12 weeks for the first 72 weeks, then every ~24 weeks thereafter, assessed until disease progression. Assessed until 19 Sep 2016 DCO.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	19.3
Placebo Tablets (Global Cohort)	5.5

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Efficacy of Olaparib by Time From Randomization to Study Treatment Discontinuation or Death (TDT)

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	19.4
Placebo Tablets (Global Cohort)	5.6
Olaparib 300mg Tablets (China Cohort)	13.4
Placebo Tablets (China Cohort)	4.7

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Efficacy of Olaparib by Time to First Subsequent Therapy or Death (TFST)

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of time from randomization to first subsequent therapy or death (TFST). (NCT01874353)
Timeframe: Time elapsed from randomization to first subsequent therapy or death. Assessed every 12 weeks following treatment discontinuation. Assessed until 03 Feb 2020 DCO; up to a maximum of 75 months.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	27.4
Placebo Tablets (Global Cohort)	7.2
Olaparib 300mg Tablets (China Cohort)	13.9
Placebo Tablets (China Cohort)	5.5

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Change From Baseline in Health-Related Quality of Life (HRQoL) as Assessed by the the Trial Outcome Index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O)

To compare the effects of olaparib maintenance monotherapy compared to placebo on Health-related Quality of Life (HRQoL) as assessed by the trial outcome index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O) in BRCA mutated relapsed ovarian cancer patients who are in complete or partial response following platinum based chemotherapy. The TOI ranges from 0-100 and a higher score indicates a higher HRQoL. (NCT01874353)
Timeframe: Questionnaires completed by patient at baseline, Day 29 and then every 12 weeks for 12 months. Assessed until 19 Sep 2016 DCO.

Intervention	Change in TOI over 12 months (Least Squares Mean)
Olaparib 300mg Tablets (Global Cohort)	-2.90
Placebo Tablets (Global Cohort)	-2.87

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Efficacy of Olaparib by Time to Second Subsequent Therapy or Death (TSST)

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated high risk advanced ovarian cancer patients who are in clinical complete response or partial response following first line platinum based chemotherapy by assessment of time from randomization to second subsequent therapy or death (TSST). (NCT01874353)
Timeframe: Time elapsed from randomization to second subsequent therapy or death. Assessed every 12 weeks following treatment discontinuation. Assessed until 03 Feb 2020 DCO; up to a maximum of 75 months.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	35.8
Placebo Tablets (Global Cohort)	18.9
Olaparib 300mg Tablets (ChinaCohort)	19.0
Placebo Tablets (China Cohort)	26.4

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Progression Free Survival (PFS) Using Investigator Assessment According to Modified Response Evaluation Criteria In Solid Tumours (RECIST 1.1)

To determine the efficacy by progression free survival (PFS) (using investigator assessment according to modified Response Evaluation Criteria In Solid Tumours (RECIST 1.1)) of olaparib maintenance monotherapy compared to placebo in BRCA mutated relapsed ovarian cancer patients who are in complete or partial response following platinum based chemotherapy. (NCT01874353)
Timeframe: Radiologic scans performed at baseline then every ~12 weeks up to 72 weeks, then every ~ 24 weeks thereafter until objective radiological disease progression. Assessed until 19 Sep 2016 DCO (16 Jan 2017 DCO for China Cohort); up to a maximum of 36 months.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	19.1
Placebo Tablets (Global Cohort)	5.5
Olaparib 300mg Tablets (China Cohort)	13.8
Placebo Tablets (China Cohort)	5.5

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Efficacy in Patients Following Platinum Based Chemotherapy by Assessment of Time to Earliest Progression by RECIST or Cancer Antigen (CA-125) or Death

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated relapsed ovarian cancer patients who are in complete or partial response following platinum based chemotherapy by assessment of time to earliest progression by RECIST or CA-125 or death. (NCT01874353)
Timeframe: CA-125 at baseline then every 4 wks. Radiologic scans at baseline then every ~12 wks up to 72 wks, then every ~ 24 wks until objective radiological disease progression. Assessed until 19Sep2016 DCO (16Jan2017 DCO for China Cohort); up to a max of 36 mths.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	16.9
Placebo Tablets (Global Cohort)	4.9
Olaparib 300mg Tablets (China Cohort)	12.9
Placebo Tablets (China Cohort)	3.7

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Efficacy in Patients Following Platinum Based Chemotherapy by Assessment of Time From Randomization to Second Progression

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated relapsed ovarian cancer patients who are in complete response or partial response following first line platinum based chemotherapy by assessment of time from randomization up to second progression (NCT01874353)
Timeframe: Scans at baseline then every 12 wks for 72 wks, then every 24 wks until first progression. Assessments then per local practice every 12 wks until second progression. Assessed until 19Sep2016 DCO (16Jan2017 DCO for China Cohort); up to a max of 36 mths

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	NA
Placebo Tablets (Global Cohort)	18.4
Olaparib 300mg Tablets (China Cohort)	NA
Placebo Tablets (China Cohort)	17.3

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Efficacy in Patients Following Platinum Based Chemotherapy by Assessment of Overall Survival

To determine the efficacy of olaparib maintenance monotherapy compared to placebo in BRCA mutated relapsed ovarian cancer patients who are in complete or partial response following platinum based chemotherapy by assessment of overall survival (OS). (NCT01874353)
Timeframe: Survival assessed every 4 weeks until treatment discontinues, then every 12 weeks. Assessed until 03 Feb 2020 DCO; up to a maximum of 75 months.

Intervention	Months (Median)
Olaparib 300mg Tablets (Global Cohort)	51.7
Placebo Tablets (Global Cohort)	38.8
Olaparib 300mg Tablets (China Cohort)	41.7
Placebo Tablets (China Cohort)	36.4

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To Determine the Exposure to Olaparib by Pharmacokinetic Analysis

To determine the exposure to olaparib in patients receiving olaparib maintenance monotherapy (NCT01874353)
Timeframe: Pharmacokinetics sampling to be performed in a subset of patients. Sampling times: Day 1 pre-dose & 1 hour; Day 15 pre-dose & 1 hour; Day 29 pre-dose. Assessed until 19 Sep 2016 DCO.

Intervention	mcg/mL (Geometric Mean)
	Day 1 - Pre-dose	Day 1 - 1 hour	Day 15 - Pre-dose	Day 15 - 1 hour	Day 29 - Pre-dose
Olaparib 300mg Tablets	NA	3.26	0.92	5.12	0.94

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Apparent Clearance Following Oral Administration (CL/F)

Summary of Geometric Least Squares (GLS) Means (NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	L/hr (Geometric Least Squares Mean)
Normal Hepatic Function	5.73
Mild Hepatic Impairment	4.98
Moderate Hepatic Impairment	5.33

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Apparent Volume of Distribution (Vz/F)

(NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	L (Geometric Mean)
Normal Hepatic Function	144.0
Mild Hepatic Impairment	119.1
Moderate Hepatic Impairment	105.4

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Area Under the Plasma Concentration Time Curve From Zero to Infinity (AUC)

Summary of Geometric Least Squares (GLS) Mean (NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	μg*h/mL (Geometric Least Squares Mean)
Normal Hepatic Function	52.33
Mild Hepatic Impairment	60.25
Moderate Hepatic Impairment	56.29

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Area Under the Plasma Concentration Time Curve From Zero to the Last Measureable Time Point(AUC 0-t)

Summary of Geometric Least Squares (GLS) Mean for ratio of mild hepatic impairment compared to normal (NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	μg*h/mL (Geometric Least Squares Mean)
Normal Hepatic Function	51.82
Mild Hepatic Impairment	59.64
Moderate Hepatic Function	55.97

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Ratio of Area Under the Plasma Concentration Time Curve From Zero to Infinity (AUC) - Mild vs Normal and Moderate vs Normal

Summary of Ratio of Geometric Least Squares (GLS) Means (NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	ratio (Geometric Least Squares Mean)
GLSMean Ratio of Mild to Normal	1.15
GLSMean Ratio of Moderate to Normal	1.08

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Ratio of Apparent Clearance Following Oral Administration (CL/F)

Intervention	ratio (Geometric Least Squares Mean)
GLSMean Ration of Mild to Normal	0.87
GLSMean Ratio of Moderate to Normal	0.93

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Time to Reach Maximum Plasma Concentration (Tmax)

(NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	h (Median)
Normal Hepatic Function	1.53
Mild Hepatic Impairment	2.05
Moderate Hepatic Impairment	1.54

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Maximum Plasma Concentration (Cmax)

Summary of Geometric Least Squares (GLS) Mean for normal, mild and moderate hepatic impairment (NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	μg/mL (Geometric Least Squares Mean)
Normal Hepatic Function	7.32
Mild Hepatic Impairment	8.25
Moderate Hepatic Function	6.40

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Terminal Half-life (t½)

(NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	h (Geometric Mean)
Normal Hepatic Function	17.41
Mild Hepatic Impairment	16.58
Moderate Hepatic Impairment	13.70

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Ratio of Maximum Plasma Concentration (Cmax) - Mild vs Normal and Moderate vs Normal

Summary of ratio of Geometric Least Squares (GLS) Means (NCT01894243)
Timeframe: Blood samples are collected at pre-dose, 0.25 , 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post olaparib dose in Part A.

Intervention	ratio (Geometric Least Squares Mean)
GLSMean Ratio of Mild to Normal	1.13
GLSMean Ratio of Moderate to Normal	0.87

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Ratio of Area Under the Plasma Concentration Time Curve From Zero to the Last Measureable Time Point(AUC 0-t)

Intervention	ratio (Geometric Least Squares Mean)
GLSMean Ratio of Mild to Normal	1.15
GLSMean Ratio of Moderate to Normal	1.08

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AUC0-t of Olaparib

Area under plasma concentration-time curve from zero to the last measurable time point of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	μg*h/mL (Geometric Mean)
Normal Renal Function	39.97
Mild Renal Impairment	62.80
Moderate Renal Impairment	69.19

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CL/F of Olaparib

Apparent plasma clearance of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	L/hour (Mean)
Normal Renal Function	7.598
Mild Renal Impairment	5.285
Moderate Renal Impairment	4.788

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CL/F of Unbound Olaparib

Calculated from dose divided by free AUC (NCT01894256)
Timeframe: Part A: Day 1, 1 hour post-dose

Intervention	L/hour (Median)
Normal Renal Function	127.7
Mild Renal Impairment	71.41
Moderate Renal Impairment	59.95

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CLR of Olaparib

Renal clearance of olaparib, calculated as the ratio of amount of drug excreted over 24 hours to AUC0-24 (NCT01894256)
Timeframe: Part A: Day 1, 0-12 hours and 12-24 hours post-dose

Intervention	L/hour (Mean)
Normal Renal Function	1.4810
Mild Renal Impairment	0.6137
Moderate Renal Impairment	0.2989

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Free AUC of Olaparib

AUC of unbound olaparib; calculated by multiplying total AUC by estimated protein binding (NCT01894256)
Timeframe: Part A: Day 1, 1 hour post-dose

Intervention	μg*h/mL (Geometric Mean)
Normal Renal Function	2.819
Mild Renal Impairment	4.771
Moderate Renal Impairment	5.590

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Free Cmax of Olaparib

Cmax of unbound olaparib; calculated by multiplying total Cmax value by estimated protein binding (NCT01894256)
Timeframe: Part A: Day 1, 1 hour post-dose

Intervention	μg/mL (Geometric Mean)
Normal Renal Function	0.4604
Mild Renal Impairment	0.5904
Moderate Renal Impairment	0.7296

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Protein Binding of Olaparib

Degree to which olaparib binds to the proteins within blood plasma (NCT01894256)
Timeframe: Part A: Day 1, 1 hour post-dose

Intervention	% plasma (Mean)
Normal Renal Function	7.593
Mild Renal Impairment	6.530
Moderate Renal Impairment	8.022

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t1/2 of Olaparib

Terminal half-life of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	Hours (Mean)
Normal Renal Function	24.26
Mild Renal Impairment	17.45
Moderate Renal Impairment	16.09

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Tmax of Olaparib

Time to reach maximum plasma concentration of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	Hours (Median)
Normal Renal Function	1.99
Mild Renal Impairment	1.55
Moderate Renal Impairment	2.00

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Vz/F of Olaparib

Apparent volume of distribution of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	L (Mean)
Normal Renal Function	283.4
Mild Renal Impairment	131.2
Moderate Renal Impairment	125.7

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Cmax of Olaparib

Maximum plasma drug concentration of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	μg/mL (Geometric Mean)
Normal Renal Function	7.227
Mild Renal Impairment	9.081
Moderate Renal Impairment	9.977

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AUC of Olaparib

Area under plasma concentration-time curve from zero to infinity of olaparib (NCT01894256)
Timeframe: Part A: pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72 and 96 hours post-dose

Intervention	μg*h/mL (Geometric Mean)
Normal Renal Function	43.70
Mild Renal Impairment	70.56
Moderate Renal Impairment	76.44

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Number of Patients Objective Response

Number of patients with objective response. Per RECIST 1.1, complete response (CR) is disappearance of all target lesions since baseline; partial response (PR) is at least a 30% decrease in the sum of the diameters of target lesions. Overall Response = CR + PR. (NCT01924533)
Timeframe: Scans taken at baseline and then follow up assessments taken every 8 weeks up to Week 40 and then every 16 weeks until objective disease progression as defined by RECIST 1.1, assessed up to 3 years

Intervention	participants (Number)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	12
Placebo Tablets bd + Paclitaxel 80 mg/m^2	5

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Progression-Free Survival (PFS)

Time from randomization until the date of objective radiological disease progression according to RECIST (v1.1) or death by any cause in the absence of progression. Objective progression is defined as at least a 20% increase in the sum of the diameters of the target lesions (compared to previous minimum sum) or an overall non-target lesion assessment of progression or a new lesion. (NCT01924533)
Timeframe: Scans taken at baseline and then follow up assessments taken every 8 weeks up to Week 40 and then every 16 weeks until objective disease progression as defined by RECIST 1.1, assessed up to 3 years

Intervention	participants (Number)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	47
Placebo Tablets bd + Paclitaxel 80 mg/m^2	29
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	11
Placebo Tablets bd + Paclitaxel 80 mg/m^2	7

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Duration of Response

Time from the first documentation of CR/PR until the date of progression, or the last evaluable RECIST assessment for patients taht do not progress or progress after two or more missed visits (NCT01924533)
Timeframe: Scans taken at baseline and then follow up assessments taken every 8 weeks up to Week 40 and then every 16 weeks until objective disease progression as defined by RECIST 1.1, assessed up to 3 years

Intervention	days (Median)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	166.0
Placebo Tablets bd + Paclitaxel 80 mg/m^2	64.0
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	171.0
Placebo Tablets bd + Paclitaxel 80 mg/m^2	108.0

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Time to Response

Time from randomization to the first onset of a confirmed objective tumour response (NCT01924533)
Timeframe: Scans taken at baseline and then follow up assessments taken every 8 weeks up to Week 40 and then every 16 weeks until objective disease progression as defined by RECIST 1.1, assessed up to 3 years

Intervention	days (Median)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	57.0
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	57.5
Placebo Tablets bd + Paclitaxel 80 mg/m^2	57.0

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Number of Patients With Deterioration of Health Related Quality of Life (HRQoL) as Assessed by the European Organisation for Research and Treatment of Cancer (EORTC) Quality of Questionnaire Core 30 Item Module (QLQ-C30) Global HRQoL Scale

Number of patients with a clinically important deterioration in the global HRQoL score or death by any cause in the absence of a clincially meaningful symptom deterioration (NCT01924533)
Timeframe: Pre-treatment , Day 29 and then every 4 weeks until discontinuation, assessed up to 3 years

Intervention	participants (Number)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	160
Placebo Tablets bd + Paclitaxel 80 mg/m^2	177
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	29
Placebo Tablets bd + Paclitaxel 80 mg/m^2	33

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Number of Patients With Objective Response.

Intervention	participants (Number)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	44
Placebo Tablets bd + Paclitaxel 80 mg/m^2	28

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Overall Survival

Time from the date of randomization until death due to any cause (NCT01924533)
Timeframe: Survival contact from the date of randomization and then every 8 weeks following objective disease progression and in the 7 days following OS Data Cut off (DCO); Time point(s) at which outcome measure is assessed up to 4 years

Intervention	participants (Number)
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	82
Placebo Tablets bd + Paclitaxel 80 mg/m^2	62
Olaparib 100 mg Tablets bd + Paclitaxel 80 mg/m^2	19
Placebo Tablets bd + Paclitaxel 80 mg/m^2	11

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Part B: Median Best Percentage Change From Baseline in Prostate Specific Antigen (PSA) Levels

"The best percentage change from baseline in PSA levels was determined to assess the anti-tumour activity of olaparib when given in addition to abiraterone, compared with placebo given in addition to abiraterone.~The best percentage change was defined as the biggest reduction in PSA level compared with baseline or smallest increase in the absence of a decrease." (NCT01972217)
Timeframe: From baseline, then every 4 weeks up to Week 52, and then every 12 weeks.

Intervention	Percentage change in PSA level (Median)
Part B: Olaparib + Abiraterone	-54.16
Part B: Placebo + Abiraterone	-49.85

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Part B: Median Overall Survival (OS)

"OS was determined to assess the efficacy of olaparib when given in addition to abiraterone, compared with placebo given in addition to abiraterone.~OS was performed at the time of the analysis of rPFS, and the median OS, calculated using the Kaplan-Meier technique, is presented." (NCT01972217)
Timeframe: From baseline, every 12 weeks up to Week 72, then every 24 weeks up to 24 months.

Intervention	Months (Median)
Part B: Olaparib + Abiraterone	22.7
Part B: Placebo + Abiraterone	20.9

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Part B: Median Radiological Progression-Free Survival (rPFS) Time

"The efficacy of olaparib when given in combination with abiraterone was assessed by rPFS, defined as the time from randomisation to disease progression using Response Evaluation Criteria in Solid Tumours (RECIST) version 1.1 (for soft tissue disease) and Prostate Cancer Working Group 2 (PCWG-2) (for bone disease) criteria, or death.~Progression using RECIST 1.1 criteria was defined as at least 20% increase from baseline in the sum of diameters of target lesions, progression of existing non-target lesions, or the appearance of at least 1 new lesion.~Progression using PCWG-2 criteria was determined if 2 or more new metastatic bone lesions were observed (with a total of at least 4 new lesions since baseline assessment if observed at the 12 week scan, or persistence of or increase in number of lesions if observed after the 12 week scan as determined by a confirmatory scan at least 6 weeks later or at next scheduled visit)." (NCT01972217)
Timeframe: From baseline, every 12 weeks up to Week 72, then every 24 weeks up to 24 months.

Intervention	Months (Median)
Part B: Olaparib + Abiraterone	13.8
Part B: Placebo + Abiraterone	8.2

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Part B: Median Time to Second Progression or Death (PFS2)

The efficacy of olaparib when given in combination with abiraterone was assessed by PFS2, defined by local standard clinical practice and included objective radiological progression by RECIST 1.1 (soft tissue), symptomatic progression, rise in PSA level or death in the absence of overall progression. (NCT01972217)
Timeframe: From randomisation until analysis cut-off date (up to approximately 3 years).

Intervention	Months (Median)
Part B: Olaparib + Abiraterone	23.3
Part B: Placebo + Abiraterone	18.5

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Part B: Percentage of Patients With at Least One Objective Response (Objective Response Rate [ORR])

"The overall radiological ORR was calculated to assess the anti-tumour activity of olaparib in combination with abiraterone, compared with placebo in combination with abiraterone.~The best overall ORR was defined as the percentage of patients with at least 1 visit response of complete response (CR) or partial response (PR) in soft tissue disease assessed by RECIST 1.1 and also bone scan status of non-progressive disease or non-evaluable for their bone scans assessed by PCWG-2.~CR: Disappearance of all target lesions. Reduction of pathological lymph nodes to <10 millimetres.~PR: At least a 30% decrease in the sum of diameters of target lesions from baseline.~The percentage of patients with a response is presented." (NCT01972217)
Timeframe: From baseline, then every 4 weeks up to Week 52, and then every 12 weeks.

Intervention	Percentage of patients (Number)
Part B: Olaparib + Abiraterone	27.3
Part B: Placebo + Abiraterone	31.6

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Part A PK: Abiraterone Cmax,ss

"Following multiple dosing to steady state of abiraterone 1000 mg once daily, the Cohort 2 abiraterone Cmax,ss is presented for abiraterone monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	nanograms per millilitre (ng/mL) (Geometric Mean)
	Abiraterone alone	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	145.8	86.12

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Part A PK: Abiraterone Cmin,ss

"Following multiple dosing to steady state of abiraterone 1000 mg once daily, the Cohort 2 abiraterone Cmin,ss is presented for abiraterone monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	ng/mL (Geometric Mean)
	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	7.983

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Part B: Percentage of Patients Experiencing AEs

"The safety and tolerability of olaparib when given in combination with abiraterone was assessed during Part B of the study. The percentage of patients experiencing AEs, including information on seriousness, severity, study treatment relationship and those leading to discontinuation for all doses of olaparib and for abiraterone are presented.~Severity of AEs was assessed using the NCI Common Terminology CTCAE v4.0. AEs were assigned to a Grade from 1 through 5 as follows:~Grade 1: Mild; Grade 2: Moderate; Grade 3: Severe or medically significant but not immediately life-threatening requiring hospitalisation; Grade 4: Life-threatening consequences; Grade 5: Death related to AE.~'c-r' = causally related. 'discont' = discontinuation. 'ola/pla' = olaparib/placebo." (NCT01972217)
Timeframe: From first dose of study treatment following randomisation in Part B up to 30 days following last dose of study treatment (up to approximately 3 years).

Intervention	Percentage of patients (Number)
	Any AE c-r to ola/pla + abiraterone	Any AE c-r to ola/pla only	Any AE c-r to abiraterone only	Any AE CTCAE Grade 3 or higher	Any AE CTCAE Grade 3 or higher c-r to ola/pla	Any AE CTCAE Grade 3 or higher c-r to abiraterone	Any AE with outcome = death	Any AE with outcome = death c-r to ola/pla	Any AE with outcome = death c-r to abiraterone	Any SAE	Any SAE c-r to ola/pla	Any SAE c-r to abiraterone	Any AE causing discont of ola/pla	Any AE causing discont of treatment c-r to ola/pla	Any AE causing discont treatment c-r abiraterone
Part B: Olaparib + Abiraterone	45.1	18.3	1.4	53.5	23.9	16.9	5.6	1.4	0	35.2	9.9	5.6	29.6	16.9	8.5
Part B: Placebo + Abiraterone	12.7	9.9	7.0	28.2	5.6	1.4	1.4	0	0	19.7	1.4	0	9.9	5.6	1.4

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Part A PK: Abiraterone Cmin,ss

Intervention	ng/mL (Geometric Mean)
	Abiraterone alone	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	8.376	6.358

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Part B: Percentage of Patients With PSA Responses

"The percentages of patients with single visit responses and with confirmed responses are presented to assess the anti-tumour activity of olaparib when given in addition to abiraterone, compared with placebo given in addition to abiraterone.~A single visit response was defined as any post-dose visit PSA level reduced by 50% or more compared with baseline.~A confirmed response was defined as a reduction in PSA level of 50% or more on 2 consecutive occasions at least 4 weeks apart compared with baseline.~Patients may have had more than 1 single visit response or confirmed response but were counted once." (NCT01972217)
Timeframe: From baseline, then every 4 weeks up to Week 24, and then every 12 weeks.

Intervention	Percentage of patients (Number)
	Single visit response	Confirmed response
Part B: Olaparib + Abiraterone	50.7	47.9
Part B: Placebo + Abiraterone	47.9	42.3

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Part A PK Analysis: Olaparib Area Under the Plasma Concentration-Time Curve at Steady State (AUCss)

"Following multiple dosing to steady state of olaparib 300 mg bid, the Cohort 2 olaparib AUCss is presented for olaparib monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	mcg*h/mL (Geometric Mean)
	Olaparib alone	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	45.27	40.83

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Part B: Percentage of Patients With Progression Events or Death (rPFS)

"The efficacy of olaparib when given in combination with abiraterone was assessed by rPFS, defined as the time from randomisation to disease progression using RECIST version 1.1 (for soft tissue disease) and PCWG-2 (for bone disease) criteria, or death.~Progression using RECIST 1.1 criteria was defined as at least 20% increase from baseline in the sum of diameters of target lesions, progression of existing non-target lesions, or the appearance of at least 1 new lesion.~Progression using PCWG-2 criteria was determined if 2 or more new metastatic bone lesions were observed (with a total of at least 4 new lesions since baseline assessment if observed at the 12 week scan, or persistence of or increase in number of lesions if observed after the 12 week scan as determined by a confirmatory scan at least 6 weeks later or at next scheduled visit).~The percentage of patients with progression events is presented overall and according to RECIST 1.1 and/or PCWG-2 criteria, or death." (NCT01972217)
Timeframe: From baseline, every 12 weeks up to Week 72, then every 24 weeks up to 24 months.

Intervention	Percentage of patients (Number)
Part B: Olaparib + Abiraterone	64.8
Part B: Placebo + Abiraterone	76.1

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Median Time to First Subsequent Therapy (TFST) and Median Time to Second Subsequent Therapy (TSST)

"The TFST and TSST were determined to assess the anti-tumour activity of olaparib when given in combination with abiraterone, compared with placebo given in addition to abiraterone.~TFST was defined as the time from randomisation to the earlier of first subsequent anti-cancer therapy start date following study treatment discontinuation, or death.~TSST was defined as the time from randomisation to the earlier of the second subsequent anti-cancer therapy start date following study treatment discontinuation, or death." (NCT01972217)
Timeframe: From randomisation until analysis cut-off date (up to approximately 3 years).

Intervention	Months (Median)
	TFST	TSST
Part B: Olaparib + Abiraterone	13.5	19.6
Part B: Placebo + Abiraterone	9.7	18.0

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Part A Pharmacokinetics (PK): Olaparib Maximum Plasma Concentration at Steady State (Cmax,ss)

"Following multiple dosing to steady state of olaparib 300 mg bid, the Cohort 2 olaparib Cmax,ss is presented for olaparib monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	micrograms per millilitre (mcg/mL) (Geometric Mean)
	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	7.724

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Part A Pharmacokinetics (PK): Olaparib Maximum Plasma Concentration at Steady State (Cmax,ss)

Intervention	micrograms per millilitre (mcg/mL) (Geometric Mean)
	Olaparib alone	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	7.781	6.504

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Part A PK: Abiraterone Cmax,ss

Intervention	nanograms per millilitre (ng/mL) (Geometric Mean)
	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	130.7

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Part A PK: Abiraterone AUCss

"Following multiple dosing to steady state of abiraterone 1000 mg once daily, the Cohort 2 abiraterone AUCss is presented for abiraterone monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	ng*h/mL (Geometric Mean)
	Abiraterone alone	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	825.5	524.6

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Part A PK: Abiraterone AUCss

Intervention	ng*h/mL (Geometric Mean)
	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	718.9

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Part A PK Analysis: Olaparib Time to Reach Maximum Plasma Concentration at Steady State (Tmax,ss)

"Following multiple dosing to steady state of olaparib 300 mg bid, the Cohort 2 olaparib tmax,ss is presented for olaparib monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	Hours (h) (Median)
	Olaparib alone	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	2.000	2.080

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Part A PK Analysis: Olaparib Time to Reach Maximum Plasma Concentration at Steady State (Tmax,ss)

Intervention	Hours (h) (Median)
	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	2.000

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Part A PK Analysis: Olaparib Minimum Plasma Concentration at Steady State (Cmin,ss)

"Following multiple dosing to steady state of olaparib 300 mg bid, the Cohort 2 olaparib Cmin,ss is presented for olaparib monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	mcg/mL (Geometric Mean)
	Olaparib alone	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	1.264	0.9170

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Part A PK Analysis: Olaparib Minimum Plasma Concentration at Steady State (Cmin,ss)

Intervention	mcg/mL (Geometric Mean)
	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	1.279

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Part A PK: Abiraterone Tmax,ss

"Following multiple dosing to steady state of abiraterone 1000 mg once daily, the Cohort 2 abiraterone tmax,ss is presented for abiraterone monotherapy and for olaparib given in combination with abiraterone.~Only patients with data available for analysis at each time point are presented." (NCT01972217)
Timeframe: PK sampling for Cohort 2 Group 1 was between Days 3 and 7 for olaparib, and Days 4 and 8 for olaparib and abiraterone. PK sampling for Cohort 2 Group 2 was between Days 5 and 7 for abiraterone, and Days 6 and 8 for olaparib and abiraterone.

Intervention	Hours (Median)
	Olaparib + abiraterone
Part A Cohort 2 Group 1: Olaparib, Olaparib + Abiraterone	3.000

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Part A PK: Abiraterone Tmax,ss

Intervention	Hours (Median)
	Abiraterone alone	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	2.525	2.500

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Part A: Percentage of Patients Experiencing Adverse Events (AEs)

"The safety and tolerability of olaparib in combination with abiraterone was assessed during Part A of the study. The percentage of patients experiencing AEs, including information on seriousness, severity, study treatment relationship and those leading to discontinuation for all doses of olaparib and for abiraterone are presented.~Severity of AEs was assessed using the National Cancer Institute (NCI) Common Terminology Criteria for Adverse events (CTCAE) v4.0. AEs were assigned to a Grade from 1 through 5 as follows:~Grade 1: Mild; Grade 2: Moderate; Grade 3: Severe or medically significant but not immediately life-threatening requiring hospitalisation; Grade 4: Life-threatening consequences; Grade 5: Death related to AE.~'c-r' = causally related 'discont' = discontinuation." (NCT01972217)
Timeframe: Cohort 1 and 2: From baseline in Part A (Day 1 for each cohort) up to 30 days following last dose of study treatment.

Intervention	Percentage of patients (Number)
	Any AE c-r to olaparib + abiraterone	Any AE c-r to olaparib only	Any AE c-r to abiraterone only	Any AE CTCAE Grade 3 or higher	Any AE CTCAE Grade 3 or higher c-r to olaparib	Any AE CTCAE Grade 3 or higher c-r to abiraterone	Any AE with outcome = death	Any serious AE (SAE)	Any SAE c-r to olaparib	Any SAE c-r to abiraterone	Any AE causing discont of olaparib	Any AE causing discont of olaparib c-r to olaparib	Any AE causing discont olaparib c-r to abiraterone
Part A Cohort 1: Olaparib 200 mg + Abiraterone	66.7	33.3	0	66.7	0	0	0	66.7	0	0	0	0	0
Part A Cohort 2: Olaparib 300 mg + Abiraterone	46.2	7.7	15.4	23.1	7.7	7.7	0	23.1	0	0	7.7	0	0

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Part A PK Analysis: Olaparib Area Under the Plasma Concentration-Time Curve at Steady State (AUCss)

Intervention	mcg*h/mL (Geometric Mean)
	Olaparib + abiraterone
Part A Cohort 2 Group 2: Abiraterone, Olaparib + Abiraterone	49.51

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Part B: Median Best Percentage Change From Baseline in Circulating Tumour Cell (CTC) Level

"The median best percentage change from baseline in CTC levels was determined to assess the anti-tumour activity of olaparib when given in combination with abiraterone, compared with placebo given in addition to abiraterone.~The best percentage change was defined as the biggest CTC level reduction compared with baseline or smallest increase in the absence of a decrease." (NCT01972217)
Timeframe: From baseline, then every 4 weeks up to Week 24, and then every 12 weeks.

Intervention	Percentage change in CTC level (Median)
Part B: Olaparib + Abiraterone	-1.0
Part B: Placebo + Abiraterone	-1.0

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Part A: Number of Patients With Dose Limiting Toxicities (DLTs)

"DLTs were assessed by a Safety Review Committee (SRC) after a minimum of 3 patients had received at least 14 days of treatment in Part A.~A DLT was defined as any toxicity which was not a recognised AE of abiraterone or prednisolone, and was not attributable to the disease or disease-related processes under investigation, which occurred during a minimum period of 14 days treatment and which included: 1. haematological toxicity CTCAE v4.0 Grade 4 or higher present for more than 4 days (except anaemia); 2. non-haematological toxicity CTCAE v4.0 Grade 3 or higher including infection, corrected QT interval prolongation; 3. any other toxicity that was greater than that at baseline, was clinically significant and/or unacceptable, did not respond to supportive care, resulted in a disruption of dosing schedule of 7 days or more, or was judged to be a DLT by the SRC.~A DLT excluded alopecia and isolated laboratory changes of any grade without clinical sequelae or clinical significance." (NCT01972217)
Timeframe: From Day 1 for Cohort 1 and from Day 4 for Cohort 2 up to 14 days treatment with olaparib + abiraterone for 3 patients.

Intervention	Patients (Number)
Part A Cohort 1: Olaparib 200 mg + Abiraterone	2
Part A Cohort 2: Olaparib 300 mg + Abiraterone	4

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Time to First Subsequent Cancer Therapy or Death (TFST) at Extended OS

Time from randomisation to the earliest of first subsequent cancer therapy start date following study treatment discontinuation, or death. (NCT02000622)
Timeframe: Subsequent cancer therapy status reviewed every 8 weeks following study treatment discontinuation until Sep 2017 (final OS DCO), then every 3 months. Assessed up to a maximum of 64 months.

Intervention	Months (Median)
Olaparib 300 mg bd	9.4
Chemotherapy	4.3

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Overall Survival (OS) at Final OS

Time from randomisation until death due to any cause. (NCT02000622)
Timeframe: Survival status reviewed every 3 weeks until treatment discontinued, then every 8 weeks. Assessed up to a maximum of 40 months.

Intervention	Months (Median)
Olaparib 300 mg bd	19.3
Chemotherapy	17.1

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Adjusted Mean Change in Global Health Status/Quality of Life (QoL) Score From the European Organisation for Research and Treatment of Cancer - Quality of Life Questionnaire (EORTC QLQ-C30)

Change from baseline in global health status/quality of life (QoL) score assessed using a mixed model for repeated measures (MMRM) analysis, including all post-baseline global health status/QoL scores up to the latest scheduled visit where at least 20 patients on each treatment arm have a score. Global health status/QoL score is on a scale from 0 to 100. A higher score represents an improved health status/QoL. (NCT02000622)
Timeframe: EORTC QLQ-C30 assessments performed at baseline then every ~6 weeks until objective radiological disease progression. Assessed up to a maximum of 30 months.

Intervention	Score on a scale (Mean)
Olaparib 300 mg bd	3.9
Chemotherapy	-3.6

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Time to Second Subsequent Cancer Therapy or Death (TSST) at Extended OS

Time from randomisation to the earliest of second subsequent cancer therapy start date following study treatment discontinuation, or death. (NCT02000622)
Timeframe: Subsequent cancer therapy status reviewed every 8 weeks following study treatment discontinuation until Sep 2017 (final OS DCO), then every 3 months. Assessed up to a maximum of 64 months.

Intervention	Months (Median)
Olaparib 300 mg bd	14.3
Chemotherapy	10.5

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Time to Second Subsequent Cancer Therapy or Death (TSST)

Intervention	Months (Median)
Olaparib 300 mg bd	14.3
Chemotherapy	10.5

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Time to Second Progression or Death (PFS2)

Time from randomisation to the earliest of the progression event subsequent to the first objective radiological progression, or death. Second progression may involve any of; objective radiological or symptomatic progression or death. Objective radiological progression is defined using Response Evaluation Criteria In Solid Tumours (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. Symptomatic progression is assessed by investigators based on clinical examination. (NCT02000622)
Timeframe: Second progression status reviewed every 8 weeks following the first objective radiological progression as per investigator assessment. Assessed up to a maximum of 30 months.

Intervention	Months (Median)
Olaparib 300 mg bd	13.2
Chemotherapy	9.3

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Objective Response Rate (ORR) Using Blinded Independent Central Review (BICR) Data Assessed by Modified Response Evaluation Criteria In Solid Tumours (RECIST v1.1)

Number of responders according to blinded independent central review (BICR) assessment. Per Response Evaluation Criteria In Solid Tumours Criteria (RECIST v1.1) for target lesions assessed by CT or MRI: Complete Response (CR) is defined as the disappearance of all target lesions; Partial Response (PR) is defined as >=30% decrease in the sum of the longest diameter of target lesions; Overall Response = CR + PR. (NCT02000622)
Timeframe: Radiological scans performed at baseline then every ~6 weeks up to 24 weeks, then every ~ 12 weeks thereafter until objective radiological disease progression. Assessed up to a maximum of 30 months.

Intervention	Participants (Number)
Olaparib 300 mg bd	100
Chemotherapy	19

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Progression-free Survival (PFS) Using Blinded Independent Central Review (BICR) According to Modified Response Evaluation Criteria In Solid Tumours (RECIST v1.1) in Patients Confirmed as Myriad CDx gBRCAm

Time from randomisation to the earliest of objective radiological progression or death by any cause in the absence of objective progression. Objective radiological progression is defined using Response Evaluation Criteria In Solid Tumours Criteria (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. Assessed in patients with a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and future BRCA mutation assays (gene sequencing and large rearrangement analysis). (NCT02000622)
Timeframe: Radiological scans performed at baseline then every ~6 weeks up to 24 weeks, then every ~ 12 weeks thereafter until objective radiological disease progression. Assessed up to a maximum of 30 months.

Intervention	Months (Median)
Olaparib 300 mg bd	7.4
Chemotherapy	4.2

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Time to First Subsequent Cancer Therapy or Death (TFST)

Intervention	Months (Median)
Olaparib 300 mg bd	9.4
Chemotherapy	4.2

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Overall Survival (OS)

Intervention	Months (Median)
Olaparib 300 mg bd	19.3
Chemotherapy	19.6

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Overall Survival (OS) at Extended OS

Time from randomisation until death due to any cause. (NCT02000622)
Timeframe: Survival status reviewed every 3 weeks until treatment discontinued, then every 8 weeks until Sep 2017 (final OS DCO), then every 3 months. Assessed up to a maximum of 64 months.

Intervention	Months (Median)
Olaparib 300 mg bd	19.3
Chemotherapy	17.1

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Progression-free Survival (PFS) Using Blinded Independent Central Review (BICR) According to Modified Response Evaluation Criteria In Solid Tumours (RECIST v1.1)

Time from randomisation to the earliest of objective radiological progression or death by any cause in the absence of objective progression. Objective radiological progression is defined using Response Evaluation Criteria In Solid Tumours (RECIST v1.1), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT02000622)
Timeframe: Radiological scans performed at baseline then every ~6 weeks up to 24 weeks, then every ~ 12 weeks thereafter until objective radiological disease progression. Assessed up to a maximum of 30 months.

Intervention	Months (Median)
Olaparib 300 mg bd	7.0
Chemotherapy	4.2

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Change From Baseline for EORTC QLQ-C30 (European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core Questions 30) Scores for Participants Who Completed Neoadjuvant Chemotherapy

Change from baseline for EORTC QLQ-C30 Global health status QOL (Quality of Life) Score at 6, 12, 18 and 24 months for patients who completed neoadjuvant chemotherapy. Adjusted least-square mean changes and 95% CI are obtained from mixed model for repeated measures (MMRM) analysis of the change from baseline. Only patients with evaluable baseline forms are included. EORTC QLQ-C30 scores range from 0 to 100 with higher score indicating better quality of life. (NCT02032823)
Timeframe: 6, 12, 18 and 24 months after randomisation (data cut off: 12 July 2021)

Intervention	Scores on a scale (Mean)
	Change from baseline EORTC QLQ-C30 Global health status score to 6 months	Change from baseline EORTC QLQ-C30 Global health status score to 12 months	Change from baseline EORTC QLQ-C30 Global health status score to 18 months	Change from baseline EORTC QLQ-C30 Global health status score to 24 months
Olaparib	-0.4	0.5	3.3	2.8
Placebo	0.4	2.7	4.4	6.1

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Change From Baseline for FACIT-Fatigue (Functional Assessment of Chronic Illness Therapy-Fatigue) Score for Participants Who Completed Adjuvant Chemotherapy

Change from baseline for FACIT-Fatigue Score at 6, 12, 18 and 24 months for patients who completed adjuvant chemotherapy. Adjusted least-square mean changes and 95% CI are obtained from mixed model for repeated measures (MMRM) analysis of the change from baseline. Only patients with evaluable baseline forms are included. FACIT-Fatigue score ranges from 0 to 52 with higher score indicating less fatigue. (NCT02032823)
Timeframe: 6, 12, 18 and 24 months after randomisation (data cut off: 12 July 2021)

Intervention	Scores on a scale (Mean)
	Change from baseline FACIT-Fatigue Score to 6 months	Change from baseline FACIT-Fatigue Score to 12 months	Change from baseline FACIT-Fatigue Score to 18 months	Change from baseline FACIT-Fatigue Score to 24 months
Olaparib	-0.7	-0.8	0.9	1.3
Placebo	0.6	0.5	1.2	1.6

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Change From Baseline for FACIT-Fatigue (Functional Assessment of Chronic Illness Therapy-Fatigue) Score for Participants Who Completed Neoadjuvant Chemotherapy

Change from baseline for FACIT-Fatigue Score at 6, 12, 18 and 24 months for patients who completed neoadjuvant chemotherapy. Adjusted least-square mean changes and 95% Confidence Interval (CI) are obtained from mixed model for repeated measures (MMRM) analysis of the change from baseline. Only patients with evaluable baseline forms are included. FACIT-Fatigue score ranges from 0 to 52 with higher score indicating less fatigue. (NCT02032823)
Timeframe: 6, 12, 18 and 24 months after randomisation (data cut off: 12 July 2021)

Intervention	Scores on a scale (Mean)
	Change from baseline FACIT-Fatigue Score to 6 months	Change from baseline FACIT-Fatigue Score to 12 months	Change from baseline FACIT-Fatigue Score to 18 months	Change from baseline FACIT-Fatigue Score to 24 months
Olaparib	-1.5	-1.5	1.3	1.6
Placebo	-0.2	0.0	1.4	2.0

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Distant Disease Free Survival (DDFS)

A DDFS event is defined as documented evidence of first distant recurrence of breast cancer or death from any cause (NCT02032823)
Timeframe: From date of randomisation to data cut off: 27 March 2020 (approximately 5 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib	89
Placebo	152

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Invasive Disease Free Survival (IDFS)

An IDFS event is defined as the first occurrence of loco-regional or distant recurrence or new cancer or death from any cause. (NCT02032823)
Timeframe: From date of randomisation to data cut off: 27 March 2020 (approximately 5 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib	106
Placebo	178

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Overall Survival (OS)

An OS event is defined as death by any cause. (NCT02032823)
Timeframe: From date of randomisation to data cut off: 12 July 2021 (approximately 7 years 3 months)

Intervention	Participants (Count of Participants)
Olaparib	75
Placebo	109

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Number of Participants With Contralateral Invasive and Non-invasive Breast Cancer, New Primary Ovarian Cancer, New Primary Fallopian Tube Cancer and New Primary Peritoneal Cancer

Number of patients with contralateral invasive breast cancer, contralateral non-invasive breast cancer, new primary ovarian cancer, new primary fallopian tube cancer and new primary peritoneal cancer. Analysis of contralateral breast cancers exclude patients with a bilateral mastectomy prior to randomisation. Analysis of new primary ovarian cancers excludes male patients and patients with a bilateral oophorectomy prior to randomisation. Analysis of new primary fallopian tube cancer excludes male patients and patients with a bilateral salpingectomy prior to randomisation. Analysis of new primary peritoneal cancers excludes male patients. (NCT02032823)
Timeframe: From date of randomisation to data cut off: 12 July 2021 (approximately 7 years 3 months)

Intervention	Participants (Count of Participants)
	Contralateral invasive breast cancer	Contralateral non-invasive breast cancer	New primary ovarian cancer	New primary fallopian tube cancer	New primary peritoneal cancer
Olaparib	19	2	1	1	0
Placebo	21	4	5	4	0

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Change From Baseline for EORTC QLQ-C30 (European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core Questions 30) Scores for Participants Who Completed Adjuvant Chemotherapy

Change from baseline for EORTC QLQ-C30 Global health status QOL (Quality of Life) Score at 6, 12, 18 and 24 months for patients who completed adjuvant chemotherapy. Adjusted least-square mean changes and 95% CI are obtained from mixed model for repeated measures (MMRM) analysis of the change from baseline. Only patients with evaluable baseline forms are included. EORTC QLQ-C30 scores range from 0 to 100 with higher score indicating better quality of life. (NCT02032823)
Timeframe: 6, 12, 18 and 24 months after randomisation (data cut off: 12 July 2021)

Intervention	Scores on a scale (Mean)
	Change from baseline EORTC QLQ-C30 Global health status score to 6 months	Change from baseline EORTC QLQ-C30 Global health status score to 12 months	Change from baseline EORTC QLQ-C30 Global health status score to 18 months	Change from baseline EORTC QLQ-C30 Global health status score to 24 months
Olaparib	-0.5	0.6	2.9	4.5
Placebo	2.2	3.1	5.1	4.8

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Effect of Tamoxifen on Exposure to Olaparib - Cmax ss

Olaparib Cmax ss in the presence and absence of co-administered tamoxifen, and associated Cmax ss treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 hours post morning dose on Day 5 and Day 31

Intervention	mcg/mL (Geometric Mean)
Cohort 1 - Olaparib (Treatment Period 1)	9.456
Cohort 1 - Olaparib + Tamoxifen (Treatment Period 3)	7.216

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Effect of Tamoxifen on Exposure to Olaparib - AUC0-τ

Olaparib AUC0-τ, in the presence and absence of co-administered tamoxifen, and associated AUC0-τ treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 hours post morning dose on Day 5 and Day 31

Intervention	mcg*h/mL (Geometric Mean)
Cohort 1 - Olaparib (Treatment Period 1)	62.12
Cohort 1 - Olaparib + Tamoxifen (Treatment Period 3)	42.27

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Effect of Olaparib on Exposure to Letrozole - Cmax ss

Letrozole Cmax ss in the presence and absence of co-administered olaparib, and associated Cmax ss treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 1, 2, 4, 6, 8, 12 and 24 hours post-dose on Day 38 and Day 43

Intervention	mcg/mL (Geometric Mean)
Cohort 3 - Letrozole Alone (Treatment Period 2)	118.9
Cohort 3 - Olaparib + Letrozole (Treatment Period 3)	111.8

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Effect of Olaparib on Exposure to Tamoxifen - AUC0-τ

Tamoxifen, N-DMT and endoxifen AUC0-τ, in the presence and absence of co-administered olaparib, and associated AUC0-τ treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 1, 2, 4, 5, 6, 8, 12 and 24 hours post-dose on Day 26 and Day 31

Intervention	microgram x hour/millilitre (mcg*h/mL) (Geometric Mean)
	PK analysis of tamoxifen	PK analysis of N-DMT	PK analysis of endoxifen
Cohort 1 - Olaparib + Tamoxifen (Treatment Period 3)	2751	2955	115.8
Cohort 1 - Tamoxifen Alone (Treatment Period 2)	2233	3189	119.3

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Effect of Olaparib on Exposure to Tamoxifen - Cmax ss

Tamoxifen, N-desmethyl tamoxifen (N-DMT) and endoxifen Cmax ss in the presence and absence of co-administered olaparib, and associated Cmax ss treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 1, 2, 4, 5, 6, 8, 12 and 24 hours post-dose on Day 26 and Day 31

Intervention	mcg/mL (Geometric Mean)
	PK analysis of tamoxifen	PK analysis of N-DMT	PK analysis of endoxifen
Cohort 1 - Olaparib + Tamoxifen (Treatment Period 3)	154.2	149.1	5.727
Cohort 1 - Tamoxifen Alone (Treatment Period 2)	130.3	162.9	5.923

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Effect of Olaparib on Exposure to Letrozole - AUC0-τ

Letrozole AUC0-τ, in the presence and absence of co-administered olaparib, and associated AUC0-τ treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 1, 2, 4, 6, 8, 12 and 24 hours post-dose on Day 38 and Day 43

Intervention	mcg*h/mL (Geometric Mean)
Cohort 3 - Letrozole Alone (Treatment Period 2)	2292
Cohort 3 - Olaparib + Letrozole (Treatment Period 3)	2167

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Effect of Olaparib on Exposure to Anastrozole - Cmax ss

Anastrozole maximum plasma concentration at steady state (Cmax ss) in the presence and absence of co-administered olaparib, and associated Cmax ss treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 1, 2, 4, 6, 8, 12 and 24 hours post-dose on Day 19 and Day 24

Intervention	micrograms per millilitre (mcg/mL) (Geometric Mean)
Cohort 2 - Anastrozole Alone (Treatment Period 2)	40.98
Cohort 2 - Olaparib + Anastrozole (Treatment Period 3)	35.83

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Effect of Olaparib on Exposure to Anastrozole - AUC0-τ

Anastrozole Area under plasma concentration-time curve over the dosing interval at steady state (AUC0-τ), in the presence and absence of co-administered olaparib, and associated AUC0-τ treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 1, 2, 4, 6, 8, 12 and 24 hours post-dose on Day 19 and Day 24

Intervention	mcg*h/mL (Geometric Mean)
Cohort 2 - Anastrozole Alone (Treatment Period 2)	696.8
Cohort 2 - Olaparib + Anastrozole (Treatment Period 3)	582.5

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Effect of Letrozole on Exposure to Olaparib - Cmax ss

Olaparib Cmax ss in the presence and absence of co-administered letrozole, and associated Cmax ss treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 hours post morning dose on Day 5 and Day 43

Intervention	mcg/mL (Geometric Mean)
Cohort 3 - Olaparib (Treatment Period 1)	10.05
Cohort 3 - Olaparib + Letrozole (Treatment Period 3)	10.48

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Effect of Letrozole on Exposure to Olaparib - AUC0-τ

Olaparib AUC0-τ, in the presence and absence of co-administered letrozole, and associated AUC0-τ treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 hours post morning dose on Day 5 and Day 43

Intervention	mcg*h/mL (Geometric Mean)
Cohort 3 - Olaparib (Treatment Period 1)	61.77
Cohort 3 - Olaparib + Letrozole (Treatment Period 3)	67.82

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Effect of Anastrozole on Exposure to Olaparib - AUC0-τ

Olaparib AUC0-τ, in the presence and absence of co-administered anastrozole, and associated AUC0-τ treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 hours post morning dose on Day 5 and Day 24

Intervention	mcg*h/mL (Geometric Mean)
Cohort 2 - Olaparib (Treatment Period 1)	55.49
Cohort 2 - Olaparib + Anastrozole (Treatment Period 3)	44.33

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Effect of Anastrozole on Exposure to Olaparib - Cmax ss

Olaparib Cmax ss in the presence and absence of co-administered anastrozole, and associated Cmax ss treatment ratios (NCT02093351)
Timeframe: Pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 hours post morning dose on Day 5 and Day 24

Intervention	mcg/mL (Geometric Mean)
Cohort 2 - Olaparib (Treatment Period 1)	9.490
Cohort 2 - Olaparib + Anastrozole (Treatment Period 3)	8.256

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Adjusted Mean Change From Baseline up to 6 Months in Global Quality of Life (QoL) Score From the EORTC-QLQ-C30 Questionnaire

"To assess the effect of olaparib on health-related quality of life (QoL) as measured by the EORTC-QLQ-C30 global QoL scale. The EORTC-QLQ-C30 is defined as EORTC QLQ-C30: a questionnaire (30 questions) used to evaluate disease symptoms, functional impacts (eg, physical functioning), and HRQoL and to characterize clinical benefit from the patient perspective. The HRQoL score ranges from 0 to 100.~A higher score indicates better QoL. A score change of 10 points was pre-defined as clinically meaningful.~bd twice daily." (NCT02184195)
Timeframe: From baseline up to 6 months

Intervention	Unit on scale (Mean)
Olaparib 300 mg Twice Daily (bd)	-1.03
Placebo	1.18

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Number of Participants With Objective Response Rate (ORR) by BICR Using Modified RECIST 1.1

To determine efficacy by assessment of objective response rate according to modified RECIST 1.1 of olaparib maintenance monotherapy compared to placebo. The ORR is defined as the number of with a BoR of CR and PR according to the BICR data divided by the number of patients in the treatment group with measurable disease at baseline. (NCT02184195)
Timeframe: Up to 4 years

Intervention	Participants (Count of Participants)
Olaparib 300 mg Twice Daily (bd)	22
Placebo	11

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Overall Survival (OS)

To determine the efficacy by assessment of OS of olaparib maintenance monotherapy compared to placebo. The OS was defined as the time from the date of randomization until death due to any cause. (NCT02184195)
Timeframe: Upto 4 years

Intervention	Months (Median)
Olaparib 300 mg Twice Daily (bd)	19.0
Placebo	19.2

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Progression-free Survival (PFS) by Blinded Independent Central Review (BICR) Using Modified Response Evaluation Criteria in Solid Tumours. This Study Used Modified RECIST Version (v) 1.1 (RECIST v1.1)

To determine the efficacy of olaparib maintenance monotherapy compared to placebo by PFS. The PFS was defined as the time from randomisation until the date of objective radiological disease progression according to modified RECIST v1.1 or death (by any cause in the absence of disease progression) regardless of whether the patient withdrew from randomized therapy or received another anticancer therapy prior to disease progression. (NCT02184195)
Timeframe: Up to 4 years

Intervention	Months (Median)
Olaparib 300 mg Twice Daily (bd)	7.4
Placebo	3.8

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Time From Randomisation to First Subsequent Therapy or Death (TFST)

To determine the efficacy by assessment of TFST of olaparib maintenance monotherapy compared to placebo. The TFST was defined as time to first subsequent therapy or death. (NCT02184195)
Timeframe: Up to 4 years

Intervention	Months (Median)
Olaparib 300 mg Twice Daily (bd)	9.0
Placebo	5.4

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Time From Randomisation to Second Progression (PFS2)

To determine efficacy by assessment of PFS2 of olaparib maintenance monotherapy compared to placebo. The PFS2 was defined as the time from the date of randomisation to the earliest of the progression event subsequent to that used for the primary variable PFS or death. (NCT02184195)
Timeframe: Up to 4 years

Intervention	Months (Median)
Olaparib 300 mg Twice Daily (bd)	16.9
Placebo	9.3

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Time From Randomisation to Second Subsequent Therapy or Death (TSST)

To determine the efficacy by assessment of TSST of olaparib maintenance monotherapy compared to placebo. The TSST was defined as time to second subsequent therapy or death. (NCT02184195)
Timeframe: Up to 4 years

Intervention	Months (Median)
Olaparib 300 mg Twice Daily (bd)	14.9
Placebo	9.6

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Time From Randomisation to Study Treatment Discontinuation or Death (TDT)

To determine the efficacy by assessment of TDT compared to placebo. compared to placebo. The TDT was defined as time to study treatment discontinuation or death. (NCT02184195)
Timeframe: Up to 4 years

Intervention	Months (Median)
Olaparib 300 mg Twice Daily (bd)	7.5
Placebo	3.8

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Disease Control Rate (DCR) by BICR Using Modified RECIST 1.1

Efficacy by assessment of disease control rate according to modified RECIST 1.1 of olaparib maintenance monotherapy compared to placebo. (NCT02184195)
Timeframe: At 16 weeks

Intervention	Participants (Number)
	Yes	No	Not evaluable/missing
Olaparib 300 mg Twice Daily (bd)	51	34	7
Placebo	24	34	4

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Number of Participants With Adverse Events (AEs)

To assess the safety and tolerability of olaparib maintenance monotherapy. SAE: serious adverse events CTCAE: Common Terminology Criteria for Adverse Events (NCT02184195)
Timeframe: Up to 4 years

Intervention	Participants (Number)
	Any AE	Any AE of CTCAE Grade 3 or higher	Any AE with outcome = death	Any SAE (including events with outcome = death)	AnyAE leading to withdrawal of olaparib/placebo	Any AE leading to dose interruption	Any AE leading to dose reduction
Olaparib 300 mg Twice Daily (bd)	89	44	1	28	8	38	16
Placebo	56	15	0	10	1	4	3

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Time From Randomization To First Subsequent Therapy Or Death (TFST)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by time from randomisation to first subsequent therapy or death (TFST)~TFST is defined as the time from the date of randomisation to the earlier of first subsequent chemotherapy start date or death.~Anti-cancer treatments include chemotherapy and targeted agents." (NCT02282020)
Timeframe: Anti-cancer treatments initiated post discontinuation of study treatment and investigator's opinion of response and date of progression recorded, assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Months (Median)
Olaparib 300 mg BID	15.4
Single Agent Chemotherapy	10.9

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Objective Response Rate (ORR)

"To determine the efficacy of olaparib vs. physician's choice single agent chemotherapy by assessment of Objective Response Rate (ORR) using blinded independent central review (BICR)~Response Evaluation Criteria In Solid Tumors (RECIST) 1.1 criteria was used by a Blinded Independent Central Review (BICR) to assess participant response to treatment~ORR is the number of participants with Complete Response (CR) or Partial Response (PR) in the Measurable Disease Analysis Set (MDAS). Complete response is declared when all lesions have disappeared or all lesions have disappeared and all nodal disease is < 10 mm each. Partial response is declared when there is a decrease in sum of diameters of target lesions ≥ 30%." (NCT02282020)
Timeframe: RECIST follow-up assessments performed every 8 weeks (±1 week), up to 48 weeks, then every 12 weeks (±1 week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	109
Single Agent Chemotherapy	37

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Duration of Response (DoR)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by duration of response (DoR) by BICR using RECIST 1.1 criteria for evaluable patients.~Duration of response is the time from the first documentation of complete response (CR) or partial response (PR) until the date of progression or death, or the last evaluable RECIST assessment for participants that do not progress or progress after 2 missed assessments. Response Evaluation Criteria In Solid Tumors (RECIST) 1.1 criteria was used to assess participant response to treatment." (NCT02282020)
Timeframe: RECIST follow-up assessments performed every 8 weeks (±1 week), up to 48 weeks, then every 12 weeks (±1 week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Months (Median)
Olaparib 300 mg BID	9.4
Single Agent Chemotherapy	10.2

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Mean Change From Baseline In Trial Outcome Index (TOI) Score

"To compare the efficacy of single agent olaparib versus physician's choice single agent chemotherapy on the Health-related Quality of Life (HRQoL) as measured by the trial outcome index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O)~The TOI score was derived from the sum of the scores of the 25 items included in the physical well-being (7 items), functional well-being (7 items), and additional concerns ovarian cancer subscale (11 items) of the FACT-O questionnaire Version 4. TOI score ranges from 0 to 100, a higher score indicates a higher HRQoL. A negative change in score from baseline indicated a worsening in symptoms." (NCT02282020)
Timeframe: Baseline (Day 1) to Week 48 (±1 week). DCO: 10Oct2018

Intervention	Scores on a scale (Mean)
Olaparib 300 mg BID	-2.4
Selected Chemotherapy	-3.6

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Number of Participants Who Discontinued Study Treatment or Died in BRCA Gene Population

BRCA gene population includes participants identified as having a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and future BRCA mutation assays (eg, gene sequencing and large rearrangement analysis). (NCT02282020)
Timeframe: Patients randomised to Olaparib administer their tablets orally at a dose of 300 mg twice daily and continue Olaparib until objective disease progression. Assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	151
Single Agent Chemotherapy	76

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Number of Participants Who Experience at Least One Adverse Event (AE)

An AE is the development of an undesirable medical condition or the deterioration of a pre-existing medical condition following or during exposure to a pharmaceutical product, whether or not considered causally related to the product. (NCT02282020)
Timeframe: Safety Follow-up 30 days after last dose of IP, assessed from the date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	175
Single Agent Chemotherapy	73

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Number of Participants Who Experienced Disease Progression or Death in BRCA Gene Population by Blinded Independent Central Review (BICR)

"BRCA gene population includes participants identified as having a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and future BRCA mutation assays (eg, gene sequencing and large rearrangement analysis).~Progressive disease was defined as at least 20% increase in the sum of diameters of target lesions, taking as reference the smallest sum of study. In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm." (NCT02282020)
Timeframe: RECIST follow-up assessments performed every 8 weeks (±1 week), up to 48 weeks, then every 12 weeks (±1 week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	105
Single Agent Chemotherapy	48

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Overall Survival (OS)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by overall survival (OS).~Overall survival is defined as the time from the date of randomisation until death due to any cause." (NCT02282020)
Timeframe: Visits to occur every 12 weeks from the date of first progression, assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Months (Median)
Olaparib 300 mg BID	34.9
Single Agent Chemotherapy	32.9

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Number of Participants Who Experienced Second Progression or Death (PFS2) in BRCA Gene Population

BRCA gene population includes participants identified as having a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and future BRCA mutation assays (eg, gene sequencing and large rearrangement analysis). (NCT02282020)
Timeframe: Visits to occur every 12 weeks from the date of first progression, assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	110
Single Agent Chemotherapy	48

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Number of Participants Who Received Subsequent Chemotherapy or Died in BRCA Gene Population

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	138
Selected Chemotherapy	66

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Number of Participants Who Show an Improvement in TOI Score

"To compare the efficacy of single agent olaparib versus physician's choice single agent chemotherapy on the Health-related Quality of Life (HRQoL) as measured by the trial outcome index (TOI) of the Functional Assessment of Cancer Therapy - Ovarian (FACT-O)~The TOI score was derived from the sum of the scores of the 25 items included in the physical well-being (7 items), functional well-being (7 items), and additional concerns ovarian cancer subscale (11 items) of the FACT-O questionnaire Version 4. TOI score ranges from 0 to 100, a higher score indicates a higher health-related quality of life (HRQoL). A change in at least 10 points was considered clinically relevant." (NCT02282020)
Timeframe: Baseline (Day 1) to Week 48 (±1 week). DCO: 10Oct2018

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	25
Single Agent Chemotherapy	5

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Time From Randomization To Study Treatment Discontinuation Or Death (TDT)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by time to study treatment discontinuation or death (TDT)~TDT was defined as the time from randomization to the earlier of the date of study treatment discontinuation or death." (NCT02282020)
Timeframe: Patients randomised to Olaparib administer their tablets orally at a dose of 300 mg twice daily and continue Olaparib until objective disease progression. Assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Months (Median)
Olaparib 300 mg BID	13.1
Single Agent Chemotherapy	5.1

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Geometric Mean Plasma Concentration of Olaparib

Summary of plasma concentrations (ug/mL) of olaparib (NCT02282020)
Timeframe: Day 1, 1 hour post-dose and Day 29 pre-dose. DCO: 10Oct2018

Intervention	μg/mL (Geometric Mean)
	Day 1, 1 hour post-dose	Day 29, pre-dose
Olaparib 300 mg BID	4.76	1.78

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Time to Response (TTR)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by time to response (TTR) by BICR using RECIST 1.1 criteria for evaluable patients.~TTR was defined as the time from randomization until the date of first documented response by Blinded independent central review (BICR) assessment." (NCT02282020)
Timeframe: RECIST follow-up assessments performed every 8 weeks (±1 week), up to 48 weeks, then every 12 weeks (±1 week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Months (Median)
Olaparib 300 mg BID	2.0
Single Agent Chemotherapy	3.5

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Time To Earliest Progression By RECIST 1.1 Or Cancer Antigen (CA) -125 Or Death

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by time to earliest progression by RECIST 1.1 or CA-125 or death.~Response Evaluation Criteria In Solid Tumors (RECIST) 1.1 criteria was used to assess participant response to treatment. CA-125 progression was assessed per Gynecological Cancer Intergroup (GCIG)." (NCT02282020)
Timeframe: RECIST and CA-125 follow-up assessments performed every 8 weeks (±1week), up to 48 weeks, then every 12 weeks (±1week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Months (Median)
Olaparib 300 mg BID	11.1
Single Agent Chemotherapy	7.9

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Number of Participants Who Received Second Subsequent Chemotherapy or Died in BRCA Gene Population

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	127
Single Agent Chemotherapy	56

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Objective Response Rate (ORR) in Breast Cancer Susceptibility (BRCA) Gene Population by Blinded Independent Central Review (BICR)

"BRCA gene population includes participants identified as having a deleterious or suspected deleterious variant in either of the BRCA genes using variants identified with current and future BRCA mutation assays (eg, gene sequencing and large rearrangement analysis).~The number of participants with complete or partial response per Response Evaluation Criteria In Solid Tumors (RECIST) 1.1 criteria. Partial response is declared when there is a decrease in sum of target disease ≥ 30%. Complete response is declared when all lesions have disappeared or all lesions have disappeared and all nodal disease is < 10 mm each." (NCT02282020)
Timeframe: RECIST follow-up assessments performed every 8 weeks (±1 week), up to 48 weeks, then every 12 weeks (±1 week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	103
Single Agent Chemotherapy	36

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Time From Randomization To Second Subsequent Therapy Or Death (TSST)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by time from randomisation to second subsequent therapy or death (TSST)~TSST was defined as the time from the date of randomisation to the earlier of second subsequent chemotherapy start date or death.~Anti-cancer treatments include chemotherapy and targeted agents." (NCT02282020)
Timeframe: Anti-cancer treatments initiated post discontinuation of study treatment and investigator's opinion of response and date of progression recorded, assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Months (Median)
Olaparib 300 mg BID	25.2
Single Agent Chemotherapy	19.9

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Overall Survival (OS) in BRCA Gene Population

Intervention	Count of Participants (Number)
Olaparib 300 mg BID	111
Single Agent Chemotherapy	45

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Progression Free Survival (PFS)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by progression free survival (PFS) using BICR assessment according to RECIST 1.1 criteria~PFS is defined as the time from randomization until the date of objective radiological disease progression according to RECIST 1.1 or death (by any cause in the absence of disease progression) regardless of whether the participant withdrew from randomized therapy or received another anti-cancer therapy prior to disease progression (i.e., date of RECIST progression/death or censoring - date of randomization +1)." (NCT02282020)
Timeframe: RECIST follow-up assessments performed every 8 weeks (±1 week), up to 48 weeks, then every 12 weeks (±1 week) from randomisation, assessed from date of first patient randomised to data cut off: 10Oct2018 (approx. 3 years 8 months)

Intervention	Months (Median)
Olaparib 300 mg BID	13.4
Single Agent Chemotherapy	9.2

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Time From Randomisation to Second Progression (PFS2)

"To determine the efficacy of single agent olaparib vs. physician's choice single agent chemotherapy by second progression (PFS2).~Time from randomization to PFS2 is defined as the time from the date of randomization to the earliest of the progression events subsequent to first progression or death. The date of second progression was recorded by the investigator and defined according to local standard clinical practice, and could involve objective radiological, clinical, cancer antigen-125 (CA-125) progression or death. CA-125 progression was assessed per Gynecological Cancer Intergroup (GCIG) criteria." (NCT02282020)
Timeframe: Visits to occur every 12 weeks from the date of first progression, assessed from date of first patient randomised to data cut off: 16Apr2021 (approx. 6 years 2 months)

Intervention	Months (Median)
Olaparib 300 mg BID	23.6
Single Agent Chemotherapy	19.6

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Progression-Free Survival (PFS) by HRR Status in Platinum-Sensitive Ovarian Cancer

"PFS determined per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1), where disease progression represents at least a 20% increase in the sum of diameters of target lesions, appearance of one or more new lesions, or unequivocal progression of existing non-target lesions.~Homologous recombination repair (HRR) status was measured by the BROCA-HR assay. BROCA-HR is a targeted NGS platform including all known gynecologic cancer susceptibility genes and other DNA repair or related genes as well as a 3100 single nucleotide polymorphism panel to increase coverage for loss of heterozygosity (LOH) analysis. HRR status was associated as a pooled group against PFS using the Kaplan-Meier product-limit estimator with 95% confidence bands derived using Greenwood's formula." (NCT02345265)
Timeframe: Interval from start of treatment to documented disease progression per Response Evaluation Criteria in Solid Tumors (RECIST) v1.1 or death from any cause, whichever occurs first, assessed up to 32 months.

Intervention	months (Median)
HRRmt	16.79
HRRwt	16.43

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Objective Response Rate (ORR) in Platinum-Resistant Ovarian Cancer

Responses determined per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for target lesions and assessed by CT or MRI, where Objective Response (OR) represents either a Complete Response (CR; disappearance of all target lesions) or a Partial Response (PR; at least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum diameters); Objective Response (OR) = CR + PR. (NCT02345265)
Timeframe: Up to 32 months

Intervention	percentage of participants (Number)
Platinum-Resistant Ovarian Cancer	22.86

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Steady State PK Parameter--tmax, ss at Day 8

Steady state pharmacokinetic parameter summary for olaparib by dose and visit after multiple doses - tmax, ss (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 h post morning dose of Day 8

Intervention	hour (Median)
Cohort 1	1.50
Cohort 2, Olaparib Alone	2.00

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Steady State PK Parameter--Cmax, ss and Cmin, ss at Day 9

Steady state pharmacokinetic parameter summary for olaparib by dose and visit after multiple doses - Cmax, ss and Cmin, ss (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose, 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 h post morning dose of Day 9

Intervention	µg/mL (Geometric Mean)
	Cmax, ss	Cmin, ss
Cohort 2(Olaparib 100 mg + Paclitaxel)	3.031	0.1915

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Steady State PK Parameter--Cmax, ss and Cmin, ss at Day 8

Steady state pharmacokinetic parameter summary for olaparib by dose and visit after multiple doses - Cmax, ss and Cmin, ss (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 h post morning dose of Day 8

Intervention	µg/mL (Geometric Mean)
	Cmax, ss	Cmin, ss
Cohort 1	8.268	0.7996
Cohort 2 (Olaparib Alone)	3.752	0.3162

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Steady State PK Parameter--RAC and TCP at Day 8

Steady state pharmacokinetic parameter summary for olaparib by dose and visit after multiple doses - RAC and TCP (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 h post morning dose of Day 8

Intervention	Ratio (Mean)
	RAC	TCP
Cohort 1	1.436	1.253
Cohort 2, Olaparib Alone	1.565	1.349

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Steady State PK Parameter--AUCss at Day 9

Steady state pharmacokinetic parameter summary for olaparib by dose and visit after multiple doses - AUC (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 h post morning dose of Day 9

Intervention	µg*h/mL (Geometric Mean)
	AUCss	AUC0-t
Cohort 2(Olaparib 100 mg + Paclitaxel)	12.44	12.42

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Steady State PK Parameter--AUCss at Day 8

Intervention	µg*h/mL (Geometric Mean)
	AUCss	AUC0-t
Cohort 1	43.95	43.91
Cohort 2, Olaparib Alone	16.73	16.68

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Single Dose PK Parameter--AUC

Single dose PK parameter summary for olaparib in monotherapy by dose - AUC (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24 (Day 2) and 48 h (Day 3)

Intervention	µg*h/mL (Geometric Mean)
	AUC0-12	AUC0-t	AUC
Cohort 1	31.68	36.37	36.53
Cohort 2	10.86	12.63	12.75

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Steady State PK Parameter--tmax, ss at Day 9

Intervention	hour (Median)
Cohort 2(Olaparib 100 mg + Paclitaxel)	1.48

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Steady State PK Parameter--CLss/F at Day 8

Steady state pharmacokinetic parameter summary for olaparib by dose and visit after multiple doses - CLss/F (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8 and 12 h post morning dose of Day 8

Intervention	L/h (Mean)
Cohort 1	7.512
Cohort 2, Olaparib Alone	6.745

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Single Dose PK Parameter--Vz/F

Single dose PK parameter summary for olaparib in monotherapy by dose - Vz/F (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24 (Day 2) and 48 h (Day 3)

Intervention	L (Mean)
Cohort 2	88.32
Cohort 1	74.78

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Single Dose PK Parameter--tmax

Single dose PK parameter summary for olaparib in monotherapy by dose - tmax (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24 (Day 2) and 48 h (Day 3)

Intervention	hour (Median)
Cohort 2	1.95
Cohort 1	1.50

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Single Dose PK Parameter--t1/2, λz

Single dose PK parameter summary for olaparib in monotherapy by dose - t1/2, λz (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24 (Day 2) and 48 h (Day 3)

Intervention	hour (Mean)
Cohort 2	7.165
Cohort 1	6.519

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Single Dose PK Parameter--Cmax

Single dose PK parameter summary for olaparib in monotherapy by dose - Cmax (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24 (Day 2) and 48 h (Day 3)

Intervention	µg/mL (Geometric Mean)
Cohort 1	6.875
Cohort 2	2.972

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Single Dose PK Parameter--CL/F

Single dose PK parameter summary for olaparib in monotherapy by dose - CL/F (PK analysis set) (NCT02430311)
Timeframe: PK samples were collected pre-dose and at 0.25, 0.5, 1, 1.5, 2, 3, 4, 6, 8, 12, 24 (Day 2) and 48 h (Day 3)

Intervention	L/h (Mean)
Cohort 2	9.217
Cohort 1	8.107

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Overall Survival

Overall survival (OS) was defined as the number of months between study enrollment and death from any cause. Patients still alive at the last follow-up were censored on the date of last contact. Japanese cohort not included in overall survival analysis, the cohort was only included in toxicity assessments. (NCT02446600)
Timeframe: Approximately 30 months

Intervention	months (Median)
Arm I (Platinum-based Chemotherapy)	31.3
Arm II (Olaparib)	29.2
Arm III (Olaparib, Cediranib Maleate)	30.5

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Patient Reported Scores of Disease-related Symptoms as Measured by the National Comprehensive Cancer Network/Functional Assessment of Cancer Therapy Ovarian Symptom Index-18 Disease-Related Symptom-Physical

Disease-related physical symptoms were measured by the Disease-Related Symptom-Physical (DRS-P) subscale of the National Comprehensive Cancer Network/Functional Assessment of Cancer Therapy Ovarian Symptom Index-18 (NCCN/FOSI-18). The DRS-P subscale is composed of 9 items. For the negative statements (or questions), reversal was performed prior to score calculation. According to the FACIT measurement system, a subscale score was the summation of the individual item scores if more than 50% of subscale items were answered. When unanswered items existed, a subscale score was prorated by multiplying the mean of the answered item scores by the number of items in the subscale. The DRS-P score ranges 0-36 with a larger score suggesting better QOL (Quality of Life) or less symptoms. This analysis did not include the Japanese cohort. (NCT02446600)
Timeframe: Prior to cycle 1, week 12, week 24, week 36, week 48, week 60, week 72, week 84, week 96 and 108 weeks after starting treatment

Intervention	score on a scale (Mean)
	Baseline	12 Weeks	24 Weeks	36 Weeks	48 Weeks	60 Weeks	72 Weeks	84 Weeks	96 Weeks	108 Weeks
Arm I (Platinum-based Chemotherapy)	17.1	16.5	16.3	16.9	16.9	16.5	17.1	17.4	17.0	17.3
Arm II (Olaparib)	17.8	17.4	17.4	17.2	17.1	16.9	17.3	17.2	16.9	17.4
Arm III (Olaparib, Cediranib Maleate)	17.9	15.9	16.3	16.3	16.5	16.3	16.3	16.6	17.0	17.2

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Progression Free Survival Determined Using Response Evaluation Criteria in Solid Tumors Version 1.1 Criteria

Progression free survival (PFS) was defined as the number of months between study enrollment and documentation of disease progression (RECIST 1.1) or death from any cause. Patients still alive and disease free at the last follow-up were censored on the date of last CT Scan, or the CT Scan date prior to two missed assessments. Japanese cohort not included in progression free survival analysis, only included in toxicity assessments. (NCT02446600)
Timeframe: The protocol required lesion assessments every 9 weeks from cycle 1, day 1 for the first year, then every 12 weeks thereafter until disease progression. An average of approximately 10 months.

Intervention	months (Median)
Arm I (Platinum-based Chemotherapy)	10.3
Arm II (Olaparib)	8.2
Arm III (Olaparib, Cediranib Maleate)	10.4

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Frequency and Severity of Adverse Effects

Number of treated patients with Adverse Events (grade 3 or higher) observed while receiving randomized therapy, by Preferred term with incidence rate greater than 5%. (NCT02446600)
Timeframe: During treatment period and up to 100 days after stopping the study treatment, up to 39 months.

,,,

Intervention	Participants (Count of Participants)
	Anemia	Fatigue	Neutrophil count decreased	Platelet count decreased	Urinary tract infection	White blood cell decreased
Arm I (Platinum-based Chemotherapy)	23	3	51	24	10	22
Arm II (Olaparib)	28	12	3	2	11	3
Arm III (Olaparib, Cediranib Maleate)	11	31	7	3	15	2
Japanese Cohort	1	0	1	0	0	1

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Time to Second Progression (PFS2) or Death; Assessed at Primary Analysis

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of PFS2. The PFS2 was defined as the time from the date of enrolment to the earliest progression event subsequent to that used for the primary variable PFS or death (by any cause) in the absence of progression. Patients whose progression event for PFS was death had this counted as a progression event for PFS2 also. The date of second progression was recorded by the Investigator and defined according to local standard clinical practice and could involve any of the following: objective radiological, symptomatic, cancer antigen-125 (CA-125) progression or death. Pre-specified analysis of PFS2 was performed at the time of the primary analysis; a further analysis of PFS2 was performed at the final analysis (and reported as a separate outcome measure). (NCT02476968)
Timeframe: Tumour assessments (and blood samples for CA-125, if applicable) at baseline then every 12 weeks relative to date of enrolment until second progression. Assessed until primary analysis DCO of 17 April 2020 (up to maximum of 55 months).

Intervention	months (Median)
Overall BRCAm	30.9
sBRCAm	24.7

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TSST; Assessed at Final Analysis

Intervention	months (Median)
Overall BRCAm	38.4
sBRCAm	32.1

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Change From Baseline in Functional Living Index-Emesis (FLIE) Questionnaire Total Scores Over Time

The FLIE captures the impact of nausea and vomiting on patient's QoL. The FLIE consists of 18 items (9 nausea-specific and 9 vomiting-specific items), rated from 1 to 7. Two domain scores and a total score are derived; the total score ranges 18-126 and a higher score indicates a lower impact (and better QoL). A positive change in score from baseline indicates an improvement. (NCT02476968)
Timeframe: FLIE questionnaires at baseline, weekly until Day 29 (Week 4), then every 12 weeks for 24 months or DCO for primary analysis, whichever came first. FLIE questionnaires also collected at discontinuation of study treatment visit and 30 days post last dose.

Intervention	scores on a scale (Mean)
	Week 1	Week 2	Week 3	Week 4	Week 16	Week 28	Week 40	Week 52	Week 64	Week 76	Week 88	Week 100	Discontinuation of olaparib visit	30 days post discontinuation
Overall BRCAm	-6.1	-4.5	-4.1	-4.8	-2.3	-1.6	-0.1	0.9	-0.2	0.9	2.2	0.4	-0.7	-5.2
sBRCAm	-1.6	-2.6	-3.9	-5.4	-6.3	-3.0	-3.2	-1.9	-1.0	0.6	-1.3	0.1	-8.8	-5.6

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Time to Second Subsequent Therapy (Treatment) or Death (TSST); Assessed at Primary Analysis

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of TSST. The TSST was defined as the time from the date of enrolment to the earlier of the date of second subsequent anti-cancer therapy start date, or death date. Pre-specified analysis of TSST was performed at the time of the primary analysis; a further analysis of TSST was performed at the final analysis (and reported as a separate outcome measure). (NCT02476968)
Timeframe: From enrolment to second subsequent therapy or death. Assessed every 12 weeks following treatment discontinuation. Assessed until primary analysis DCO of 17 April 2020 (up to maximum of 55 months).

Intervention	months (Median)
Overall BRCAm	47.6
sBRCAm	NA

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Change From Baseline in Functional Assessment of Cancer Therapy - Ovarian (FACT-O) Trial Outcome Index (TOI) Scores Over Time

To assess the Quality of Life (QoL) of patients with BRCAm and sBRCAm ovarian cancer by evaluation of FACT-O TOI. The TOI score was derived from the sum of the scores of the 25 items included in the physical well-being (7 items), functional well-being (7 items), and additional concerns ovarian cancer subscale (11 items) of the FACT-O questionnaire version 4. The FACT-O TOI score ranges from 0-100, with a higher score indicating better QoL. A change (increase or decrease) in score of at least 10 points from baseline was defined as clinically meaningful. A positive change in score from baseline indicates an improvement. (NCT02476968)
Timeframe: QoL questionnaires at baseline, Day 29 (Week 4), then every 12 weeks for 24 months or DCO for primary analysis, whichever came first. QoL questionnaires also collected at discontinuation of study treatment visit and 30 days post last dose.

Intervention	scores on a scale (Mean)
	Week 4	Week 16	Week 28	Week 40	Week 52	Week 64	Week 76	Week 88	Week 100	Discontinuation of olaparib visit	30 days post discontinuation
Overall BRCAm	-2.2	-1.3	1.2	1.6	3.2	1.8	1.4	2.0	-0.2	-4.7	-8.0
sBRCAm	-1.9	-0.3	3.2	4.1	4.9	0.8	0.3	1.5	-3.5	-7.4	-4.3

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Progression-Free Survival (PFS)

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of PFS. The PFS was defined as the time from the date of enrolment until date of objective radiological disease progression (assessed by the Investigator via Response Evaluation Criteria in Solid Tumors, version 1.1 [RECIST 1.1]), or death (by any cause in absence of disease progression) regardless of whether the patient withdrew from therapy or received another anti-cancer therapy prior to disease progression. Objective progression was defined as at least a 20% increase in the sum of the diameters of the target lesions (compared to previous minimum sum) and an absolute increase of > 5 millimeters, or an overall non-target lesion assessment of progression or a new lesion. The data cut-off (DCO) for the primary analysis of the study occurred after approximately 60% maturity of PFS in the sBRCAm and all BRCAm patient populations. (NCT02476968)
Timeframe: Tumour assessments at baseline then every 12 weeks relative to date of enrolment until RECIST 1.1-defined progression. Assessed until primary analysis DCO of 17 April 2020 (up to maximum of 55 months).

Intervention	months (Median)
Overall BRCAm	18.0
sBRCAm	16.6

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OS; Assessed at Final Analysis

Intervention	months (Median)
Overall BRCAm	46.8
sBRCAm	43.2

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Overall Survival (OS); Assessed at Primary Analysis

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of OS. The OS was defined as the time from the date of enrolment until death due to any cause regardless of whether the patient withdrew from therapy or received another anti-cancer therapy. Any patient not known to have died at the time of analysis was censored based on the last recorded date on which the patient was known to be alive. Pre-specified analysis of OS was performed at the time of primary analysis of PFS; a further analysis of OS was performed after approximately 60% maturity of OS in the sBRCAm and all BRCAm patient populations (and reported as a separate outcome measure). (NCT02476968)
Timeframe: From baseline until death due to any cause. Assessed until primary analysis DCO of 17 April 2020 (up to maximum of 55 months).

Intervention	months (Median)
Overall BRCAm	47.6
sBRCAm	NA

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PFS2 or Death; Assessed at Final Analysis

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of PFS2. The PFS2 was defined as the time from the date of enrolment to the earliest progression event subsequent to that used for the primary variable PFS or death (by any cause) in the absence of progression. Patients whose progression event for PFS was death had this counted as a progression event for PFS2 also. The date of second progression was recorded by the Investigator and defined according to local standard clinical practice and could involve any of the following: objective radiological, symptomatic, CA-125 progression or death. (NCT02476968)
Timeframe: Tumour assessments (and blood samples for CA-125, if applicable) at baseline then every 12 weeks relative to date of enrolment until second progression (up to maximum of 6 years).

Intervention	months (Median)
Overall BRCAm	34.0
sBRCAm	29.3

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Change From Baseline in Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F) Total Scores Over Time

To assess the QoL of patients with BRCAm and sBRCAm ovarian cancer by evaluation of FACIT-F. The FACIT-F is a 13-item questionnaire to assess patients' fatigue experience and its impact on their daily lives over the past 7 days. The FACIT-F total score ranges from 0-52, with a higher score indicating a lower level of fatigue (and better QoL). Changes in scores of ≥3 points were defined to be clinically meaningful. A positive change in score from baseline indicates an improvement. (NCT02476968)
Timeframe: QoL questionnaires at baseline, Day 29 (Week 4), then every 12 weeks for 24 months or DCO for primary analysis, whichever came first. QoL questionnaires also collected at discontinuation of study treatment visit and 30 days post last dose.

Intervention	scores on a scale (Mean)
	Week 4	Week 16	Week 28	Week 40	Week 52	Week 64	Week 76	Week 88	Week 100	Discontinuation of olaparib visit	30 days post discontinuation
Overall BRCAm	-2.9	-2.5	-1.2	-0.3	0.6	0.8	-0.3	0.3	-0.4	-2.3	-5.2
sBRCAm	-2.9	-2.7	-0.6	0.9	1.3	0.5	-1.1	-0.9	-1.3	-2.7	-3.8

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TFST; Assessed at Final Analysis

Intervention	months (Median)
Overall BRCAm	32.1
sBRCAm	31.7

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Time to Discontinuation of Treatment or Death (TDT)

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of TDT. The TDT was defined as the time from the date of enrolment to the earlier of the date of study treatment discontinuation or death. (NCT02476968)
Timeframe: From enrolment to study treatment discontinuation or death (up to maximum of 6 years).

Intervention	months (Median)
Overall BRCAm	19.8
sBRCAm	19.0

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Time to First Subsequent Therapy (Treatment) or Death (TFST); Assessed at Primary Analysis

To assess the real-world clinical effectiveness of olaparib maintenance monotherapy in patients with BRCAm and sBRCAm ovarian cancer by assessment of TFST. The TFST was defined as the time from the date of enrolment to the earlier of first subsequent anti-cancer therapy start date (excluding radiotherapy), or death date. Pre-specified analysis of TFST was performed at the time of the primary analysis; a further analysis of TFST was performed at the final analysis (and reported as a separate outcome measure). (NCT02476968)
Timeframe: From enrolment to first subsequent therapy or death. Assessed every 12 weeks following treatment discontinuation. Assessed until primary analysis DCO of 17 April 2020 (up to maximum of 55 months).

Intervention	months (Median)
Overall BRCAm	37.6
sBRCAm	31.5

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Protein Expression of Biomarkers Related to PARP-inhibition

"We assessed the change from baseline in the H-score of several biomarkers targeted by olaparib-based therapy on endometrial tumor tissues after 28 (+/- 5) days of treatment. In detail, expression of protein involved in the DNA repair (PARP1, ɣH2AX), angiogenesis (VEG, HIF-1α, PTEN), apoptosis (p65, p50, p53), glucose metabolism (GLUT1), proliferation (PH3), and regulation of gene transcription (ARID1A) were evaluated by an H-score according to the following formula:~H-score= 1x(%light staining) + 2x(%moderate staining) + 3x(%strong staining).~The final score ranges from 0 to 300, where 0 indicates absence of staining and 300 the maximum staining." (NCT02506816)
Timeframe: Baseline and Day 28 (+/- 5)

Intervention	score on a scale (Mean)
	PARP1 pre-treatment - post-treatment	y-H2AX pre-treatment - post-treatment	VEGF pre-treatment - post-treatment	HIF-1α pre-treatment - post-treatment	PTEN pre-treatment - post-treatment	P65 pre-treatment - post-treatment	P50 pre-treatment - post-treatment	P53 pre-treatment - post-treatment	GLUT1 active pre-treatment - post-treatment	PHH3 pre-treatment - post-treatment	ARID1A pre-treatment - post-treatment
Olaparib	10.3	-46.21	-9.4	76.9	3.2	-0.2	0.1	0.1	-20.8	3.1	20

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Plasma Levels of Olaparib

Plasma concentration of olaparib administered at dosis of 300mg twice in a day (600mg/day). Values of plasma level of olaparib on days 7,14,21 and 28 were collected at time when maximum of drug concentration is reached. Data are reported as µg/mL. (NCT02506816)
Timeframe: Days 7,14,21 and 28

Intervention	µg/mL (Mean)
	Day 07	Day 14	Day 21	Day 28
Olaparib	6.55	5.61	6.49	4.7

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Expression of Cell Cycle-related Proteins

"We assessed the change from baseline in the histological score (H-score) of the cell cycle-related proteins on endometrial tumor tissues after 28 (+/- 5) days of olaparib-based therapy. In detail, expression of the cyclin D1, Ki67, and caspase-3 active proteins evaluated by an H-score according to the following formula:~H-score= 1x(%light staining) + 2x(%moderate staining) + 3x(%strong staining).~The final score ranges from 0 to 300, where 0 indicates absence of staining (corresponding to the lowest tumor proliferation rate and better outcome) and 300 the maximum staining (corresponding to the highest tumor proliferation score and worse outcome)." (NCT02506816)
Timeframe: Baseline and Day 28 (+/- 5)

Intervention	score on a scale (Mean)
	Cyclin D1 pre-treatment - post-treatment	Ki67 pre-treatment - post-treatment	Caspase-3 active pre-treatment - post-treatment
Olaparib	46.1	0.8	0.7

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Number of Participants With Olaparib-Associated Toxicities

To assess the tolerability for all treated patients (N=36) according to NCI-CTCAE v.4.03. (NCT02506816)
Timeframe: Up to 28 days (+/- 5)

Intervention	Participants (Count of Participants)
Olaparib	3

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Part A: Number of Subjects Reporting Adverse Events (AEs)

Treatment-emergent AEs (TEAEs) defined as events occurring on or after cycle 1, day 1 up to and including 30 days after last dose (approximately 114 days). (NCT02561832)
Timeframe: From day 1 cycle 1, up to and including 30 days after last dose

Intervention	Participants (Number)
Cohort 1	8
Cohort 2	7

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Second Stage Cohort: Serum Concentrations of Bevacizumab

Blood samples were collected to determine the serum concentration of bevacizumab. (NCT02734004)
Timeframe: Pre-dose and within 10 minutes of end of infusion on Days 1 and 85; Pre-dose on Days 29 and 169; and 90 days post last dose of bevacizumab. Assessed until DCO 17 Sep 2021

Intervention	mcg/mL (Geometric Mean)
	Day 1: Pre-dose	Day 1: End of infusion	Day 29: Pre-dose	Day 85: Pre-dose	Day 85: End of infusion	Day 169: Pre-dose	90 days post last dose
Second Stage: Ovarian Cancer Triplet	NA	243.7	104.6	145.5	364.0	147.9	5.094

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Initial Stage Cohorts: Percentage Change From Baseline in Target Tumor Size at Weeks 12 and 28

The percentage change in target tumor size at each timepoint (based on RECIST 1.1 target lesion measurements) was obtained for each participant taking the difference between the sum of the target lesions at each timepoint and the sum of the target lesions at baseline divided by the sum of the target lesions at baseline times 100. Baseline was defined as the last evaluable assessment prior to starting olaparib treatment. (NCT02734004)
Timeframe: Baseline (Day 1) and Weeks 12 and 28. Assessed until DCO 14 Jun 2019

,,,

Intervention	percentage change in tumor size (Mean)
	Week 12	Week 28
Initial Stage: Breast Cancer	-26.13	-40.85
Initial Stage: Gastric Cancer	20.81	-41.00
Initial Stage: Ovarian Cancer	-35.86	-53.74
Initial Stage: Small Cell Lung Cancer	17.23	-2.05

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Initial and Second Stage Cohorts: Best Percentage Change From Baseline in Target Tumor Size

The best percentage change from baseline in target tumor size was based on RECIST 1.1 target lesion measurements taken at each RECIST 1.1 assessment. All measurements until PD or the last evaluable assessment in the absence of PD was included in the calculation. Baseline was defined as the last evaluable assessment prior to starting olaparib treatment for initial stage cohorts. Baseline was defined as the last assessment prior to Cycle 1 Day 1 for second stage cohorts. (NCT02734004)
Timeframe: From baseline (Day 1) until confirmed PD/death. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	percentage change in tumor size (Mean)
Initial Stage: Small Cell Lung Cancer	6.27
Initial Stage: Breast Cancer	-47.60
Initial Stage: Ovarian Cancer	-55.55
Initial Stage: Gastric Cancer	1.64
Second Stage: Ovarian Cancer Expansion	-72.78
Second Stage: Ovarian Cancer Triplet	-53.30
Second Stage: Ovarian Cancer Doublet	-20.42

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Initial and Second Stage Cohorts: OS

The OS was defined as the time from the start of study treatment (Day 1; start of olaparib monotherapy for initial stage cohorts) until death due to any cause. The OS was calculated using the Kaplan-Meier technique. (NCT02734004)
Timeframe: From baseline (Day 1) until death from any cause. Assessed until DCO 14 Jun 2019 for initial stage cohorts except for ovarian cancer cohort and DCO 17 Sep 2021 for initial stage ovarian cancer cohort and second stage cohorts

Intervention	months (Median)
Initial Stage: Small Cell Lung Cancer	7.6
Initial Stage: Breast Cancer	20.5
Initial Stage: Ovarian Cancer	35.5
Initial Stage: Gastric Cancer	6.4
Second Stage: Ovarian Cancer Expansion	NA
Second Stage: Ovarian Cancer Triplet	31.9
Second Stage: Ovarian Cancer Doublet	26.1

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Initial and Second Stage Cohorts: Duration of Response (DoR)

The DoR (based on RECIST 1.1 as assessed by the Investigator) was defined as the time from the date of first documented response until date of documented progression or death in the absence of PD. The DoR was calculated using Kaplan-Meier technique. (NCT02734004)
Timeframe: RECIST performed at baseline, at 4 weeks after first dose of olaparib monotherapy (for initial stage cohort only) and every 8 weeks +/-7 days thereafter. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	months (Median)
Initial Stage: Small Cell Lung Cancer	3.6
Initial Stage: Breast Cancer	9.2
Initial Stage: Ovarian Cancer	10.2
Initial Stage: Gastric Cancer	14.8
Second Stage: Ovarian Cancer Expansion	14.8
Second Stage: Ovarian Cancer Triplet	11.1
Second Stage: Ovarian Cancer Doublet	6.9

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Initial and Second Stage Cohorts: ORR

The ORR (based on RECIST 1.1 as assessed by the Investigator) was defined as the percentage of participants with at least 1 visit response of CR or PR prior to PD or last evaluable assessment in the absence of progression. The 95% CI were calculated using Exact Clopper-Pearson confidence limits for the binomial proportion. (NCT02734004)
Timeframe: RECIST performed at baseline, at 4 weeks after first dose of olaparib monotherapy (for initial stage cohort only) and every 8 weeks +/-7 days thereafter. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	percentage of participants (Number)
Initial Stage: Small Cell Lung Cancer	10.5
Initial Stage: Breast Cancer	63.3
Initial Stage: Ovarian Cancer	71.9
Initial Stage: Gastric Cancer	10.3
Second Stage: Ovarian Cancer Triplet	87.1
Second Stage: Ovarian Cancer Doublet	34.4

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Initial and Second Stage Cohorts: Progression-Free Survival (PFS)

The PFS (based on RECIST 1.1 as assessed by the Investigator) was defined as the time from start of study treatment (Day 1; start of olaparib monotherapy for initial stage cohorts) until the date of objective PD or death (by any cause in the absence of disease progression) regardless of whether the patient withdraws from therapy or receives another anticancer therapy prior to disease progression. The PFS was calculated using Kaplan-Meier technique. (NCT02734004)
Timeframe: RECIST performed at baseline, at 4 weeks after first dose of olaparib monotherapy (for initial stage cohort only) and every 8 weeks +/-7 days thereafter. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	months (Median)
Initial Stage: Small Cell Lung Cancer	2.4
Initial Stage: Breast Cancer	8.2
Initial Stage: Ovarian Cancer	12.0
Initial Stage: Gastric Cancer	2.6
Second Stage: Ovarian Cancer Expansion	15.0
Second Stage: Ovarian Cancer Triplet	14.7
Second Stage: Ovarian Cancer Doublet	5.5

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Second Stage Cohorts: Percentage Change From Baseline in Target Tumor Size at Weeks 24 and 56

The percentage change in target tumor size at each timepoint (based on RECIST 1.1 target lesion measurements) was obtained for each participant taking the difference between the sum of the target lesions at each timepoint and the sum of the target lesions at baseline divided by the sum of the target lesions at baseline times 100. Baseline was defined as the last assessment prior to Cycle 1 Day 1. (NCT02734004)
Timeframe: Baseline (Day 1) and Weeks 24 and 56. Assessed until DCO 17 Sep 2021

Intervention	percentage change in tumor size (Mean)
	Week 24	Week 56
Second Stage: Ovarian Cancer Doublet	-35.63	-39.54
Second Stage: Ovarian Cancer Expansion	-66.30	-77.74
Second Stage: Ovarian Cancer Triplet	-43.00	-60.00

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Initial and Second Stage Cohorts: Time to Study Treatment Discontinuation or Death (TDT)

The TDT was defined as the time from start of study treatment (Day 1; start of olaparib monotherapy for initial stage cohorts) to the earlier of the date of study treatment discontinuation or death. The TDT was calculated using the Kaplan-Meier technique. (NCT02734004)
Timeframe: From baseline (Day 1) until treatment discontinuation/death. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	months (Median)
Initial Stage: Small Cell Lung Cancer	2.8
Initial Stage: Breast Cancer	7.8
Initial Stage: Ovarian Cancer	13.1
Initial Stage: Gastric Cancer	2.8
Second Stage: Ovarian Cancer Expansion	19.3
Second Stage: Ovarian Cancer Triplet	15.9
Second Stage: Ovarian Cancer Doublet	6.6

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Initial Stage Cohorts: DCR at Week 28

The DCR at 28 weeks was defined as the percentage of participants who had CR + PR + SD at 28 weeks. Participants demonstrated SD for a minimum interval of 27 weeks (minus 1 week to allow for an early assessment within the assessment window, i.e. 189 days) following the start of treatment. The DCR was determined using Investigator assessments according to RECIST v1.1. (NCT02734004)
Timeframe: RECIST performed at baseline, at 4 weeks after first dose of olaparib monotherapy and every 8 weeks +/-7 days thereafter. Assessed until DCO 14 Jun 2019.

Intervention	percentage of participants (Number)
Initial Stage: Small Cell Lung Cancer	5.3
Initial Stage: Breast Cancer	50.0
Initial Stage: Ovarian Cancer	65.6
Initial Stage: Gastric Cancer	7.7

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Initial Stage Cohorts: Disease Control Rate (DCR) at Week 12

The DCR at 12 weeks was defined as the percentage of participants who had complete response (CR) + partial response (PR) + stable disease (SD) at 12 weeks. Participants demonstrated SD for a minimum interval of 11 weeks (minus 1 week to allow for an early assessment within the assessment window, i.e. 77 days) following the start of treatment. The DCR was determined using Investigator assessments according to Response Evaluation Criteria in Solid Tumors version 1.1 (RECIST v1.1). (NCT02734004)
Timeframe: RECIST performed at baseline, at 4 weeks after first dose of olaparib monotherapy and every 8 weeks +/-7 days thereafter. Assessed until DCO 14 Jun 2019.

Intervention	percentage of participants (Number)
Initial Stage: Small Cell Lung Cancer	28.9
Initial Stage: Breast Cancer	80.0
Initial Stage: Ovarian Cancer	81.3
Initial Stage: Gastric Cancer	25.6

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Second Stage Cohort: Objective Response Rate (ORR)

The ORR (based on RECIST 1.1 as assessed by the Investigator) was defined as the percentage of participants with at least 1 visit response of CR or PR prior to PD or last evaluable assessment in the absence of progression. The 95% confidence interval (CI) were calculated using Exact Clopper-Pearson confidence limits for the binomial proportion. (NCT02734004)
Timeframe: RECIST performed at baseline, and every 8 weeks +/-7 days thereafter. Assessed until 17 Sep 2021.

Intervention	percentage of participants (Number)
Second Stage: Ovarian Cancer Expansion	92.2

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Second Stage Cohorts: DCR at Week 24

The DCR at 24 weeks was defined as the percentage of participants who had CR + PR + SD at 24 weeks. Participants demonstrated SD for a minimum interval of 23 weeks (minus 1 week to allow for an early assessment within the assessment window, i.e. 161 days) following the start of treatment. The DCR was determined using Investigator assessments according to RECIST v1.1. (NCT02734004)
Timeframe: RECIST performed at baseline, and every 8 weeks +/-7 days thereafter. Assessed until 17 Sep 2021.

Intervention	percentage of participants (Number)
Second Stage: Ovarian Cancer Triplet	74.2
Second Stage: Ovarian Cancer Doublet	28.1

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Second Stage Cohorts: DCR at Week 56

The DCR at 56 weeks was defined as the percentage of participants who had CR + PR + SD at 56 weeks. Participants demonstrated SD for a minimum interval of 55 weeks (minus 1 week to allow for an early assessment within the assessment window, i.e. 385 days) following the start of treatment. The DCR was determined using Investigator assessments according to RECIST v1.1. (NCT02734004)
Timeframe: RECIST performed at baseline, and every 8 weeks +/-7 days thereafter. Assessed until 17 Sep 2021.

Intervention	percentage of participants (Number)
Second Stage: Ovarian Cancer Expansion	41.2
Second Stage: Ovarian Cancer Triplet	38.7
Second Stage: Ovarian Cancer Doublet	9.4

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Second Stage Expansion Cohort: DCR at Week 24

Intervention	percentage of participants (Number)
Second Stage: Ovarian Cancer Expansion	88.2

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Initial and Second Stage Cohorts: Serum Concentrations of Olaparib

Blood samples were collected to determine the serum concentration of olaparib. (NCT02734004)
Timeframe: Pre-dose and 0.5-1 hour postdose on Days 1 and 22 of monotherapy; Pre-dose and 0.5-1, 1-3, 3-6 and 6-12 hours postdose on Day 15 of combination therapy. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	mcg/mL (Geometric Mean)
	Combination therapy - Day 15: Pre-dose	Combination therapy - Day 15: 0.5-1 hour postdose	Combination therapy - Day 15: 1-3 hour postdose	Combination therapy - Day 15: 3-6 hour postdose	Combination therapy - Day 15: 6-12 hour postdose
Second Stage: Ovarian Cancer Triplet	1.400	5.922	7.644	5.717	3.023

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Initial and Second Stage Cohorts: Number of Participants With Anti-Drug Antibody (ADA) Response to MEDI4736

Blood samples were measured for the presence of ADAs and ADA-neutralizing antibodies (nAb) for MEDI4736 using validated assays. ADA prevalence was defined as the percentage of participants with positive ADA result at any time, baseline or post-baseline. ADA incidence (treatment-emergent ADA) was defined as the sum of both treatment-induced (post-baseline ADA positive only) and treatment-boosted ADA. Treatment-boosted ADA was defined as baseline ADA titer that was boosted to 4-fold or higher following drug administration. Persistently positive was defined as positive at >=2 post-baseline assessments (with >=16 weeks between first and last positive) or positive at last post-baseline assessment. Transiently positive was defined as having at least 1 post-baseline ADA positive assessment and not fulfilling the conditions of persistently positive. (NCT02734004)
Timeframe: Pre-dose on Days 1, 15, 57, 85, 113 and 169; and 90 days post-last dose of MEDI4736. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

,,,,,

Intervention	Participants (Count of Participants)
	ADA prevalence	ADA incidence	ADA positive post-baseline and positive at baseline	ADA positive post-baseline and not detected at baseline	ADA not detected post-baseline and positive at baseline	Treatment-boosted ADA	Persistent positive	Transient positive	Any nAb positive among any ADA positive
Initial Stage: Breast Cancer	1	0	0	0	0	0	0	0	0
Initial Stage: Gastric Cancer	0	0	0	0	0	0	0	0	0
Initial Stage: Ovarian Cancer	0	0	0	0	0	0	0	0	0
Initial Stage: Small Cell Lung Cancer	0	0	0	0	0	0	0	0	0
Second Stage: Ovarian Cancer Doublet	0	0	0	0	0	0	0	0	0
Second Stage: Ovarian Cancer Triplet	0	0	0	0	0	0	0	0	0

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Initial and Second Stage Cohorts: Serum Concentrations of MEDI4736

Blood samples were collected to determine the serum concentration of MEDI4736. (NCT02734004)
Timeframe: Pre-dose and within 10 minutes of end of infusion on Days 1, 85 and 113; Pre-dose on Days 29, 57 and 169; and 90 days post last dose of MEDI4736. Assessed until DCO 14 Jun 2019 and 17 Sep 2021 for initial and second stage cohorts, respectively

Intervention	microgram per milliliter (mcg/mL) (Geometric Mean)
	Day 1: Pre-dose	Day 1: End of infusion	Day 29: Pre-dose	Day 85: Pre-dose	Day 85: End of infusion	Day 169: Pre-dose	90 days post last dose
Second Stage: Ovarian Cancer Doublet	NA	397.1	78.23	142.8	482.9	186.6	20.50
Second Stage: Ovarian Cancer Expansion	NA	409.3	93.56	152.8	610.6	206.3	17.94
Second Stage: Ovarian Cancer Triplet	NA	498.8	96.50	145.2	589.3	162.6	17.47

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Initial and Second Stage Cohorts: Serum Concentrations of MEDI4736

,,,

Intervention	microgram per milliliter (mcg/mL) (Geometric Mean)
	Day 1: Pre-dose	Day 1: End of infusion	Day 57: Pre-dose	Day 113: Pre-dose	Day 113: End of infusion	Day 169: Pre-dose	90 days post last dose
Initial Stage: Small Cell Lung Cancer	NA	483.5	144.7	119.5	504.8	133.1	6.907
Initial Stage: Breast Cancer	NA	542.5	165.2	220.7	671.5	231.5	12.24
Initial Stage: Gastric Cancer	NA	391.8	114.7	196.9	679.1	230.7	17.23
Initial Stage: Ovarian Cancer	NA	417.9	171.3	231.3	585.5	261.6	22.35

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Initial and Second Stage Cohorts: Serum Concentrations of Olaparib

Intervention	mcg/mL (Geometric Mean)
	Combination therapy - Day 15: Pre-dose	Combination therapy - Day 15: 0.5-1 hour postdose
Second Stage: Ovarian Cancer Doublet	0.9718	6.549
Second Stage: Ovarian Cancer Expansion	1.544	5.439

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Initial and Second Stage Cohorts: Serum Concentrations of Olaparib

,,,

Intervention	mcg/mL (Geometric Mean)
	Monotherapy - Day 1: Pre-dose	Monotherapy - Day 1: 0.5-1 hour postdose	Monotherapy - Day 22: Pre-dose	Monotherapy - Day 22: 0.5-1 hour postdose	Combination therapy - Day 15: Pre-dose	Combination therapy - Day 15: 0.5-1 hour postdose	Combination therapy - Day 15: 1-3 hour postdose	Combination therapy - Day 15: 3-6 hour postdose	Combination therapy - Day 15: 6-12 hour postdose
Initial Stage: Breast Cancer	NA	2.093	0.8500	5.370	0.6526	2.805	4.018	5.217	2.820
Initial Stage: Gastric Cancer	NA	2.321	2.053	5.350	1.744	3.226	4.804	5.491	3.679
Initial Stage: Ovarian Cancer	NA	5.016	1.242	6.130	1.773	4.288	5.897	6.322	3.661
Initial Stage: Small Cell Lung Cancer	NA	3.647	1.374	7.212	1.848	5.008	8.038	7.811	5.186

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Median Duration of Response (DoR) by ICR and Investigator Assessment Using RECIST 1.1

DoR was defined as the time from date of first documented response (which was subsequently confirmed) until date of documented progression or death in the absence of disease progression (i.e. date of progression free survival [PFS] event or censoring - date of first response + 1). The end of response coincided with the date of progression or death from any cause used for the PFS endpoint. The time of initial response was defined as the latest of the dates used towards the first visit that was CR or PR that was subsequently confirmed. If a patient did not progress following a response, the PFS censoring time was used. The Investigator assessment was based on the FAS and the ICR used the EFR analysis set. The median DoR for each assessment is presented and was calculated using the Kaplan-Meier technique. (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs). RECIST assessments were performed at baseline and every 8 weeks (+/- 1 week) after first doses of IPs until disease progression.

Intervention	weeks (Median)
	ICR assessment (EFR analysis set)	Investigator assessment (FAS)
Cediranib + Olaparib	36.0	45.0

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Median PFS by ICR and Investigator Assessment Using RECIST 1.1

"PFS was defined as the time from date of first dose of IP until the date of objective disease progression or death (by any cause in the absence of progression) regardless of whether the patient withdrew from treatment or received another anti-cancer therapy prior to progression (i.e. date of PFS event or censoring - date of first dose + 1). Patients who had not progressed or died at the time of analysis were censored at the time of the latest date of assessment from their last evaluable RECIST assessment.~The median PFS, calculated using the Kaplan-Meier technique, is presented for the ICR and the Investigator assessment, both based on the FAS." (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs). RECIST assessments were performed at baseline and every 8 weeks (+/- 1 week) after first doses of IPs until disease progression.

Intervention	months (Median)
	ICR assessment (FAS)	Investigator assessment (FAS)
Cediranib + Olaparib	5.1	3.8

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Mean Objective Response Rate (ORR) by Independent Central Review (ICR) Using Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST 1.1)

"The ORR was defined as the percentage of patients with objective response (complete response [CR] or partial response [PR]) according to RECIST 1.1 and was assessed by ICR. Only patients whose CR/PR response was confirmed by a second scan at least 4 weeks after the initial response, with no evidence of progression between the initial and CR/PR confirmation visit were included.~CR: Disappearance of all target lesions (TLs) and non-TLs (NTLS) since baseline; any pathological lymph nodes selected as TLs must have a reduction in short axis to <10 millimeters (mm).~PR: At least a 30% decrease in the sum of the diameters of TL, referencing the baseline sum of diameters.~Data obtained up until progression, or last evaluable assessment in the absence of progression were included in the assessment of ORR." (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs). RECIST assessments were performed at baseline and every 8 weeks (+/- 1 week) after first doses of IPs until disease progression.

Intervention	percentage of patients (Number)
Cediranib + Olaparib	15.3

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Median Overall Survival (OS)

OS was defined as the time from the date of first dose of IP until death due to any cause regardless of whether the patient withdrew from treatment or received another anti-cancer therapy (i.e. date of death or censoring - date of first dose + 1). Any patient not known to have died at the time of analysis was censored based on the last recorded date on which the patient was known to be alive. The median OS was calculated using the Kaplan-Meier technique. (NCT02889900)
Timeframe: From baseline until death due to any cause, assessed until primary analysis DCO (8 months after last patient received their first dose of IPs).

Intervention	months (Median)
Cediranib + Olaparib	13.2

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Median Time to Treatment Discontinuation or Death (TDT)

The median time to discontinuation of IPs or death was defined as the time from the date of first dose of IP to the earlier of the date of discontinuation of both IPs, or death date. If 1 IP was discontinued before the other, the TDT reflected the time from the date of first dose to the earliest IP discontinuation date. The median TDT was calculated using the Kaplan-Meier technique. (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs).

Intervention	months (Median)
Cediranib + Olaparib	3.5

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ORR by Investigator Assessment Using RECIST 1.1

"The percentage of patients with a response (CR/PR), including patients with both confirmed and unconfirmed responses, based on investigator assessed RECIST 1.1 data is presented. Confirmed responses included patients whose CR/PR response was confirmed by a second scan at least 4 weeks after the initial response, with no evidence of progression between the initial and CR/PR confirmation visit.~CR: Disappearance of all TLs and NTLs since baseline; any pathological lymph nodes selected as TLs must have a reduction in short axis to <10 mm.~PR: At least a 30% decrease in the sum of the diameters of TL, referencing the baseline sum of diameters." (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs). RECIST assessments were performed at baseline and every 8 weeks (+/- 1 week) after first doses of IPs until disease progression.

Intervention	percentage of patients (Number)
Cediranib + Olaparib	26.7

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Best Observed Change From Baseline in EORTC QLQ-OV28

"The EORTC QLQ-OV28 is specific for ovarian cancer and consists of 28 items assessing abdominal/gastrointestinal symptoms (6 items), peripheral neuropathy (2 items), other chemotherapy side effects (5 items), hormonal symptoms (2 items), body image (2 items), attitudes to disease/treatment (3 items), sexuality (4 items) and 4 other single items.~Each scale was scored from 0 to 100 with higher scores on the symptom scales indicating greater symptom burden.~The best observed change from baseline is presented for each EORTC QLQ-OV28 scale, where a 10-point change in the score was used to identify patients who improved, stayed the same or deteriorated. The number of patients with a best observed change from baseline response of improved, stayed the same, or deteriorated in the EORTC QLQ-OV28 is presented." (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs). EORTC QLQ-OV28 assessments were performed at baseline and every 8 weeks relative to first dose until discontinuation of IPs.

Intervention	Participants (Count of Participants)
	Abdominal / Gastrointestinal: improved	Abdominal / Gastrointestinal: stayed the same	Abdominal / Gastrointestinal: deteriorated	Attitude to disease / treatment: improved	Attitude to disease / treatment: stayed the same	Attitude to disease / treatment: deteriorated	Body image: improved	Body image: stayed the same	Body image: deteriorated	Chemotherapy side effects: improved	Chemotherapy side effects: stayed the same	Chemotherapy side effects: deteriorated	Hormonal: improved	Hormonal: stayed the same	Hormonal: deteriorated	Other single items: improved	Other single items: stayed the same	Other single items: deteriorated	Peripheral neuropathy: improved	Peripheral neuropathy: stayed the same	Peripheral neuropathy: deteriorated	Sexuality: improved	Sexuality: stayed the same	Sexuality: deteriorated
Cediranib + Olaparib	2	18	12	3	16	13	7	19	6	1	24	7	2	25	5	1	19	12	1	24	7	2	26	4

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Best Observed Change From Baseline in European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ) C30 Scales

"The EORTC QLQ-C30 questionnaire assesses health-related quality of life (HRQoL). The questions are grouped into a global health status/QoL scale, 5 functional scales (physical, role, emotional, cognitive and social), 3 multi-item symptom scales (fatigue, pain, nausea/ vomiting), 5 single items assessing cancer symptoms (dyspnea, loss of appetite, insomnia, constipation, diarrhea), and 1 item on the financial impact of the disease.~Each scale/item is scored from 0 to 100. Higher scores on the global health status/QoL scale and functional scales indicate better health status/function. Higher scores on the symptom scales/items indicate a greater symptom burden.~A 10-point change in the score was used to identify patients who improved, stayed the same or deteriorated from baseline. The number of patients with a best observed change from baseline response of improved, stayed the same or deteriorated for each EORTC QLQ-C30 scale/item is presented." (NCT02889900)
Timeframe: From baseline to primary analysis DCO (8 months after last patient received their first dose of IPs). EORTC QLQ-C30 assessments were performed at baseline and every 8 weeks relative to first dose until discontinuation of IPs.

Intervention	Participants (Count of Participants)
	Appetite loss: improved	Appetite loss: stayed the same	Appetite loss: deteriorated	Cognitive functioning: improved	Cognitive functioning: stayed the same	Cognitive functioning: deteriorated	Constipation: improved	Constipation: stayed the same	Constipation: deteriorated	Diarrhea: improved	Diarrhea: stayed the same	Diarrhea: deteriorated	Dyspnea: improved	Dyspnea: stayed the same	Dyspnea: deteriorated	Emotional functioning: improved	Emotional functioning: stayed the same	Emotional functioning: deteriorated	Fatigue: improved	Fatigue: stayed the same	Fatigue: deteriorated	Financial difficulties: improved	Financial difficulties: stayed the same	Financial difficulties: deteriorated	Global Health Status / QoL: improved	Global Health Status / QoL: stayed the same	Global Health Status / QoL: deteriorated	Insomnia: improved	Insomnia: stayed the same	Insomnia: deteriorated	Nausea / vomiting: improved	Nausea / vomiting: stayed the same	Nausea / vomiting: deteriorated	Pain: improved	Pain: stayed the same	Pain: deteriorated	Physical functioning: improved	Physical functioning: stayed the same	Physical functioning: deteriorated	Role functioning: improved	Role functioning: stayed the same	Role functioning: deteriorated	Social functioning: improved	Social functioning: stayed the same	Social functioning: deteriorated
Cediranib + Olaparib	0	22	14	2	23	11	2	27	7	0	22	14	2	24	10	2	31	3	4	11	21	2	32	2	1	19	16	3	26	7	4	19	13	9	21	6	0	24	12	1	18	17	1	22	13

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Disease Control Rate (DCR) by ICR and Investigator Assessment Using RECIST 1.1

"The DCR was defined as the percentage of patients who had a best overall response of CR, PR or Stable Disease (SD) at 6 months.~CR: Disappearance of all TLs and NTLs since baseline; any pathological lymph nodes selected as TLs must have a reduction in short axis to <10 mm.~PR: At least a 30% decrease in the sum of the diameters of TL, referencing the baseline sum of diameters.~SD: Neither sufficient shrinkage of TLs to qualify for PR nor sufficient increase to qualify for progressive disease (PD) (at least a 20% increase in the sum of diameters of TLs with an absolute increase of at least 5 mm and progression of existing NTLs). Patients had to have demonstrated SD for at least 23 weeks following the start of treatment. The Investigator assessment was based on the FAS and the ICR used the EFR analysis set. The percentage of patients with disease control for each assessment is presented." (NCT02889900)
Timeframe: From baseline up to 6 months after first doses of IPs. RECIST assessments were performed at baseline and every 8 weeks (+/- 1 week) after first doses of IPs until disease progression.

Intervention	percentage of patients (Number)
	ICR assessment (EFR analysis set)	Investigator assessment (FAS)
Cediranib + Olaparib	23.7	26.7

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Maximum Tolerated Dose (MTD) of Olaparib Administered in Combination With Onalespib

"MTD was determined by testing increasing doses of the combination of olaparib PO and onalespib IV within dose escalation cohorts consisting of 3 to 6 evaluable participants. MTD reflects the highest dose combination that did not cause a Dose-Limiting Toxicity (DLT) in > 33% of participants. DLTs were defined based on the National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0.~Enrollment to this study was suspended prior to completion of the dose escalation due to discontinuation of further development of onalespib. A true single MTD therefore could not be determined. The two dose levels included in this outcome measure represent the highest well-tolerated dose combinations (Dose Level 2 [DL2]: Olaparib 300 mg PO BID and Onalespib 40 mg/m^2 IV; and Dose Level 2a [DL2a]: Olaparib 200 mg PO BID and Onalespib 80 mg/m^2 IV)." (NCT02898207)
Timeframe: Up to 35 days for each dose level cohort

Intervention	mg (Number)
	Dose Level 2 Olaparib PO BID	Dose Level 2a Olaparib PO BID
All Evaluable Participants	300	200

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Number of Participants Who Experienced Dose-Limiting Toxicities (DLTs)

DLTs were based on the NCI Common Terminology Criteria for Adverse Events (CTCAE) v.5.0 and were defined as any grade 3 or 4 non-hematologic toxicity (excluding grade 3: fatigue; diarrhea, constipation, and nausea and/or vomiting controlled with supportive measured within 24 hours; hypophosphatemia; hyponatremia; hypomagnesemia; and rash that resolves to < grade 3 within < 5 days), grade 4 neutropenia of > 7 day duration, febrile neutropenia, grade 4 thrombocytopenia or bleeding associated with grade 3 thrombocytopenia, requirement for repeated blood transfusion within 4-6 weeks, any other grade 4 hematologic toxicity, any study treatment-related death, any grade 3 or 4 event considered to be dose-limiting in the opinion of the investigator, and the inability to take 75% or more of the planned dose for olaparib and 4 out of 6 doses for onalespib within the DLT period due to treatment-related adverse events. (NCT02898207)
Timeframe: Within Cycles 0 and 1 (up to 35 days).

Intervention	Participants (Count of Participants)
Dose Level 0: Olaparib 200 mg and Onalespib 20 mg/m^2	0
Dose Level 1: Olaparib 200 mg and Onalespib 40 mg/m^2	0
Dose Level 2: Olaparib 300 mg and Onalespib 40 mg/m^2	0
Dose Level 3: Olaparib 300 mg and Onalespib 80 mg/m^	0
Dose Level 2a: Olaparib 200 mg and Onalespib 80 mg/m^2	2
Dose Level 3a: Olaparib 200 mg and Onalespib 120 mg/m^2	1

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Number of Participants Progression-Free for At Least 24 Weeks by RECIST 1.1

Responses determined per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT or MRI, where Progressive Disease (PD) represents (relative to baseline) at least a 20% increase in the sum of diameters of target lesions, appearance of one or more new lesions, or unequivocal progression of existing non-target lesions. The duration of progression-free status was defined as the interval from the date of enrollment to date of either PD or date of last disease assessment. (NCT02898207)
Timeframe: Up to 24 weeks

Intervention	Participants (Count of Participants)
Dose Level 0: Olaparib 200 mg and Onalespib 20 mg/m^2	1
Dose Level 1: Olaparib 200 mg and Onalespib 40 mg/m^2	2
Dose Level 2: Olaparib 300 mg and Onalespib 40 mg/m^2	1
Dose Level 3: Olaparib 300 mg and Onalespib 80 mg/m^2	1
Dose Level 2a: Olaparib 200 mg and Onalespib 80 mg/m^2	1
Dose Level 3a: Olaparib 200 mg and Onalespib 120 mg/m^2	1

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Number of Participants With Objective Responses by RECIST 1.1

Responses determined per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by CT or MRI, where Objective Response (OR) represents either a Complete Response (CR; disappearance of all target lesions) or a Partial Response (PR; at least a 30% decrease in the sum of the longest diameter of target lesions, taking as reference the baseline sum diameters). (NCT02898207)
Timeframe: Up to 63 weeks

Intervention	Participants (Count of Participants)
Dose Level 0: Olaparib 200 mg and Onalespib 20 mg/m^2	0
Dose Level 1: Olaparib 200 mg and Onalespib 40 mg/m^2	0
Dose Level 2: Olaparib 300 mg and Onalespib 40 mg/m^2	0
Dose Level 3: Olaparib 300 mg and Onalespib 80 mg/m^2	0
Dose Level 2a: Olaparib 200 mg and Onalespib 80 mg/m^2	0
Dose Level 3a: Olaparib 200 mg and Onalespib 120 mg/m^2	0

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Number of Participants Who Experienced Treatment-Related Toxicities

Treatment-related toxicities in this outcome include non-hematologic and hematologic adverse events that were either Grade 3+ or occurred in at least 10% of all treated participants, and were considered at least possibly related to olaparib and/or onalespib. Adverse events were graded according to the NCI Common Terminology Criteria for Adverse Events (CTCAE) v.5.0. (NCT02898207)
Timeframe: Up to 67 weeks

,,,,,

Intervention	Participants (Count of Participants)
	Diarrhea : Maximum Grade 1-2	Diarrhea : Maximum Grade 3	Nausea : Maximum Grade 1-2	Nausea : Maximum Grade 3	Anemia : Maximum Grade 1-2	Anemia : Maximum Grade 3	Thrombocytopenia/platelet count decrease : Maximum Grade 1-2	Thrombocytopenia/platelet count decrease : Maximum Grade 3	Fatigue : Maximum Grade 1-2	Vomiting : Maximum Grade 1-2	Vomiting : Maximum Grade 3	Abdominal pain : Maximum Grade 1-2	Abdominal pain : Maximum Grade 3	Anorexia : Maximum Grade 1-2	Neutrophil count decreased : Maximum Grade 1-2	Neutrophil count decreased : Maximum Grade 4	Lymphocyte count decreased : Maximum Grade 1-2	Lymphocyte count decreased : Maximum Grade 3	Floaters : Maximum Grade 1-2	Dysgeusia : Maximum Grade 1-2
Dose Level 0: Olaparib 200 mg and Onalespib 20 mg/m^2	3	0	1	1	2	0	0	0	1	1	1	1	0	1	0	0	0	0	0	0
Dose Level 1: Olaparib 200 mg and Onalespib 40 mg/m^2	3	0	2	0	3	0	3	0	3	1	0	1	0	1	0	0	0	0	1	1
Dose Level 2: Olaparib 300 mg and Onalespib 40 mg/m^2	3	0	4	0	2	0	1	0	3	3	0	0	1	1	1	0	0	0	0	0
Dose Level 2a: Olaparib 200 mg and Onalespib 80 mg/m^2	3	0	3	0	1	0	0	0	1	1	0	2	0	1	0	0	1	0	0	0
Dose Level 3: Olaparib 300 mg and Onalespib 80 mg/m^2	5	0	6	0	4	2	3	1	2	2	0	0	0	0	1	0	1	0	1	1
Dose Level 3a: Olaparib 200 mg and Onalespib 120 mg/m^2	4	1	2	0	1	3	3	1	2	0	0	0	0	1	1	1	1	1	2	2

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Maximum Tolerated Dose (MTD) of Onalespib Administered in Combination With Olaparib

MTD was determined by testing increasing doses of the combination of olaparib PO and onalespib IV within dose escalation cohorts consisting of 3 to 6 evaluable participants. MTD reflects the highest dose combination that did not cause a Dose-Limiting Toxicity (DLT) in > 33% of participants. DLTs were defined based on the National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. (NCT02898207)
Timeframe: Up to 35 days for each dose level cohort

Intervention	mg/m2 (Number)
	Dose Level 2 Onalespib IV on Days 1, 2, 8, 9, 15, and 16	Dose Level 2a Onalespib IV on Days 1, 2, 8, 9, 15, and 16
All Evaluable Participants	40	80

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Serum Concentrations of Durvalumab and Tremelimumab

Serum concentrations of Durvalumab and Tremelimumab are reported. (NCT02937818)
Timeframe: Durvalumab: Cycle 1 (each cycle was 4 weeks) Day 1(post-dose); Cycle 2 Day 1(pre-dose); Cycle 5 Day 1 (pre-dose); Tremelimumab: Cycle 1 (each cycle was 4 weeks) Day 1 (post-dose); Cycle 2 Day 1 (pre-dose); Cycle 5 Day 1 (No dose); Cycle 7 Day 1 (No dose)

Intervention	μg/mL (Geometric Mean)
	Durvalumab: Cycle 1 Day 1 (Post-dose)	Durvalumab: Cycle 2 Day 1 (Pre-dose)	Durvalumab: Cycle 5 Day 1 (Pre-dose)	Tremelimumab: Cycle 1 Day 1 (Post-dose)	Tremelimumab: Cycle 2 Day 1 (Pre-dose)	Tremelimumab: Cycle 5 Day 1 (No dose)	Tremelimumab: Cycle 7 Day 1 (No dose)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	391.192	55.590	116.846	18.299	2.650	5.005	0.784

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Plasma Concentrations of Adavosertib and Carboplatin

Plasma concentrations of Adavosertib and Carboplatin are reported. (NCT02937818)
Timeframe: Adavosertib: Cycle 1 (each cycle was 21 days) Day 3 (pre-dose and post-dose); Cycle 3 Day 3 (pre-dose and post-dose); Carboplatin: Cycle 1 (each cycle was 21 days) Day 1 (post-dose)

Intervention	nM (Geometric Mean)
	Adavosertib: Cycle 1 Day 3 (Pre-dose)	Adavosertib: Cycle 1 Day 3 (Post-dose)	Adavosertib: Cycle 3 Day 3 (Pre-dose)	Adavosertib: Cycle 3 Day 3 (Post-dose)	Carboplatin: Cycle 1 Day 1 (Post-dose)
Arm B: Adavosertib + Carboplatin	551.489	728.342	606.571	805.270	12834.615

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Partial Area Under the Concentration-time Curve (AUC0-6)

Partial area under the concentration-time curve for ceralasertib and olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 1 (post-dose) and Cycle 1 Day 7 (pre-dose and post-dose)

Intervention	h*µg/mL (Geometric Mean)
	Cycle 1, Day 1	Cycle 1, Day 7
Ceralasertib (AZD6738)	18.346	23.666
Olaparib	26.356	42.016

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Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

An AE is the development of an undesirable medical condition or the deterioration of a pre-existing medical condition following or during exposure to a pharmaceutical product, whether or not considered causally related to the product. SAE is an AE that results in any untoward medical occurrence that results in death, is life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability, or is a significant medical event. (NCT02937818)
Timeframe: Day 1 until disease progression, and follow-up visit (Up to 3.5 Years)

,,,

Intervention	Participants (Count of Participants)
	Any AE	Any AE causally related to any study treatment	Any AE with outcome = death	Any SAE	Any AE leading to discontinuation of any study treatment
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	17	9	0	8	4
Arm A: Durvalumab + Tremelimumab (Original Cohort)	16	10	1	6	2
Arm B: Adavosertib + Carboplatin	8	8	1	4	1
Arm C: Ceralasertib (AZD6738) + Olaparib	18	16	1	7	1

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Area Under the Concentration-time Curve From Time Zero to the Last Measurable Concentration (AUC0-t)

Area under the concentration-time curve from time zero to the last measurable concentration for Ceralasertib and Olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 1 (post-dose) and Cycle 1 Day 7 (pre-dose and post-dose)

Intervention	h*µg/mL (Geometric Mean)
	Cycle 1, Day 1	Cycle 1, Day 7
Ceralasertib (AZD6738)	18.575	24.061
Olaparib	26.973	62.535

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Time to Response (TTR)

The TTR (per RECIST 1.1 as assessed by the Investigator) was defined as the time from the date of first dose until the first date of documented response. (NCT02937818)
Timeframe: Until disease progression or data cut-off or Death (Up to 3.5 Years)

Intervention	Months (Median)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	1.8
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	1.8
Arm C: Ceralasertib (AZD6738) + Olaparib	1.7

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Time to Maximum Concentration at Steady State (Tmax,ss)

Time to maximum concentration at steady state for Ceralasertib and Olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 7 (pre-dose and post-dose)

Intervention	Hour (Median)
Ceralasertib (AZD6738)	1.875
Olaparib	2.708

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Time to Maximum Concentration (Tmax)

Time to maximum concentration for ceralasertib and olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 1 (post-dose)

Intervention	Hour (Median)
Ceralasertib (AZD6738)	1.250
Olaparib	1.800

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Progression Free Survival (PFS)

The PFS (per RECIST 1.1 according to the Investigator's assessment) was defined as the time from the date of the first dose of study treatment until the date of objective disease progression or death (by any cause in the absence of progression) regardless of whether the participant withdrew from allocated therapy or received another anti-cancer therapy prior to progression. (NCT02937818)
Timeframe: Until disease progression or data cut-off or Death (Up to 3.5 Years)

Intervention	Months (Median)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	1.91
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	1.77
Arm B: Adavosertib + Carboplatin	2.60
Arm C: Ceralasertib (AZD6738) + Olaparib	2.92

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Percentage of Participants With Disease Control at 12 Weeks

The disease control rate (DCR) at 12 weeks was defined as the percentage of participants who had a best objective response of CR or PR in the first 13 weeks or who had demonstrated stable disease (SD) for a minimum interval of 11 weeks following the start of study treatment. The DCR was determined programmatically based on RECIST 1.1 using site Investigator data and all data up until the first progression event. (NCT02937818)
Timeframe: At 12 Weeks

Intervention	Percentage of Participants (Number)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	38.1
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	15.0
Arm B: Adavosertib + Carboplatin	30.0
Arm C: Ceralasertib (AZD6738) + Olaparib	38.1

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Overall Survival (OS)

The OS was defined as the time from the date of the first dose of study treatment until death due to any cause. (NCT02937818)
Timeframe: Until disease progression or data cut-off or Death (Up to 3.5 Years)

Intervention	Months (Median)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	5.95
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	3.37
Arm B: Adavosertib + Carboplatin	4.67
Arm C: Ceralasertib (AZD6738) + Olaparib	7.56

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Apparent Clearance of Drug at Steady State at Steady State (CLss/F)

Area under the concentration-time curve at steady state at steady state for Ceralasertib and Olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 7 (pre-dose and post-dose)

Intervention	Litre/hour (Geometric Mean)
Ceralasertib (AZD6738)	NA
Olaparib	4.416

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Number of Participants With Overall Response

Overall Response Rate (ORR) using Investigator assessments according to Response Evaluation Criteria In Solid Tumors (RECIST) 1.1. ORR was defined as the number (percentage) of participants with a confirmed Complete Response (CR) or confirmed Partial Response (PR) and was estimated for each treatment arm with corresponding 2-sided 95% exact confidence intervals (CIs). A confirmed response of CR/PR meant that a response of CR/PR was recorded at one visit and confirmed by repeat imaging, preferably at the next regularly scheduled imaging visit, and not less than 4 weeks after the visit when the response was first observed, with no evidence of progression between the initial and CR/PR confirmation visit. (NCT02937818)
Timeframe: Until disease progression [PD] (Up to 3.5 Years)

Intervention	Participants (Count of Participants)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	2
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	1
Arm B: Adavosertib + Carboplatin	0
Arm C: Ceralasertib (AZD6738) + Olaparib	1

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Area Under the Concentration-time Curve at Steady State (AUCss)

Intervention	h*µg/mL (Geometric Mean)
Ceralasertib (AZD6738)	NA
Olaparib	67.929

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Minimum Concentration at Steady State (Cmin,ss)

Minimum concentration at steady state for Ceralasertib and Olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 7 (pre-dose and post-dose)

Intervention	µg/mL (Geometric Mean)
Ceralasertib (AZD6738)	1.119
Olaparib	2.376

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Maximum Concentration at Steady State (Cmax,ss)

Maximum concentration at steady state for Ceralasertib and Olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 7 (pre-dose and post-dose)

Intervention	µg/mL (Geometric Mean)
Ceralasertib (AZD6738)	5.176
Olaparib	9.189

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Maximum Concentration (Cmax)

Maximum concentration for ceralasertib and olaparib are reported. (NCT02937818)
Timeframe: Cycle 1 (each cycle was 28 days in length) Day 1 (post-dose)

Intervention	µg/mL (Geometric Mean)
Ceralasertib (AZD6738)	4.215
Olaparib	6.558

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Duration of Response (DoR)

The DoR was defined as the time from the date of first documented response (which was subsequently confirmed) CR/PR until the date of documented progression, or death in the absence of disease progression. The DoR in participants with confirmed objective response are reported. (NCT02937818)
Timeframe: Until disease progression or data cut-off or Death (Up to 3.5 Years)

Intervention	Months (Median)
Arm A: Durvalumab + Tremelimumab (Original Cohort)	NA
Arm A: Durvalumab + Tremelimumab (Expansion Cohort)	3
Arm C: Ceralasertib (AZD6738) + Olaparib	8.5

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Overall Survival (OS)

OS will be summarized and analyzed descriptively via summary frequencies and Kaplan-Meier estimators. (NCT02953457)
Timeframe: 35 months

Intervention	Months (Median)
Treatment I (Olaparib, Tremelimumab, Durvalumab)	14.9
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab)- Platinum Resistant Patients	9.1
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Sensitive Patients	21.6

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Incidence of Dose-limiting Toxicities (DLTs) Defined as the Rate of Drug-related Grade 3-5 Adverse Events Assessed Using the National Cancer Institute Common Terminology Criteria for Adverse Events Version 4.03 (Phase I)

The maximum tolerated dose is defined as the highest dose studied, for which the observed incidence of DLT is less than 33%. Number of Participants with Dose-limiting Toxicities (DLTs) in Phase I and Phase II will be reported. (NCT02953457)
Timeframe: Up to 8 weeks

Intervention	Participants (Count of Participants)
Phase I Treatment (Olaparib, Tremelimumab, Durvalumab)	2
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Resistant Patients	0
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Sensitive Patients	0

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6 Month Progression Free Survival (PFS) in the Platinum Sensitive Group (Phase II)

6-month progression-free survival rate is the probability of patients remaining alive and progression-free at 6 months from study entry estimated using Kaplan-Meier methods. Per RECIST 1.0 criteria: progressive disease (PD) is at least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesion (NCT02953457)
Timeframe: At 6 months

Intervention	Proportion of participants (Number)
Phase I Treatment (Olaparib, Tremelimumab, Durvalumab)	0.27
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Resistant Patients	0.21
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Sensitive Patients	0.60

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3 Month Progression Free Survival (PFS) in the All Eligible Patients by Group/Arm

Progression free survival (PFS) rate will be assessed at 3 months in the platinum resistant group using Kaplan-Meier methods. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT02953457)
Timeframe: At 3 months

Intervention	Proportion of participants (Number)
Phase I Treatment (Olaparib, Tremelimumab, Durvalumab)	0.5
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Resistant Patients	0.42
Phase II Treatment (Olaparib, Tremelimumab, Durvalumab) - Platinum Sensitive Patients	0.88

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Progression Free Survival

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using progression free survival (NCT02983799)
Timeframe: From first dose to earlier date of assessment of objective progression or death by any cause in the absence of progression (up to 36 months)

Intervention	Months (Median)
Cohort 1	11
Cohort 2	10.8
COHORT 3	7.2
COHORT 4	5.4
Unassigned	9.2

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HRD Status as Per HRRm Gene Panel Assessment Will be Correlated With Clinical Outcome (ORR) for Subjects Enrolled in the 2 Cohorts With BRCAwt (Cohorts 3 and 4)

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using HRRm gene panel status related to clinical outcome (NCT02983799)
Timeframe: At baseline

Intervention	Percent (Number)
Cohort 3, HRRm Pos	11.1
Cohort 3, HRRm Neg	32.1
Cohort 4, HRRm Pos	8.3
Cohort 4, HRRm Neg	10.5

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Overall Survival

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using overall survival (NCT02983799)
Timeframe: From date of first dose to date of death from any cause (up to 48 months)

Intervention	Months (Median)
Cohort 1	NA
Cohort 2	NA
COHORT 3	NA
COHORT 4	23.8
Unassigned	18

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Time to Any Progression

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using time to any progression (NCT02983799)
Timeframe: From first dose to earlier date of CA-125 progression or RECIST v1.1 progression, or death by any cause in absence of progression (up to 36 months)

Intervention	Months (Median)
Cohort 1	10.9
Cohort 2	11.1
COHORT 3	7.2
COHORT 4	5.3
Unassigned	7.3

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Objective Response Rate, Defined as the Percentage of Subjects With a Best Overall Response of Confirmed Complete Response (CR) or Partial Response (PR)

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using ORR according to RECIST v1.1 criteria (Investigator determined) (NCT02983799)
Timeframe: From first dose up until progression, or last evaluable assessment in the absence of progression (up to 36 months)

Intervention	Percent (Number)
Cohort 1	69.3
Cohort 2	64.0
COHORT 3	29.4
COHORT 4	10.1
Unassigned	30.8

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CA-125 Response Rate, Defined as the Percentage of Subjects With a CA-125 Response According to GCIG Criteria Divided by the Number of Subjects Evaluable for CA-125 Response

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using CA-125 response rate (NCT02983799)
Timeframe: From baseline to Day 1 of each cycle and end of study treatment visit (up to 36 months)

Intervention	Percent (Number)
Cohort 1	93.2
Cohort 2	70.0
COHORT 3	47.9
COHORT 4	26.6
Unassigned	66.7

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Disease Control Rate Defined as the Percentage of Subjects Who Have a Best Overall Response of CR or PR or SD at Greater Than or Equal to 8 Weeks Divided by the Number of Subjects in the Efficacy Analysis Set, Prior to Any PD Event

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using disease control rate (DCR). DCR is defined as the percentage of subjects with a best overall response of CR or PR (at any time up to and including the defined analysis cut-off point) or who have demonstrated stable disease (SD) for at least 8 weeks from first dose, divided by the number of subjects in the efficacy analysis set. (NCT02983799)
Timeframe: From first dose up until progression, or last evaluable assessment in the absence of progression

Intervention	Percent (Number)
Cohort 1	96.0
Cohort 2	100.0
COHORT 3	79.4
COHORT 4	75.3
Unassigned	92.3

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Duration of Response, for Those Subjects With a Confirmed Response of CR or PR

To determine the clinical effectiveness of olaparib treatment in each of 4 cohorts assessed using duration of response (NCT02983799)
Timeframe: From the date of the measurement criteria for CR or PR are first met until the date of documented progression or death in the absence of disease progression (up to 36 months)

Intervention	Months (Median)
Cohort 1	9.4
Cohort 2	14.7
COHORT 3	10.0
COHORT 4	5.3
Unassigned	7.5

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Radiological Progression Free Survival (rPFS) by Blinded Independent Central Review (BICR) - Cohort A Only

The time from randomisation until the date of objective radiological disease progression (determined by RECIST 1.1 (soft tissue) and Prostate Cancer Working Group 3 (PCWG-3) (bone)) or death (by any cause in the absence of progression) regardless of whether the patient withdrew from randomised therapy or received another anti-cancer therapy prior to progression. Progression is defined using (i) Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) for soft tissue, as a >=20% increase in the sum of diameters of target lesions and an absolute increase of >=5mm taking as reference the smallest sum of diameters since treatment started including the baseline sum of diameters; (ii) Prostate Cancer Working Group 3 (PGWG-3) for bone as >= 2 new bone lesions on the 1st week 8 scan compared to baseline. The confirmatory scan, >=6 weeks later, must show >=2 more new bone lesions (for a total of >=4 new bone lesions since baseline). (NCT02987543)
Timeframe: Tumor assessments every 8 weeks from randomisation until radiographic progression assessed by BICR (median duration of treatment of 7 and 4 months for Olaparib and Investigators Choice of NHA respectively).

Intervention	Months (Median)
Cohort A Olaparib 300mg bd	7.39
Cohort A Investigators Choice of NHA	3.55

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Time to Pain Progression - Cohort A Only

Time from randomisation to time point at which worsening in pain is observed (ie date of pain progression - date of randomisation + 1). Based on average Brief Pain Inventory - short form (BPI-SF) worst pain [Item 3] and Analgesic Quantification Algorithm [AQA] score. (NCT02987543)
Timeframe: Every 4 weeks from randomisation (for 7 consecutive days) throughout the study (median duration of treatment of 7 and 4 months for Olaparib and Investigators Choice of NHA respectively).

Intervention	Months (Median)
Cohort A Olaparib 300mg bd	NA
Cohort A Investigators Choice of NHA	9.92

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Radiological Progression Free Survival (rPFS) by Blinded Independent Central Review (BICR) - Cohort A+B

The time from randomisation until the date of objective radiological disease progression (by RECIST 1.1 and Prostate Cancer Working Group 3 (PGWG-3)) or death (by any cause in the absence of progression) regardless of whether the patient withdrew from randomised therapy or received another anti-cancer therapy prior to progression. (NCT02987543)
Timeframe: Tumor assessments every 8 weeks from randomisation until radiographic progression assessed by BICR (median duration of treatment of 7 and 4 months for Olaparib and Investigators Choice of NHA respectively).

Intervention	Months (Median)
Cohort A Olaparib 300mg bd	5.82
Cohort A Investigators Choice of NHA	3.52

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Efficacy: Time to Second Subsequent Treatment Commencement (TSST)

TSST was assessed as time from randomisation to second subsequent treatment commencement or death if this occurs before commencement of second subsequent treatment. Any patient not known to have had a further second subsequent therapy or death was censored at the last known time to have not received second subsequent therapy (NCT03106987)
Timeframe: From follow-up i.e. 30 days after last dose of study medication till end of study (assessed every 12 weeks upto 3.8 years)

Intervention	Months (Median)
Olaparib (BRCA1/2 +ve)	13.1
Placebo (BRCA1/2 +ve)	11.7
Olaparib (BRCA1/2 -ve)	15.4
Placebo (BRCA1/2 -ve)	12.7

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Efficacy: Change From Baseline in Health-related Quality of Life (HRQoL)

Health related quality of life (HRQoL) of Olaparib maintenance retreatment compared to placebo as measured by the Functional Assessment of Cancer Therapy - Ovarian (FACT-O) Trial Outcome Index (TOI) was determined. HRQoL was analysed using the FACT-O tool by mixed model for repeated measures (MMRM) analysis of the change from baseline in TOI score. FACT-O TOI is scored from O to 100 with higher scores denoting better quality of life. The higher the score, the better the HRQoL. (NCT03106987)
Timeframe: At Baseline, and from Day 1 until objective disease progression (assessed upto 2 years)

Intervention	Change in scores (Mean)
Olaparib (BRCA1/2 +ve)	-1.27
Placebo (BRCA1/2 +ve)	1.67
Olaparib (BRCA1/2 -ve)	-2.08
Placebo (BRCA1/2 -ve)	0.58

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Efficacy: Time to Progression by Gynecologic Cancer Intergroup (GCIG) Criteria

Time to progression by RECIST or CA-125 or death is defined as the time from randomisation to the earlier date of RECIST progression or CA-125 progression or death by any cause. Patients without a CA-125 progression or a RECIST progression who are still alive at the time of analysis will be censored at the time of their last evaluable RECIST assessment and/or their last available CA-125 measurement, whichever is the earliest at the time of analysis. Patients that do not have any evaluable RECIST assessments or any CA-125 results post-randomisation will be censored at the date of randomisation (NCT03106987)
Timeframe: At screening (Visit 1) and at every 12 weeks (±7 days), until objective disease progression, based on progressive serial elevation of serum CA-125 according to the GCIG criteria, or until discontinuation for other reasons (assessed upto 3.8 years)

Intervention	Months (Median)
Olaparib (BRCA1/2 +ve)	2.8
Placebo (BRCA1/2 +ve)	2.8
Olaparib (BRCA1/2 -ve)	2.9
Placebo (BRCA1/2 -ve)	2.79

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Efficacy: Overall Survival (OS)

OS was defined as the time from the date of randomisation until death due to any cause. Any patient not known to have died at the time of analysis was censored based on the last recorded date on which the patient was known to be alive (NCT03106987)
Timeframe: From randomisation till Long-term follow-up (12-weekly beyond 30 days after last dose of study treatment) assessed upto 3.8 years

Intervention	Months (Median)
Olaparib (BRCA1/2 +ve)	20.1
Placebo (BRCA1/2 +ve)	20.9
Olaparib (BRCA1/2 -ve)	23.2
Placebo (BRCA1/2 -ve)	30.2

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Efficacy: Progression-free Survival (PFS)

PFS (per RECIST 1.1) was defined as the time from randomisation until the date of Investigator assessed objective radiological disease progression or death (by any cause in the absence of disease progression). Objective progression (per RECIST 1.1) is defined as at least a 20% increase in the sum of the diameters of the target lesions and an absolute increase of >5 mm, or an overall non-target lesion assessment of progression or a new lesion. Patients who have not progressed or died at the time of analysis were censored at the time of the latest date of assessment from their last evaluable RECIST assessment. (NCT03106987)
Timeframe: At randomization visit and at every 12 weeks (+/- 7 days) until objective radiological disease progression as determined by the investigator or other discontinuation criteria are met (assessed upto 3.8 years)

Intervention	Months (Median)
Olaparib (BRCA1/2 +ve)	4.3
Placebo (BRCA1/2 +ve)	2.8
Olaparib (BRCA1/2 -ve)	5.3
Placebo (BRCA1/2 -ve)	2.8

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Number of Patients With Adverse Events (AEs), and Serious Adverse Events (SAEs)

All AEs/serious adverse events (SAEs) reported during the study were recorded. (NCT03106987)
Timeframe: At Baseline and from Day 1 till follow-up i.e. 30 days after last dose of study medication (assessed upto 3.8 years)

,,,

Intervention	Participants (Count of Participants)
	Any Treatment emergent adverse event (TEAE)	Any TEAE causally related to treatment	Any TEAE of Common Terminology Criteria for Adverse Events (CTCAE) grade 3 or higher	Any TEAE of CTCAE grade 3 or higher, causally related to treatment	Any TEAE with outcome = death	Any TEAE with outcome = death, causally related to treatment	Any treatment-emergent SAE (including events with outcome = death)	Any treatment-emergent SAE (including events with outcome = death), causally related to treatment	Any TEAE leading to discontinuation of study medication	Any TEAE leading to discontinuation of study medication, causally related to treatment	Any TEAE leading to dose modification	Any TEAE leading to dose modification, causally related to treatment
Olaparib (BRCA1/2 -ve)	66	53	15	5	0	0	11	3	1	0	28	21
Olaparib (BRCA1/2 +ve)	64	50	11	5	0	0	5	1	2	1	18	14
Placebo (BRCA1/2 -ve)	31	14	3	1	0	0	2	0	0	0	2	1
Placebo (BRCA1/2 +ve)	33	23	2	1	0	0	0	0	0	0	6	5

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Number of Patients With Adverse Event of Special Interest (AESI).

All AESIs reported during the study were recorded. (NCT03106987)
Timeframe: At Baseline and from Day 1 till long-term follow-up i.e. 12-weekly beyond 30 days after last dose of study treatment (assessed upto 3.8 years)

Intervention	Participants (Count of Participants)
Olaparib (BRCA1/2 +ve)	1
Placebo (BRCA1/2 +ve)	1
Olaparib (BRCA1/2 -ve)	1
Placebo (BRCA1/2 -ve)	0

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Efficacy: Time to Study Treatment Discontinuation (TDT)

TDT was assessed as time from randomisation to study treatment discontinuation or death if this occurs before discontinuation of study treatment. Any patient not known to have died at the time of analysis and not known to have discontinued study treatment was censored based on the last recorded date on which the patient was known to be alive (NCT03106987)
Timeframe: From follow-up 30 days after last dose of study medication till long-term follow-up i.e. 12-weekly beyond 30 days after last dose of study treatment

Intervention	Months (Median)
Olaparib (BRCA1/2 +ve)	4.5
Placebo (BRCA1/2 +ve)	3.4
Olaparib (BRCA1/2 -ve)	5.6
Placebo (BRCA1/2 -ve)	3.1

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Efficacy: Time to First Subsequent Treatment Commencement (TFST)

TFST was assessed as time from randomisation to first subsequent treatment commencement or death if this occurs before commencement of first subsequent treatment. Any patient not known to have had a further subsequent therapy or death was censored at the last known time to have not received subsequent therapy (NCT03106987)
Timeframe: From follow-up i.e. 30 days after last dose of study medication till end of study (assessed every 12 weeks upto 3.8 years)

Intervention	Months (Median)
Olaparib (BRCA1/2 +ve)	5.8
Placebo (BRCA1/2 +ve)	5.1
Olaparib (BRCA1/2 -ve)	7.9
Placebo (BRCA1/2 -ve)	4.3

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Clinical Benefit Rate (CBR) as Measured by the Number of Participants Achieving Complete Response (CR), Partial Response (PR) or Stable Disease for ≥ 24 Weeks (SD) as Defined by RECIST 1.1. (Olaparib Alone)

To determine the efficacy of maintenance olaparib following platinum-based chemotherapy as assessed by clinical benefit rate (CBR) based on RECIST 1.1 (Response Evaluation Criteria In Solid Tumors Criteria). Per RECIST v1.1 for target lesions and assessed by CT or MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive Disease (PD); Clinical Benefit (CB) = CR + PR + SD for >= 24 weeks. (NCT03167619)
Timeframe: Assessed every 8 weeks from date of randomization until documented disease progression or last patient contact, approximately 1 year

Intervention	Participants (Count of Participants)
A - Olaparib Alone	9

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Clinical Benefit Rate (CBR) as Measured by the Number of Participants Achieving Complete Response (CR), Partial Response (PR) or Stable Disease for ≥ 24 Weeks (SD) as Defined by RECIST 1.1. (Olaparib in Combination With Durvalumab)

To determine the efficacy of maintenance olaparib in combination with durvalumab following platinum-based chemotherapy as assessed by clinical benefit rate (CBR) based on RECIST 1.1 (Response Evaluation Criteria In Solid Tumors Criteria). Per RECIST v1.1 for target lesions and assessed by CT or MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Stable Disease (SD), neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for Progressive Disease (PD); Clinical Benefit (CB) = CR + PR + SD for >= 24 weeks. (NCT03167619)
Timeframe: Assessed every 8 weeks from date of randomization until documented disease progression or last patient contact, approximately 1 year

Intervention	Participants (Count of Participants)
B - Olaparib Plus Durvalumab	8

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Efficacy of Olaparib in Combination With Durvalumab as Assessed by PFS (Progression-free Survival)

PFS, as defined as the time from randomization to the first occurrence of disease progression (as determined using RECIST v1.1 criteria and assessed by the investigator) or death from any cause on study for olaparib in combination with durvalumab. Death on study is defined as death from any cause within 30 days of the last dose of study treatment regimen. Reported as (disease progression or death) events per month. (NCT03167619)
Timeframe: From date of randomization until the date of documented progression or date of death, whichever came first, approximately 1 year.

Intervention	events/month (Mean)
B - Olaparib Plus Durvalumab	0.11

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Overall Response Rate (ORR) as Measured by Number of Participants Achieving Complete Response (CR) or Partial Response (PR) as Defined by RECIST 1.1 (Olaparib Alone)

To determine the efficacy of maintenance olaparib following platinum-based chemotherapy as assessed by overall response rate (ORR) based on RECIST 1.1 (Response Evaluation Criteria In Solid Tumors Criteria). Per RECIST v1.1 for target lesions and assessed by CT or MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT03167619)
Timeframe: Assessed every 8 weeks from date of randomization until documented disease progression or last patient contact, approximately 1 year

Intervention	Participants (Count of Participants)
A - Olaparib Alone	5

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Efficacy of Olaparib Alone as Assessed by PFS (Progression-free Survival) Reported as Events Per Month

PFS, defined as the time from randomization to the first occurrence of disease progression or death from any cause on study for olaparib alone. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.1) as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. Death on study is defined as death from any cause within 30 days of the last dose of study treatment regimen. Reported as events (disease progression or death) per month. (NCT03167619)
Timeframe: From date of randomization until the date of documented progression or date of death, whichever came first, approximately 1 year.

Intervention	events/month (Mean)
A - Olaparib Alone	0.18

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Overall Survival (Olaparib in Combination With Durvalumab)

To determine the efficacy of maintenance olaparib in combination with durvalumab following platinum based chemotherapy as assessed by overall survival (OS). (NCT03167619)
Timeframe: From date of randomization until death or last patient contact, approximately 2 years

Intervention	months (Median)
B - Olaparib Plus Durvalumab	18.27

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Overall Survival (Olaparib Alone)

To determine the efficacy of maintenance olaparib following platinum based chemotherapy as assessed by overall survival (OS). (NCT03167619)
Timeframe: From date of randomization until death or last patient contact, approximately 2 years

Intervention	months (Median)
A - Olaparib Alone	21.68

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Overall Response Rate (ORR) as Measured by Number of Participants Achieving Complete Response (CR) or Partial Response (PR) as Defined by RECIST 1.1 (Olaparib in Combination With Durvalumab)

To determine the efficacy of maintenance olaparib in combination with durvalumab following platinum-based chemotherapy as assessed by overall response rate (ORR) based on RECIST 1.1 (Response Evaluation Criteria In Solid Tumors Criteria). Per RECIST v1.1 for target lesions and assessed by CT or MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT03167619)
Timeframe: Assessed every 8 weeks from date of randomization until documented disease progression or last patient contact, approximately 1 year

Intervention	Participants (Count of Participants)
B - Olaparib Plus Durvalumab	3

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Clinical Response Rate (CRR) in Germline BRCA Mutated Participants

The clinical effectiveness of olaparib treatment in HER2-ve metastatic breast cancer participants in a real-world setting by assessment of clinical response rate and duration of clinical response in germline BRCA mutated participants was determined. CRR is defined as the percentage of patients assessed by the Investigator as responding. Response in gBRCAm patients were based on the Investigator's assessment. Data obtained up until progression, or last evaluable assessment in the absence of progression, will be included in the assessment of CRR. However, any responses, which occurred after a further anticancer therapy was received, will not be included in the numerator for the CRR calculation. (NCT03286842)
Timeframe: At every visit until disease progression or death or end of study (up to 3 years)

Intervention	Percentage of participants (Number)
Olaparib gBRCAm Cohort	49.6

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Duration of Clinical Response (DoCR) in Germline BRCA Mutated Participants

The clinical effectiveness of olaparib treatment in HER2-ve metastatic breast cancer participants in a real-world setting by assessment of clinical response rate and duration of clinical response in germline BRCA mutated participants was determined. DoCR is defined as the time from the date the Investigator first assessed the patient as responding to the date the Investigator assessed the patient as progressing or the date of death from any cause. The end of response should coincide with the date of progression or death used for the PFS endpoint. The time of the initial response will be defined as the latest of the dates contributing towards the first visit response. If a patient does not progress following a response, they will be censored at the PFS censoring date. (NCT03286842)
Timeframe: At every visit until disease progression or death or end of study (up to 3 years)

Intervention	Months (Median)
Olaparib gBRCAm Cohort	8.0

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Overall Survival (OS) in Germline BRCA Mutated Participants

The clinical effectiveness of olaparib treatment in HER2-ve metastatic breast cancer participants in a real-world setting by assessment of overall survival in germline BRCA mutated participants was determined. OS is defined as the time from first dose of olaparib to the date of death from any cause. (NCT03286842)
Timeframe: At every visit and until death or end of study (up to 3 years)

Intervention	months (Median)
Olaparib gBRCAm Cohort	24.94

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Progression-free Survival (PFS) in Real-world Setting in Germline BRCA Mutated Participants

The clinical effectiveness of olaparib treatment in HER2-ve metastatic breast cancer participants in a real-world setting through assessment of PFS in germline BRCA mutated patients was evaluated. PFS is defined as the time from first dose of olaparib to the date of progression or death from any cause. In this study, disease progression in gBRCAm patients will be based on Investigator assessment, i.e. radiological ( e.g. RECIST) progression, symptomatic progression, or clear progression of non-measurable disease, as long as progression can be documented. (NCT03286842)
Timeframe: At every visit until the earliest of disease progression, death or end of study (up to 3 years)

Intervention	months (Median)
Olaparib gBRCAm Cohort	8.18

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Time to First Subsequent Treatment or Death (TFST) in Germline BRCA Mutated Participants

Intervention	months (Median)
Olaparib gBRCAm Cohort	9.40

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Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

The safety and tolerability of olaparib treatment in HER2-ve metastatic breast cancer patients in a real-word setting was evaluated. (NCT03286842)
Timeframe: From Screening (Day -28 to Day -1) until post DCO [up to 3 years]

Intervention	Participants (Count of Participants)
	Any AE	Any AE casually related to study treatment	Any AE of CTCAE grade 3 or higher	Any AE of CTCAE grade 3 or higher, causally related to study treatment	Any AE with outcome = death	Any AE with outcome = death, causally related to study treatment	Any SAE (including events with outcome = death)	Any SAE (including events with outcome = death), causally related to study treatment	Any AE leading to discontinuation of study treatment	Any AE leading to discontinuation of study treatment, causally related to study treatment
Olaparib gBRCAm Cohort	243	214	69	44	0	0	32	10	16	11
Olaparib sBRCAm Cohort	3	3	2	1	0	0	1	0	0	0

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Time to Study Treatment Discontinuation or Death (TDT) in Germline BRCA Mutated Participants

Intervention	months (Median)
Olaparib gBRCAm Cohort	7.98

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Time to Second Subsequent Treatment or Death (TSST) in Germline BRCA Mutated Participants

Intervention	months (Median)
Olaparib gBRCAm Cohort	14.72

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Time to Second Progression or Death (PFS2) in Germline BRCA Mutated Participants

The clinical effectiveness of olaparib treatment in HER2-ve metastatic breast cancer participants in a real-world setting by assessment of time to use of subsequent therapies, second progression, and study treatment discontinuation in germline BRCA mutated participants was determined. PFS2 is defined as the time from first dose of olaparib to the earliest progression event subsequent to that used for the primary variable PFS or death from any cause. Patients alive and for whom a second disease progression has not been observed will be censored at the last time known to be alive and without a second disease progression. In this study, disease progression in gBRCAm patients will be based on Investigator assessment, i.e. radiological ( e.g. RECIST) progression, symptomatic progression, or clear progression of non-measurable disease, as long as progression can be documented (NCT03286842)
Timeframe: At every visit until second progression or death or end of study (up to 3 years)

Intervention	months (Median)
Olaparib gBRCAm Cohort	14.49

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Overall Survival (OS)

Overall survival was defined as the time from the date of randomisation until death due to any cause. Any patient not known to have died at the time of data cut-off was censored based on the last recorded date on which the patient was known to be alive. Here, the study patient population was stratified as follows: BRCAm patients; non BRCAm HRRm patients; non HRRm patients. (NCT03330847)
Timeframe: From the date of randomisation until time of data cut-off date or death due to any cause (assessed up to 32 months)

Intervention	Months (Median)
	BRCAm patients	non BRCAm HRRm patients	non HRRm patients
Olaparib + Adavosertib	22.8	8.0	10.6
Olaparib + Ceralasertib	15.5	12.4	10.3
Olaparib Monotherapy	20.4	8.4	9.2

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Objective Response Rate (ORR) (Per BICR and Per Sensitivity Analysis)

The ORR was defined using BICR data to define a visit response of CR or PR, with denominator defined as number of patients in FAS. For sensitivity analysis, ORR is defined as the percentage of patients with at least one investigator-assessed visit response of CR or PR, with denominator defined as number of patients in FAS. These are summarized using adjusted response rates, which are computed with a logistic regression including factors study treatment and prior platinum-based therapy (no, yes), i.e. these response rates are adjusted for prior platinum-based therapy, which is one of the randomisation stratification factors. The adjusted response rates have been presented as a percentage of patients. (NCT03330847)
Timeframe: From date of randomization until date of first documented progression or last evaluable assessment, or start of subsequent anti-cancer therapy (Whichever occurred first [assessed up to 32 months])

Intervention	Percentage of patients (Number)
	BRCAm patients per BICR	non BRCAm HRRm patients per BICR	non HRRm patients per BICR	HRRm patients per BICR	All patients per BICR	BRCAm patients per sensitivity analysis	non BRCAm HRRm per sensitivity analysis	non HRRm per sensitivity analysis
Olaparib + Adavosertib	44.9	0.0	11.1	28.5	18.3	53.1	14.3	11.1
Olaparib + Ceralasertib	48.4	20.0	15.4	38.0	27.3	49.0	20.0	21.2
Olaparib Monotherapy	42.7	15.0	3.9	33.2	20.1	41.0	15.0	2.0

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Number of Patients With Objective Response (Per BICR and Per Sensitivity Analysis)

The objective response was defined as patients with at least one BICR assessed visit response of CR or PR. For sensitivity analysis, objective response was defined as the patients with at least one visit response of CR or PR based on Investigator data. These are unadjusted percentages of responders (100 * number of responders / number of patients in full analysis set). The objective response was assessed per RECIST 1.1 guidelines for: measurable lesions (measured at baseline as ≥ 10 mm in the longest diameter (except lymph nodes which must have short axis ≥ 15 mm) using CT or MRI, non-measurable lesions (all other lesions, including small lesions (longest diameter <10 mm or pathological lymph nodes with ≥10 to <15mm short axis at baseline), based on target lesions [TL] (maximum of 5 measurable lesions (with a maximum of 2 lesions per organ), non-target lesions [NTL] (lesions (or sites of disease) not recorded as TL should be identified as NTL at baseline) and any new lesions. (NCT03330847)
Timeframe: From date of randomization until date of first documented progression or last evaluable assessment, or start of subsequent anti-cancer therapy (Whichever occurred first [assessed up to 32 months])

Intervention	Participants (Count of Participants)
	BRCAm patients per BICR	non BRCAm HRRm patients per BICR	non HRRm patients per BICR	HRRm patients per BICR	All patients per BICR	BRCAm patients per sensitivity analysis	non BRCAm HRRm per sensitivity analysis	non HRRm per sensitivity analysis
Olaparib + Adavosertib	6	0	3	6	9	7	1	3
Olaparib + Ceralasertib	20	4	8	24	32	20	4	11
Olaparib Monotherapy	19	3	2	22	24	18	3	1

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Duration of Response (DoR) [Per BICR and Per Sensitivity Analysis]

The DoR was defined as the time from the date of first documented response according to BICR data until date of documented progression according to BICR data or death in the absence of disease progression. For sensitivity analysis, DoR was defined as the time from the date of first documented response according to Investigator assessment until date of documented progression according to Investigator assessment or death in the absence of disease progression. Here, the median DoR and the 25th and 75th percentile of DoR are presented. The DoR from onset of response was calculated using Kaplan-Meier technique. Here, the study patient population was stratified as follows: BRCAm patients; non BRCAm HRRm patients; non HRRm patients. (NCT03330847)
Timeframe: From date of first documented response until date of first documented progression or last evaluable assessment (assessed up to 32 months)

Intervention	Weeks (Median)
	BRCAm patients per BICR	non BRCAm HRRm patients per BICR	non HRRm patients per BICR	BRCAm patients per sensitivity analysis	non BRCAm HRRm per sensitivity analysis	non HRRm per sensitivity analysis
Olaparib + Ceralasertib	32.0	17.1	24.1	32.6	16.5	11.7
Olaparib Monotherapy	20.0	16.8	11.4	20.0	16.3	13.6

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Duration of Response (DoR) [Per BICR and Per Sensitivity Analysis]

Intervention	Weeks (Median)
	BRCAm patients per BICR	non HRRm patients per BICR	BRCAm patients per sensitivity analysis	non BRCAm HRRm per sensitivity analysis	non HRRm per sensitivity analysis
Olaparib + Adavosertib	33.4	16.6	41.1	48.1	31.6

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Plasma Drug Concentrations of Olaparib

Plasma drug concentrations of olaparib are evaluated to assess exposure to olaparib in all patients. (NCT03330847)
Timeframe: Pre-dose at Cycle 1 Day 7 [olaparib monotherapy or ceralasertib+olaparib] or Cycle 1 Day 10 [adavosertib+olaparib] (each cycle is 21 days for olaparib+adavosertib, and 28 days for olaparib monotherapy and olaparib+ceralasertib)

Intervention	ug/mL (Mean)
Olaparib Monotherapy	2.97
Olaparib + Ceralasertib	2.90
Olaparib + Adavosertib	3.22

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Plasma Drug Concentrations of Ceralasertib and Adavosertib

Plasma drug concentrations of ceralasertib and adavosertib are evaluated to assess exposure to ceralasertib and adavosertib in all patients. (NCT03330847)
Timeframe: Pre-dose at Cycle 1 Day 7 [ceralasertib+olaparib] or Cycle 1 Day 10 [adavosertib+olaparib] (each cycle is 21 days for olaparib+adavosertib, and 28 days for olaparib+ceralasertib)

Intervention	ng/mL (Mean)
Olaparib + Ceralasertib	870.05
Olaparib + Adavosertib	290.46

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Percentage Change From Baseline in Target Lesion Tumour Size [Per BICR and Per Sensitivity Analysis]

Tumour size was the sum of the longest diameters of the target lesions (TLs). The percentage change in TL tumour size at Week 16 was obtained for each patient as follows (considering a visit window around the scheduled day of the Week 16 assessment): (TL at Week 16 minus TL at baseline) divided by (TL at baseline) multiplied by 100. Here, the percentage change data have been reported as per BICR and as per sensitivity analysis per investigator assessments. Here, the study patient population was stratified as follows: BRCAm patients; non BRCAm HRRm patients; non HRRm patients. (NCT03330847)
Timeframe: Baseline, at Week 16

Intervention	Percentage change (Mean)
	BRCAm patients per BICR	non BRCAm HRRm patients per BICR	non HRRm patients per BICR	BRCAm patients per sensitivity analysis	non BRCAm HRRm per sensitivity analysis	non HRRm per sensitivity analysis
Olaparib + Adavosertib	-34.1	42.3	9.2	-23.7	73.9	9.3
Olaparib + Ceralasertib	-33.8	4.9	5.7	-29.5	-2.1	3.9
Olaparib Monotherapy	-27.7	4.9	40.3	-21.9	6.2	20.1

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Number of Patients With Treatment Emergent Adverse Events (TEAEs)

Treatment-emergent adverse events reported after treatment with olaparib monotherapy, the combination of ceralasertib and olaparib or the combination of adavosertib and olaparib. The data includes adverse events (AEs) with an onset or worsening date on or after the date of first dose and up to and including 30 days following the date of last dose of study medication. (NCT03330847)
Timeframe: From screening until Follow-up 30 Days after last dose of study treatment (assessed up to 32 months)

Intervention	Participants (Count of Participants)
	Any AE	Any AE causally related to olaparib	Any AE causally related to non-olaparib	Any AE causally related to non-olaparib and olaparib	Any AE with outcome = death	Any AE with outcome = death, causally related to olaparib	Any AE with outcome = death, causally related to non-olaparib	Any AE with outcome = death, causally related to non-olaparib and olaparib	Any SAE	Any SAE causally related to olaparib	Any SAE causally related to non-olaparib	Any SAE causally related to non-olaparib and olaparib	Any AE leading to discontinuation of study treatment	AEs leading to reduction of study treatment	AEs leading to reduction of olaparib	AEs leading to reduction of non-olaparib	AEs leading to reduction of non-olaparib and olaparib
Olaparib + Adavosertib	46	43	45	42	1	0	0	0	17	9	14	9	9	19	11	12	3
Olaparib + Ceralasertib	107	95	92	91	2	0	0	0	24	9	7	7	12	32	30	16	11
Olaparib Monotherapy	105	91	NA	NA	1	0	NA	NA	21	4	NA	NA	2	15	15	NA	NA

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Progression-free Survival (Per BICR)

Progression-free survival was defined as time from randomization until the date of objective disease progression or death, regardless of whether the patient withdrew from randomized therapy or received another anti-cancer therapy prior to progression. Progression was determined by BICR using RECIST 1.1. Patients who had not progressed or died at the time of analysis were censored at the time of the latest date of assessment from their last evaluable RECIST assessment. If patients had no evaluable visits or baseline data, the patient was censored at Study Day 1, unless death occurred within 17 weeks i.e., death within 17 weeks was relative to randomization. Here, the study patient population was presented as follows: HRRm and all enrolled patients. (NCT03330847)
Timeframe: From randomization until date of first documented progression or censoring date or date of death from any cause, whichever came first (assessed up to 32 months)

Intervention	Months (Median)
	HRRm patients per BICR	All patients per BICR
Olaparib + Adavosertib	3.7	3.8
Olaparib + Ceralasertib	5.6	5.3
Olaparib Monotherapy	5.6	3.6

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Progression-free Survival Per Stratum (BICR)

Progression-free survival was defined as time from randomization until the date of objective disease progression or death, regardless of whether the patient withdrew from randomized therapy or received another anti-cancer therapy prior to progression. Progression was determined by Blinded independent central review (BICR) using Response Evaluation Criteria In Solid Tumours Version (RECIST 1.1). Patients who had not progressed or died at the time of analysis were censored at the time of the latest date of assessment from their last evaluable RECIST assessment. If patients had no evaluable visits or baseline data, the patient was censored at Study Day 1, unless death occurred within 17 weeks i.e., death within 17 weeks was relative to randomization. Here, the study patient population was stratified as follows: Breast cancer susceptible gene mutation (BRCAm) patients; non BRCAm homologous recombination repair gene mutation (HRRm) patients; non HRRm patients. (NCT03330847)
Timeframe: Until date of first documented progression or censoring date or date of death from any cause, whichever came first (assessed up to 32 months)

Intervention	Months (Median)
	BRCAm patients	non BRCAm HRRm patients	non HRRm patients
Olaparib + Adavosertib	3.8	2.1	4.4
Olaparib + Ceralasertib	7.4	3.9	3.6
Olaparib Monotherapy	7.3	1.9	1.9

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Progression-free Survival Per Stratum (Sensitivity Analysis)

Progression-free survival was defined as time from randomization until the date of objective disease progression or death, regardless of whether the patient withdrew from randomized therapy or received another anti-cancer therapy prior to progression. Progression was determined by the site Investigator. Patients who had not progressed or died at the time of analysis were censored at the time of the latest date of assessment from their last evaluable RECIST 1.1 assessment. If patients had no evaluable visits or baseline data, the patient was censored at Study Day 1, unless death occurred within 17 weeks i.e., death within 17 weeks was relative to randomization. Here, the study patient population was stratified as follows: BRCAm patients; non BRCAm HRRm patients; non HRRm patients. (NCT03330847)
Timeframe: Until date of first documented progression or censoring date or date of death from any cause, whichever came first (assessed up to 32 months)

Intervention	Months (Median)
	BRCAm patients	non BRCAm HRRm patients	non HRRm patients
Olaparib + Adavosertib	5.4	2.9	2.9
Olaparib + Ceralasertib	7.5	3.7	3.5
Olaparib Monotherapy	7.4	3.4	1.9

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Time to First Subsequent Therapy or Death (TFST)

TFST is defined as the time from date of first dose to date of first subsequent treatment commencement or death due to any cause if this occurs before commencement of first subsequent treatment. Calculated using the Kaplan-Meier technique. CI for median TFST was derived based on Brookmeyer-Crowley method. (NCT03402841)
Timeframe: Up to a maximum of 43 months

Intervention	months (Median)
Olaparib	13.9

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Time to Treatment Discontinuation or Death (TDT)

TDT is defined as the time from date of first dose to date of study drug discontinuation or death due to any cause if this occurs before study drug discontinuation. Calculated using the Kaplan-Meier technique. CI for median TDT was derived based on Brookmeyer-Crowley method. (NCT03402841)
Timeframe: Up to a maximum of 43 months

Intervention	months (Median)
Olaparib	9.6

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Overall Survival (OS)

OS is defined as the time from the date of first dose of olaparib to the date of death from any cause. Calculated using the Kaplan-Meier technique. CI for median OS was derived based on Brookmeyer-Crowley method. (NCT03402841)
Timeframe: Up to a maximum of 43 months

Intervention	months (Median)
Olaparib	32.7

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Chemotherapy-free Interval (CT-FI)

CT-FI is defined as the time from the date of the last dose of platinum chemotherapy prior to olaparib maintenance therapy until the date of initiation of the next anticancer therapy. Calculated using the Kaplan-Meier technique. CI for median CT-FI was derived based on Brookmeyer-Crowley method. (NCT03402841)
Timeframe: Up to a maximum of 43 months

Intervention	months (Median)
Olaparib	17.9

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Percentage of Patients With a 10-Point Deterioration From Baseline in TOI Score at Any Point During the Treatment Period

"10-point deterioration was defined as a FACT-O TOI response of 10-point deterioration at any time point over the course of treatment. The TOI is an established single targeted index composed of the following scales of the FACT-O: physical and functional well-being and additional concerns. The range of possible scores for the FACT-O TOI is 0-100, with a higher score indicating better HRQoL. A decrease in score of at least 10 points from baseline was defined as a clinically meaningful deterioration." (NCT03402841)
Timeframe: Baseline up to a maximum of 32 months

Intervention	percentage of patients (Number)
Olaparib	42.6

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Percentage of Patients With Any Improvement From Baseline in Trial Outcome Index (TOI) Score at Any Point During the Treatment Period

"Improvement was defined as a functional assessment of cancer therapy - ovarian (FACT-O) TOI response of any improvement at any time point over the course of treatment. The TOI is an established single targeted index composed of the following scales of the FACT-O: physical and functional well-being and additional concerns. The range of possible scores for the FACT-O TOI is 0-100, with a higher score indicating better health related quality of life (HRQoL). An increase in score from baseline indicates an improvement in HRQoL." (NCT03402841)
Timeframe: Baseline up to a maximum of 32 months

Intervention	percentage of patients (Number)
Olaparib	64.3

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PFS by Homologous Recombination Deficiency (HRD)/ Breast Cancer Susceptibility Gene Mutation (Mutated) (BRCAm) Status

HRD/BRCAm status was based on the central blood and tumour assessments. Assessed according to modified RECIST 1.1 or death (by any cause in the absence of progression). Progression was determined by investigator assessment, RECIST 1.1. Calculated using the Kaplan-Meier technique. CI for median PFS was derived based on Brookmeyer-Crowley method. (NCT03402841)
Timeframe: Up to maximum of 32 months

Intervention	months (Median)
	HRD status positive and/or sBRCAm subgroup	HRD status positive, non-BRCAm subgroup	HRD status negative subgroup	sBRCAm subgroup	gBRCAm subgroup
Olaparib	11.1	9.7	7.3	16.4	12.1

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Progression Free Survival (PFS)

PFS is defined as the time from date of first dose until the date of objective radiological disease progression. Assessed according to modified Response Evaluation Criteria In Solid Tumours Version 1.1 (RECIST 1.1) or death (by any cause in the absence of progression). Progression was determined by investigator assessment, RECIST 1.1. Calculated using the Kaplan-Meier technique. Confidence intervals (CI) for median PFS was derived based on Brookmeyer-Crowley method. (NCT03402841)
Timeframe: Up to maximum of 32 months

Intervention	months (Median)
Olaparib	9.2

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PSA Progression-free Survival of Olaparib and Radical Prostatectomy for Patients With Locally Advanced Prostate Cancer and Defects in DNA Repair Genes.

Evaluation by treating physician (NCT03432897)
Timeframe: Post treatment (approximately 8-12 weeks) and approximately every 6 months for 2 years.

Intervention	months (Number)
Treatment	7

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Number of Participants With Prostate Specific Antigen (PSA) Response

"Response:Reduction of at least 50% in the prostate-specific antigen level from baseline Progression:A 25% increase in PSA from baseline~Baseline then approximately 8 weeks later and 2 weeks post Olaparib, approximately 10-14 weeks after baseline and then approximately every 6 months for 2 years in follow-up." (NCT03432897)
Timeframe: Throughout the trial for approximately 2 years

Intervention	Participants (Count of Participants)
Treatment	0

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Objective Response Rate (ORR)

"Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST): Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Progressive Disease (PD) >= 20% increase in tumor burden relative to nadir or the appearance of one or more new lesions; Stable Disease (SD), not meet criteria for CR/PR/PD.~ORR is defined as the proportion of all subjects with confirmed PR or CR according to RECIST 1.1." (NCT03448718)
Timeframe: Up to a maximum of 17 months

Intervention	Percentage of participants (Number)
Olaparib Monotherapy	0

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Overall Survival (OS)

Overall survival is defined as the time from treatment start until death or date of last contact. (NCT03448718)
Timeframe: Time of treatment start until death or date of last contact, up to a maximum of 23 months.

Intervention	Months (Median)
Olaparib Monotherapy	9.5

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Progression-Free Survival (PFS)

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST): Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Progressive Disease (PD) >= 20% increase in tumor burden relative to nadir or the appearance of one or more new lesions; Stable Disease (SD), not meet criteria for CR/PR/PD. PFS is defined as time from registration until disease progression met by RECIST 1.1 or death from any cause. (NCT03448718)
Timeframe: Time of treatment start until the criteria for disease progression or death. Up to a maximum of 17 months.

Intervention	Months (Median)
Olaparib Monotherapy	1.9

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Adverse Events

Number of participants with treatment related adverse events are reported by CTCAEv4 term and grade. (NCT03448718)
Timeframe: AE had been recorded from time of signed informed consent until 30 days after discontinuation of study drug(s) or until a new anti-cancer treatment starts, whichever occurs first, up to a maximum of 18 months.

Intervention	Participants (Number)
	WBC count decreased	Lymphocyte count decreased	Neutrophil count decreased	Platelet count decreased	Anemia	Fatigue	Fever	Dizziness	Anorexia	Myalgia	Nausea	Vomiting	Diarrhea	Constipation	Abdominal pain	Allergic reaction	Confusion	Papulopustular rash	Skin disorders, other	Sore throat	Chronic kidney disease	Creatinine increased
Olaparib Monotherapy	1	2	2	3	5	4	1	1	2	1	4	3	2	1	1	1	1	1	1	1	1	2

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Progression-free Survival (PFS)

Progression-free survival based on investigator assessments according to RECIST 1.1 (NCT03459846)
Timeframe: Assessments performed at baseline and every 8 weeks from date of randomization until date of objective disease progression or death (by any cause in the absence of progression), assessed up to the data cut-off date (15 Oct 2020), up to a max. of 31 months

Intervention	Months (Median)
Durva + Olaparib	4.2
Durva + Placebo	3.5

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Duration of Response (DoR)

Per Response Evaluation Criteria in Solid Tumours (RECIST v1.1) assessed by MRI or CT: Complete Response (CR): Disappearance of all target and non-target lesions and no new lesions; Partial Response (PR): >= 30% decrease in the sum of diameters of Target Lesions (compared to baseline) and no new lesions. DoR is the time from the date of first documented response until the date of documented progression or death in the absence of disease progression (NCT03459846)
Timeframe: Tumor assessments every 8 weeks after randomization for the first 48 weeks and then every 12 weeks thereafter until the date of objective disease progression. Assessed up to the data cut-off date (15 October 2020), to a maximum of 31 months

Intervention	Months (Median)
Durva + Olaparib	8.9
Durva + Placebo	14.8

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Radiographic Response Rate

Per the Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 guidelines, a radiographic response (as determined on CT or MRI) will be defined as: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT03516812)
Timeframe: Up to 2 years

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Testosterone Enanthate or Cypionate)	8

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Percent of Patients With a Prostate-specific Antigen (PSA) Decline of at Least 50% Below Baseline PSA50 Response Rate

PSA response will be defined as a decline in PSA ≥ 50% compared to baseline in patients who received at least 12 weeks of treatment. Will be calculated as the percentage with 95% confidence interval (CI) of the total number of subjects that achieved a PSA response. (NCT03516812)
Timeframe: Median time to PSA50 response was 22 weeks.

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Testosterone Enanthate or Cypionate)	14

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Number of Participants With Germline Deoxyribonucleic Acid (DNA) Repair Mutation Who Experienced Partial or Complete Response.

Number of participants with germline deoxyribonucleic acid (DNA) repair mutation who experienced partial or complete response. Response was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, and the Malignant Pleural Mesothelioma (MPM) criteria. Partial Response is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters. Complete Response is disappearance of all target lesions. (NCT03531840)
Timeframe: 6 months after enrollment of last patient

Intervention	Participants (Count of Participants)
	Partial Response	Complete Response
Comparison Group 1:Participants With a Germline Mutation in Deoxyribonucleic Acid (DNA) Repair Genes	1	0

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Number of Participants With an Objective Response

Number of participants overall who experienced partial or complete response. Response was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, and the Malignant Pleural Mesothelioma (MPM) criteria. Partial Response is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters. Complete Response is disappearance of all target lesions. (NCT03531840)
Timeframe: 6 months after enrollment of last patient

,,,

Intervention	Participants (Count of Participants)
	Partial Response	Complete Response
Comparison Group 1:Participants With a Germline Mutation in Deoxyribonucleic Acid (DNA) Repair Genes	1	0
Comparison Group 2: Participants With BRCA1 Associated Protein-1 (BAP1) Somatic Mutations	0	0
Comparison Group 3: Participants With Neither Germline Mutations Nor BAP 1 Somatic Mutations	0	0
Participants Not Classified Under Comparison Groups	0	0

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Number of Participants With Serious and Non-serious Adverse Events Assessed by the Common Terminology Criteria for Adverse Events (CTCAE v5.0)

Here is the count of participants with serious and non-serious adverse events assessed by the Common Terminology Criteria for Adverse Events (CTCAE v5.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT03531840)
Timeframe: Adverse events were recorded from the study start date until prior to the study completion date, approximately 27 months and 11 days.

Intervention	Participants (Count of Participants)
Comparison Group 1:Participants With a Germline Mutation in Deoxyribonucleic Acid (DNA) Repair Genes	5
Comparison Group 2: Participants With BRCA1 Associated Protein-1 (BAP1) Somatic Mutations	6
Comparison Group 3: Participants With Neither Germline Mutations Nor BAP 1 Somatic Mutations	8
Participants Not Classified Under Comparison Groups	4

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Number of Participants With Dose Limiting-toxicities (DLT's)

Dose Limiting-toxicities (DLT's) is defined as (NCT03531840)
Timeframe: 21 days after enrollment of last subject

Intervention	Participants (Count of Participants)
Comparison Group 1:Participants With a Germline Mutation in Deoxyribonucleic Acid (DNA) Repair Genes	0
Comparison Group 2: Participants With BRCA1 Associated Protein-1 (BAP1) Somatic Mutations	0
Comparison Group 3: Participants With Neither Germline Mutations Nor BAP 1 Somatic Mutations	0
Participants Not Classified Under Comparison Groups	0

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Percentage of Subjects With Neither Germline Deoxyribonuclecic Acid (DNA) Repair Mutations Nor Somatic Breast Cancer Type 1 Associated Protein-1 (BAP1) Mutations Who Experienced Partial or Complete Response.

Percentage of subjects with neither germline DNA repair mutations nor somatic BAP1 mutations who experienced partial or complete response.Response was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, and the Malignant Pleural Mesothelioma (MPM) criteria. Partial Response is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters. Complete Response is disappearance of all target lesions. (NCT03531840)
Timeframe: 6 months after enrollment of last patient

Intervention	percentage of participants (Number)
	Partial Response	Complete Response
Comparison Group 3: Participants With Neither Germline Mutations Nor BAP 1 Somatic Mutations	0	0

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Percentage of Participants With Breast Cancer Type 1 Associated Protein-1 (BAP1) Somatic Mutations Who Experienced Partial or Complete Response.

Percentage of participants with germline deoxyribonucleic acid (DNA) repair mutation who experienced partial or complete response. Response was assessed by the Response Evaluation Criteria in Solid Tumors (RECIST) v1.1, and the Malignant Pleural Mesothelioma (MPM) criteria. Partial Response is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum of diameters. Complete Response is disappearance of all target lesions. (NCT03531840)
Timeframe: 6 months after enrollment of last patient

Intervention	percentage of participants (Number)
	Partial Response	Complete Response
Comparison Group 2: Participants With BRCA1 Associated Protein-1 (BAP1) Somatic Mutations	0	0

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Pathologic Complete Response (pCR) Rate

Percent of patients who achieve a pCR at the time of prostatectomy, after 12 weeks of neoadjuvant therapy with olaparib. PCR is defined as the absence of morphologically identifiable carcinoma in the prostatectomy specimen. Assessment will be based on the recommendations of the International Society of Urological Pathology (ISUP). (NCT03570476)
Timeframe: At time of prostatectomy (at 12 weeks)

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Radical Prostatectomy)	0

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Number of Participants With Adverse Events

Will be evaluated according to Common Terminology Criteria for Adverse Events (CTCAE). (NCT03570476)
Timeframe: Up to 30 days after the last dose of olaparib

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Radical Prostatectomy)	0

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Rate of Positive Surgical Margins

The rate of detectable tumor in pathology specimens obtained at prostatectomy. (NCT03570476)
Timeframe: At time of prostatectomy (at 12 weeks)

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Radical Prostatectomy)	0

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Number of Participants With Time to Pain Progression (TTPP) Event

A TTPP event is defined as pain progression based on the Brief Pain Inventory-Short Form (BPI-SF) Item 3 (range 0-10, a higher score indicates worse pain) and opiate analgesic use (Analgesic quantification algorithm [AQA] score, range 0-7, a higher score indicates increased opioid use). For patients who are asymptomatic at baseline (average worst pain score of 0 and not taking opioids): A ≥2 point change from baseline in average (4-7 days) worst pain score observed at 2 consecutive visits or initiation of opioid use; For patients who are symptomatic at baseline (average worst pain score >0 and/or receiving opioids): A ≥2 point change from baseline in average (4-7 days) worst pain score observed at 2 consecutive visits and an average worst pain score ≥4, and no decrease in average opioid use (≥1-point decrease in AQA score from a starting value of ≥2), or increase in opioid use (≥1-point increase, or ≥2-point increase if the starting value is 0) at 2 consecutive follow-up visits. (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	68
Placebo bd + Abiraterone 1000 mg qd	60

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Number of Participants With First Symptomatic Skeletal Related Event (SSRE)

"An SSRE event is defined as the first sympomatic skeletal-related event defined by~Use of radiation therapy to prevent or relieve skeletal symptoms.~Occurrence of new symptomatic pathological bone fractures (vertebral or non-vertebral)." (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	46
Placebo bd + Abiraterone 1000 mg qd	51

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Number of Participants With Time to First Subsequent Anticancer Therapy or Death (TFST) Event

A TFST (excluding radiotherapy) event is defined as the start of the first subsequent anticancer therapy after discontinuation of randomised treatment or death from any cause. (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	255
Placebo bd + Abiraterone 1000 mg qd	285

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Brief Pain Inventory-Short Form (BPI-SF)

The BPI-SF is a validated, 15-item domain-specific instrument designed to assess the severity of pain and the impact/interference of pain on daily functions. BPI-SF worst pain, pain severity and pain interference score changes can be a minimum of -10 and a maximum of 10. A negative change from baseline value indicates improvement. (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Score (Least Squares Mean)
	Change from baseline in BPI-SF worst pain	Change from baseline in BPI-SF pain severity score	Change from baseline in BPI-SF pain interference score
Olaparib 300 mg bd + Abiraterone 1000 mg qd	-0.09	-0.08	0.01
Placebo bd + Abiraterone 1000 mg qd	0.03	-0.02	0.13

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Functional Assessment of Cancer Therapy- Prostate Cancer (FACT-P)

"Functional Assessment of Cancer Therapy-Prostate Cancer (FACT-P) total score and Functional Assessment of Cancer Therapy-General (FACT-G) total score.~Total FACT-P score is the sum of Physical Well-being (PWB), Social Well-being (SWB), Emotional Well-being (EWB), Functional Well-being (FWB) and Prostate cancer subscale (PCS). FACT-P total score change from baseline values can be a minimum of -156 and a maximum of 156. A positive value indicates improvement.~FACT-G total score is the sum of PWB, SWB, EWB and FWB. FACT-G Total score change from baseline values can be a minimum of -108 and a maximum of 108. A positive value indicates improvement." (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Score (Least Squares Mean)
	Change from baseline in FACT-P Total	Change from baseline in FACT-G Total
Olaparib 300 mg bd + Abiraterone 1000 mg qd	-5.84	-5.06
Placebo bd + Abiraterone 1000 mg qd	-5.30	-4.35

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Number of Participants With Second Progression or Death (PFS2) Event

An event for PFS2 is defined as the second progression on next-line anticancer therapy or death, whichever occurs earlier. (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	103
Placebo bd + Abiraterone 1000 mg qd	126

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Number of Participants With Opiate Use

An event for opiate use is defined as the first opiate use for cancer related pain. (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months)

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	58
Placebo bd + Abiraterone 1000 mg qd	45

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Number of Participants With Overall Survival (OS) Event

An OS event is defined as death by any cause, regardless of whether the patient withdraws from randomised therapy or receives another anticancer therapy. (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO3): 12Oct2022 (Approx. 3 years 11 months). DCO3 is the final data cut-off for the OS analysis and therefore no further updates will be made.

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	176
Placebo bd + Abiraterone 1000 mg qd	205

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Number of Participants With Radiological Progression Free Survival (rPFS) Event by Investigator Assessment

"An rPFS event is defined as progression determined by Response Evaluation Criteria in Solid Tumours version 1.1 [RECIST 1.1] and/or Prostate Cancer Working Group 3 [PCWG-3] or death (by any cause in the absence of progression), regardless of whether the patient withdraws from randomised therapy or receives another anticancer therapy prior to progression.~Per RECIST v1.1, progression is defined as the sum of TLs has a 20% and absolute ≥ 5mm increase from nadir, and/or unequivocal progression in any non target lesions, and/or any new lesion identified.~Per PCWG3, progression on a bone scan is defined as 2 or more new lesions observed from the first visit after baseline compared to baseline, or from all other visits compared to first visit after baseline. A confirmatory scan is required." (NCT03732820)
Timeframe: Assessed from date of randomisation to data cut off (DCO1): 30Jul2021 (Approx. 2 years 9 months)

Intervention	Participants (Count of Participants)
Olaparib 300 mg bd + Abiraterone 1000 mg qd	168
Placebo bd + Abiraterone 1000 mg qd	226

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Number of Participants With Treatment-Related Adverse Events

Number of Participants with Treatment-Related Adverse Events as Assessed by Common Terminology Criteria for Adverse Events (CTCAE) (NCT03775486)
Timeframe: From randomization until date of objective radiological disease progression or death, or last evaluable assessment in the absence of progression, up to 18 months

Intervention	Participants (Count of Participants)
Durvalumab/Olaparib Combination Therapy	83
Durvalumab/Placebo Therapy	54

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Change From Baseline in EORTC Quality of Life Questionnaire (QLQ) QLQ-C30

"Disease-related symptoms and health-related quality of life (HRQoL) assessed by change from baseline (for maintenance phase) in EORTC QLQ-C30. Average adjusted mean over first 11 cycles is presented.~The EORTC QLQ-C30 was scored according to the published scoring manual. An outcome variable consisting of a score from 0 to 100 was derived for each of the symptom scales, each of the function scales, and the global health status/QoL scale in the EORTC QLQ-C30. Higher scores on the global health status and function scales indicate better health status/function.~A high scale score represents a higher response level. Thus a high score for a functional scale represents a high / healthy level of functioning, a high score for the global health status / quality of life (QoL) represents a high QoL, but a high score for a symptom scale / item represents a high level of symptomatology / problems." (NCT03775486)
Timeframe: Includes all assessments occurring within the first 12 months of randomization or until disease progression, up to 18 months.

Intervention	change from baseline score (Mean)
	EORTC QLQ-C30: Fatigue	EORTC QLQ-C30: Appetite loss
Durvalumab/Olaparib Combination Therapy	0.15	-0.13
Durvalumab/Placebo Therapy	-1.49	-3.35

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Change From Baseline in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-Lung Cancer (LC)13

"Disease-related symptoms assessed by change from baseline (for maintenance phase) in EORTC QLQ-LC13. Average adjusted mean over first 11 cycles is presented.~The EORTC QLQ-LC13 was scored according to the published scoring manual. An outcome variable consisting of a score from 0 to 100 was derived for each of the symptom scales in the EORTC QLQ-LC13. Higher scores on symptom scales represent greater symptom severity." (NCT03775486)
Timeframe: From randomization until date of objective radiological disease progression or death, or last evaluable assessment in the absence of progression, up to 18 months

Intervention	change from baseline score (Mean)
	EORTC QLQ-LC13: Dyspnoea	EORTC QLQ-LC13: Coughing	EORTC QLQ-LC13: Pain in chest
Durvalumab/Olaparib Combination Therapy	-1.27	-2.14	1.31
Durvalumab/Placebo Therapy	-0.76	-3.09	3.57

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Concentration of Durvalumab

Concentration (pharmacokinetics) of durvalumab (NCT03775486)
Timeframe: Assessed from start of initial therapy up to 2 years.

Intervention	μg/mL (Geometric Mean)
	Cycle 01 Day 01 (Initial Therapy Phase) Post dose	Cycle 02 Day 01 (Initial Therapy Phase) Pre dose	Cycle 04 Day 01 (Initial Therapy Phase) Pre dose	Cycle 01 (Maintenance Phase) Post dose	Cycle 02 (Maintenance Phase) Pre dose	Cycle 05 (Maintenance Phase) Pre dose	Cycle 08 (Maintenance Phase) Pre dose	Cycle 11 (Maintenance Phase) Pre dose	Cycle 14 (Maintenance Phase) Pre dose	Cycle 17 (Maintenance Phase) Pre dose	Cycle 20 (Maintenance Phase) Pre dose	Month 03 (Maintenance Phase) Pre dose
Durvalumab/Olaparib Combination Therapy	417.152	76.812	155.461	535.078	159.157	166.644	198.932	210.794	276.612	264.096	528.046	12.289
Durvalumab/Placebo Therapy	453.724	76.959	154.947	524.306	160.315	147.848	154.057	186.092	182.042	217.137	112.276	12.769

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Overall Survival

"Overall survival (OS) across the maintenance phase.~OS is defined as time from date of randomization until the date of death by any cause" (NCT03775486)
Timeframe: From randomization until the date of death due to any cause, up to 18 months.

Intervention	Participants (Count of Participants)
	Death	Censored participants (still in survival at follow up or terminated study prior to death)
Durvalumab/Olaparib Combination Therapy	44	90
Durvalumab/Placebo Therapy	45	90

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Presence of Anti-drug Antibodies (ADAs) for Durvalumab

Presence of anti-drug antibodies (ADAs) for durvalumab, as assessed at 3, 6, 12, 16 and 20 weeks after start of treatment and every 12 weeks thereafter until 3 and 6 months after last dose of durvalumab (NCT03775486)
Timeframe: Assessed from start of initial therapy up to 2 years.

Intervention	Participants (Count of Participants)
	ADA prevalence (any ADA positive, baseline or post-baseline)	ADA incidence (treatment-induced or treatment-boosted)	ADA positive post-baseline and positive at baseline	ADA positive post-baseline and not detected at baseline (treatment-induced)	ADA not detected at post-baseline and positive at baseline	Treatment-boosted ADA	Persistent positive	Transient positive	Neutralizing anti-drug antibody positive at any visit
Durvalumab/Olaparib Combination Therapy	11	5	0	5	6	0	0	5	1
Durvalumab/Placebo Therapy	9	4	1	4	4	0	3	2	1

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Progression-free Survival

"Progression-free survival (PFS) based on investigator assessments according to Response Evaluation Criteria in Solid Tumours version 1.1.~PFS is defined as time from date of randomization until the date of objective radiological disease progression using Response Evaluation Criteria in Solid Tumours version 1.1 (RECIST 1.1) or death (by any cause in the absence of progression)." (NCT03775486)
Timeframe: From randomization until date of objective radiological disease progression or death, or last evaluable assessment in the absence of progression, up to 18 months

Intervention	Participants (Count of Participants)
	RECIST progression: Target Lesions	RECIST progression: Non Target Lesions	RECIST progression: New Lesions	Death in the absence of progression	Censored subjects: Censored RECIST progression	Censored subjects: Censored death	Censored subjects: Progression-free at time of analysis	Censored subjects: Progression-free prior to lost to follow-up	Censored subjects: Progression-free prior to withdrawal of consent	Censored subjects: Progression-free prior to discontinuation due to other reason	Censored subjects: No post-baseline evaluable tumor assessment
Durvalumab/Olaparib Combination Therapy	40	28	44	8	0	1	44	0	3	0	2
Durvalumab/Placebo Therapy	63	30	39	9	0	0	34	0	2	0	2

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Progression-free Survival in Homologous Recombination Repair Related Gene Mutation (HRRm) Population

Progression-free survival in homologous recombination repair related gene mutation (HRRm) population defined as time from date of randomization until the date of objective radiological disease progression in HRRm population using Response Evaluation Criteria in Solid Tumours version 1.1 (RECIST 1.1) or death (by any cause in the absence of progression). (NCT03775486)
Timeframe: From randomization until date of objective radiological disease progression or death, or last evaluable assessment in the absence of progression, up to 18 months

Intervention	Participants (Count of Participants)
	RECIST progression: Target Lesions	RECIST progression: Non Target Lesions	RECIST progression: New Lesions	Death in the absence of progression	Censored subjects: Censored RECIST progression	Censored subjects: Censored death	Censored subjects: Progression-free at time of analysis	Censored subjects: Progression-free prior to lost to follow-up	Censored subjects: Progression-free prior to withdrawal of consent	Censored subjects: Progression-free prior to discontinuation due to other reason	Censored subjects: No post-baseline evaluable tumor assessment
Durvalumab/Olaparib Combination Therapy	1	2	3	0	0	0	2	0	0	0	0
Durvalumab/Placebo Therapy	5	2	3	0	0	0	2	0	0	0	0

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Time to Deterioration in EORTC Quality of Life Questionnaire (QLQ) QLQ-C30

"Disease-related symptoms and health-related quality of life (HRQoL) assessed by time to deterioration (for maintenance phase) in EORTC QLQ-C30.~NA is not applicable. The upper confidence limit was not calculable because of an insufficient number of participants with events." (NCT03775486)
Timeframe: From randomization until date of first symptom deterioration that is confirmed, up to 18 months.

Intervention	time to deterioration (months) (Median)
	EORTC QLQ-C30: Fatigue	EORTC QLQ-C30: Nausea And Vomiting	EORTC QLQ-C30: Pain	EORTC QLQ-C30: Dyspnoea	EORTC QLQ-C30: Insomnia	EORTC QLQ-C30: Appetite Loss	EORTC QLQ-C30: Constipation	EORTC QLQ-C30: Diarrhoea	Physical Functioning	Role Functioning	Emotional Functioning	Cognitive Functioning	Social Functioning	Global Health Status/Quality of Life
Durvalumab/Olaparib Combination Therapy	8.8	12.2	10.2	12.2	13.8	11.7	12.2	13.8	12.0	10.0	12.2	10.2	9.3	10.2
Durvalumab/Placebo Therapy	10	12.6	9.7	11.0	10.6	11.5	12.0	11.5	12.0	10.6	11.0	10.6	10.0	9.7

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Time to Deterioration in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-Lung Cancer (LC)13

"Disease-related symptoms assessed by time to deterioration (for maintenance phase) in European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire (QLQ)-Lung Cancer (LC)13.~Symptom deterioration is defined as an increase in the score from baseline of less than or equal to 10) that is confirmed at a subsequent assessment, or death (by any cause) in the absence of a clinically meaningful symptom deterioration.~NA is not applicable. The upper confidence limit was not calculable because of an insufficient number of participants with events." (NCT03775486)
Timeframe: From randomization until date of objective radiological disease progression or death, or last evaluable assessment in the absence of progression, up to 18 months

Intervention	months (Median)
	EORTC QLQ-LC13: Dyspnoea	EORTC QLQ-LC13: Coughing	EORTC QLQ-LC13: Haemoptysis	EORTC QLQ-LC13: Pain In Chest	EORTC QLQ-LC13: Pain In Arm Or Shoulder	EORTC QLQ-LC13: Pain In Other Parts
Durvalumab/Olaparib Combination Therapy	10.0	11.7	15.0	13.8	15.0	10.3
Durvalumab/Placebo Therapy	9.7	10.6	12.6	11.5	9.7	10.6

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Duration of Response

"Duration of response (DoR) defined as time from the date of first documented response following randomization until the first date of documented progression or death in the absence of disease progression.~Percentage of participants remaining in response at 3, 6, 9 and 12 months estimated using the Kaplan-Meier method." (NCT03775486)
Timeframe: From date of first documented response until objective radiological disease progression or death, up to 18 months.

Intervention	percent (Number)
	Percentage of participants remaining in response at 3 months	Percentage of participants remaining in response at 6 months	Percentage of participants remaining in response at 9 months	Percentage of participants remaining in response at 12 months
Durvalumab/Olaparib Combination Therapy	90.5	79.1	69.2	69.2
Durvalumab/Placebo Therapy	85.1	65.7	65.7	65.7

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Overall Survival (OS)

Overall survival (OS) is defined as the time from randomization to death due to any cause. The nonparametric Kaplan-Meier method was used to estimate the survival curves. (NCT03834519)
Timeframe: Up to ~31 months

Intervention	Months (Median)
Pembrolizumab + Olaparib	15.8
Next-generation Hormonal Agent Monotherapy (NHA)	14.6

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Radiographic Progression-Free Survival (rPFS)

rPFS is defined as the time from randomization to the first documented progressive disease (PD) per PCWG-modified RECIST 1.1 based on BICR or death due to any cause, whichever occurred first. Per PCWG-modified RECIST 1.1, PD is defined as ≥20% increase in the sum of diameters of target lesions. In addition to the relative increase of 20%, the sum must also have demonstrated an absolute increase of ≥5 mm. The appearance of one or more new lesions or ≥2 new bone lesions was also considered PD. PCWG-modified RECIST is similar to RECIST 1.1 with the exception that a confirmation assessment of PD (>4 weeks after the initial PD) is required for participants who remain on treatment following a documented PD per RECIST 1.1 and PCWG rules include new bone lesions. The rPFS per PCWG-modified RECIST as assessed by BICR for all participants is presented. The nonparametric Kaplan-Meier method was used to estimate the survival curves. (NCT03834519)
Timeframe: Up to ~31 months

Intervention	Months (Median)
Pembrolizumab + Olaparib	4.4
Next-generation Hormonal Agent Monotherapy (NHA)	4.2

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Number of Patients Experiencing Adverse Events

Recorded at each clinical visit and will be categorized according to National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. Number of patients experiencing a grade 3 or greater adverse event will be reported. (NCT03880019)
Timeframe: Up to 2 years after study treatment

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Temozolomide)	20

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Confirmed Objective Response Rate (ORR) (Complete Response + Partial Response)

Will be measured by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 criteria assessed by MRI: Complete Response (CR), disappearance of all target lesions, any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm (<1 cm); Partial Response (PR), at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. A response rate of 10% is considered inactive and unworthy of further study. A response rate of 35% would be promising for further study among patients with advanced uterine leiomyosarcoma (LMS) treated with at least one prior systemic regimen. A response rate of 35% for the temozolomide (TMZ) + poly(adenosine diphosphate[ADP]-ribose) polymerase inhibitor (PARPi) combination would also be suggestive of superior efficacy over TMZ monotherapy in sarcoma. Will be reported with a 95% confidence interval. (NCT03880019)
Timeframe: Within first 6 months of study treatment

Intervention	Participants (Count of Participants)
Treatment (Olaparib, Temozolomide)	5

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Dose-limiting Toxicity (DLT) (Safety Lead-In)

The outcome measure presents the count of participants who experienced a DLT. If more than six of the first 25 patients treated with Tremelimumab and Olaparib are unable to complete at least 3 cycles of treatment due to DLTs then the study will be stopped. If not, then enrollment will continue until 45 patients are enrolled. If more than 11 of the first 45 patients treated with the combination regimen are unable to complete the first 3 cycles of treatment, then enrollment will be stopped, otherwise, the trial till proceed to the third component (i.e. a phase 2 comparison of study treatments). (NCT04034927)
Timeframe: At least 4 weeks after initiating treatment, no longer than 12 weeks (three complete treatment cycles). Maximum follow-up was 12 weeks.

Intervention	Participants (Count of Participants)
Arm I (Olaparib)	0
Arm II (Olaparib, Tremelimumab)	6

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Number of Participants Died

Overall survival (OS) will be presented as survival events (deaths). (NCT04034927)
Timeframe: Overall survival will be monitored from enrollment to randomization to the date of death due to any cause. The median follow-up is 22 months. Since the study was stopped early, the time frame for OS follow-up was significantly reduced.

Intervention	Participants (Count of Participants)
Arm I (Olaparib)	9
Arm II (Olaparib, Tremelimumab)	11

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Number of Participants With Adverse Event of Grade 3 or Higher

Safety data will be summarized for all treated subjects. All adverse events, including severe adverse events (SAEs) and treatment-related adverse events, will be categorized and graded for severity according to National Cancer Institute Common Terminology Criteria for Adverse Events version 5.0. This will be presented as the count of participants who experienced an adverse event (AE) of grade 3 or higher. (NCT04034927)
Timeframe: During treatment period and up to 30 days after treatment end. The mean follow-up for adverse events was 6.4 months. Note: survival is monitored for a longer period of time (i.e. up to five years) as compared to the period for collecting adverse events.

Intervention	Participants (Count of Participants)
Arm I (Olaparib)	15
Arm II (Olaparib, Tremelimumab)	20

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Objective Response (RECIST 1.1)

The objective response (RECIST 1.1) is the count of subjects with a best overall complete response (CR) or partial response (PR) among those with target lesions at the time of enrollment. : Summary of RECIST 1.1 criteria for progression for this trial: At least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression). (NCT04034927)
Timeframe: The median follow-up is 22 months. Since the study was stopped early, the follow-up time frame for objective response was significantly reduced.

Intervention	Participants (Count of Participants)
Arm I (Olaparib)	11
Arm II (Olaparib, Tremelimumab)	9

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Progression Free Survival (PFS)

The count of participants who have progressed or died (death due to any cause). Progression is defined by the Response Evaluation Criteria in Solid Tumors (RECIST) criteria. Summary of RECIST 1.1 criteria for progression for this trial: At least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study (this includes the baseline sum if that is the smallest on study). In addition to the relative increase of 20%, the sum must also demonstrate an absolute increase of at least 5 mm. (Note: the appearance of one or more new lesions is also considered progression). (NCT04034927)
Timeframe: PFS is monitored for progression or death due to any cause, whichever occurs first. The median follow-up time is 22 months. Since the study was stopped early, the follow-up for progression-free survival was significantly reduced.

Intervention	Participants (Count of Participants)
Arm I (Olaparib)	24
Arm II (Olaparib, Tremelimumab)	23

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Count of Participants With Adverse Events Greater or Equal to 3

To determine the safety of TMZ in combination with olaparib, the number of participants with ≥ grade 3 treatment related adverse events by CTCAE v5.0 coding will be assessed. (NCT04166435)
Timeframe: Up to 2 years from last treatment

Intervention	Participants (Count of Participants)
Temozolomide + Olaparib	7

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Overall Survival

To estimate overall survival (OS), patients will be followed for up to 24 months. (NCT04166435)
Timeframe: Up to 2 years from last treatment

Intervention	months (Median)
Temozolomide + Olaparib	9.4

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Progression Free Survival

To estimate the progression free survival (PFS), patients will be followed for up to 24 months. (NCT04166435)
Timeframe: Up to 2 years from last treatment

Intervention	months (Median)
Temozolomide + Olaparib	3

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Substance	Relationship Strength	Studies	Trials	Classes	Roles
phosphoserine Phosphoserine: The phosphoric acid ester of serine.	2.21	1	0	non-proteinogenic alpha-amino acid; O-phosphoamino acid; serine derivative	human metabolite
aminolevulinic acid Aminolevulinic Acid: A compound produced from succinyl-CoA and GLYCINE as an intermediate in heme synthesis. It is used as a PHOTOCHEMOTHERAPY for actinic KERATOSIS.. 5-aminolevulinic acid : The simplest delta-amino acid in which the hydrogens at the gamma position are replaced by an oxo group. It is metabolised to protoporphyrin IX, a photoactive compound which accumulates in the skin. Used (in the form of the hydrochloride salt)in combination with blue light illumination for the treatment of minimally to moderately thick actinic keratosis of the face or scalp.	2.6	1	0	4-oxo monocarboxylic acid; amino acid zwitterion; delta-amino acid	antineoplastic agent; dermatologic drug; Escherichia coli metabolite; human metabolite; mouse metabolite; photosensitizing agent; plant metabolite; prodrug; Saccharomyces cerevisiae metabolite
adenine [no description available]	2.61	2	0	6-aminopurines; purine nucleobase	Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
cadaverine [no description available]	2.11	1	0	alkane-alpha,omega-diamine	Daphnia magna metabolite; Escherichia coli metabolite; mouse metabolite; plant metabolite
carbamates [no description available]	2.15	1	0	amino-acid anion
choline [no description available]	2.31	1	0	cholines	allergen; Daphnia magna metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; neurotransmitter; nutrient; plant metabolite; Saccharomyces cerevisiae metabolite
coumarin 2H-chromen-2-one: coumarin derivative	2.6	1	0	coumarins	fluorescent dye; human metabolite; plant metabolite
salicylic acid Scalp: The outer covering of the calvaria. It is composed of several layers: SKIN; subcutaneous connective tissue; the occipitofrontal muscle which includes the tendinous galea aponeurotica; loose connective tissue; and the pericranium (the PERIOSTEUM of the SKULL).	2.6	1	0	monohydroxybenzoic acid	algal metabolite; antifungal agent; antiinfective agent; EC 1.11.1.11 (L-ascorbate peroxidase) inhibitor; keratolytic drug; plant hormone; plant metabolite
2-keto-4-methylthiobutyric acid 2-keto-4-methylthiobutyric acid: RN given refers to parent cpd; structure. 4-methylthio-2-oxobutanoic acid : A 2-oxo monocarboxylic acid derived from L-methionine via the action of methionine transaminase.	2.08	1	0	omega-(methylthio)-2-oxocarboxylic acid
dimethyl sulfoxide Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during CRYOPRESERVATION. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation.. dimethyl sulfoxide : A 2-carbon sulfoxide in which the sulfur atom has two methyl substituents.	2.41	1	0	sulfoxide; volatile organic compound	alkylating agent; antidote; Escherichia coli metabolite; geroprotector; MRI contrast agent; non-narcotic analgesic; polar aprotic solvent; radical scavenger
hydrogen Hydrogen: The first chemical element in the periodic table with atomic symbol H, and atomic number 1. Protium (atomic weight 1) is by far the most common hydrogen isotope. Hydrogen also exists as the stable isotope DEUTERIUM (atomic weight 2) and the radioactive isotope TRITIUM (atomic weight 3). Hydrogen forms into a diatomic molecule at room temperature and appears as a highly flammable colorless and odorless gas.. dihydrogen : An elemental molecule consisting of two hydrogens joined by a single bond.	2.1	1	0	elemental hydrogen; elemental molecule; gas molecular entity	antioxidant; electron donor; food packaging gas; fuel; human metabolite
thioctic acid Thioctic Acid: An octanoic acid bridged with two sulfurs so that it is sometimes also called a pentanoic acid in some naming schemes. It is biosynthesized by cleavage of LINOLEIC ACID and is a coenzyme of oxoglutarate dehydrogenase (KETOGLUTARATE DEHYDROGENASE COMPLEX). It is used in DIETARY SUPPLEMENTS.	2.6	1	0	dithiolanes; heterocyclic fatty acid; thia fatty acid	fundamental metabolite; geroprotector
niacinamide nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.	3.91	3	0	pyridine alkaloid; pyridinecarboxamide; vitamin B3	anti-inflammatory agent; antioxidant; cofactor; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; EC 3.5.1.98 (histone deacetylase) inhibitor; Escherichia coli metabolite; geroprotector; human urinary metabolite; metabolite; mouse metabolite; neuroprotective agent; Saccharomyces cerevisiae metabolite; Sir2 inhibitor
phosphorylcholine Phosphorylcholine: Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.. phosphocholine : The phosphate of choline; and the parent compound of the phosphocholine family.	2.21	1	0	phosphocholines	allergen; epitope; hapten; human metabolite; mouse metabolite
picolinic acid picolinic acid: iron-chelating agent that inhibits DNA synthesis; may interfere with iron-dependent production of stable free organic radical which is essential for ribonucleotide reductase formation of deoxyribonucleotides; RN given refers to parent cpd; structure in Merck Index, 9th ed, #7206. picolinic acid : A pyridinemonocarboxylic acid in which the carboxy group is located at position 2. It is an intermediate in the metabolism of tryptophan.	2.6	1	0	pyridinemonocarboxylic acid	human metabolite; MALDI matrix material
thiamine thiamine(1+) : A primary alcohol that is 1,3-thiazol-3-ium substituted by (4-amino-2-methylpyrimidin-5-yl)methyl, methyl and 2-hydroxyethyl groups at positions 3, 4 and 5, respectively.	2.6	1	0	primary alcohol; vitamin B1	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
thymine [no description available]	2.31	1	0	pyrimidine nucleobase; pyrimidone	Escherichia coli metabolite; human metabolite; mouse metabolite
urea pseudourea: clinical use; structure. isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.	2.78	3	0	isourea; monocarboxylic acid amide; one-carbon compound	Daphnia magna metabolite; Escherichia coli metabolite; fertilizer; flour treatment agent; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
pk 11195 PK-11195 : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 1-(2-chlorophenyl)isoquinoline-3-carboxylic acid with the amino group of sec-butylmethylamine	2.08	1	0	aromatic amide; isoquinolines; monocarboxylic acid amide; monochlorobenzenes	antineoplastic agent
pd 173074 [no description available]	2.54	2	0	aromatic amine; biaryl; dimethoxybenzene; pyridopyrimidine; tertiary amino compound; ureas	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist
zopolrestat zopolrestat: structure given in first source	3.31	1	0
3-aminobenzamide [no description available]	3.93	3	0	benzamides; substituted aniline	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
pleconaril WIN 63843: structure given in first source	2.6	1	0
4-(2-aminoethyl)benzenesulfonylfluoride [no description available]	2.6	1	0
phenytoin [no description available]	2.6	1	0	imidazolidine-2,4-dione	anticonvulsant; drug allergen; sodium channel blocker; teratogenic agent
5-(n,n-hexamethylene)amiloride 5-(N,N-hexamethylene)amiloride: inhibitor of Na+-H+ exchange; has anti-HIV-1 activity. 5-(N,N-hexamethylene)amiloride : A member of the class of pyrazines that is amiloride in which the two amino hydrogens at position N-5 are replaced by a hexamethylene moiety, resulting in the formation of an azepane ring.	2.13	1	0	aromatic amine; azepanes; guanidines; monocarboxylic acid amide; organochlorine compound; pyrazines	antineoplastic agent; apoptosis inducer; odorant receptor antagonist; sodium channel blocker
phenanthridone phenanthridone: coal tar derivative; structure given in first source. phenanthridone : A member of the class of phenanthridines that is phenanthridine with an oxo substituent at position 6. A poly(ADP-ribose) polymerase (PARP) inhibitor, it has been shown to exhibit immunosuppressive activity.	2.1	1	0	lactam; phenanthridines	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; immunosuppressive agent; mutagen
tacrine Tacrine: A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.. tacrine : A member of the class of acridines that is 1,2,3,4-tetrahydroacridine substituted by an amino group at position 9. It is used in the treatment of Alzheimer's disease.	3.31	1	0	acridines; aromatic amine	EC 3.1.1.7 (acetylcholinesterase) inhibitor
abt 702 [no description available]	2.08	1	0	bipyridines
acetazolamide Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)	2.6	1	0	monocarboxylic acid amide; sulfonamide; thiadiazoles	anticonvulsant; diuretic; EC 4.2.1.1 (carbonic anhydrase) inhibitor
alprenolol Alprenolol: One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.. alprenolol : A secondary alcohol that is propan-2-ol substituted by a 2-allylphenoxy group at position 1 and an isopropylamino group at position 3. It is a beta-adrenergic antagonist used as a antihypertensive, anti-arrhythmia and a sympatholytic agent.	2.72	2	0	secondary alcohol; secondary amino compound	anti-arrhythmia drug; antihypertensive agent; beta-adrenergic antagonist; sympatholytic agent
amantadine amant: an antiviral compound consisting of an adamantane derivative chemically linked to a water-solube polyanioic matrix; structure in first source	2.6	1	0	adamantanes; primary aliphatic amine	analgesic; antiparkinson drug; antiviral drug; dopaminergic agent; NMDA receptor antagonist; non-narcotic analgesic
theophylline [no description available]	2.25	1	0	dimethylxanthine	adenosine receptor antagonist; anti-asthmatic drug; anti-inflammatory agent; bronchodilator agent; drug metabolite; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; fungal metabolite; human blood serum metabolite; immunomodulator; muscle relaxant; vasodilator agent
2-aminothiazole 2-aminothiazole: RN given refers to parent cpd; structure. 1,3-thiazol-2-amine : A primary amino compound that is 1,3-thiazole substituted by an amino group at position 2.	2.6	1	0	1,3-thiazoles; primary amino compound
amodiaquine Amodiaquine: A 4-aminoquinoline compound with anti-inflammatory properties.. amodiaquine : A quinoline having a chloro group at the 7-position and an aryl amino group at the 4-position.	2.6	1	0	aminoquinoline; organochlorine compound; phenols; secondary amino compound; tertiary amino compound	anticoronaviral agent; antimalarial; drug allergen; EC 2.1.1.8 (histamine N-methyltransferase) inhibitor; non-steroidal anti-inflammatory drug; prodrug
amsacrine Amsacrine: An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.. amsacrine : A sulfonamide that is N-phenylmethanesulfonamide substituted by a methoxy group at position 3 and an acridin-9-ylamino group at position 4. It exhibits antineoplastic activity.	2.15	1	0	acridines; aromatic ether; sulfonamide	antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
anastrozole [no description available]	4.48	1	1	nitrile; triazoles	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
aspirin Aspirin: The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5). acetylsalicylate : A benzoate that is the conjugate base of acetylsalicylic acid, arising from deprotonation of the carboxy group.. acetylsalicylic acid : A member of the class of benzoic acids that is salicylic acid in which the hydrogen that is attached to the phenolic hydroxy group has been replaced by an acetoxy group. A non-steroidal anti-inflammatory drug with cyclooxygenase inhibitor activity.	2.6	1	0	benzoic acids; phenyl acetates; salicylates	anticoagulant; antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; EC 1.1.1.188 (prostaglandin-F synthase) inhibitor; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug; plant activator; platelet aggregation inhibitor; prostaglandin antagonist; teratogenic agent
baclofen [no description available]	2.6	1	0	amino acid zwitterion; gamma-amino acid; monocarboxylic acid; monochlorobenzenes; primary amino compound	central nervous system depressant; GABA agonist; muscle relaxant
benzamide benzamide : An aromatic amide that consists of benzene bearing a single carboxamido substituent. The parent of the class of benzamides.	2.66	2	0	benzamides
berberine [no description available]	2.21	1	0	alkaloid antibiotic; berberine alkaloid; botanical anti-fungal agent; organic heteropentacyclic compound	antilipemic drug; antineoplastic agent; antioxidant; EC 1.1.1.141 [15-hydroxyprostaglandin dehydrogenase (NAD(+))] inhibitor; EC 1.1.1.21 (aldehyde reductase) inhibitor; EC 1.13.11.52 (indoleamine 2,3-dioxygenase) inhibitor; EC 1.21.3.3 (reticuline oxidase) inhibitor; EC 2.1.1.116 [3'-hydroxy-N-methyl-(S)-coclaurine 4'-O-methyltransferase] inhibitor; EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor; EC 2.7.11.10 (IkappaB kinase) inhibitor; EC 3.1.1.4 (phospholipase A2) inhibitor; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor; EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; geroprotector; hypoglycemic agent; metabolite; potassium channel blocker
bicalutamide bicalutamide: approved for treatment of advanced prostate cancer. N-[4-cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide : A member of the class of (trifluoromethyl)benzenes that is 4-amino-2-(trifluoromethyl)benzonitrile in which one of the amino hydrogens is substituted by a 3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanoyl group.. bicalutamide : A racemate comprising of equal amounts of (R)-bicalutamide and (S)-bicalutamide. It is an oral non-steroidal antiandrogen used in the treatment of prostate cancer and hirsutism.	2.08	1	0	(trifluoromethyl)benzenes; monocarboxylic acid amide; monofluorobenzenes; nitrile; sulfone; tertiary alcohol
bromazepam Bromazepam: One of the BENZODIAZEPINES that is used in the treatment of ANXIETY DISORDERS.	2.11	1	0	organic molecular entity
busulfan [no description available]	7.59	2	0	methanesulfonate ester	alkylating agent; antineoplastic agent; carcinogenic agent; insect sterilant; teratogenic agent
verapamil Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.. verapamil : A racemate comprising equimolar amounts of dexverapamil and (S)-verapamil. An L-type calcium channel blocker of the phenylalkylamine class, it is used (particularly as the hydrochloride salt) in the treatment of hypertension, angina pectoris and cardiac arrhythmia, and as a preventive medication for migraine.. 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile : A tertiary amino compound that is 3,4-dimethoxyphenylethylamine in which the hydrogens attached to the nitrogen are replaced by a methyl group and a 4-cyano-4-(3,4-dimethoxyphenyl)-5-methylhexyl group.	2.51	2	0	aromatic ether; nitrile; polyether; tertiary amino compound
camostat camostat : A benzoate ester resulting from the formal condensation of the carboxy group of 4-guanidinobenzoic acid with the hydroxy group of 2-(dimethylamino)-2-oxoethyl (4-hydroxyphenyl)acetate. It is a potent inhibitor of the human transmembrane protease serine 2 (TMPRSS2) and its mesylate salt is currently under investigation for its effectiveness in COVID-19 patients.	2.6	1	0	benzoate ester; carboxylic ester; diester; guanidines; tertiary carboxamide	anti-inflammatory agent; anticoronaviral agent; antifibrinolytic drug; antihypertensive agent; antineoplastic agent; antiviral agent; serine protease inhibitor
camphor, (+-)-isomer [no description available]	2.6	1	0	bornane monoterpenoid; cyclic monoterpene ketone	plant metabolite
candesartan candesartan: a nonpeptide angiotensin II receptor antagonist. candesartan : A benzimidazolecarboxylic acid that is 1H-benzimidazole-7-carboxylic acid substituted by an ethoxy group at position 2 and a ({2'-(1H-tetrazol-5-yl)[1,1'-biphenyl]-4-yl}methyl) group at position 1. It is a angiotensin receptor antagonist used for the treatment of hypertension.	2.6	1	0	benzimidazolecarboxylic acid; biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
carbamazepine Carbamazepine: A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties.. carbamazepine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.	2.11	1	0	dibenzoazepine; ureas	analgesic; anticonvulsant; antimanic drug; drug allergen; EC 3.5.1.98 (histone deacetylase) inhibitor; environmental contaminant; glutamate transporter activator; mitogen; non-narcotic analgesic; sodium channel blocker; xenobiotic
celecoxib [no description available]	3.63	2	0	organofluorine compound; pyrazoles; sulfonamide; toluenes	cyclooxygenase 2 inhibitor; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug
cetylpyridinium Cetylpyridinium: Cationic bactericidal surfactant used as a topical antiseptic for skin, wounds, mucous membranes, instruments, etc.; and also as a component in mouthwash and lozenges.	2.6	1	0	pyridinium ion
chelerythrine chelerythrine : A benzophenanthridine alkaloid isolated from the root of Zanthoxylum simulans, Chelidonium majus L., and other Papaveraceae.	2.08	1	0	benzophenanthridine alkaloid; organic cation	antibacterial agent; antineoplastic agent; EC 2.7.11.13 (protein kinase C) inhibitor
chlorambucil Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia.	3.12	1	0	aromatic amine; monocarboxylic acid; nitrogen mustard; organochlorine compound; tertiary amino compound	alkylating agent; antineoplastic agent; carcinogenic agent; drug allergen; immunosuppressive agent
chloroquine Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.. chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.	2.93	3	0	aminoquinoline; organochlorine compound; secondary amino compound; tertiary amino compound	anticoronaviral agent; antimalarial; antirheumatic drug; autophagy inhibitor; dermatologic drug
chloroxylenol chloroxylenol: topical antiseptic; RN given refers to parent cpd; structure. 4-chloro-3,5-dimethylphenol : A member of the class of phenols that is 3,5-xylenol which is substituted at position 4 by chlorine. It is bactericidal against most Gram-positive bacteria but less effective against Staphylococci and Gram-negative bacteria, and often inactive against Pseudomonas species. It is ineffective against bacterial spores.	2.6	1	0	monochlorobenzenes; phenols	antiseptic drug; disinfectant; molluscicide
chlorpromazine Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.	2.6	1	0	organochlorine compound; phenothiazines; tertiary amine	anticoronaviral agent; antiemetic; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; phenothiazine antipsychotic drug
ciprofibrate [no description available]	2.6	1	0	cyclopropanes; monocarboxylic acid; organochlorine compound	antilipemic drug
clomipramine Clomipramine: A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.. clomipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine which is substituted by chlorine at position 3 and in which the hydrogen attached to the nitrogen is replaced by a 3-(dimethylamino)propyl group. One of the more sedating tricyclic antidepressants, it is used as the hydrochloride salt for the treatment of depression as well as obsessive-compulsive disorder and phobias.	2.6	1	0	dibenzoazepine	anticoronaviral agent; antidepressant; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; serotonergic antagonist; serotonergic drug; serotonin uptake inhibitor
cx546 1-(1,4-benzodioxan-6-ylcarbonyl)piperidine: structure in first source	2.1	1	0
danthron danthron: structure. chrysazin : A dihydroxyanthraquinone that is anthracene-9,10-dione substituted by hydroxy groups at positions 1 and 8.	2.6	1	0	dihydroxyanthraquinone	apoptosis inducer; plant metabolite
deferiprone Deferiprone: A pyridone derivative and iron chelator that is used in the treatment of IRON OVERLOAD in patients with THALASSEMIA.. deferiprone : A member of the class of 4-pyridones that is pyridin-4(1H)-one substituted at positions 1 and 2 by methyl groups and at position 3 by a hydroxy group. A lipid-soluble iron-chelator used for treatment of thalassaemia.	2.6	1	0	4-pyridones	iron chelator; protective agent
diclofenac Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.. diclofenac : A monocarboxylic acid consisting of phenylacetic acid having a (2,6-dichlorophenyl)amino group at the 2-position.	2.11	1	0	amino acid; aromatic amine; dichlorobenzene; monocarboxylic acid; secondary amino compound	antipyretic; drug allergen; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
dipyridamole Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752). dipyridamole : A pyrimidopyrimidine that is 2,2',2'',2'''-(pyrimido[5,4-d]pyrimidine-2,6-diyldinitrilo)tetraethanol substituted by piperidin-1-yl groups at positions 4 and 8 respectively. A vasodilator agent, it inhibits the formation of blood clots.	2.6	1	0	piperidines; pyrimidopyrimidine; tertiary amino compound; tetrol	adenosine phosphodiesterase inhibitor; EC 3.5.4.4 (adenosine deaminase) inhibitor; platelet aggregation inhibitor; vasodilator agent
disulfiram [no description available]	2.63	2	0	organic disulfide; organosulfur acaricide	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor; EC 3.1.1.1 (carboxylesterase) inhibitor; EC 3.1.1.8 (cholinesterase) inhibitor; EC 5.99.1.2 (DNA topoisomerase) inhibitor; ferroptosis inducer; fungicide; NF-kappaB inhibitor
valproic acid Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.. valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.	3.82	2	0	branched-chain fatty acid; branched-chain saturated fatty acid	anticonvulsant; antimanic drug; EC 3.5.1.98 (histone deacetylase) inhibitor; GABA agent; neuroprotective agent; psychotropic drug; teratogenic agent
doxazosin Doxazosin: A prazosin-related compound that is a selective alpha-1-adrenergic blocker.. doxazosin : A member of the class of quinazolines that is quinazoline substituted by an amino group at position 4, methoxy groups at positions 6 and 7 and a piperazin-1-yl group at position 2 which in turn is substituted by a 2,3-dihydro-1,4-benzodioxin-2-ylcarbonyl group at position 4. An antihypertensive agent, it is used in the treatment of high blood pressure.	2.6	1	0	aromatic amine; benzodioxine; monocarboxylic acid amide; N-acylpiperazine; N-arylpiperazine; quinazolines	alpha-adrenergic antagonist; antihyperplasia drug; antihypertensive agent; antineoplastic agent; vasodilator agent
ebselen ebselen : A benzoselenazole that is 1,2-benzoselenazol-3-one carrying an additional phenyl substituent at position 2. Acts as a mimic of glutathione peroxidase.	2.6	1	0	benzoselenazole	anti-inflammatory drug; antibacterial agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antioxidant; apoptosis inducer; EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; EC 3.1.3.25 (inositol-phosphate phosphatase) inhibitor; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; EC 3.5.4.1 (cytosine deaminase) inhibitor; EC 5.1.3.2 (UDP-glucose 4-epimerase) inhibitor; enzyme mimic; ferroptosis inhibitor; genotoxin; hepatoprotective agent; neuroprotective agent; radical scavenger
etidronate Etidronic Acid: A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.. etidronic acid : A 1,1-bis(phosphonic acid) that is (ethane-1,1-diyl)bis(phosphonic acid) having a hydroxy substituent at the 1-position. It inhibits the formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces.	2.6	1	0	1,1-bis(phosphonic acid)	antineoplastic agent; bone density conservation agent; chelator
2-hexyloxybenzamide 2-hexyloxybenzamide: structure	2.6	1	0	aromatic ether; benzamides	antifungal agent
brl 42810 [no description available]	2.6	1	0	2-aminopurines; acetate ester	antiviral drug; prodrug
fluphenazine [no description available]	2.6	1	0	N-alkylpiperazine; organofluorine compound; phenothiazines	anticoronaviral agent; dopaminergic antagonist; phenothiazine antipsychotic drug
fluorouracil Fluorouracil: A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.. 5-fluorouracil : A nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth.	8.28	11	1	nucleobase analogue; organofluorine compound	antimetabolite; antineoplastic agent; environmental contaminant; immunosuppressive agent; radiosensitizing agent; xenobiotic
furosemide Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.	2.08	1	0	chlorobenzoic acid; furans; sulfonamide	environmental contaminant; loop diuretic; xenobiotic
gabexate Gabexate: A serine proteinase inhibitor used therapeutically in the treatment of pancreatitis, disseminated intravascular coagulation (DIC), and as a regional anticoagulant for hemodialysis. The drug inhibits the hydrolytic effects of thrombin, plasmin, and kallikrein, but not of chymotrypsin and aprotinin.	2.6	1	0	benzoate ester
glutaral Glutaral: One of the protein CROSS-LINKING REAGENTS that is used as a disinfectant for sterilization of heat-sensitive equipment and as a laboratory reagent, especially as a fixative.. glutaraldehyde : A dialdehyde comprised of pentane with aldehyde functions at C-1 and C-5.	2.6	1	0	dialdehyde	cross-linking reagent; disinfectant; fixative
gossypol Gossypol: A dimeric sesquiterpene found in cottonseed (GOSSYPIUM). The (-) isomer is active as a male contraceptive (CONTRACEPTIVE AGENTS, MALE) whereas toxic symptoms are associated with the (+) isomer.	2.08	1	0
fasudil fasudil: intracellular calcium antagonist; structure in first source. fasudil : An isoquinoline substituted by a (1,4-diazepan-1-yl)sulfonyl group at position 5. It is a Rho-kinase inhibitor and its hydrochloride hydrate form is approved for the treatment of cerebral vasospasm and cerebral ischemia.	2.58	2	0	isoquinolines; N-sulfonyldiazepane	antihypertensive agent; calcium channel blocker; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; geroprotector; neuroprotective agent; nootropic agent; vasodilator agent
haloperidol Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.	2.6	1	0	aromatic ketone; hydroxypiperidine; monochlorobenzenes; organofluorine compound; tertiary alcohol	antidyskinesia agent; antiemetic; dopaminergic antagonist; first generation antipsychotic; serotonergic antagonist
miltefosine miltefosine: hexadecyl phosphocholine derivative of cisplatin; did not substantially activate HIV long terminal repeat; less toxic than cisplatin. miltefosine : A phospholipid that is the hexadecyl monoester of phosphocholine.	2.6	1	0	phosphocholines; phospholipid	anti-inflammatory agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antiprotozoal drug; apoptosis inducer; immunomodulator; protein kinase inhibitor
hexylresorcinol [no description available]	2.6	1	0	resorcinols
beta-thujaplicin beta-thujaplicin: structure. beta-thujaplicin : A monoterpenoid that is cyclohepta-2,4,6-trien-1-one substituted by a hydroxy group at position 2 and an isopropyl group at position 4. Isolated from Thuja plicata and Chamaecyparis obtusa, it exhibits antimicrobial activities.	2.6	1	0	cyclic ketone; enol; monoterpenoid	antibacterial agent; antifungal agent; antineoplastic agent; antiplasmodial drug; plant metabolite
hycanthone Hycanthone: Potentially toxic, but effective antischistosomal agent, it is a metabolite of LUCANTHONE.. hycanthone : A thioxanthen-9-one compound having a hydroxymethyl substituent at the 1-position and a 2-[(diethylamino)ethyl]amino substituent at the 4-position. It was formerly used (particularly as the monomethanesulfonic acid salt) as a schistosomicide for individual or mass treatement of infection with Schistosoma haematobium and S. mansoni, but due to its toxicity and concern about possible carcinogenicity, it has been replaced by other drugs such as praziquantel.	2.6	1	0	thioxanthenes	mutagen; schistosomicide drug
hydrochlorothiazide Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.. hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.	2.6	1	0	benzothiadiazine; organochlorine compound; sulfonamide	antihypertensive agent; diuretic; environmental contaminant; xenobiotic
hydroxyurea [no description available]	3.31	5	0	one-carbon compound; ureas	antimetabolite; antimitotic; antineoplastic agent; DNA synthesis inhibitor; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; genotoxin; immunomodulator; radical scavenger; teratogenic agent
ibuprofen Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine	2.6	1	0	monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; environmental contaminant; geroprotector; non-narcotic analgesic; non-steroidal anti-inflammatory drug; radical scavenger; xenobiotic
ifosfamide [no description available]	2.11	1	0	ifosfamides	alkylating agent; antineoplastic agent; environmental contaminant; immunosuppressive agent; xenobiotic
indirubin-3'-monoxime indirubin-3'-monoxime: has antiangiogenic activity. indirubin-3'-monoxime : A member of the class of biindoles that is indirubin in which the keto group at position 3' has undergone condensation with hydroxylamine to form the corresponding oxime.	2.08	1	0
indomethacin Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES.. indometacin : A member of the class of indole-3-acetic acids that is indole-3-acetic acid in which the indole ring is substituted at positions 1, 2 and 5 by p-chlorobenzoyl, methyl, and methoxy groups, respectively. A non-steroidal anti-inflammatory drug, it is used in the treatment of musculoskeletal and joint disorders including osteoarthritis, rheumatoid arthritis, gout, bursitis and tendinitis.	2.61	2	0	aromatic ether; indole-3-acetic acids; monochlorobenzenes; N-acylindole	analgesic; drug metabolite; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; gout suppressant; non-steroidal anti-inflammatory drug; xenobiotic metabolite; xenobiotic
avapro Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.. irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.	2.6	1	0	azaspiro compound; biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
itraconazole [no description available]	2.6	1	0	piperazines
ketoprofen Ketoprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.. ketoprofen : An oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2.	2.11	1	0	benzophenones; oxo monocarboxylic acid	antipyretic; drug allergen; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; environmental contaminant; non-steroidal anti-inflammatory drug; xenobiotic
kojic acid [no description available]	2.6	1	0	4-pyranones; enol; primary alcohol	Aspergillus metabolite; EC 1.10.3.1 (catechol oxidase) inhibitor; EC 1.10.3.2 (laccase) inhibitor; EC 1.13.11.24 (quercetin 2,3-dioxygenase) inhibitor; EC 1.14.18.1 (tyrosinase) inhibitor; EC 1.4.3.3 (D-amino-acid oxidase) inhibitor; NF-kappaB inhibitor; skin lightening agent
lapachol lapachol : A hydroxy-1,4-naphthoquinone that is 1,4-naphthoquinone substituted by hydroxy and 3-methylbut-2-en-1-yl groups at positions 2 and 3, respectively. It is a natural compound that exhibits antibacterial and anticancer properties, first isolated in 1882 from the bark of Tabebuia avellanedae.	2.6	1	0
leflunomide Leflunomide: An isoxazole derivative that inhibits dihydroorotate dehydrogenase, the fourth enzyme in the pyrimidine biosynthetic pathway. It is used an immunosuppressive agent in the treatment of RHEUMATOID ARTHRITIS and PSORIATIC ARTHRITIS.. leflunomide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-methyl-1,2-oxazole-4-carboxylic acid with the anilino group of 4-(trifluoromethyl)aniline. The prodrug of teriflunomide.	2.08	1	0	(trifluoromethyl)benzenes; isoxazoles; monocarboxylic acid amide	antineoplastic agent; antiparasitic agent; EC 1.3.98.1 [dihydroorotate oxidase (fumarate)] inhibitor; EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor; hepatotoxic agent; immunosuppressive agent; non-steroidal anti-inflammatory drug; prodrug; pyrimidine synthesis inhibitor; tyrosine kinase inhibitor
letrozole [no description available]	4.83	2	1	nitrile; triazoles	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
lg 100268 LG 100268: a retinoid X receptor (RXR) selective compound; structure given in first source	2.08	1	0
loperamide Loperamide: One of the long-acting synthetic ANTIDIARRHEALS; it is not significantly absorbed from the gut, and has no effect on the adrenergic system or central nervous system, but may antagonize histamine and interfere with acetylcholine release locally.. loperamide : A synthetic piperidine derivative, effective against diarrhoea resulting from gastroenteritis or inflammatory bowel disease.	2.6	1	0	monocarboxylic acid amide; monochlorobenzenes; piperidines; tertiary alcohol	anticoronaviral agent; antidiarrhoeal drug; mu-opioid receptor agonist
loratadine Loratadine: A second-generation histamine H1 receptor antagonist used in the treatment of allergic rhinitis and urticaria. Unlike most classical antihistamines (HISTAMINE H1 ANTAGONISTS) it lacks central nervous system depressing effects such as drowsiness.. loratadine : A benzocycloheptapyridine that is 6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridine substituted by a chloro group at position 8 and a 1-(ethoxycarbonyl)piperidin-4-ylidene group at position 11. It is a H1-receptor antagonist commonly employed in the treatment of allergic disorders.	2.6	1	0	benzocycloheptapyridine; ethyl ester; N-acylpiperidine; organochlorine compound; tertiary carboxamide	anti-allergic agent; cholinergic antagonist; geroprotector; H1-receptor antagonist
losartan Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position	2.6	1	0	biphenylyltetrazole; imidazoles	angiotensin receptor antagonist; anti-arrhythmia drug; antihypertensive agent; endothelin receptor antagonist
2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one: specific inhibitor of phosphatidylinositol 3-kinase; structure in first source	2.31	1	0	chromones; morpholines; organochlorine compound	autophagy inhibitor; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; geroprotector
4-(dimethylamino)-n-(7-(hydroxyamino)-7-oxoheptyl)benzamide 4-(dimethylamino)-N-(7-(hydroxyamino)-7-oxoheptyl)benzamide: structure in first source. 4-(dimethylamino)-N-[7-(hydroxyamino)-7-oxoheptyl]benzamide : A benzamide resulting from the formal condensation of the carboxy group of 4-(dimethylamino)benzoic acid with the amino group of 7-amino-N-hydroxyheptanamide. It is a potent inhibitor of histone deacetylases and induces cell cycle arrest and apoptosis in several human cancer cell lines.	2.6	1	0	benzamides; hydroxamic acid; secondary carboxamide; tertiary amino compound	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
mafenide Mafenide: A sulfonamide that inhibits the enzyme CARBONIC ANHYDRASE and is used as a topical anti-bacterial agent, especially in burn therapy.	2.6	1	0	aromatic amine
metformin Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.	3.09	4	0	guanidines	environmental contaminant; geroprotector; hypoglycemic agent; xenobiotic
methazolamide Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.	2.6	1	0	sulfonamide; thiadiazoles
methocarbamol Methocarbamol: A centrally acting muscle relaxant whose mode of action has not been established. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1206). methocarbamol : A racemate comprising equimolar amounts of (R)- and (S)-methocarbamol. A centrally acting skeletal muscle relaxant, it is used as an adjunct in the short-term symptomatic treatment of painful muscle spasm. The (R)-enantiomer is more active than the (S)-enantiomer.. 2-hydroxy-3-(2-methoxyphenoxy)propyl carbamate : A carbamate ester that is glycerol in which one of the primary alcohol groups has been converted to its 2-methoxyphenyl ether while the other has been converted to the corresponding carbamate ester.	2.6	1	0	aromatic ether; carbamate ester; secondary alcohol
methyl methanesulfonate [no description available]	3.43	6	0	methanesulfonate ester	alkylating agent; apoptosis inducer; carcinogenic agent; genotoxin; mutagen
mitoxantrone Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8.	2.58	2	0	dihydroxyanthraquinone	analgesic; antineoplastic agent
monodansylcadaverine monodansylcadaverine: inhibits cross linkage of fibrin. monodansylcadaverine : A sulfonamide obtained by formal condensation of the sulfo group of 5-(dimethylamino)naphthalene-1-sulfonic acid with one of the amino groups of cadaverine.	2.11	1	0	aminonaphthalene; primary amino compound; sulfonamide; tertiary amino compound	EC 2.3.2.13 (protein-glutamine gamma-glutamyltransferase) inhibitor; fluorochrome; protective agent
entinostat [no description available]	7.9	3	0	benzamides; carbamate ester; primary amino compound; pyridines; substituted aniline	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
ethylmaleimide Ethylmaleimide: A sulfhydryl reagent that is widely used in experimental biochemical studies.	2.6	1	0	maleimides	anticoronaviral agent; EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor; EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor; EC 2.7.1.1 (hexokinase) inhibitor
nabumetone Nabumetone: A butanone non-steroidal anti-inflammatory drug and cyclooxygenase-2 (COX2) inhibitor that is used in the management of pain associated with OSTEOARTHRITIS and RHEUMATOID ARTHRITIS.. nabumetone : A methyl ketone that is 2-butanone in which one of the methyl hydrogens at position 4 is replaced by a 6-methoxy-2-naphthyl group. A prodrug that is converted to the active metabolite, 6-methoxy-2-naphthylacetic acid, following oral administration. It is shown to have a slightly lower risk of gastrointestinal side effects than most other non-steroidal anti-inflammatory drugs.	2.6	1	0	methoxynaphthalene; methyl ketone	cyclooxygenase 2 inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug; prodrug
nafamostat nafamostat: inhibitor of trypsin, plasmin, pancreatic kallikrein, plasma kallikrein & thrombin; strongly inhibits esterolytic activities of C1r & C1 esterase complement-mediated hemolysis; antineoplastic	2.6	1	0	benzoic acids; guanidines
nevirapine Nevirapine: A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.. nevirapine : A dipyridodiazepine that is 5,11-dihydro-6H-dipyrido[3,2-b:2',3'-e][1,4]diazepine which is substituted by methyl, oxo, and cyclopropyl groups at positions 4, 6, and 11, respectively. A non-nucleoside reverse transcriptase inhibitor with activity against HIV-1, it is used in combination with other antiretrovirals for the treatment of HIV infection.	2.6	1	0	cyclopropanes; dipyridodiazepine	antiviral drug; HIV-1 reverse transcriptase inhibitor
nicardipine Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.. nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.. 2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.	2.11	1	0	benzenes; C-nitro compound; diester; dihydropyridine; methyl ester; tertiary amino compound
nizatidine [no description available]	2.11	1	0	1,3-thiazoles; C-nitro compound; carboxamidine; organic sulfide; tertiary amino compound	anti-ulcer drug; cholinergic drug; H2-receptor antagonist
olprinone olprinone: RN refers to HCl; structure given in first source	2.08	1	0	bipyridines
omeprazole Omeprazole: A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.. omeprazole : A racemate comprising equimolar amounts of (R)- and (S)-omeprazole.. 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted by a [4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group at position 2 and a methoxy group at position 5.	2.58	2	0	aromatic ether; benzimidazoles; pyridines; sulfoxide
osalmide osalmide: structure	2.6	1	0	organic molecular entity
oxethazaine [no description available]	2.6	1	0	amino acid amide
palmidrol palmidrol: a cannabinoid receptor-inactive eCB-related molecule used as prophylactic in helping to prevent respiratory viral infection. palmitoyl ethanolamide : An N-(long-chain-acyl)ethanolamine that is the ethanolamide of palmitic (hexadecanoic) acid.	2.6	1	0	endocannabinoid; N-(long-chain-acyl)ethanolamine; N-(saturated fatty acyl)ethanolamine	anti-inflammatory drug; anticonvulsant; antihypertensive agent; neuroprotective agent
papaverine Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.	2.6	1	0	benzylisoquinoline alkaloid; dimethoxybenzene; isoquinolines	antispasmodic drug; vasodilator agent
pd 98059 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one: inhibits MAP kinase kinase (MEK) activity, p42 MAPK and p44 MAPK; structure in first source. 2-(2-amino-3-methoxyphenyl)chromen-4-one : A member of the class of monomethoxyflavones that is 3'-methoxyflavone bearing an additional amino substituent at position 2'.	2.11	1	0	aromatic amine; monomethoxyflavone	EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; geroprotector
pentoxifylline [no description available]	2.6	1	0	oxopurine
perhexiline Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.	2.6	1	0	piperidines	cardiovascular drug
phenazopyridine Phenazopyridine: A local anesthetic that has been used in urinary tract disorders. Its use is limited by problems with toxicity (primarily blood disorders) and potential carcinogenicity.. phenazopyridine : A diaminopyridine that is 2,6-diaminopyridine substituted at position 3 by a phenylazo group. A local anesthetic that has topical analgesic effect on mucosa lining of the urinary tract. Its use is limited by problems with toxicity (primarily blood disorders) and potential carcinogenicity.	2.6	1	0	diaminopyridine; monoazo compound	anticoronaviral agent; carcinogenic agent; local anaesthetic; non-narcotic analgesic
4-phenylbutyric acid 4-phenylbutyric acid: RN refers to the parent cpd. 4-phenylbutyric acid : A monocarboxylic acid the structure of which is that of butyric acid substituted with a phenyl group at C-4. It is a histone deacetylase inhibitor that displays anticancer activity. It inhibits cell proliferation, invasion and migration and induces apoptosis in glioma cells. It also inhibits protein isoprenylation, depletes plasma glutamine, increases production of foetal haemoglobin through transcriptional activation of the gamma-globin gene and affects hPPARgamma activation.	2.6	1	0	monocarboxylic acid	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor; prodrug
phenylmethylsulfonyl fluoride Phenylmethylsulfonyl Fluoride: An enzyme inhibitor that inactivates IRC-50 arvin, subtilisin, and the fatty acid synthetase complex.. phenylmethanesulfonyl fluoride : An acyl fluoride with phenylmethanesulfonyl as the acyl group.	2.6	1	0	acyl fluoride	serine proteinase inhibitor
pimobendan pimobendan: produces arterial & venous dilatation in dogs; structure given in first source	2.6	1	0	benzimidazoles; pyridazinone	cardiotonic drug; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor; vasodilator agent
pioglitazone Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.	2.08	1	0	aromatic ether; pyridines; thiazolidinediones	antidepressant; cardioprotective agent; EC 2.7.1.33 (pantothenate kinase) inhibitor; EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; geroprotector; hypoglycemic agent; insulin-sensitizing drug; PPARgamma agonist; xenobiotic
piperazine [no description available]	2.69	2	0	azacycloalkane; piperazines; saturated organic heteromonocyclic parent	anthelminthic drug
pj-34 PJ34 : A member of the class of phenanthridines that is 5,6-dihydrophenanthridine substituted at positions 2 and 6 by (N,N-dimethylglycyl)amino and oxo groups, respectively. It is a potent inhibitor of poly(ADP-ribose) polymerases PARP1 and PARP2 (IC50 of 110 nM and 86 nM, respectively) and exhibits anti-cancer, cardioprotective and neuroprotective properties.	2.66	2	0	phenanthridines; secondary carboxamide; tertiary amino compound	angiogenesis inhibitor; anti-inflammatory agent; antiatherosclerotic agent; antineoplastic agent; apoptosis inducer; cardioprotective agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; neuroprotective agent
praziquantel azinox: Russian drug	2.6	1	0	isoquinolines
probenecid Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.. probenecid : A sulfonamide in which the nitrogen of 4-sulfamoylbenzoic acid is substituted with two propyl groups.	2.6	1	0	benzoic acids; sulfonamide	uricosuric drug
probucol Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).. probucol : A dithioketal that is propane-2,2-dithiol in which the hydrogens attached to both sulfur atoms are replaced by 3,5-di-tert-butyl-4-hydroxyphenyl groups. An anticholesteremic drug with antioxidant and anti-inflammatory properties, it is used to treat high levels of cholesterol in blood.	2.6	1	0	dithioketal; polyphenol	anti-inflammatory drug; anticholesteremic drug; antilipemic drug; antioxidant; cardiovascular drug
promazine Promazine: A phenothiazine with actions similar to CHLORPROMAZINE but with less antipsychotic activity. It is primarily used in short-term treatment of disturbed behavior and as an antiemetic.. promazine : A phenothiazine deriative in which the phenothiazine tricycle has a 3-(dimethylaminopropyl) group at the N-10 position.	2.6	1	0	phenothiazines; tertiary amine	antiemetic; dopaminergic antagonist; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; H1-receptor antagonist; muscarinic antagonist; phenothiazine antipsychotic drug; serotonergic antagonist
promethazine Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals.. promethazine : A tertiary amine that is a substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropan-2-amine moiety.	2.6	1	0	phenothiazines; tertiary amine	anti-allergic agent; anticoronaviral agent; antiemetic; antipruritic drug; H1-receptor antagonist; local anaesthetic; sedative
propranolol Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.. propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.	2.6	1	0	naphthalenes; propanolamine; secondary amine	anti-arrhythmia drug; antihypertensive agent; anxiolytic drug; beta-adrenergic antagonist; environmental contaminant; human blood serum metabolite; vasodilator agent; xenobiotic
3-[(3,5-dibromo-4-hydroxyphenyl)methylidene]-5-iodo-1H-indol-2-one [no description available]	2.08	1	0	indoles
riluzole Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.	2.08	1	0	benzothiazoles
rimantadine Rimantadine: An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza.	2.6	1	0	alkylamine
rolipram [no description available]	2.6	1	0	pyrrolidin-2-ones	antidepressant; EC 3.1.4.* (phosphoric diester hydrolase) inhibitor
sb 206553 SB 206553: a high-affinity 5-HT(2C/2B) antagonist; structure given in first source	2.08	1	0	pyrroloindole
sb 220025 SB 220025: inhibits p38 mitogen-activated protein kinase; structure in first source. SB220025 : Am member of the class of imidazoles carrying piperidin-4-yl, 4-fluophenyl and 2-aminopyrimidin-4-yl substituents at posiitons 1, 4 and 5 respectively.	2.08	1	0	aminopyrimidine; imidazoles; organofluorine compound; piperidines	angiogenesis inhibitor; anti-inflammatory agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
sb 202190 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole: structure given in first source; inhibits p38 MAP kinase	2.52	2	0	imidazoles; organofluorine compound; phenols; pyridines	apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
scriptaid scriptide: provokes translocation of GLUT4 to increase glucose uptake; structure in first source	2.6	1	0	isoquinolines
sebacic acid sebacic acid : An alpha,omega-dicarboxylic acid that is the 1,8-dicarboxy derivative of octane.	2.6	1	0	alpha,omega-dicarboxylic acid; dicarboxylic fatty acid	human metabolite; plant metabolite
sk&f 86002 6-(4-fluorophenyl)-2,3-dihydro-5-(4-pyridinyl)imidazo(2,1-b)thiazole: inhibits p38 MAP kinase	2.08	1	0	imidazoles
fenofibrate [no description available]	2.6	1	0	benzochromenone; delta-lactone; naphtho-alpha-pyrone	platelet aggregation inhibitor; Sir2 inhibitor
imatinib [no description available]	4	3	0	aromatic amine; benzamides; N-methylpiperazine; pyridines; pyrimidines	antineoplastic agent; apoptosis inducer; tyrosine kinase inhibitor
vorinostat Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.. vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).	3.73	9	0	dicarboxylic acid diamide; hydroxamic acid	antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
sulfasalazine Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907). sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.	2.08	1	0
suprofen Suprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic.. suprofen : An aromatic ketone that is thiophene substituted at C-2 by a 4-(1-carboxyethyl)benzoyl group.	2.6	1	0	aromatic ketone; monocarboxylic acid; thiophenes	antirheumatic drug; drug allergen; EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor; non-narcotic analgesic; non-steroidal anti-inflammatory drug; peripheral nervous system drug
2-[4-(1,2-diphenylbut-1-enyl)phenoxy]-N,N-dimethylethanamine [no description available]	2.08	1	0	stilbenoid
temozolomide [no description available]	9.21	31	4	imidazotetrazine; monocarboxylic acid amide; triazene derivative	alkylating agent; antineoplastic agent; prodrug
thalidomide Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.. thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide.. 2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group.	2.76	2	0	phthalimides; piperidones
ticlopidine Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.. ticlopidine : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group.	2.6	1	0	monochlorobenzenes; thienopyridine	anticoagulant; fibrin modulating drug; hematologic agent; P2Y12 receptor antagonist; platelet aggregation inhibitor
triamterene Triamterene: A pteridinetriamine compound that inhibits SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS.. triamterene : Pteridine substituted at positions 2, 4 and 7 with amino groups and at position 6 with a phenyl group. A sodium channel blocker, it is used as a diuretic in the treatment of hypertension and oedema.	2.6	1	0	pteridines	diuretic; sodium channel blocker
trifluoperazine [no description available]	2.6	1	0	N-alkylpiperazine; N-methylpiperazine; organofluorine compound; phenothiazines	antiemetic; calmodulin antagonist; dopaminergic antagonist; EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor; EC 5.3.3.5 (cholestenol Delta-isomerase) inhibitor; phenothiazine antipsychotic drug
triflupromazine Triflupromazine: A phenothiazine used as an antipsychotic agent and as an antiemetic.. triflupromazine : A member of the class of phenothiazines that is 10H-phenothiazine having a trifluoromethyl subsitituent at the 2-position and a 3-(dimethylamino)propyl group at the N-10 position.	2.6	1	0	organofluorine compound; phenothiazines; tertiary amine	anticoronaviral agent; antiemetic; dopaminergic antagonist; first generation antipsychotic
trigonelline trigonelline: in hydra among other organisms; RN given refers to hydroxide inner salt; structure. N-methylnicotinic acid : A pyridinium ion consisting of nicotinic acid having a methyl substituent on the pyridine nitrogen.. N-methylnicotinate : An iminium betaine that is the conjugate base of N-methylnicotinic acid, arising from deprotonation of the carboxy group.	2.6	1	0	alkaloid; iminium betaine	food component; human urinary metabolite; plant metabolite
trimethobenzamide trimethobenzamide: major descriptor (64-84); on-line search BENZAMIDES (64-84); Index Medicus search TRIMETHOBENZAMIDE (64-84); RN given refers to parent cpd. trimethobenzamide : The amide obtained by formal condensation of 3,4,5-trihydroxybenzoic acid with 4-[2-(N,N-dimethylamino)ethoxy]benzylamine. It is used to prevent nausea and vomitting in humans.	2.6	1	0	benzamides; tertiary amino compound	antiemetic
trimethoprim Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.	2.6	1	0	aminopyrimidine; methoxybenzenes	antibacterial drug; diuretic; drug allergen; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; environmental contaminant; xenobiotic
troglitazone Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.	2.08	1	0	chromanes; thiazolidinone	anticoagulant; anticonvulsant; antineoplastic agent; antioxidant; EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; hypoglycemic agent; platelet aggregation inhibitor; vasodilator agent
tyrphostin a9 [no description available]	2.6	1	0	alkylbenzene	geroprotector
delavirdine Delavirdine: A potent, non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1.. delavirdine : The amide resulting from the formal condensation of 5-[(methylsulfonyl)amino]-1H-indole-2-carboxylic acid and 4-amino group of 1-[3-(isopropylamino)pyridin-2-yl]piperazine, delavirdine is a non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1. Viral resistance emerges rapidly when delavirdine is used alone, so it is therefore used (as the methanesulfonic acid salt) with other antiretrovirals for combination therapy of HIV infection.	2.6	1	0	aminopyridine; indolecarboxamide; N-acylpiperazine; sulfonamide	antiviral drug; HIV-1 reverse transcriptase inhibitor
vesnarinone [no description available]	2.6	1	0	organic molecular entity
mitomycin Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.. mitomycin : A family of aziridine-containing natural products isolated from Streptomyces caespitosus or Streptomyces lavendulae.	8.95	4	0	mitomycin	alkylating agent; antineoplastic agent
prednisolone Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone.	4.72	1	1	11beta-hydroxy steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; C21-steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	adrenergic agent; anti-inflammatory drug; antineoplastic agent; drug metabolite; environmental contaminant; immunosuppressive agent; xenobiotic
thymidine [no description available]	2.72	2	0	pyrimidine 2'-deoxyribonucleoside	Escherichia coli metabolite; human metabolite; metabolite; mouse metabolite
prednisone Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid.	6.76	5	2	11-oxo steroid; 17alpha-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; C21-steroid; glucocorticoid; primary alpha-hydroxy ketone; tertiary alpha-hydroxy ketone	adrenergic agent; anti-inflammatory drug; antineoplastic agent; immunosuppressive agent; prodrug
estrone Hydroxyestrones: Estrone derivatives substituted with one or more hydroxyl groups in any position. They are important metabolites of estrone and other estrogens.	2.31	1	0	17-oxo steroid; 3-hydroxy steroid; phenolic steroid; phenols	antineoplastic agent; bone density conservation agent; estrogen; human metabolite; mouse metabolite
idoxuridine [no description available]	2.6	1	0	organoiodine compound; pyrimidine 2'-deoxyribonucleoside	antiviral drug; DNA synthesis inhibitor
biguanides Biguanides: Derivatives of biguanide (the structure formula HN(C(NH)NH2)2) that are primarily used as oral HYPOGLYCEMIC AGENTS for the treatment of DIABETES MELLITUS, TYPE 2 and PREDIABETES.. biguanides : A class of oral hypoglycemic drugs used for diabetes mellitus or prediabetes treatment. They have a structure based on the 2-carbamimidoylguanidine skeleton.	7.25	1	0	guanidines
serine Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.. serine : An alpha-amino acid that is alanine substituted at position 3 by a hydroxy group.	2.54	2	0	L-alpha-amino acid; proteinogenic amino acid; serine family amino acid; serine zwitterion; serine	algal metabolite; Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
chloramphenicol Amphenicol: Chloramphenicol and its derivatives.	2.6	1	0	C-nitro compound; carboxamide; diol; organochlorine compound	antibacterial drug; antimicrobial agent; Escherichia coli metabolite; geroprotector; Mycoplasma genitalium metabolite; protein synthesis inhibitor
glutamine Glutamine: A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from GLUTAMIC ACID and AMMONIA. It is the principal carrier of NITROGEN in the body and is an important energy source for many cells.. L-glutamine : An optically active form of glutamine having L-configuration.. glutamine : An alpha-amino acid that consists of butyric acid bearing an amino substituent at position 2 and a carbamoyl substituent at position 4.	2.59	2	0	amino acid zwitterion; glutamine family amino acid; glutamine; L-alpha-amino acid; polar amino acid zwitterion; proteinogenic amino acid	EC 1.14.13.39 (nitric oxide synthase) inhibitor; Escherichia coli metabolite; human metabolite; metabolite; micronutrient; mouse metabolite; nutraceutical; Saccharomyces cerevisiae metabolite
lysine Lysine: An essential amino acid. It is often added to animal feed.. lysine : A diamino acid that is caproic (hexanoic) acid bearing two amino substituents at positions 2 and 6.. L-lysine : An L-alpha-amino acid; the L-isomer of lysine.	2.6	1	0	aspartate family amino acid; L-alpha-amino acid zwitterion; L-alpha-amino acid; lysine; organic molecular entity; proteinogenic amino acid	algal metabolite; anticonvulsant; Escherichia coli metabolite; human metabolite; micronutrient; mouse metabolite; nutraceutical; plant metabolite; Saccharomyces cerevisiae metabolite
adenosine diphosphate Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.	11.29	5	1	adenosine 5'-phosphate; purine ribonucleoside 5'-diphosphate	fundamental metabolite; human metabolite
carbostyril Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.. quinolin-2(1H)-one : A quinolone that is 1,2-dihydroquinoline substituted by an oxo group at position 2.	2.82	3	0	monohydroxyquinoline; quinolone	bacterial xenobiotic metabolite
phenylethyl alcohol Phenylethyl Alcohol: An antimicrobial, antiseptic, and disinfectant that is used also as an aromatic essence and preservative in pharmaceutics and perfumery.. 2-phenylethanol : A primary alcohol that is ethanol substituted by a phenyl group at position 2.	2.6	1	0	benzenes; primary alcohol	Aspergillus metabolite; fragrance; plant growth retardant; plant metabolite; Saccharomyces cerevisiae metabolite
tyrosine Tyrosine: A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.. tyrosine : An alpha-amino acid that is phenylalanine bearing a hydroxy substituent at position 4 on the phenyl ring.	2.25	1	0	amino acid zwitterion; erythrose 4-phosphate/phosphoenolpyruvate family amino acid; L-alpha-amino acid; proteinogenic amino acid; tyrosine	EC 1.3.1.43 (arogenate dehydrogenase) inhibitor; fundamental metabolite; micronutrient; nutraceutical
zoxazolamine Zoxazolamine: A uricosuric and muscle relaxant. Zoxazolamine acts centrally as a muscle relaxant, but the mechanism of its action is not understood.	2.6	1	0	benzoxazole
methionine Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.	2.08	1	0	aspartate family amino acid; L-alpha-amino acid; methionine zwitterion; methionine; proteinogenic amino acid	antidote to paracetamol poisoning; human metabolite; micronutrient; mouse metabolite; nutraceutical
cycloheximide Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.. cycloheximide : A dicarboximide that is 4-(2-hydroxyethyl)piperidine-2,6-dione in which one of the hydrogens attached to the carbon bearing the hydroxy group is replaced by a 3,5-dimethyl-2-oxocyclohexyl group. It is an antibiotic produced by the bacterium Streptomyces griseus.	2.6	1	0	antibiotic fungicide; cyclic ketone; dicarboximide; piperidine antibiotic; piperidones; secondary alcohol	anticoronaviral agent; bacterial metabolite; ferroptosis inhibitor; neuroprotective agent; protein synthesis inhibitor
ficusin Ficusin: A naturally occurring furocoumarin, found in PSORALEA. After photoactivation with UV radiation, it binds DNA via single and double-stranded cross-linking.. psoralen : The simplest member of the class of psoralens that is 7H-furo[3,2-g]chromene having a keto group at position 7. It has been found in plants like Psoralea corylifolia and Ficus salicifolia.	2.6	1	0	psoralens	plant metabolite
tubercidin Tubercidin: An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.. tubercidin : An N-glycosylpyrrolopyrimidine that is adenosine in which the in the 5-membered ring that is not attached to the ribose moiety is replaced by a carbon. Tubercidin is produced in the culture broth of Streptomyces tubericidus.	2.6	1	0	antibiotic antifungal agent; N-glycosylpyrrolopyrimidine; ribonucleoside	antimetabolite; antineoplastic agent; bacterial metabolite
cytarabine [no description available]	2.17	1	0	beta-D-arabinoside; monosaccharide derivative; pyrimidine nucleoside	antimetabolite; antineoplastic agent; antiviral agent; immunosuppressive agent
trifluridine Trifluridine: An antiviral derivative of THYMIDINE used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis due to HERPES SIMPLEX virus. (From Martindale, The Extra Pharmacopoeia, 30th ed, p557). trifluridine : A pyrimidine 2'-deoxyribonucleoside compound having 5-trifluoromethyluracil as the nucleobase. An antiviral drug used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis.	2.82	2	0	nucleoside analogue; organofluorine compound; pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent; antiviral drug; EC 2.1.1.45 (thymidylate synthase) inhibitor
9,10-anthraquinone 9,10-anthraquinone : An anthraquinone that is anthracene in which positions 9 and 10 have been oxidised to carbonyls.	2.6	1	0	anthraquinone
fluorene [no description available]	2.25	1	0	ortho-fused polycyclic arene; ortho-fused tricyclic hydrocarbon
salicylanilide salicylanilide: RN given refers to parent cpd. salicylanilide : An amide of salicylic acid and of aniline; it is therefore both a salicylamide and an anilide.	2.6	1	0	benzanilide fungicide; salicylamides; salicylanilides
gramine gramine : An aminoalkylindole that is indole carrying a dimethylaminomethyl substituent at postion 3.	2.6	1	0	aminoalkylindole; indole alkaloid; tertiary amino compound	antibacterial agent; antiviral agent; plant metabolite; serotonergic antagonist
aminacrine Aminacrine: A highly fluorescent anti-infective dye used clinically as a topical antiseptic and experimentally as a mutagen, due to its interaction with DNA. It is also used as an intracellular pH indicator.. 9-aminoacridine : An aminoacridine that is acridine in which the hydrogen at position 9 is replaced by an amino group. A fluorescent dyd and topical antiseptic agent, it is used (usually as the hydrochloride salt) in eye drops for the treatment of superficial eye infections.	2.6	1	0	aminoacridines; primary amino compound	acid-base indicator; antiinfective agent; antiseptic drug; fluorescent dye; MALDI matrix material; mutagen
quinoxalines quinoxaline : A naphthyridine in which the nitrogens are at positions 1 and 4.	2.21	1	0	mancude organic heterobicyclic parent; naphthyridine; ortho-fused heteroarene
xanthenes Xanthenes: Compounds with three aromatic rings in linear arrangement with an OXYGEN in the center ring.	2.05	1	0	xanthene
methyl gallate methyl gallate: has both immunosuppressive and phytogenic antineoplastic activities; isolated from Acer saccharinum. methyl 3,4,5-trihydroxybenzoate : A gallate ester obtained by the formal condensation of gallic acid with methanol. It exhibits anti-oxidant, anti-tumor, anti-microbial and anti-inflammatory properties.	2.6	1	0	gallate ester	anti-inflammatory agent; antioxidant; plant metabolite
quinuclidines Quinuclidines: A class of organic compounds which contain two rings that share a pair of bridgehead carbon atoms and contains an amine group.	2.13	1	0	quinuclidines; saturated organic heterobicyclic parent
monobenzone monobenzone: structure. monobenzone : The monobenzyl ether of hydroquinone. It is used as a topical drug for medical depigmentation.	2.6	1	0	benzyl ether	allergen; dermatologic drug; melanin synthesis inhibitor
pyrroles 1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.	3.95	2	1	pyrrole; secondary amine
thiophenes Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.	3.41	6	0	mancude organic heteromonocyclic parent; monocyclic heteroarene; thiophenes; volatile organic compound	non-polar solvent
pyrazolanthrone pyrazolanthrone: JNK (c-Jun N-terminal kinase) inhibitor; structure in first source. anthra[1,9-cd]pyrazol-6(2H)-one : A member of the class of anthrapyrazoles that is anthra[1,9-cd]pyrazole substituted at position 6 by an oxo group. An inhibitor of c-Jun N-terminal kinase.	2.17	1	0	anthrapyrazole; aromatic ketone; cyclic ketone	antineoplastic agent; c-Jun N-terminal kinase inhibitor; geroprotector
ditiocarb Ditiocarb: A chelating agent that has been used to mobilize toxic metals from the tissues of humans and experimental animals. It is the main metabolite of DISULFIRAM.. diethyldithiocarbamic acid : A member of the class of dithiocarbamic acids that is diethylcarbamic acid in which both of the oxygens are replaced by sulfur.	2.6	1	0	dithiocarbamic acids	chelator; copper chelator
catechin Catechin: An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.. catechin : Members of the class of hydroxyflavan that have a flavan-3-ol skeleton and its substituted derivatives.. rac-catechin : A racemate comprising equimolar amounts of (+)- and (-)-catechin. (+)-catechin : The (+)-enantiomer of catechin and a polyphenolic antioxidant plant metabolite.	2.6	1	0	catechin	antioxidant; plant metabolite
quinazolines Quinazolines: A group of aromatic heterocyclic compounds that contain a bicyclic structure with two fused six-membered aromatic rings, a benzene ring and a pyrimidine ring.. quinazoline : A mancude organic heterobicyclic parent that is naphthalene in which the carbon atoms at positions 1 and 3 have been replaced by nitrogen atoms.. quinazolines : Any organic heterobicyclic compound based on a quinazoline skeleton and its substituted derivatives.	13.53	32	13	azaarene; mancude organic heterobicyclic parent; ortho-fused heteroarene; quinazolines
acridines Acridines: Compounds that include the structure of acridine.. acridine : A polycyclic heteroarene that is anthracene in which one of the central CH groups is replaced by a nitrogen atom.	2.13	1	0	acridines; mancude organic heterotricyclic parent; polycyclic heteroarene	genotoxin
indazoles Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.	8.97	46	0	indazole
cyclopentane Cyclopentanes: A group of alicyclic hydrocarbons with the general formula R-C5H9.. cyclopentanes : Cyclopentane and its derivatives formed by substitution.	2.15	1	0	cycloalkane; cyclopentanes; volatile organic compound	non-polar solvent
thiazoles [no description available]	6.44	4	2	1,3-thiazoles; mancude organic heteromonocyclic parent; monocyclic heteroarene
pyrazines Pyrazines: A heterocyclic aromatic organic compound with the chemical formula C4H4N2.. pyrazine : A diazine that is benzene in which the carbon atoms at positions 1 and 4 have been replaced by nitrogen atoms.	4.69	5	1	diazine; pyrazines	Daphnia magna metabolite
hydrazine diamine : Any polyamine that contains two amino groups.	2.72	2	0	azane; hydrazines	EC 4.3.1.10 (serine-sulfate ammonia-lyase) inhibitor
azacitidine Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.. 5-azacytidine : An N-glycosyl-1,3,5-triazine that is 4-amino-1,3,5-triazin-2(1H)-one substituted by a beta-D-ribofuranosyl residue via an N-glycosidic linkage. An antineoplastic agent, it is used in the treatment of myeloid leukaemia.	2.83	3	0	N-glycosyl-1,3,5-triazine; nucleoside analogue	antineoplastic agent
aminoimidazole carboxamide Aminoimidazole Carboxamide: An imidazole derivative which is a metabolite of the antineoplastic agents BIC and DIC. By itself, or as the ribonucleotide, it is used as a condensation agent in the preparation of nucleosides and nucleotides. Compounded with orotic acid, it is used to treat liver diseases.. 5-aminoimidazole-4-carboxamide : An aminoimidazole in which the amino group is at C-5 with a carboxamido group at C-4.	2.13	1	0	aminoimidazole; monocarboxylic acid amide	mouse metabolite
lucanthone Lucanthone: One of the SCHISTOSOMICIDES, it has been replaced largely by HYCANTHONE and more recently PRAZIQUANTEL. (From Martindale The Extrapharmacopoeia, 30th ed., p46). lucanthone : A thioxanthen-9-one compound having a methyl substituent at the 1-position and a 2-[(diethylamino)ethyl]amino substituent at the 4-position. Formerly used for the treatment of schistosomiasis. It is a prodrug, being metabolised to hycanthone.	2.6	1	0	thioxanthenes	adjuvant; antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; mutagen; photosensitizing agent; prodrug; schistosomicide drug
cepharanthine cepharanthine: isoquinoline alkaloid from tubers of STEPHANIA; stimulates recovery of immunologic function in lymphatic system after administration of antineoplastic agents or x-irradiation. cepharanthine : A bisbenzylisoquinoline alkaloid from tubers of Stephania; stimulates recovery of immunologic function in lymphatic system after administration of antineoplastic agents or x-irradiation.	2.6	1	0	bisbenzylisoquinoline alkaloid; isoquinolines
aloe emodin aloe emodin: structure distinct from emodin; this does not mean emodin from aloe. Aloe emodin : A dihydroxyanthraquinone that is chrysazin carrying a hydroxymethyl group at position 3. It has been isolated from plant species of the genus Aloe.	2.6	1	0	aromatic primary alcohol; dihydroxyanthraquinone	antineoplastic agent; plant metabolite
chrysophanic acid chrysophanic acid: RN given refers to parent cpd; structure in Merck, 9th ed, #2260. chrysophanol : A trihydroxyanthraquinone that is chrysazin with a methyl substituent at C-3. It has been isolated from Aloe vera and exhibits antiviral and anti-inflammatory activity.	2.6	1	0	dihydroxyanthraquinone	anti-inflammatory agent; antiviral agent; plant metabolite
emetine Emetine: The principal alkaloid of ipecac, from the ground roots of Uragoga (or Cephaelis) ipecacuanha or U. acuminata, of the Rubiaceae. It is used as an amebicide in many different preparations and may cause serious cardiac, hepatic, or renal damage and violent diarrhea and vomiting. Emetine inhibits protein synthesis in EUKARYOTIC CELLS but not PROKARYOTIC CELLS.. emetine : A pyridoisoquinoline comprising emetam having methoxy substituents at the 6'-, 7'-, 10- and 11-positions. It is an antiprotozoal agent and emetic. It inhibits SARS-CoV2, Zika and Ebola virus replication and displays antimalarial, antineoplastic and antiamoebic properties.	2.6	1	0	isoquinoline alkaloid; pyridoisoquinoline	antiamoebic agent; anticoronaviral agent; antiinfective agent; antimalarial; antineoplastic agent; antiprotozoal drug; antiviral agent; autophagy inhibitor; emetic; expectorant; plant metabolite; protein synthesis inhibitor
osthol osthol: from Cnidium monnieri and Angelica pubescens (both Apiaceae); structure given in first source	2.6	1	0	botanical anti-fungal agent; coumarins	metabolite
flavanone flavanone: RN given refers to cpd with unspecified isomeric designation; structure in first source. flavanone : The simplest member of the class of flavanones that consists of flavan bearing an oxo substituent at position 4.	2.6	1	0	flavanones
phloretic acid phloretic acid: structure. N-hydroxysuccinimide ester : An ester of N-hydroxysuccinimide.. phloretic acid : A hydroxy monocarboxylic acid consisting of propionic acid having a 4-hydroxyphenyl group at the 3-position.	2.6	1	0	hydroxy monocarboxylic acid	plant metabolite
alpha-aminopyridine alpha-aminopyridine: RN given refers to parent cpd; structure in Merck Index, 9th ed, #485. aminopyridine : Compounds containing a pyridine skeleton substituted by one or more amine groups.	5.37	11	1
oleanolic acid [no description available]	2.6	1	0	hydroxy monocarboxylic acid; pentacyclic triterpenoid	plant metabolite
podophyllotoxin Podophyllum: A genus of poisonous American herbs, family BERBERIDACEAE. The roots yield PODOPHYLLOTOXIN and other pharmacologically important agents. The plant was formerly used as a cholagogue and cathartic. It is different from the European mandrake, MANDRAGORA.	2.08	1	0	furonaphthodioxole; lignan; organic heterotetracyclic compound	antimitotic; antineoplastic agent; keratolytic drug; microtubule-destabilising agent; plant metabolite; tubulin modulator
angelicin angelicin: used as tranquillizer; sedative; or anticonvulsant; structure	2.6	1	0	furanocoumarin
diperodon diperodon: RN given refers to parent cpd; structure given in first source	2.6	1	0	carbamate ester
malondialdehyde Malondialdehyde: The dialdehyde of malonic acid.. malonaldehyde : A dialdehyde that is propane substituted by two oxo groups at the terminal carbon atoms respectively. A biomarker of oxidative damage to lipids caused by smoking, it exists in vivo mainly in the enol form.	2.17	1	0	dialdehyde	biomarker
trinitrobenzenesulfonic acid Trinitrobenzenesulfonic Acid: A reagent that is used to neutralize peptide terminal amino groups.. 2,4,6-trinitrobenzenesulfonic acid : The arenesulfonic acid that is benzenesulfonic acid with three nitro substituents in the 2-, 4- and 6-positions.	2.31	1	0	arenesulfonic acid; C-nitro compound	epitope; explosive; reagent
formestane [no description available]	2.08	1	0	17-oxo steroid; 3-oxo-Delta(4) steroid; enol; hydroxy steroid	antineoplastic agent; EC 1.14.14.14 (aromatase) inhibitor
megestrol acetate [no description available]	2.6	1	0	20-oxo steroid; 3-oxo-Delta(4) steroid; acetate ester; steroid ester	antineoplastic agent; appetite enhancer; contraceptive drug; progestin; synthetic oral contraceptive
acetylcysteine N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.	2.6	1	0	acetylcysteine; L-cysteine derivative; N-acetyl-L-amino acid	antidote to paracetamol poisoning; antiinfective agent; antioxidant; antiviral drug; ferroptosis inhibitor; geroprotector; human metabolite; mucolytic; radical scavenger; vulnerary
hydroxychloroquine sulfate [no description available]	2.58	2	0
deoxycytidine [no description available]	8.49	12	2	pyrimidine 2'-deoxyribonucleoside	Escherichia coli metabolite; human metabolite; mouse metabolite; Saccharomyces cerevisiae metabolite
deoxycytidine monophosphate Deoxycytidine Monophosphate: Deoxycytidine (dihydrogen phosphate). A deoxycytosine nucleotide containing one phosphate group esterified to the deoxyribose moiety in the 2'-,3'- or 5- positions.. 2'-deoxycytosine 5'-monophosphate : A pyrimidine 2'-deoxyribonucleoside 5'-monophosphate having cytosine as the nucleobase.	2.31	1	0	2'-deoxycytidine phosphate; pyrimidine 2'-deoxyribonucleoside 5'-monophosphate	Escherichia coli metabolite; mouse metabolite
ethambutol Ethambutol: An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863). ethambutol : An ethylenediamine derivative that is ethane-1,2-diamine in which one hydrogen attached to each of the nitrogens is sutstituted by a 1-hydroxybutan-2-yl group (S,S-configuration). It is a bacteriostatic antimycobacterial drug, effective against Mycobacterium tuberculosis and some other mycobacteria. It is used (as the dihydrochloride salt) in combination with other antituberculous drugs in the treatment of pulmonary and extrapulmonary tuberculosis; resistant strains of M. tuberculosis are readily produced if ethambutol is used alone.	2.6	1	0	ethanolamines; ethylenediamine derivative	antitubercular agent; environmental contaminant; xenobiotic
metformin hydrochloride metformin hydrochloride : A hydrochloride resulting from the reaction of metformin with one molar equivalent of hydrogen chloride.	2.6	1	0	hydrochloride	environmental contaminant; hypoglycemic agent; xenobiotic
arsenic trioxide Arsenic Trioxide: An inorganic compound with the chemical formula As2O3 that is used for the treatment of ACUTE PROMYELOCYTIC LEUKEMIA in patients who have relapsed from, or are resistant to, conventional drug therapy.	7.41	1	0
antimycin a [no description available]	2.6	1	0	benzamides; formamides; macrodiolide; phenols	antifungal agent; mitochondrial respiratory-chain inhibitor; piscicide
5,5'-dimethyl-2,2'-bipyridyl 5,5'-dimethyl-2,2'-bipyridyl: structure in first source	2.6	1	0	bipyridines
dichlorobenzyl alcohol 2,4-dichlorobenzyl alcohol : A member of the class of benzyl alcohols that is benzyl alcohol in which the hydrogens at positions 2 and 4 are replaced by chlorines.	2.6	1	0	benzyl alcohols; dichlorobenzene	antiseptic drug
amiloride hydrochloride, anhydrous amiloride hydrochloride : A hydrochloride obtained by combining amiloride with one molar equivalent of hydrochloric acid.	2.08	1	0	hydrochloride	diuretic; sodium channel blocker
amiloride Amiloride: A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705). amiloride : A member of the class of pyrazines resulting from the formal monoacylation of guanidine with the carboxy group of 3,5-diamino-6-chloropyrazine-2-carboxylic acid.	2.13	1	0	aromatic amine; guanidines; organochlorine compound; pyrazines	diuretic; sodium channel blocker
acadesine [no description available]	2.08	1	0	1-ribosylimidazolecarboxamide; aminoimidazole; nucleoside analogue	antineoplastic agent; platelet aggregation inhibitor
stavudine Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.. stavudine : A nucleoside analogue obtained by formal dehydration across positions 2 and 3 of thymidine. An inhibitor of HIV-1 reverse transcriptase	2.6	1	0	dihydrofuran; nucleoside analogue; organic molecular entity	antimetabolite; antiviral agent; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
dideoxyadenosine Dideoxyadenosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is an inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal side effect is nephrotoxicity. In vivo, dideoxyadenosine is rapidly metabolized to DIDANOSINE (ddI) by enzymatic deamination; ddI is then converted to dideoxyinosine monophosphate and ultimately to dideoxyadenosine triphosphate, the putative active metabolite.	2.6	1	0	adenosines; purine 2',3'-dideoxyribonucleoside	EC 3.5.4.4 (adenosine deaminase) inhibitor; EC 4.6.1.1 (adenylate cyclase) inhibitor
cladribine [no description available]	2.08	1	0	organochlorine compound; purine 2'-deoxyribonucleoside	antineoplastic agent; immunosuppressive agent
vidarabine adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.	2.6	1	0	beta-D-arabinoside; purine nucleoside	antineoplastic agent; bacterial metabolite; nucleoside antibiotic
3-deazaadenosine 3-deazaadenosine: RN given refers to parent cpd.	2.6	1	0
lutetium Lutetium: An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175.	2.13	1	0	d-block element atom; lanthanoid atom
palladium Palladium: A chemical element having an atomic weight of 106.4, atomic number of 46, and the symbol Pd. It is a white, ductile metal resembling platinum, and following it in abundance and importance of applications. It is used in dentistry in the form of gold, silver, and copper alloys.. palladium : Chemical element (nickel group element atom) with atomic number 46.	2.11	1	0	metal allergen; nickel group element atom; platinum group metal atom
platinum Platinum: A heavy, soft, whitish metal, resembling tin, with atomic number 78, atomic weight 195.084, symbol Pt. It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as alutiae.	9.15	21	5	elemental platinum; nickel group element atom; platinum group metal atom
ruthenium Ruthenium: A hard, brittle, grayish-white rare earth metal with an atomic symbol Ru, atomic number 44, and atomic weight 101.07. It is used as a catalyst and hardener for PLATINUM and PALLADIUM.	8.11	3	0	iron group element atom; platinum group metal atom
zalcitabine Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.. zalcitabine : A pyrimidine 2',3'-dideoxyribonucleoside compound having cytosine as the nucleobase.	2.6	1	0	pyrimidine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; HIV-1 reverse transcriptase inhibitor
camptothecin NSC 100880: carboxylate (opened lactone) form of camptothecin; RN refers to (S)-isomer; structure given in first source	14.18	22	3	delta-lactone; pyranoindolizinoquinoline; quinoline alkaloid; tertiary alcohol	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; genotoxin; plant metabolite
tricalcium phosphate tricalcium phosphate: a form of tricalcium phosphate used as bioceramic bone replacement material; see also records for alpha-tricalcium phosphate, beta-tricalcium phosphate, calcium phosphate; apatitic tricalcium phosphate Ca9(HPO4)(PO4)5(OH) is the calcium orthophosphate leading to beta tricalcium phosphate Ca3(PO4)2 (b-TCP). calcium phosphate : A calcium salt composed of calcium and phosphate/diphosphate ions; present in milk and used for the mineralisation of calcified tissues.	2.6	1	0	calcium phosphate
deuterium Deuterium: The stable isotope of hydrogen. It has one neutron and one proton in the nucleus.	2.1	1	0	dihydrogen
ancitabine Ancitabine: Congener of CYTARABINE that is metabolized to cytarabine and thereby maintains a more constant antineoplastic action.. ancitabine : An organic heterotricyclic compound resulting from the formal condensation of the oxo group of cytidine to the 2' position with loss of water to give the corresponding cyclic ether. A prodrug, it is metabolised to the antineoplastic agent cytarabine, so is used to maintain a more constant antineoplastic action.	2.6	1	0	diol; organic heterotricyclic compound	antimetabolite; antineoplastic agent; prodrug
chloropyramine chloropyramine: RN given refers to parent cpd; structure	2.6	1	0	aminopyridine
levamisole Levamisole: An antihelminthic drug that has been tried experimentally in rheumatic disorders where it apparently restores the immune response by increasing macrophage chemotaxis and T-lymphocyte function. Paradoxically, this immune enhancement appears to be beneficial in rheumatoid arthritis where dermatitis, leukopenia, and thrombocytopenia, and nausea and vomiting have been reported as side effects. (From Smith and Reynard, Textbook of Pharmacology, 1991, p435-6). levamisole : A 6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole that has S configuration. It is used (generally as the monohydrochloride salt) to treat parasitic worm infections in pigs, sheep and cattle and was formerly used in humans as an adjuvant to chemotherapy for the treatment of various cancers. It is also widely used as an adulterant to coccaine.	2.6	1	0	6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole	antinematodal drug; antirheumatic drug; EC 3.1.3.1 (alkaline phosphatase) inhibitor; immunological adjuvant; immunomodulator
n'-nitrosonornicotine N'-nitrosonornicotine: structure; a potent carcinogen in laboratory animals	2.6	1	0	pyridines; pyrrolidines
daunorubicin Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.. anthracycline : Anthracyclines are polyketides that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.. daunorubicin : A natural product found in Actinomadura roseola.	2.6	1	0	aminoglycoside antibiotic; anthracycline; p-quinones; tetracenequinones	antineoplastic agent; bacterial metabolite
phenyl acetate phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.	2.31	1	0	benzenes; phenyl acetates
alkenes [no description available]	2.1	1	0
adenosine diphosphate ribose Adenosine Diphosphate Ribose: An ester formed between the aldehydic carbon of RIBOSE and the terminal phosphate of ADENOSINE DIPHOSPHATE. It is produced by the hydrolysis of nicotinamide-adenine dinucleotide (NAD) by a variety of enzymes, some of which transfer an ADP-ribosyl group to target proteins.	3.07	3	0	ADP-sugar	Escherichia coli metabolite; mouse metabolite
zidovudine Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase.	2.58	2	0	azide; pyrimidine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; HIV-1 reverse transcriptase inhibitor
paclitaxel Taxus: Genus of coniferous yew trees or shrubs, several species of which have medicinal uses. Notable is the Pacific yew, Taxus brevifolia, which is used to make the anti-neoplastic drug taxol (PACLITAXEL).	13.2	30	11	taxane diterpenoid; tetracyclic diterpenoid	antineoplastic agent; human metabolite; metabolite; microtubule-stabilising agent
etoposide [no description available]	12.09	8	1	beta-D-glucoside; furonaphthodioxole; organic heterotetracyclic compound	antineoplastic agent; DNA synthesis inhibitor
ribavirin Rebetron: Rebetron is tradename	2.6	1	0	1-ribosyltriazole; aromatic amide; monocarboxylic acid amide; primary carboxamide	anticoronaviral agent; antiinfective agent; antimetabolite; antiviral agent; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
n-(2-hydroxypropyl)methacrylamide Duxon: RN given refers to unlabeled cpd	2.31	1	0
pyridoxal phosphate [no description available]	2.6	1	0	pyridinecarbaldehyde
nimustine Nimustine: Antineoplastic agent especially effective against malignant brain tumors. The resistance which brain tumor cells acquire to the initial effectiveness of this drug can be partially overcome by the simultaneous use of membrane-modifying agents such as reserpine, calcium antagonists such as nicardipine or verapamil, or the calmodulin inhibitor, trifluoperazine. The drug has also been used in combination with other antineoplastic agents or with radiotherapy for the treatment of various neoplasms.. nimustine : An organochlorine compound that is urea in which the two hydrogens on one of the amino groups are replaced by nitroso and 2-chloroethyl groups and one hydrogen from the other amino group is replaced by a 4-amino-2-methylpyrimidin-5-ylmethyl] group. An antineoplastic agent especially effective against malignant brain tumors.	2.54	2	0	aminopyrimidine; N-nitrosoureas; organochlorine compound	alkylating agent; antineoplastic agent
lonidamine lonidamine: structure. lonidamine : A member of the class of indazoles that is 1H-indazole that is substituted at positions 1 and 3 by 2,4-dichlorobenzyl and carboxy groups, respectively.	2.08	1	0	dichlorobenzene; indazoles; monocarboxylic acid	antineoplastic agent; antispermatogenic agent; EC 2.7.1.1 (hexokinase) inhibitor; geroprotector
nitazoxanide nitazoxanide: a 5-nitrothiazolyl derivative used for a broad range of intestinal parasitic infections including CRYPTOSPORIDIUM and GIARDIA; it is a redox-active nitrothiazolyl-salicylamide prodrug	2.6	1	0	benzamides; carboxylic ester
s-2678 XI-006: diminishes MDM4 promoter activity; structure in first source	2.11	1	0
captopril Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.	2.6	1	0	alkanethiol; L-proline derivative; N-acylpyrrolidine; pyrrolidinemonocarboxylic acid	antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
staurosporine [no description available]	2.31	1	0	indolocarbazole alkaloid; organic heterooctacyclic compound	apoptosis inducer; bacterial metabolite; EC 2.7.11.13 (protein kinase C) inhibitor; geroprotector
oltipraz oltipraz : A 1,2-dithiole that is 3H-1,2-dithiole-3-thione substituted at positions 4 and 5 by methyl and pyrazin-2-yl groups respectively.	2.6	1	0	1,2-dithiole; pyrazines	angiogenesis modulating agent; antimutagen; antineoplastic agent; antioxidant; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor; neurotoxin; protective agent; schistosomicide drug
fiacitabine fiacitabine: anti-herpes virus agent which also inhibits growth of certain human tumor cell lines in vitro.	2.6	1	0
bisantrene bisantrene: RN given refers to parent cpd; synonyms CL 216942 & NSC 337766 refers to di-HCl. bisantrene : A hydrazone resulting from the formal condensation of both of the aldehyde groups of anthracene-9,10-dicarbaldehyde with 2-hydrazinyl-4,5-dihydro-1H-imidazole.	7.41	1	0	anthracenes; hydrazone; imidazolidines	antineoplastic agent
simvastatin Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.	2.08	1	0	delta-lactone; fatty acid ester; hexahydronaphthalenes; statin (semi-synthetic)	EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor; EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor; ferroptosis inducer; geroprotector; prodrug
mifepristone Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.	2.6	1	0	3-oxo-Delta(4) steroid; acetylenic compound; tertiary amino compound	abortifacient; contraceptive drug; hormone antagonist; synthetic oral contraceptive
itraconazole Itraconazole: A triazole antifungal agent that inhibits cytochrome P-450-dependent enzymes required for ERGOSTEROL synthesis.. itraconazole : An N-arylpiperazine that is cis-ketoconazole in which the imidazol-1-yl group is replaced by a 1,2,4-triazol-1-yl group and in which the actyl group attached to the piperazine moiety is replaced by a p-[(+-)1-sec-butyl-5-oxo-1,5-dihydro-4H-1,2,4-triazol-4-yl]phenyl group. A potent P-glycoprotein and CYP3A4 inhibitor, it is used as an antifungal drug for the treatment of various fungal infections, including aspergillosis, blastomycosis, candidiasis, chromoblastomycosis, coccidioidomycosis, cryptococcosis, histoplasmosis, and sporotrichosis.	2.08	1	0	aromatic ether; conazole antifungal drug; cyclic ketal; dichlorobenzene; dioxolane; N-arylpiperazine; triazole antifungal drug; triazoles	EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor; Hedgehog signaling pathway inhibitor; P450 inhibitor
pravadoline [no description available]	2.08	1	0
ranolazine Ranolazine: An acetanilide and piperazine derivative that functions as a SODIUM CHANNEL BLOCKER and prevents the release of enzymes during MYOCARDIAL ISCHEMIA. It is used in the treatment of ANGINA PECTORIS.. N-(2,6-dimethylphenyl)-2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetamide : An aromatic amide obtained by formal condensation of the carboxy group of 2-{4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]piperazin-1-yl}acetic acid with the amino group of 2,6-dimethylaniline.. ranolazine : A racemate comprising equal amounts of (R)- and (S)-ranolazine. Used for treatment of chronic angina.	2.6	1	0	aromatic amide; monocarboxylic acid amide; monomethoxybenzene; N-alkylpiperazine; secondary alcohol
brequinar brequinar : A quinolinemonocarboxylic acid that is quinoline substituted by 2'-fluoro[1,1'-biphenyl]-4-yl, methyl, carboxy and fluoro groups at positions 2, 3, 4, and 6, respectively. It is an inhibitor of dihydroorotate dehydrogenase, an enzyme that is required for de novo pyrimidine biosynthesis. The compound exhibits antineoplastic and antiviral properties.	2.6	1	0	biphenyls; monocarboxylic acid; monofluorobenzenes; quinolinemonocarboxylic acid	anticoronaviral agent; antimetabolite; antineoplastic agent; antiviral agent; EC 1.3.5.2 [dihydroorotate dehydrogenase (quinone)] inhibitor; immunosuppressive agent; pyrimidine synthesis inhibitor
imiquimod Imiquimod: A topically-applied aminoquinoline immune modulator that induces interferon production. It is used in the treatment of external genital and perianal warts, superficial CARCINOMA, BASAL CELL; and ACTINIC KERATOSIS.. imiquimod : An imidazoquinoline fused [4,5-c] carrying isobutyl and amino substituents at N-1 and C-4 respectively. A prescription medication, it acts as an immune response modifier and is used to treat genital warts, superficial basal cell carcinoma, and actinic keratosis.	2.6	1	0	imidazoquinoline	antineoplastic agent; interferon inducer
adefovir adefovir: inhibitor of African swine fever virus. adefovir(1-) : A organophosphonate oxoanion obtained by removal of a proton from the phosphonate group of adefovir, a nucleoside reverse transcriptase inhibitor. It is the major microspecies at pH 7.3 (according to Marvin v 6.2.0.).. adefovir : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens has been replaced by a 2-(6-amino-9H-purin-9-yl)ethoxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(t-butoxycarbonyloxymethyl) ester (dipivoxil ester) prodrug is used to treat chronic hepatitis B viral infection.	2.6	1	0	6-aminopurines; ether; phosphonic acids	antiviral drug; DNA synthesis inhibitor; drug metabolite; HIV-1 reverse transcriptase inhibitor; nephrotoxic agent
zileuton [no description available]	2.08	1	0	1-benzothiophenes; ureas	anti-asthmatic drug; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; ferroptosis inhibitor; leukotriene antagonist; non-steroidal anti-inflammatory drug
niguldipine [no description available]	2.08	1	0	diarylmethane
cidofovir anhydrous Cidofovir: An acyclic nucleoside phosphonate that acts as a competitive inhibitor of viral DNA polymerases. It is used in the treatment of RETINITIS caused by CYTOMEGALOVIRUS INFECTIONS and may also be useful for treating HERPESVIRUS INFECTIONS.. cidofovir anhydrous : Cytosine substituted at the 1 position by a 3-hydroxy-2-(phosphonomethoxy)propyl group (S configuration). A nucleoside analogue, it is an injectable antiviral used for the treatment of cytomegalovirus (CMV) retinitis in AIDS patients.	2.6	1	0	phosphonic acids; pyrimidone	anti-HIV agent; antineoplastic agent; antiviral drug; photosensitizing agent
topotecan Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.. topotecan : A pyranoindolizinoquinoline used as an antineoplastic agent. It is a derivative of camptothecin and works by binding to the topoisomerase I-DNA complex and preventing religation of these 328 single strand breaks.	10.84	6	1	pyranoindolizinoquinoline	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor
eliprodil 1-(4-chlorophenyl)-2-[4-(4-fluorobenzyl)piperidin-1-yl]ethanol : A member of the class of piperidines that is piperidine substituted by a 2-(4-chlorophenyl)-2-hydroxyethyl group at position 1 and by a 4-fluorobenzyl group at position 4.	2.08	1	0	monochlorobenzenes; monofluorobenzenes; piperidines; secondary alcohol; tertiary amino compound
celgosivir celgosivir: inhibits glycoprotein processing & the growth of HIVs	2.6	1	0
gemcitabine gemcitabine : A 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer.	8.78	16	2	organofluorine compound; pyrimidine 2'-deoxyribonucleoside	antimetabolite; antineoplastic agent; antiviral drug; DNA synthesis inhibitor; EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor; environmental contaminant; immunosuppressive agent; photosensitizing agent; prodrug; radiosensitizing agent; xenobiotic
lamivudine [no description available]	2.6	1	0	monothioacetal; nucleoside analogue; oxacycle; primary alcohol	allergen; anti-HBV agent; antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor; HIV-1 reverse transcriptase inhibitor; prodrug
irinotecan [no description available]	6.73	11	1	carbamate ester; delta-lactone; N-acylpiperidine; pyranoindolizinoquinoline; ring assembly; tertiary alcohol; tertiary amino compound	antineoplastic agent; apoptosis inducer; EC 5.99.1.2 (DNA topoisomerase) inhibitor; prodrug
valsartan Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.	2.6	1	0	biphenylyltetrazole; monocarboxylic acid amide; monocarboxylic acid	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
zanamivir Zanamivir: A guanido-neuraminic acid that is used to inhibit NEURAMINIDASE.	2.6	1	0	guanidines	antiviral agent; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor
adefovir dipivoxil bis(pivaloyloxymethyl)-9-(2-phosphonylmethoxyethyl)adenine: structure given in first source. adefovir pivoxil : An organic phosphonate that is the dipivoxil ester of adefovir. A prodrug for adefovir, an HIV-1 reverse transcriptase inhibitor, adefovir pivoxil is used to treat chronic hepatitis B viral infection.	2.6	1	0	6-aminopurines; carbonate ester; ether; organic phosphonate	antiviral drug; DNA synthesis inhibitor; HIV-1 reverse transcriptase inhibitor; nephrotoxic agent; prodrug
emtricitabine Emtricitabine: A deoxycytidine analog and REVERSE TRANSCRIPTASE INHIBITOR with antiviral activity against HIV-1 and HEPATITIS B viruses. It is used to treat HIV INFECTIONS.. emtricitabine : An organofluorine compound that is 5-fluorocytosine substituted at the 1 position by a 2-(hydroxymethyl)-1,3-oxathiolan-5-yl group (2R,5S configuration). It is used in combination therapy for the treatment of HIV-1 infection.	2.6	1	0	monothioacetal; nucleoside analogue; organofluorine compound; pyrimidone	antiviral drug; HIV-1 reverse transcriptase inhibitor
capecitabine Capecitabine: A deoxycytidine derivative and fluorouracil PRODRUG that is used as an ANTINEOPLASTIC ANTIMETABOLITE in the treatment of COLON CANCER; BREAST CANCER and GASTRIC CANCER.. capecitabine : A carbamate ester that is cytidine in which the hydrogen at position 5 is replaced by fluorine and in which the amino group attached to position 4 is converted into its N-(penyloxy)carbonyl derivative. Capecitabine is a antineoplastic agent used in the treatment of cancers.	11.32	4	3	carbamate ester; cytidines; organofluorine compound	antimetabolite; antineoplastic agent; prodrug
octyl gallate [no description available]	2.6	1	0	gallate ester	food antioxidant; hypoglycemic agent; plant metabolite
verapamil hydrochloride verapamil hydrochloride : A racemate comprising equimolar amounts of dexverapamil hydrochloride and (S)-verapamil hydrochloride.	2.08	1	0
efavirenz efavirenz: HIV-1 reverse transcriptase inhibitor. efavirenz : 1,4-Dihydro-2H-3,1-benzoxazin-2-one substituted at the 4 position by cyclopropylethynyl and trifluoromethyl groups (S configuration) and at the 6 position by chlorine. A non-nucleoside reverse transcriptase inhibitor with activity against HIV, it is used with other antiretrovirals for combination therapy of HIV infection.	2.58	2	0	acetylenic compound; benzoxazine; cyclopropanes; organochlorine compound; organofluorine compound	antiviral drug; HIV-1 reverse transcriptase inhibitor
nelfinavir Nelfinavir: A potent HIV protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children.. nelfinavir : An aryl sulfide that is used (as its mesylate salt) for treatment of HIV and also exhibits some anticancer properties.	2.6	1	0	aryl sulfide; benzamides; organic heterobicyclic compound; phenols; secondary alcohol; tertiary amino compound	antineoplastic agent; HIV protease inhibitor
thiazolyl blue thiazolyl blue: RN & II refers to bromide. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide : The bromide salt of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium.	2.1	1	0	organic bromide salt	colorimetric reagent; dye
betulinic acid [no description available]	2.6	1	0	hydroxy monocarboxylic acid; pentacyclic triterpenoid	anti-HIV agent; anti-inflammatory agent; antimalarial; antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; plant metabolite
arctigenin arctigenin: precursor to catechols; in many plants	2.6	1	0	lignan
baicalin [no description available]	2.6	1	0	dihydroxyflavone; glucosiduronic acid; glycosyloxyflavone; monosaccharide derivative	antiatherosclerotic agent; antibacterial agent; anticoronaviral agent; antineoplastic agent; antioxidant; cardioprotective agent; EC 2.7.7.48 (RNA-directed RNA polymerase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; ferroptosis inhibitor; neuroprotective agent; non-steroidal anti-inflammatory drug; plant metabolite; prodrug
plerixafor plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2. plerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.	2.9	2	0	azacycloalkane; azamacrocycle; benzenes; crown amine; secondary amino compound; tertiary amino compound	anti-HIV agent; antineoplastic agent; C-X-C chemokine receptor type 4 antagonist; immunological adjuvant
amprenavir [no description available]	2.6	1	0	carbamate ester; sulfonamide; tetrahydrofuryl ester	antiviral drug; HIV protease inhibitor
oseltamivir Oseltamivir: An acetamido cyclohexene that is a structural homolog of SIALIC ACID and inhibits NEURAMINIDASE.. oseltamivir : A cyclohexenecarboxylate ester that is the ethyl ester of oseltamivir acid. An antiviral prodrug (it is hydrolysed to the active free carboxylic acid in the liver), it is used to slow the spread of influenza.	2.6	1	0	acetamides; amino acid ester; cyclohexenecarboxylate ester; primary amino compound	antiviral drug; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor; environmental contaminant; prodrug; xenobiotic
epigallocatechin gallate epigallocatechin gallate: a steroid 5alpha-reductase inhibitor and antimutagen in green tea (Camellia sinensis). (-)-epigallocatechin 3-gallate : A gallate ester obtained by the formal condensation of gallic acid with the (3R)-hydroxy group of (-)-epigallocatechin.	2.6	1	0	flavans; gallate ester; polyphenol	antineoplastic agent; antioxidant; apoptosis inducer; geroprotector; Hsp90 inhibitor; neuroprotective agent; plant metabolite
1,2,3,4,6-pentakis-O-galloyl-beta-D-glucose pentagalloylglucose: pentahydroxy gallic acid ester of glucose; a phytogenic antineoplastic agent and antibacterial agent. 1,2,3,4,6-pentakis-O-galloyl-beta-D-glucose : A galloyl-beta-D-glucose compound having five galloyl groups in the 1-, 2-, 3-, 4- and 6-positions.	2.6	1	0	gallate ester; galloyl beta-D-glucose	anti-inflammatory agent; antineoplastic agent; geroprotector; hepatoprotective agent; plant metabolite; radiation protective agent; radical scavenger
cephalotaxine [no description available]	2.6	1	0	benzazepine alkaloid fundamental parent; benzazepine alkaloid; cyclic acetal; enol ether; organic heteropentacyclic compound; secondary alcohol; tertiary amino compound
desipramine hydrochloride desipramine hydrochloride : The hydrochloride salt of desipramine.	2.6	1	0	hydrochloride	drug allergen
mefloquine hydrochloride [no description available]	2.6	1	0	hydrochloride
bendamustine [no description available]	2.08	1	0	benzimidazoles
aloxistatin aloxistatin: a membrane-permeable cysteine protease inhibitor. aloxistatin : An L-leucine derivative that is the amide obtained by formal condensation of the carboxy group of (2S,3S)-3-(ethoxycarbonyl)oxirane-2-carboxylic acid with the amino group of N-(3-methylbutyl)-L-leucinamide.	2.6	1	0	epoxide; ethyl ester; L-leucine derivative; monocarboxylic acid amide	anticoronaviral agent; cathepsin B inhibitor
propazole propazole: RN given refers to parent cpd; structure	2.6	1	0	benzimidazoles
caroverine caroverine: structure	2.08	1	0	quinoxaline derivative
cgs 9343b [no description available]	2.08	1	0	benzimidazoles
prulifloxacin prulifloxacin: structure given in first source	2.6	1	0	fluoroquinolone antibiotic; quinolone antibiotic
telmisartan Telmisartan: A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.. telmisartan : A member of the class of benzimidazoles used widely in the treatment of hypertension.	2.58	2	0	benzimidazoles; biphenyls; carboxybiphenyl	angiotensin receptor antagonist; antihypertensive agent; EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor; environmental contaminant; xenobiotic
bergenin bergenin: RN refers to (2R-(2alpha,3beta,4alpha,4aalpha,10bbeta))-isomer; structure	2.6	1	0	trihydroxybenzoic acid	metabolite
2-methoxyestradiol 2-methoxy-17beta-estradiol : A 17beta-hydroxy steroid, being 17beta-estradiol methoxylated at C-2.	2.08	1	0	17beta-hydroxy steroid; 3-hydroxy steroid	angiogenesis modulating agent; antimitotic; antineoplastic agent; human metabolite; metabolite; mouse metabolite
triazoles Triazoles: Heterocyclic compounds containing a five-membered ring with two carbon atoms and three nitrogen atoms with the molecular formula C2H3N3.. triazoles : An azole in which the five-membered heterocyclic aromatic skeleton contains three N atoms and two C atoms.	4.1	12	0	1,2,3-triazole
fluorodeoxyglucose f18 Fluorodeoxyglucose F18: The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)	2.17	1	0	2-deoxy-2-((18)F)fluoro-D-glucose; 2-deoxy-2-fluoro-aldehydo-D-glucose
zoledronic acid Zoledronic Acid: An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS.. zoledronic acid : An imidazole compound having a 2,2-bis(phosphono)-2-hydroxyethane-1-yl substituent at the 1-position.	2.6	1	0	1,1-bis(phosphonic acid); imidazoles	bone density conservation agent
artemisinin (+)-artemisinin : A sesquiterpene lactone obtained from sweet wormwood, Artemisia annua, which is used as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria.	2.6	1	0	organic peroxide; sesquiterpene lactone	antimalarial; plant metabolite
brinzolamide brinzolamide: an antiglaucoma agent	2.6	1	0	sulfonamide; thienothiazine	antiglaucoma drug; EC 4.2.1.1 (carbonic anhydrase) inhibitor
4-methylquinolin-2(1H)-one 4-methylquinolin-2(1H)-one : A quinolone that is quinolin-2(1H)-one substituted by a methyl group at position 4.	2.08	1	0	quinolone
1,2,3,4-tetrahydroquinoline 1,2,3,4-tetrahydroquinoline: structure in first source. 1,2,3,4-tetrahydroquinoline : A member of the class of quinolines that is the 1,2,3,4-tetrahydro derivative of quinoline.	2.1	1	0	quinolines
dipropylacetamide dipropylacetamide: structure. valpromide : A fatty amide derived from valproic acid.	2.6	1	0	fatty amide	geroprotector; metabolite; teratogenic agent
oxprenolol hydrochloride [no description available]	2.6	1	0
dexrazoxane Dexrazoxane: The (+)-enantiomorph of razoxane.	2.6	1	0	razoxane	antineoplastic agent; cardiovascular drug; chelator; immunosuppressive agent
2-phenylquinoline 2-phenylquinoline: structure in first source	2.1	1	0
opipramol hydrochloride [no description available]	2.6	1	0
moroxydine [no description available]	2.6	1	0	biguanides
alacepril [no description available]	2.08	1	0	dipeptide; thioacetate ester	EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
thioxolone tioxolone : A 1,3-benzoxathiole having a hydroxy substituent at the 6-position.	2.6	1	0	benzoxathiole	antiseborrheic
ubenimex ubenimex: growth inhibitor	2.08	1	0
honokiol [no description available]	2.6	1	0	biphenyls
nobiletin nobiletin : A methoxyflavone that is flavone substituted by methoxy groups at positions 5, 6, 7, 8, 3' and 4' respectively.	2.6	1	0	methoxyflavone	antineoplastic agent; plant metabolite
lycorine lycorine: from bulbs of LYCORIS & other plants; RN given refers to (1 alpha,2 beta)-isomer; structure in Merck Index, 9th ed, #5444. lycorine : An indolizidine alkaloid that is 3,12-didehydrogalanthan substituted by hydroxy groups at positions and 2 and a methylenedioxy group across positions 9 and 10. Isolated from Crinum asiaticum, it has been shown to exhibit antimalarial activity.	2.6	1	0	indolizidine alkaloid	anticoronaviral agent; antimalarial; plant metabolite; protein synthesis inhibitor
leupeptin [no description available]	2.6	1	0	aldehyde; tripeptide	bacterial metabolite; calpain inhibitor; cathepsin B inhibitor; EC 3.4.21.4 (trypsin) inhibitor; serine protease inhibitor
alantolactone alantolactone: allergenic sesquiterpene lactone; crystalline mixture of alantolactones from group of sesquiterpenes; structure. alantolactone : A sesquiterpene lactone that is 3a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2-one bearing two methyl substituents at positions 5 and 8a as well as a methylidene substituent at position 3.	7.82	2	0	naphthofuran; olefinic compound; sesquiterpene lactone	antineoplastic agent; apoptosis inducer; plant metabolite
tetrandrine tetrandrine: a bisbenzylisoquinoline that exhibits antifibrogenic activity	2.6	1	0	bisbenzylisoquinoline alkaloid; isoquinolines
3-deazaneplanocin 3-deazaneplanocin: S-adenosylhomocysteine hydrolase antagonist	3.51	1	0
calpeptin [no description available]	2.6	1	0	amino acid amide
fangchinoline [no description available]	2.6	1	0	aromatic ether; bisbenzylisoquinoline alkaloid; macrocycle	anti-HIV-1 agent; anti-inflammatory agent; antineoplastic agent; antioxidant; neuroprotective agent; plant metabolite
maslinic acid (2Alpha,3beta)-2,3-dihydroxyolean-12-en-28-oic acid: from Luehea divaricata and Agrimonia eupatoria	2.6	1	0	dihydroxy monocarboxylic acid; pentacyclic triterpenoid	anti-inflammatory agent; antineoplastic agent; antioxidant; plant metabolite
atovaquone Atovaquone: A hydroxynaphthoquinone that has antimicrobial activity and is being used in antimalarial protocols.. atovaquone : A naphthoquinone compound having a 4-(4-chlorophenyl)cyclohexyl group at the 2-position and a hydroxy substituent at the 3-position.	2.6	1	0	hydroxy-1,2-naphthoquinone
rosiglitazone [no description available]	7.25	1	0	aminopyridine; thiazolidinediones	EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor; ferroptosis inhibitor; insulin-sensitizing drug
loganin [no description available]	2.6	1	0	beta-D-glucoside; cyclopentapyran; enoate ester; iridoid monoterpenoid; methyl ester; monosaccharide derivative; secondary alcohol	anti-inflammatory agent; EC 3.1.1.7 (acetylcholinesterase) inhibitor; EC 3.2.1.20 (alpha-glucosidase) inhibitor; EC 3.4.23.46 (memapsin 2) inhibitor; neuroprotective agent; plant metabolite
moexipril [no description available]	2.6	1	0	peptide
aucubin [no description available]	2.6	1	0	organic molecular entity	metabolite
catalpol [no description available]	2.6	1	0	organic molecular entity	metabolite
lekoptin (S)-verapamil : A 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile that has S configuration.	2.6	1	0	2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile
s-(2,4-dinitrophenyl)glutathione S-(2,4-dinitrophenyl)glutathione : A glutathione conjugate in which the thiol hydrogen of glutathione has been replaced by a 2,4-dinitrophenyl group.	2.1	1	0	glutathione conjugate
n-methyladenosine N-methyladenosine: is a inhibitor of cell differentiation. N(6)-methyladenosine : A methyladenosine compound with one methyl group attached to N(6) of the adenine nucleobase.	2.6	1	0	methyladenosine
fulvestrant Fulvestrant: An estradiol derivative and estrogen receptor antagonist that is used for the treatment of estrogen receptor-positive, locally advanced or metastatic breast cancer.. fulvestrant : A 3-hydroxy steroid that is 17beta-estradiol in which the 7alpha hydrogen has been replaced by a nonyl group in which one of the hydrogens of the terminal methyl has been replaced by a (4,4,5,5,5-pentafluoropentyl)sulfinyl group. An estrogen receptor antagonist, it is used in the treatment of breast cancer.	2.31	1	0	17beta-hydroxy steroid; 3-hydroxy steroid; organofluorine compound; sulfoxide	antineoplastic agent; estrogen antagonist; estrogen receptor antagonist
vinpocetine [no description available]	2.08	1	0
sivelestat sivelestat: inhibitor of neutrophil elastase; structure given in first source	2.6	1	0	N-acylglycine; pivalate ester
pyronaridine [no description available]	2.6	1	0	aminoquinoline
geniposide [no description available]	2.6	1	0	terpene glycoside
deguelin deguelin: a natural product from Mundulea sericea; RN refers to (7aS-cis)-isomer; structure given in first source. deguelin : A rotenone that is 13,13a-dihydro-3H-chromeno[3,4-b]pyrano[2,3-h]chromen-7(7aH)-one substituted by methoxy groups at positions 9 and 10, and by two methyl groups at position 3 (the 7aS,13aS-stereoisomer). It exists in abundant quantities in the bark, roots, and leaves of the Leguminosae family of plants and reported to exert anti-tumour effects in various cancers.	2.08	1	0	aromatic ether; diether; organic heteropentacyclic compound; rotenones	angiogenesis inhibitor; anti-inflammatory agent; antineoplastic agent; antiviral agent; apoptosis inducer; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; mitochondrial NADH:ubiquinone reductase inhibitor; plant metabolite
daidzin daidzin: a potent, selective, and reversible inhibitor of human mitochondrial aldehyde dehydrogenase. daidzein 7-O-beta-D-glucoside : A glycosyloxyisoflavone that is daidzein attached to a beta-D-glucopyranosyl residue at position 7 via a glycosidic linkage. It is used in the treatment of alcohol dependency (antidipsotropic).	2.6	1	0	7-hydroxyisoflavones 7-O-beta-D-glucoside; hydroxyisoflavone; monosaccharide derivative	plant metabolite
triptolide [no description available]	2.08	1	0	diterpenoid; epoxide; gamma-lactam; organic heteroheptacyclic compound	antispermatogenic agent; plant metabolite
ecteinascidin 743 [no description available]	6.58	5	2	acetate ester; azaspiro compound; bridged compound; hemiaminal; isoquinoline alkaloid; lactone; organic heteropolycyclic compound; organic sulfide; oxaspiro compound; polyphenol; tertiary amino compound	alkylating agent; angiogenesis modulating agent; anti-inflammatory agent; antineoplastic agent; marine metabolite
sophocarpine [no description available]	2.6	1	0
marimastat marimastat: a matrix metalloproteinase inhibitor active in patients with advanced carcinoma of the pancreas, prostate, or ovary. marimastat : A secondary carboxamide resulting from the foraml condensation of the carboxy group of (2R)-2-[(1S)-1-hydroxy-2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the alpha-amino group of N,3-dimethyl-L-valinamide.	2.6	1	0	hydroxamic acid; secondary carboxamide	antineoplastic agent; matrix metalloproteinase inhibitor
sr 48692 SR 48692: structure in first source; a neurotensin receptor-1 antagonist	2.08	1	0	N-acyl-amino acid
elacridar Elacridar: inhibitor of MDR1 PROTEIN; structure given in first source	2.85	3	0
1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid 1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid: structure given in first source. DOTA : An azamacrocyle in which four nitrogen atoms at positions 1, 4, 7 and 10 of a twelve-membered ring are each substituted with a carboxymethyl group.	2.15	1	0	azamacrocycle	chelator; copper chelator
celastrol [no description available]	2.6	1	0	monocarboxylic acid; pentacyclic triterpenoid	anti-inflammatory drug; antineoplastic agent; antioxidant; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; Hsp90 inhibitor; metabolite
imatinib mesylate imatinib methanesulfonate : A methanesulfonate (mesylate) salt that is the monomesylate salt of imatinib. Used for treatment of chronic myelogenous leukemia and gastrointestinal stromal tumours.	2.88	3	0	methanesulfonate salt	anticoronaviral agent; antineoplastic agent; apoptosis inducer; tyrosine kinase inhibitor
gefitinib [no description available]	10.41	4	1	aromatic ether; monochlorobenzenes; monofluorobenzenes; morpholines; quinazolines; secondary amino compound; tertiary amino compound	antineoplastic agent; epidermal growth factor receptor antagonist
n-(n-(3-carboxyoxirane-2-carbonyl)leucyl)isoamylamine N-(N-(3-carboxyoxirane-2-carbonyl)leucyl)isoamylamine: inhibits calcium-activated neutral protease; see also record for E-64; RN given refers to (2-S-(2alpha,3beta)(R*)-isomer)	2.6	1	0	leucine derivative
bay x 1005 2-(4-(quinolin-2-yl-methoxy)phenyl)-2-cyclopentylacetic acid: inhibits synthesis of leukotriene B4 and 5-hydroxyeicosatetraenoic acid; inhibits five-lipoxygenase activating protein(FLAP)and leukotriene A4 hydrolase(LTA4H); structure given in first source;	2.08	1	0
vadimezan vadimezan : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by a 5,6-dimethyl-9-oxoxanthen-4-yl group.	2.6	1	0	monocarboxylic acid; xanthones	antineoplastic agent
e 64 E 64: cysteine protease inhibitor of microbial origin, which inhibits cathepsin B (EC 3.4.22.1) and cathepsin L (EC 3.4.22.-)	2.6	1	0	dicarboxylic acid monoamide; epoxy monocarboxylic acid; guanidines; L-leucine derivative; zwitterion	antimalarial; antiparasitic agent; protease inhibitor
gyki 53655 GYKI 53655: an AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate) receptor antagonist	2.08	1	0
methotrexate [no description available]	3.58	2	0	dicarboxylic acid; monocarboxylic acid amide; pteridines	abortifacient; antimetabolite; antineoplastic agent; antirheumatic drug; dermatologic drug; DNA synthesis inhibitor; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; immunosuppressive agent
umifenovir umifenovir: an antiviral agent	2.6	1	0	indolyl carboxylic acid
safinamide safinamide: short-acting inhibitor of MOA-B; FCE 26743 is (S)-isomer, FCE 28073 is (R)-isomer; structure in first source	2.6	1	0	amino acid amide
ilomastat CS 610: matrix metalloproteinase inhibitor; structure in first source. ilomastat : An N-acyl-amino acid obtained by formal condensation of the carboxy group of (2R)-2-[2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the amino group of N-methyl-L-tryptophanamide. A cell permeable broad-spectrum matrix metalloproteinase (MMP) inhibitor	2.6	1	0	hydroxamic acid; L-tryptophan derivative; N-acyl-amino acid	anti-inflammatory agent; antibacterial agent; antineoplastic agent; EC 3.4.24.24 (gelatinase A) inhibitor; neuroprotective agent
abiraterone [no description available]	9.05	13	5	3beta-hydroxy-Delta(5)-steroid; 3beta-sterol; pyridines	antineoplastic agent; EC 1.14.99.9 (steroid 17alpha-monooxygenase) inhibitor
ml-3000 [no description available]	2.08	1	0
pomalidomide 3-aminophthalimidoglutarimide: structure in first source	2.72	2	0	aromatic amine; dicarboximide; isoindoles; piperidones	angiogenesis inhibitor; antineoplastic agent; immunomodulator
cd 437 CD 437: selective for retinoic acid receptors gamma. CD437 : A naphthoic acid that is 6-phenylnaphthylene-2-carboxyic acid in which the phenyl substituent has been substituted at positions 3 and 4 by adamant-1-yl and hydroxy groups, respectively. It acts as a selective agonist of retinoic acid receptor (RAR)gamma and induces cell cycle arrest and apoptosis in various cancer cells.	2.08	1	0	adamantanes; monocarboxylic acid; naphthoic acid; phenols	apoptosis inducer; retinoic acid receptor gamma agonist
docetaxel anhydrous Docetaxel: A semisynthetic analog of PACLITAXEL used in the treatment of locally advanced or metastatic BREAST NEOPLASMS and NON-SMALL CELL LUNG CANCER.. docetaxel anhydrous : A tetracyclic diterpenoid that is paclitaxel with the N-benzyloxycarbonyl group replaced by N-tert-butoxycarbonyl, and the acetoxy group at position 10 replaced by a hydroxy group.	5.77	6	1	secondary alpha-hydroxy ketone; tetracyclic diterpenoid	antimalarial; antineoplastic agent; photosensitizing agent
perifosine [no description available]	2.53	2	0	ammonium betaine; phospholipid	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
atazanavir atazanavir : A heavily substituted carbohydrazide that is an antiretroviral drug of the protease inhibitor (PI) class used to treat infection of human immunodeficiency virus (HIV).	2.6	1	0	carbohydrazide	antiviral drug; HIV protease inhibitor
mk 767 5-((2,4-dioxo-5-thiazolidinyl)methyl)-2-methoxy-N-((4-(trifluoromethyl)phenyl)methyl)benzamide: an antihyperlipidemic agent that also functions as an insulin sensitizer, PPARalpha agonist, and PPARgamma agonist; structure in first source	2.08	1	0
vatalanib [no description available]	3.31	1	0	monochlorobenzenes; phthalazines; pyridines; secondary amino compound	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; vascular endothelial growth factor receptor antagonist
imidazole-4-carboxamide imidazole-4-carboxamide: see also related record for imidazolecarboxamide, unspecified position	2.13	1	0
vx 497 N-3-(3-(3-methoxy-4-oxazol-5-ylphenyl)ureido)benzylcarbamic acid tetrahydrofuran-3-yl ester: structure in first source	2.6	1	0
bcx 1812 [no description available]	2.6	1	0	3-hydroxy monocarboxylic acid; acetamides; cyclopentanols; guanidines	antiviral drug; EC 3.2.1.18 (exo-alpha-sialidase) inhibitor
bazedoxifene acetate [no description available]	2.08	1	0
naproxen Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.. naproxen : A methoxynaphthalene that is 2-methoxynaphthalene substituted by a carboxy ethyl group at position 6. Naproxen is a non-steroidal anti-inflammatory drug commonly used for the reduction of pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, kidney stones, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and for the treatment of primary dysmenorrhea. It works by inhibiting both the COX-1 and COX-2 enzymes.	2.6	1	0	methoxynaphthalene; monocarboxylic acid	antipyretic; cyclooxygenase 1 inhibitor; cyclooxygenase 2 inhibitor; drug allergen; environmental contaminant; gout suppressant; non-narcotic analgesic; non-steroidal anti-inflammatory drug; xenobiotic
canertinib [no description available]	2.08	1	0	monochlorobenzenes; morpholines; organofluorine compound; quinazolines	antineoplastic agent; tyrosine kinase inhibitor
birb 796 [no description available]	2.08	1	0	aromatic ether; morpholines; naphthalenes; pyrazoles; ureas	EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; immunomodulator
olmesartan olmesartan: an active metabolite of CS 866	2.6	1	0	biphenylyltetrazole	angiotensin receptor antagonist; antihypertensive agent
telbivudine [no description available]	2.6	1	0	pyrimidine 2'-deoxyribonucleoside	antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
tipifarnib [no description available]	2.08	1	0	imidazoles; monochlorobenzenes; primary amino compound; quinolone	antineoplastic agent; apoptosis inducer; EC 2.5.1.58 (protein farnesyltransferase) inhibitor
celastrol methyl ester celastrol methyl ester: isolated from Tripterygium wilfordii; potent inhibitory activity on both Kir2.1 and ERG1 potassium channels, leading to LONG QT SYNDROME	2.6	1	0	carboxylic ester
resiquimod S 28463: structure given in first source	2.6	1	0	imidazoquinoline
cyc 202 seliciclib : 2,6-Diaminopurine carrying benzylamino, (2R)-1-hydroxybutan-2-yl and isopropyl substituents at C-6, C-2-N and N-9 respectively. It is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors.	2.55	2	0	2,6-diaminopurines	antiviral drug; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
pyropheophorbide a pyropheophorbide a: RN given refers to (3S-trans)-isomer	2.31	1	0
tanshinone ii a tashinone IIA: a cardiovascular agent with antineoplastic activity; isolated from Salvia miltiorrhiza; structure in first source	2.6	1	0	abietane diterpenoid
anacardic acid anacardic acid: isolated from Anacardium occidentale; monophenol monooxygenase inhibitor. anacardic acid : A hydroxybenzoic acid that is salicylic acid substituted by a pentadecyl group at position 6. It is a major component of cashew nut shell liquid and exhibits an extensive range of bioactivities.	2.6	1	0	hydroxy monocarboxylic acid; hydroxybenzoic acid	anti-inflammatory agent; antibacterial agent; anticoronaviral agent; apoptosis inducer; EC 2.3.1.48 (histone acetyltransferase) inhibitor; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; neuroprotective agent; plant metabolite
5-hydroxymethyldeoxycytidine monophosphate 5-hydroxymethyl-2'-deoxycytidine: structure in first source	2.31	1	0
migalastat migalastat: a potent inhibitor of glycolipid biosynthesis	2.6	1	0	piperidines
sb 203580 [no description available]	2.58	2	0	imidazoles; monofluorobenzenes; pyridines; sulfoxide	EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; geroprotector; Hsp90 inhibitor; neuroprotective agent
enzastaurin [no description available]	2.08	1	0	indoles; maleimides
erlotinib [no description available]	2.58	2	0	aromatic ether; quinazolines; secondary amino compound; terminal acetylenic compound	antineoplastic agent; epidermal growth factor receptor antagonist; protein kinase inhibitor
erlotinib hydrochloride [no description available]	2.52	2	0	hydrochloride; terminal acetylenic compound	antineoplastic agent; protein kinase inhibitor
piboserod Serotonin 5-HT4 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT4 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN RECEPTOR AGONISTS.	2.08	1	0
l 163191 [no description available]	2.08	1	0
limonin [no description available]	2.6	1	0	epoxide; furans; hexacyclic triterpenoid; lactone; limonoid; organic heterohexacyclic compound	inhibitor; metabolite; volatile oil component
scutellarin scutellarin: see scutellarein for aglycone. scutellarin : The glycosyloxyflavone which is the 7-O-glucuronide of scutellarein.	2.6	1	0	glucosiduronic acid; glycosyloxyflavone; monosaccharide derivative; trihydroxyflavone	antineoplastic agent; proteasome inhibitor
bd 1047 N-(2-(3,4-Dichlorphenyl)ethyl)-N,N',N'-trimethyl-1,2-ethandiamin: sigma receptor ligand; putative sigma receptor antagonist with antidystonic activity	2.08	1	0	primary amine
etravirine [no description available]	2.6	1	0	aminopyrimidine; aromatic ether; dinitrile; organobromine compound	antiviral agent; HIV-1 reverse transcriptase inhibitor
3-(2'-pyridyldithio)benzyldiazoacetate 3-(2'-pyridyldithio)benzyldiazoacetate: structure given in first source; isomeric probe	2.6	1	0
chelidonine chelidonine: benzophenanthridine derived from scoulerine from Chelidonium majus; RN given refers to parent cpd (chelidonine, (5bR-(5balpha,6beta,12alpha))-isomer)	2.6	1	0	alkaloid antibiotic; alkaloid fundamental parent; benzophenanthridine alkaloid
4-n-butylresorcinol 4-n-butylresorcinol: structure in first source	2.6	1	0	resorcinols
lapatinib [no description available]	2.55	2	0	furans; organochlorine compound; organofluorine compound; quinazolines	antineoplastic agent; tyrosine kinase inhibitor
darunavir Darunavir: An HIV PROTEASE INHIBITOR that is used in the treatment of AIDS and HIV INFECTIONS. Due to the emergence of ANTIVIRAL DRUG RESISTANCE when used alone, it is administered in combination with other ANTI-HIV AGENTS.. darunavir : An N,N-disubstituted benzenesulfonamide bearing an unsubstituted amino group at the 4-position, used for the treatment of HIV infection. A second-generation HIV protease inhibitor, darunavir was designed to form robust interactions with the protease enzyme from many strains of HIV, including those from treatment-experienced patients with multiple resistance mutations to other protease inhibitors.	2.6	1	0	carbamate ester; furofuran; sulfonamide	antiviral drug; HIV protease inhibitor
dapivirine Dapivirine: effectively prevented human immunodeficiency virus (HIV) infection in cocultures of monocyte-derived dendritic cells and T cells, representing primary targets in sexual transmission	2.6	1	0
sorafenib [no description available]	10.22	5	0	(trifluoromethyl)benzenes; aromatic ether; monochlorobenzenes; phenylureas; pyridinecarboxamide	angiogenesis inhibitor; anticoronaviral agent; antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor; ferroptosis inducer; tyrosine kinase inhibitor
lenalidomide [no description available]	2.54	2	0	aromatic amine; dicarboximide; isoindoles; piperidones	angiogenesis inhibitor; antineoplastic agent; immunomodulator
N-[4-(3-chloro-4-fluoroanilino)-3-cyano-7-ethoxy-6-quinolinyl]-4-(dimethylamino)-2-butenamide [no description available]	2.08	1	0	aminoquinoline
sr 142806 [no description available]	2.08	1	0
vincaleukoblastine [no description available]	2.31	1	0	acetate ester; indole alkaloid fundamental parent; methyl ester; organic heteropentacyclic compound; organic heterotetracyclic compound; tertiary alcohol; tertiary amino compound; vinca alkaloid	antineoplastic agent; immunosuppressive agent; microtubule-destabilising agent; plant metabolite
nsc 74859 NSC 74859: inhibits Stat3 binding activity; structure in first source. S3I-201 : An amidobenzoic acid obtained by formal condensation of the carboxy group of [(4-methylbenzene-1-sulfonyl)oxy]acetic acid with the amino group of 4-amino-2-hydroxybenzoic acid.	2.6	1	0	amidobenzoic acid; monohydroxybenzoic acid; tosylate ester	STAT3 inhibitor
metribolone Metribolone: A synthetic non-aromatizable androgen and anabolic steroid. It binds strongly to the androgen receptor and has therefore also been used as an affinity label for this receptor in the prostate and in prostatic tumors.. 17beta-hydroxy-17-methylestra-4,9,11-trien-3-one : A synthetic non-aromatisable androgen and anabolic steroid. It binds strongly to the androgen receptor and has therefore also been used as an affinity label for this receptor in the prostate and in prostatic tumors.	2.31	1	0	17beta-hydroxy steroid; 3-oxo steroid; anabolic androgenic steroid	androgen
berbamine [no description available]	2.6	1	0	bisbenzylisoquinoline alkaloid; isoquinolines
elesclomol [no description available]	2.08	1	0	carbohydrazide; thiocarbonyl compound	antineoplastic agent; apoptosis inducer
u-104 SLC-0111: a carbonic anhydrase inhibitor; structure in first source	2.6	1	0
wortmannin [no description available]	2.57	2	0	acetate ester; cyclic ketone; delta-lactone; organic heteropentacyclic compound	anticoronaviral agent; antineoplastic agent; autophagy inhibitor; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; geroprotector; Penicillium metabolite; radiosensitizing agent
7-hydroxy-5-methyl-2-(2-oxopropyl)-8-[3,4,5-trihydroxy-6-(hydroxymethyl)-2-oxanyl]-1-benzopyran-4-one [no description available]	2.6	1	0	glycoside
nsc 663284 NSC 663284: structure in first source	2.08	1	0	quinolone
bortezomib [no description available]	3.1	4	0	amino acid amide; L-phenylalanine derivative; pyrazines	antineoplastic agent; antiprotozoal drug; protease inhibitor; proteasome inhibitor
ritonavir Ritonavir: An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. It also inhibits CYTOCHROME P-450 CYP3A.. ritonavir : An L-valine derivative that is L-valinamide in which alpha-amino group has been acylated by a [(2-isopropyl-1,3-thiazol-4-yl)methyl]methylcarbamoyl group and in which a hydrogen of the carboxamide amino group has been replaced by a (2R,4S,5S)-4-hydroxy-1,6-diphenyl-5-{[(1,3-thiazol-5-ylmethoxy)carbonyl]amino}hexan-2-yl group. A CYP3A inhibitor and antiretroviral drug from the protease inhibitor class used to treat HIV infection and AIDS, it is often used as a fixed-dose combination with another protease inhibitor, lopinavir. Also used in combination with dasabuvir sodium hydrate, ombitasvir and paritaprevir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0	1,3-thiazoles; carbamate ester; carboxamide; L-valine derivative; ureas	antiviral drug; environmental contaminant; HIV protease inhibitor; xenobiotic
tizoxanide tizoxanide: major metabolite of nitazoxanide; structure in first source	2.6	1	0	salicylamides
bardoxolone methyl methyl 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oate: structure in first source	2.08	1	0	cyclohexenones
nsc 23766 [no description available]	2.08	1	0	aminopyrimidine; aminoquinoline; primary amino compound; secondary amino compound; tertiary amino compound	antiviral agent; apoptosis inducer; EC 3.6.5.2 (small monomeric GTPase) inhibitor; muscarinic antagonist
gant 61 GANT 61: a sonic hedgehog pathway inhibitor and Gli inhibitor; structure in first source. GANT61 : An aminal that is hexahydropyrimidine which is substituted on each nitrogen by a 2-(dimethylamino)benzyl group, and at the aminal carbon by a pyridin-4-yl group. A Hedgehog signaling pathway and Gli protein inhibitor.	2.31	1	0	aminal; dialkylarylamine; pyridines; substituted aniline; tertiary amino compound	antineoplastic agent; apoptosis inducer; glioma-associated oncogene inhibitor; Hedgehog signaling pathway inhibitor
carboplatin [no description available]	13.45	36	12
arbutin hydroquinone O-beta-D-glucopyranoside : A monosaccharide derivative that is hydroquinone attached to a beta-D-glucopyranosyl residue at position 4 via a glycosidic linkage.	2.6	1	0	beta-D-glucoside; monosaccharide derivative	Escherichia coli metabolite; plant metabolite
quinidine Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.. quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy.	2.6	1	0	cinchona alkaloid	alpha-adrenergic antagonist; anti-arrhythmia drug; antimalarial; drug allergen; EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor; EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor; muscarinic antagonist; P450 inhibitor; potassium channel blocker; sodium channel blocker
conessine conessine : A steroid alkaloid that is con-5-enine substituted by a N,N-dimethylamino group at position 3. It has been isolated from the plant species of the family Apocynaceae.	2.6	1	0	steroid alkaloid; tertiary amino compound	antibacterial agent; antimalarial; H3-receptor antagonist; plant metabolite
saquinavir Saquinavir: An HIV protease inhibitor which acts as an analog of an HIV protease cleavage site. It is a highly specific inhibitor of HIV-1 and HIV-2 proteases, and also inhibits CYTOCHROME P-450 CYP3A.. saquinavir : An aspartic acid derivative obtained by formal condensation of the primary amino group of (2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)octahydroisoquinolin-2(1H)-yl]-3-hydroxy-1-phenylbutan-2-ylamine with the carboxy group of N(2)(-quinolin-2-ylcarbonyl)-L-asparagine. An inhibitor of HIV-1 protease.	2.6	1	0	L-asparagine derivative; quinolines	antiviral drug; HIV protease inhibitor
abacavir abacavir: a carbocyclic nucleoside with potent selective anti-HIV activity. abacavir : A 2,6-diaminopurine that is (1S)-cyclopent-2-en-1-ylmethanol in which the pro-R hydrogen at the 4-position is substituted by a 2-amino-6-(cyclopropylamino)-9H-purin-9-yl group. A nucleoside analogue reverse transcriptase inhibitor (NRTI) with antiretroviral activity against HIV, it is used (particularly as the sulfate) with other antiretrovirals in combination therapy of HIV infection.	2.6	1	0	2,6-diaminopurines	antiviral drug; drug allergen; HIV-1 reverse transcriptase inhibitor
linezolid [no description available]	2.6	1	0	acetamides; morpholines; organofluorine compound; oxazolidinone	antibacterial drug; protein synthesis inhibitor
ginsenoside rg1 [no description available]	2.17	1	0	12beta-hydroxy steroid; 3beta-hydroxy-4,4-dimethylsteroid; beta-D-glucoside; ginsenoside; tetracyclic triterpenoid	neuroprotective agent; pro-angiogenic agent
cephaelin cephaelin: do not confuse with cephalin of brain; after emetine this is the most important alkaloid of ipecac; protein synthesis inhibitor. cephaeline : A pyridoisoquinoline comprising emetam having a hydroxy group at the 6'-position and methoxy substituents at the 7'-, 10- and 11-positions.	2.6	1	0	pyridoisoquinoline
(-)-usnic acid (-)-usnic acid : The (-)-enantiomer of usnic acid.	2.6	1	0	usnic acid	EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
acetylleucyl-leucyl-norleucinal acetylleucyl-leucyl-norleucinal: a proteasome inhibitor. acetylleucyl-leucyl-norleucinal : A tripeptide composed of N-acetylleucyl, leucyl and norleucinal residues joined in sequence.	2.6	1	0	aldehyde; tripeptide	cysteine protease inhibitor
tretinoin Tretinoin: An important regulator of GENE EXPRESSION during growth and development, and in NEOPLASMS. Tretinoin, also known as retinoic acid and derived from maternal VITAMIN A, is essential for normal GROWTH; and EMBRYONIC DEVELOPMENT. An excess of tretinoin can be teratogenic. It is used in the treatment of PSORIASIS; ACNE VULGARIS; and several other SKIN DISEASES. It has also been approved for use in promyelocytic leukemia (LEUKEMIA, PROMYELOCYTIC, ACUTE).. retinoic acid : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraenoic acid substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).. all-trans-retinoic acid : A retinoic acid in which all four exocyclic double bonds have E- (trans-) geometry.	2.31	1	0	retinoic acid; vitamin A	anti-inflammatory agent; antineoplastic agent; antioxidant; AP-1 antagonist; human metabolite; keratolytic drug; retinoic acid receptor agonist; retinoid X receptor agonist; signalling molecule
resveratrol trans-resveratrol : A resveratrol in which the double bond has E configuration.	8.16	3	0	resveratrol	antioxidant; phytoalexin; plant metabolite; quorum sensing inhibitor; radical scavenger
tacrolimus Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.. tacrolimus (anhydrous) : A macrolide lactam containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.	2.6	1	0	macrolide lactam	bacterial metabolite; immunosuppressive agent
ferulic acid ferulate : A monocarboxylic acid anion obtained by the deprotonation of the carboxy group of ferulic acid.	2.31	1	0	ferulic acids	anti-inflammatory agent; antioxidant; apoptosis inhibitor; cardioprotective agent; MALDI matrix material; plant metabolite
pectins Pectins: High molecular weight polysaccharides present in the cell walls of all plants. Pectins cement cell walls together. They are used as emulsifiers and stabilizers in the food industry. They have been tried for a variety of therapeutic uses including as antidiarrheals, where they are now generally considered ineffective, and in the treatment of hypercholesterolemia.. alpha-D-galacturonic acid : The alpha-anomer of D-galacturonic acid.	2.25	1	0	D-galactopyranuronic acid
lycopene [no description available]	2.6	1	0	acyclic carotene	antioxidant; plant metabolite
zithromax Azithromycin: A semi-synthetic macrolide antibiotic structurally related to ERYTHROMYCIN. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis.. azithromycin : A macrolide antibiotic useful for the treatment of bacterial infections.	2.6	1	0	macrolide antibiotic	antibacterial drug; environmental contaminant; xenobiotic
gw 3965 GW 3965: a liver X receptor ligand	2.08	1	0	diarylmethane
y 27632 Y 27632: RN given for di-HCl salt; inhibits Rho-associated protein kinase; inhibits calcium sensitization to affect smooth muscle relaxation; structure in first source. Y-27632 : A monocarboxylic acid amide that is trans-[(1R)-1-aminoethyl]cyclohexanecarboxamide in which one of the nitrogens of the aminocarbony group is substituted by a pyridine nucleus. It has been shown to exhibit inhibitory activity against Rho-associated protein kinase (ROCK) enzyme.	2.08	1	0	aromatic amide
6-bromoindirubin-3'-oxime 6-bromoindirubin-3'-oxime: structure in first source. 6-bromoindirubin-3'-oxime : A member of the class of biindoles that is indirubin substituted at position 6 by a bromo group and in which the keto group at position 3' has undergone condensation with hydroxylamine to form the corresponding oxime.	2.08	1	0
purvalanol b purvalanol B: protein kinase inhibitor; structure in first source	2.08	1	0	purvalanol	protein kinase inhibitor
y-700 [no description available]	2.08	1	0
repsox RepSox: inhibits TGF-beta signaling; structure in first source appears to be incorrect	2.08	1	0	pyrazolopyridine
roflumilast [no description available]	2.6	1	0	aromatic ether; benzamides; chloropyridine; cyclopropanes; organofluorine compound	anti-asthmatic drug; phosphodiesterase IV inhibitor
L-cycloserine L-cycloserine : A 4-amino-1,2-oxazolidin-3-one that has S configuration. An antibiotic isolated from Erwinia uredovora.	2.6	1	0	4-amino-1,2-oxazolidin-3-one	anti-HIV agent; anticonvulsant; EC 2.3.1.50 (serine C-palmitoyltransferase) inhibitor
h 89 N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide: structure given in first source. N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A member of the class of isoquinolines that is the sulfonamide obtained by formal condensation of the sulfo group of isoquinoline-5-sulfonic acid with the primary amino group of N(1)-[3-(4-bromophenyl)prop-2-en-1-yl]ethane-1,2-diamine. It is a protein kinase A inhibitor.. (E)-N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide in which the double bond adopts a trans-configuration.	2.6	1	0	N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide
decitabine [no description available]	7.58	2	0	2'-deoxyribonucleoside
texas red Texas red: hydrophilic Texas red; structure given in first source	2.05	1	0	organic heteroheptacyclic compound	fluorochrome
dactinomycin Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)	2.11	1	0	actinomycin	mutagen
bevirimat bevirimat: an HIV inhibitor; disrupts late step in processing HIV Major Core Protein p24, preventing the capsid precursor p25 from being converted to mature capsid p24. bevirimat : A pentacyclic triterpenoid obtained by the formal condensation of 2,2-dimethylsuccinic acid with the 3-hydroxy group of betulinic acid. It is isolated from the Chinese herb Syzygium claviflorum. The first in the class of HIV-1 maturation inhibitors to be studied in humans, bevirimat was identified as a potent HIV drug candidate and several clinical trials were conducted, but development into a new drug was plagued by numerous resistance-related problems.	2.6	1	0	dicarboxylic acid monoester; monocarboxylic acid; pentacyclic triterpenoid	HIV-1 maturation inhibitor; metabolite
melphalan Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.. melphalan : A phenylalanine derivative comprising L-phenylalanine having [bis(2-chloroethyl)amino group at the 4-position on the phenyl ring.	2.8	3	0	L-phenylalanine derivative; nitrogen mustard; non-proteinogenic L-alpha-amino acid; organochlorine compound	alkylating agent; antineoplastic agent; carcinogenic agent; drug allergen; immunosuppressive agent
benzyloxycarbonylleucyl-leucyl-leucine aldehyde benzyloxycarbonylleucyl-leucyl-leucine aldehyde: proteasome inhibitor. N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal : A tripeptide that is L-leucyl-L-leucyl-L-leucine in which the C-terminal carboxy group has been reduced to the corresponding aldehyde and the N-terminal amino group is protected as its benzyloxycarbonyl derivative.	2.6	1	0	amino aldehyde; carbamate ester; tripeptide	proteasome inhibitor
tenofovir tenofovir (anhydrous) : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens is replaced by a [(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(isopropyloxycarbonyloxymethyl) ester (disoproxil ester) prodrug is used as the fumaric acid salt in combination therapy for the treatment of HIV infection.	2.66	2	0	nucleoside analogue; phosphonic acids	antiviral drug; drug metabolite; HIV-1 reverse transcriptase inhibitor
posaconazole [no description available]	2.6	1	0	aromatic ether; conazole antifungal drug; N-arylpiperazine; organofluorine compound; oxolanes; triazole antifungal drug; triazoles	trypanocidal drug
gw 257406x maribavir: has antiviral activity against human cytomegalovirus	2.6	1	0
rubitecan rubitecan: RN refers to (+-)-isomer; anti-HIV agent; DNA Topoisomerases, Type I inhibitor. rubitecan : A pyranoindolizinoquinoline that is camptothecin in which the hydrogen at position 9 has been replaced by a nitro group. It is a prodrug for 9-aminocamptothecin.	2.31	1	0	C-nitro compound; delta-lactone; pyranoindolizinoquinoline; semisynthetic derivative; tertiary alcohol	antineoplastic agent; EC 5.99.1.2 (DNA topoisomerase) inhibitor; prodrug
shikonin shikonin: a naphthazarin; has antineoplastic and angiogenesis inhibiting activities	2.6	1	0	hydroxy-1,4-naphthoquinone
4,4-difluoro-N-[(1S)-3-[3-(3-methyl-5-propan-2-yl-1,2,4-triazol-4-yl)-8-azabicyclo[3.2.1]octan-8-yl]-1-phenylpropyl]-1-cyclohexanecarboxamide [no description available]	2.58	2	0	tropane alkaloid
cmx 001 [no description available]	2.6	1	0
amd 8664 [no description available]	2.6	1	0
bay 41-4109 BAY 41-4109: structure in first source	2.6	1	0
bay 57-1293 pritelivir: herpes simplex virus 1 helicase-primase inhibitor	2.6	1	0
2'-c-methylcytidine 2'-C-methylcytidine: structure in first source	2.6	1	0
isoxanthohumol isoxanthohumol: structure in first source	2.6	1	0	flavanones
ammonium acetate ammonium acetate : An ammonium salt obtained by reaction of ammonia with acetic acid. A deliquescent white crystalline solid, it has a relatively low melting point (114degreeC) for a salt. Used as a food acidity regulator, although no longer approved for this purpose in the EU.	2.31	1	0	acetate salt; ammonium salt	buffer; food acidity regulator
4-(4-chloro-2-methylphenoxy)-n-hydroxybutanamide 4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide: a c-FLIP inhibitor; structure in first source	2.6	1	0	aromatic ether
mecarbinate [no description available]	2.6	1	0
s 1033 [no description available]	2.08	1	0	(trifluoromethyl)benzenes; imidazoles; pyridines; pyrimidines; secondary amino compound; secondary carboxamide	anticoronaviral agent; antineoplastic agent; tyrosine kinase inhibitor
acetyl-aspartyl-glutamyl-valyl-aspartal acetyl-aspartyl-glutamyl-valyl-aspartal: a capase inhibitor. Ac-Asp-Glu-Val-Asp-H : A tetrapeptide consisting of two L-aspartic acid residues, an L-glutamyl residue and an L-valine residue with an acetyl group at the N-terminal and with the C-terminal carboxy group reduced to an aldehyde. It is an inhibitor of caspase-3/7.	2.6	1	0	tetrapeptide	protease inhibitor
octotropine methylbromide octotropine methylbromide: minor descriptor (65-86); on line & INDEX MEDICUS search TROPANES (69-86); RN given refers to endo-isomer. anisotropine methylbromide : A quaternary ammonium salt resulting from the reaction of the amino group of anisotropine with methyl bromide.	2.6	1	0
sesquiterpenes [no description available]	2.63	2	0
mercaptopurine Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.. purine-6-thiol : A thiol that is the tautomer of mercaptopurine.. mercaptopurine : A member of the class of purines that is 6,7-dihydro-1H-purine carrying a thione group at position 6. An adenine analogue, it is used in the treatment of acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), Crohn's disease, and ulcerative colitis.	2.58	2	0	aryl thiol; purines; thiocarbonyl compound	anticoronaviral agent; antimetabolite; antineoplastic agent
jrf 12 N2,N4-dibenzylquinazoline-2,4-diamine: a selective, potent, reversible, and ATP-competitive p97 inhibitor	2.6	1	0
3,4'-dihydroxyflavone 3,4'-dihydroxyflavone: an antioxidant; structure in first source	2.6	1	0
rg108 RG108: DNA methyltransferase inhibitor; structure in first source	2.08	1	0	indolyl carboxylic acid
3-(3,4-dimethoxyphenyl)propenoic acid 3-(3,4-dimethoxyphenyl)propenoic acid: structure given in first source; RN given refers to parent cpd. 3,4-dimethoxycinnamic acid : A methoxycinnamic acid that is trans-cinnamic acid substituted by methoxy groups at positions 3' and 4' respectively.	2.6	1	0	methoxycinnamic acid
stf 083010 [no description available]	2.08	1	0
isoferulic acid isoferulic acid: isomer of ferulic acid; structure. isoferulic acid : A ferulic acid consisting of trans-cinnamic acid bearing methoxy and hydroxy substituents at positions 4 and 3 respectively on the phenyl ring.	2.6	1	0	ferulic acids	antioxidant; biomarker; metabolite
N-(3-cyano-4,5,6,7-tetrahydro-1-benzothiophen-2-yl)-1-naphthalenecarboxamide [no description available]	2.08	1	0	naphthalenecarboxamide
cyclouridine cyclouridine: structure given in third source	2.6	1	0
curcumin Curcumin: A yellow-orange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes.. curcumin : A beta-diketone that is methane in which two of the hydrogens are substituted by feruloyl groups. A natural dyestuff found in the root of Curcuma longa.	3.43	5	0	aromatic ether; beta-diketone; diarylheptanoid; enone; polyphenol	anti-inflammatory agent; antifungal agent; antineoplastic agent; biological pigment; contraceptive drug; dye; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; EC 1.1.1.21 (aldehyde reductase) inhibitor; EC 1.1.1.25 (shikimate dehydrogenase) inhibitor; EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor; EC 1.8.1.9 (thioredoxin reductase) inhibitor; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; EC 3.5.1.98 (histone deacetylase) inhibitor; flavouring agent; food colouring; geroprotector; hepatoprotective agent; immunomodulator; iron chelator; ligand; lipoxygenase inhibitor; metabolite; neuroprotective agent; nutraceutical; radical scavenger
cct018159 CCT018159: structure in first source. CCT-018159 : A member of the class of pyrazoles that is 1H-pyrazole carrying 1,4-benzodioxane-6-yl and 5-ethyl-2,4-dihydroxyphenyl substituents at positions 4 and 5 respectively.	2.08	1	0	benzodioxine; pyrazoles; resorcinols	antineoplastic agent; apoptosis inducer; Hsp90 inhibitor
secinh3 SecinH3: a small molecule antagonist of cytohesins; structure in first source	2.08	1	0	triazoles
jk184 JK184: structure in first source	2.08	1	0
thiohydantoins Thiohydantoins: Sulfur analogs of hydantoins with one or both carbonyl groups replaced by thiocarbonyl groups.	2.31	1	0
zucapsaicin [no description available]	2.6	1	0	methoxybenzenes; phenols
nbd 556 [no description available]	2.6	1	0
thioguanine anhydrous Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. tioguanine : A 2-aminopurine that is the 6-thiono derivative of 2-amino-1,9-dihydro-6H-purine. Incorporates into DNA and inhibits synthesis. Used in the treatment of leukaemia.	2.6	1	0	2-aminopurines	anticoronaviral agent; antimetabolite; antineoplastic agent
4,5,6,7-tetrachloroindan-1,3-dione 4,5,6,7-tetrachloroindan-1,3-dione: inhibits ubiquitin C-terminal hydrolase L1	2.6	1	0
tamoxifen citrate [no description available]	2.08	1	0	citrate salt	angiogenesis inhibitor; anticoronaviral agent
tamoxifen [no description available]	6.7	3	1	stilbenoid; tertiary amino compound	angiogenesis inhibitor; antineoplastic agent; bone density conservation agent; EC 1.2.3.1 (aldehyde oxidase) inhibitor; EC 2.7.11.13 (protein kinase C) inhibitor; estrogen antagonist; estrogen receptor antagonist; estrogen receptor modulator
hc-067047 HC-067047: a TRPA1 antagonist; structure in first source	2.08	1	0
bi-78d3 [no description available]	2.08	1	0	aryl sulfide
srpin340 SRPIN340: Serine-Arginine-Rich Protein Kinase Inhibitor	2.6	1	0
gsk 3787 [no description available]	2.08	1	0
pr-619 [no description available]	2.6	1	0
p5091 P5091: inhibits ubiquitin-specific protease 7; structure in first source	2.6	1	0
methyl-thiohydantoin-tryptophan methyl-thiohydantoin-tryptophan: structure in first source	2.08	1	0	organonitrogen compound; organooxygen compound
2-[2-chloro-6-ethoxy-4-[(3-methyl-5-oxo-1-phenyl-4-pyrazolylidene)methyl]phenoxy]acetic acid methyl ester [no description available]	2.08	1	0	monocarboxylic acid
4-(5-(4-methoxyphenyl)-3-phenyl-4,5-dihydro-1h-pyrazol-1-yl)benzenesulfonamide [no description available]	2.08	1	0	sulfonamide
trovirdine trovirdine: HIV-1 reverse transcriptase inhibitor	2.6	1	0
LSM-1318 [no description available]	2.08	1	0	oxa-steroid
fti 277 [no description available]	2.6	1	0
u 0126 U 0126: protein kinase kinase inhibitor; structure in first source	2.6	1	0	aryl sulfide; dinitrile; enamine; substituted aniline	antineoplastic agent; antioxidant; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; osteogenesis regulator; vasoconstrictor agent
rwj 67657 RWJ 67657: inhibits p38 mitogen-activated protein kinase; structure in first source	2.08	1	0
vicriviroc vicriviroc: structure in first source	2.6	1	0	(trifluoromethyl)benzenes
telaprevir [no description available]	2.6	1	0	cyclopentapyrrole; cyclopropanes; oligopeptide; pyrazines	antiviral drug; hepatitis C protease inhibitor; peptidomimetic
6-methyl-2-(phenylethynyl)pyridine 6-methyl-2-(phenylethynyl)pyridine: an mGlu5 antagonist. 2-methyl-6-(phenylethynyl)pyridine : A methylpyridine that coinsists of 2-methylp[yridine bearing an additional phenylethynyl group at position 6. Potent and highly selective non-competitive antagonist at the mGlu5 receptor subtype (IC50 = 36 nM) and a positive allosteric modulator at mGlu4 receptors. Centrally active following systemic administration in vivo. Reverses mechanical hyperalgesia in the inflamed rat hind paw.	2.08	1	0	acetylenic compound; methylpyridines	anxiolytic drug; metabotropic glutamate receptor antagonist
bms 387032 N-(5-(((5-(1,1-dimethylethyl)-2-oxazolyl)methyl)thio)-2-thiazolyl)-4-piperidinecarboxamide: a CDK2 inhibitor with antineoplastic activity; structure in first source. N-(5-{[(5-tert-butyl-1,3-oxazol-2-yl)methyl]sulfanyl}-1,3-thiazol-2-yl)piperidine-4-carboxamide : A secondary carboxamide resulting from the formal condensation of the carboxy group of piperidine-4-carboxylic acid with the amino group of 5-{[(5-tert-butyl-1,3-oxazol-2-yl)methyl]sulfanyl}-1,3-thiazol-2-amine. It is an ATP-competitive inhibitor of CDK2, CDK7 and CDK9 kinases and exhibits anti-cancer properties.	2.08	1	0	1,3-oxazoles; 1,3-thiazoles; organic sulfide; piperidinecarboxamide; secondary carboxamide	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
raclopride Raclopride: A substituted benzamide that has antipsychotic properties. It is a dopamine D2 receptor (see RECEPTORS, DOPAMINE D2) antagonist.	2.11	1	0	salicylamides
orlistat Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.	2.6	1	0	beta-lactone; carboxylic ester; formamides; L-leucine derivative	anti-obesity agent; bacterial metabolite; EC 2.3.1.85 (fatty acid synthase) inhibitor; EC 3.1.1.3 (triacylglycerol lipase) inhibitor
tandutinib [no description available]	2.08	1	0	aromatic ether; N-arylpiperazine; N-carbamoylpiperazine; phenylureas; piperidines; quinazolines; tertiary amino compound	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
vx-745 [no description available]	2.08	1	0	aryl sulfide; dichlorobenzene; difluorobenzene; pyrimidopyridazine	anti-inflammatory drug; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
corlanor ivabradine hydrochloride : A hydrochloride obtained by combining ivabradine with one molar equivalent of hydrochloric acid. Used to treat patients with angina who have intolerance to beta blockers and/or heart failure.	2.08	1	0	hydrochloride	cardiotonic drug
dasatinib N-(2-chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)-1,3-thiazole-5-carboxamide: a dasatinib prodrug; structure in first source. dasatinib (anhydrous) : An aminopyrimidine that is 2-methylpyrimidine which is substituted at position 4 by the primary amino group of 2-amino-1,3-thiazole-5-carboxylic acid and at position 6 by a 4-(2-hydroxyethyl)piperazin-1-yl group, and in which the carboxylic acid group has been formally condensed with 2-chloro-6-methylaniline to afford the corresponding amide. A multi-targeted kinase inhibitor, it is used, particularly as the monohydrate, for the treatment of chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia. Note that the name 'dasatinib' is used to refer to the monohydrate (USAN) as well as to anhydrous dasatinib (INN).	8.49	6	0	1,3-thiazoles; aminopyrimidine; monocarboxylic acid amide; N-(2-hydroxyethyl)piperazine; N-arylpiperazine; organochlorine compound; secondary amino compound; tertiary amino compound	anticoronaviral agent; antineoplastic agent; tyrosine kinase inhibitor
ha 1100 HA 1100: intracellular calcium antagonist	3.51	1	0
zd 6474 CH 331: structure in first source	2.08	1	0	aromatic ether; organobromine compound; organofluorine compound; piperidines; quinazolines; secondary amine	antineoplastic agent; tyrosine kinase inhibitor
ginsenosides ginsenoside : Triterpenoid saponins with a dammarane-like skeleton originally isolated from ginseng (Panax) species. Use of the term has been extended to include semi-synthetic derivatives.	2.17	1	0
compound 968 compound 968: a glutaminase inhibitor. 5-[3-bromo-4-(dimethylamino)phenyl]-2,2-dimethyl-2,3,5,6-tetrahydrobenzo[a]phenanthridin-4(1H)-one : A partially hydrogenated benzophenanthridine carrying an oxo group at C-4, geminal methyl groups at C-2 and a 3-bromo-4-(dimethylamino)phenyl group at C-5.	2.08	1	0	benzophenanthridine	EC 3.5.1.2 (glutaminase) inhibitor
yya-021 YYA-021: an HIV entry inhibitor; structure in first source	2.6	1	0
ovalbumin Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.	2.55	2	0
sb-224289 SB 224289 : A member of the class of benzamides obtained by formal condensation of the carboxy group of 2'-methyl-4'-(5-methyl-1,2,4-oxadiazol-3-yl)biphenyl-4-carboxylic acid with the secondary amino group of 1'-methyl-6,7-dihydro-5H-spiro[furo[2,3-f]indole-3,4'-piperidine]. Selective 5-HT1B receptor antagonist (pKi = 8.2). Displays >60-fold selectivity over 5-HT1D, 5-HT1A, 5-HT1E, 5-HT1F, 5-HT2A and 5-HT2C receptors in radioligand binding and functional assays. Centrally active following oral administration in vivo.	2.08	1	0	1,2,4-oxadiazole; azaspiro compound; benzamides; organic heterotetracyclic compound	serotonergic antagonist
gw 7647 GW 7647: a PPAR-alpha agonist; structure in first source. GW 7647 : A monocarboxylic acid that is 2-(phenylsulfanyl)isobutyric acid in which the phenyl group is substituted at the para- position by a 3-aza-7-cyclohexylhept-1-yl group in which the nitrogen is acylated by a (cyclohexylamino)carbonyl group.	2.08	1	0	aryl sulfide; monocarboxylic acid; ureas	PPARalpha agonist
l 663536 MK-886: orally active leukotriene biosynthesis inhibitor. 3-[3-(tert-butylsulfanyl)-1-(4-chlorobenzyl)-5-(propan-2-yl)-1H-indol-2-yl]-2,2-dimethylpropanoic acid : A member of the class of indoles that is 1H-indole substituted by a isopropyl group at position 5, a tert-butylsulfanediyl group at position 3, a 4-chlorobenzyl group at position 1 and a 2-carboxy-2-methylpropyl group at position 2. It acts as an inhibitor of arachidonate 5-lipoxygenase.	2.08	1	0	aryl sulfide; indoles; monocarboxylic acid; monochlorobenzenes	antineoplastic agent; EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor; leukotriene antagonist
1-[6-(4-chlorophenyl)-5-imidazo[2,1-b]thiazolyl]-N-[(3,4-dichlorophenyl)methoxy]methanimine [no description available]	2.08	1	0	imidazoles
N4-ethyl-N6,1,2-trimethyl-N4-phenylpyrimidin-1-ium-4,6-diamine [no description available]	2.08	1	0	aromatic amine; tertiary amino compound
2-[[2-[2-(2,3-dihydro-1,4-benzodioxin-6-ylamino)-2-oxoethyl]-1-oxo-5-isoquinolinyl]oxy]propanoic acid ethyl ester [no description available]	2.08	1	0	isoquinolines
sb 415286 3-(3-chloro-4-hydroxyphenylamino)-4-(4-nitrophenyl)-1H-pyrrole-2,5-dione: a glycogen synthase kinase-3 inhibitor; structure in first source	2.6	1	0	C-nitro compound; maleimides; monochlorobenzenes; phenols; secondary amino compound; substituted aniline	antioxidant; apoptosis inducer; EC 2.7.11.26 (tau-protein kinase) inhibitor; neuroprotective agent
sch 79797 [no description available]	2.08	1	0	quinazolines
sitagliptin sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.	2.6	1	0	triazolopyrazine; trifluorobenzene	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; environmental contaminant; hypoglycemic agent; serine proteinase inhibitor; xenobiotic
4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide: a TGF-beta type I receptor kinase activity inhibitor	2.08	1	0	benzamides; benzodioxoles; imidazoles; pyridines	EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
1-(4-Fluorophenyl)-3-(3-(4-fluorophenyl)-3-hydroxypropyl)-4-(4-hydroxyphenyl)azetidin-2-one [no description available]	2.08	1	0	monobactam
imd 0354 N-(3,5-bis(trifluoromethyl)phenyl)-5-chloro-2-hydroxybenzamide: a cardioprotective agent that inhibits IkappaB kinase beta (IKKbeta); structure in first source	2.08	1	0	benzamides
ex 527 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide: structure in first source. 6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide : A member of the class of carbazoles that is 2,3,4,9-tetrahydro-1H-carbazole which is substituted at position 1 by an aminocarbohyl group and at position 6 by a chlorine.	2.08	1	0	carbazoles; monocarboxylic acid amide; organochlorine compound
tak-220 TAK-220: structure in first source	2.6	1	0
jtk-303 [no description available]	2.6	1	0	aromatic ether; monochlorobenzenes; organofluorine compound; quinolinemonocarboxylic acid; quinolone	HIV-1 integrase inhibitor
ku 55933 2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one: specific inhibitor of the ataxia-telangiectasia mutated kinase ATM; structure in first source	2.83	3	0
nbd 557 [no description available]	2.6	1	0
quercetin [no description available]	2.58	2	0	7-hydroxyflavonol; pentahydroxyflavone	antibacterial agent; antineoplastic agent; antioxidant; Aurora kinase inhibitor; chelator; EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor; geroprotector; phytoestrogen; plant metabolite; protein kinase inhibitor; radical scavenger
luteolin [no description available]	2.17	1	0	3'-hydroxyflavonoid; tetrahydroxyflavone	angiogenesis inhibitor; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; c-Jun N-terminal kinase inhibitor; EC 2.3.1.85 (fatty acid synthase) inhibitor; immunomodulator; nephroprotective agent; plant metabolite; radical scavenger; vascular endothelial growth factor receptor antagonist
5'-o-caffeoylquinic acid trans-5-O-caffeoyl-D-quinic acid : A cinnamate ester obtained by formal condensation of the carboxy group of trans-caffeic acid with the 5-hydroxy group of quinic acid.	2.6	1	0	cinnamate ester; cyclitol carboxylic acid	plant metabolite
luteolin-7-glucoside luteolin-7-glucoside: has both antiasthmatic and antineoplastic activities; has 3C protease inhibitory activity; isolated from Ligustrum lucidum. luteolin 7-O-beta-D-glucoside : A glycosyloxyflavone that is luteolin substituted by a beta-D-glucopyranosyl moiety at position 7 via a glycosidic linkage.	2.6	1	0	beta-D-glucoside; glycosyloxyflavone; monosaccharide derivative; trihydroxyflavone	antioxidant; plant metabolite
cyclosporine [no description available]	2.6	1	0
harmine Harmine: Alkaloid isolated from seeds of PEGANUM HARMALA; ZYGOPHYLLACEAE. It is identical to banisterine, or telepathine, from Banisteria caapi and is one of the active ingredients of hallucinogenic drinks made in the western Amazon region from related plants. It has no therapeutic use, but (as banisterine) was hailed as a cure for postencephalitic PARKINSON DISEASE in the 1920's.. harmine : A harmala alkaloid in which the harman skeleton is methoxy-substituted at C-7.	2.6	1	0	harmala alkaloid	anti-HIV agent; EC 1.4.3.4 (monoamine oxidase) inhibitor; metabolite
genistein [no description available]	2.08	1	0	7-hydroxyisoflavones	antineoplastic agent; EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor; geroprotector; human urinary metabolite; phytoestrogen; plant metabolite; tyrosine kinase inhibitor
pulmicort Budesonide: A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.. budesonide : A glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis.	2.11	1	0	11beta-hydroxy steroid; 20-oxo steroid; 21-hydroxy steroid; 3-oxo-Delta(1),Delta(4)-steroid; cyclic acetal; glucocorticoid; primary alpha-hydroxy ketone	anti-inflammatory drug; bronchodilator agent; drug allergen
eprosartan eprosartan: angiotensin II receptor antagonist. eprosartan : A member of the class of imidazoles and thiophenes that is an angiotensin II receptor antagonist used for the treatment of high blood pressure.	2.6	1	0	dicarboxylic acid; imidazoles; thiophenes	angiotensin receptor antagonist; antihypertensive agent; environmental contaminant; xenobiotic
mycophenolate mofetil mycophenolate mofetil : A carboxylic ester resulting from the formal condensation between the carboxylic acid group of mycophenolic acid and the hydroxy group of 2-(morpholin-4-yl)ethanol. In the liver, it is metabolised to mycophenolic acid, an immunosuppressant for which it is a prodrug. It is widely used to prevent tissue rejection following organ transplants as well as for the treatment of certain autoimmune diseases.	2.6	1	0	carboxylic ester; ether; gamma-lactone; phenols; tertiary amino compound	anticoronaviral agent; EC 1.1.1.205 (IMP dehydrogenase) inhibitor; immunosuppressive agent; prodrug
entacapone entacapone: structure given in first source. entacapone : A monocarboxylic acid amide that is N,N-diethylprop-2-enamide in which the hydrogen at position 2 is substituted by a cyano group and the hydrogen at the 3E position is substituted by a 3,4-dihydroxy-5-nitrophenyl group.	2.6	1	0	2-nitrophenols; catechols; monocarboxylic acid amide; nitrile	antidyskinesia agent; antiparkinson drug; central nervous system drug; EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
amentoflavone [no description available]	2.69	2	0	biflavonoid; hydroxyflavone; ring assembly	angiogenesis inhibitor; antiviral agent; cathepsin B inhibitor; P450 inhibitor; plant metabolite
baicalein [no description available]	2.6	1	0	trihydroxyflavone	angiogenesis inhibitor; anti-inflammatory agent; antibacterial agent; anticoronaviral agent; antifungal agent; antineoplastic agent; antioxidant; apoptosis inducer; EC 1.13.11.31 (arachidonate 12-lipoxygenase) inhibitor; EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor; EC 3.4.21.26 (prolyl oligopeptidase) inhibitor; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; EC 4.1.1.17 (ornithine decarboxylase) inhibitor; ferroptosis inhibitor; geroprotector; hormone antagonist; plant metabolite; prostaglandin antagonist; radical scavenger
genkwanin genkwanin: structure. genkwanin : A monomethoxyflavone that is apigenin in which the hydroxy group at position 7 is methylated.	2.6	1	0	dihydroxyflavone; monomethoxyflavone	metabolite
hyperoside quercetin 3-O-beta-D-galactopyranoside : A quercetin O-glycoside that is quercetin with a beta-D-galactosyl residue attached at position 3. Isolated from Artemisia capillaris, it exhibits hepatoprotective activity.	2.6	1	0	beta-D-galactoside; monosaccharide derivative; quercetin O-glycoside; tetrahydroxyflavone	hepatoprotective agent; plant metabolite
mangostin mangostin: xanthone from rind of Garcinia mangostana Linn. fruit. alpha-mangostin : A member of the class of xanthones that is 9H-xanthene substituted by hydroxy group at positions 1, 3 and 6, a methoxy group at position 7, an oxo group at position 9 and prenyl groups at positions 2 and 8. Isolated from the stems of Cratoxylum cochinchinense, it exhibits antioxidant, antimicrobial and antitumour activities.	2.6	1	0	aromatic ether; phenols; xanthones	antimicrobial agent; antineoplastic agent; antioxidant; plant metabolite
3-methylquercetin isorhamnetin : A monomethoxyflavone that is quercetin in which the hydroxy group at position 3' is replaced by a methoxy group.	2.6	1	0	7-hydroxyflavonol; monomethoxyflavone; tetrahydroxyflavone	anticoagulant; EC 1.14.18.1 (tyrosinase) inhibitor; metabolite
kaempferide kaempferide: structure in first source. kaempferide : A monomethoxyflavone that is the 4'-O-methyl derivative of kaempferol.	2.6	1	0	7-hydroxyflavonol; monomethoxyflavone; trihydroxyflavone	antihypertensive agent; metabolite
orientin orientin: structure given in first source; RN given refers to the (D-glucopyranosyl)-isomer. orientin : A C-glycosyl compound that is luteolin substituted by a beta-D-glucopyranosyl moiety at position 8.	2.6	1	0	3'-hydroxyflavonoid; C-glycosyl compound; tetrahydroxyflavone	antioxidant; metabolite
scutellarein scutellarein: aglycone of scutellarin from Scutellaria baicalensis; carthamidin is 2S isomer of scutellarein; do not confuse with isoscutellarein and/or isocarthamidin which are respective regioisomers, or with the scutelarin protein. scutellarein : Flavone substituted with hydroxy groups at C-4', -5, -6 and -7.	2.6	1	0	tetrahydroxyflavone	metabolite
trans-2,3',4,5'-tetrahydroxystilbene trans-2,3',4,5'-tetrahydroxystilbene: hydroxystilbene oxyresveratrol	2.6	1	0	stilbenoid
polydatin trans-piceid : A stilbenoid that is trans-resveratrol substituted at position 3 by a beta-D-glucosyl residue.	2.6	1	0	beta-D-glucoside; monosaccharide derivative; polyphenol; stilbenoid	anti-arrhythmia drug; antioxidant; geroprotector; hepatoprotective agent; metabolite; nephroprotective agent; potassium channel modulator
chicoric acid chicoric acid: inhibits HIV-1 integrase	2.6	1	0	organooxygen compound	geroprotector; HIV-1 integrase inhibitor
acteoside acteoside: a protein kinase C inhibitor with hepatoprotective, anti-asthmatic, and analgesic activities; a phenylethanoid glycoside related to isoacteoside; from leaves of Lippia multiflora (Verbenaceae). acteoside : A glycoside that is the alpha-L-rhamnosyl-(1->3)-beta-D-glucoside of hydroxytyrosol in which the hydroxy group at position 4 of the glucopyranosyl moiety has undergone esterification by formal condensation with trans-caffeic acid.	2.6	1	0	catechols; cinnamate ester; disaccharide derivative; glycoside; polyphenol	anti-inflammatory agent; antibacterial agent; antileishmanial agent; neuroprotective agent; plant metabolite
dorzolamide dorzolamide: topically effective ocular hypotensive carbonic anhydrase inhibitor; RN refers to mono-HCl (4S-trans)-isomer. dorzolamide : 5,6-Dihydro-4H-thieno[2,3-b]thiopyran-2-sulfonamide 7,7-dioxide in which hydrogens at the 4 and 6 positions are substituted by ethylamino and methyl groups, respectively (4S, trans-configuration). A carbonic anhydrase inhibitor, it is used as the hydrochloride in ophthalmic solutions to lower increased intraocular pressure in the treatment of open-angle glaucoma and ocular hypertension.	2.6	1	0	sulfonamide; thiophenes	antiglaucoma drug; antihypertensive agent; EC 4.2.1.1 (carbonic anhydrase) inhibitor
sirolimus Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.. sirolimus : A macrolide lactam isolated from Streptomyces hygroscopicus consisting of a 29-membered ring containing 4 trans double bonds, three of which are conjugated. It is an antibiotic, immunosupressive and antineoplastic agent.	4.14	4	0	antibiotic antifungal drug; cyclic acetal; cyclic ketone; ether; macrolide lactam; organic heterotricyclic compound; secondary alcohol	antibacterial drug; anticoronaviral agent; antineoplastic agent; bacterial metabolite; geroprotector; immunosuppressive agent; mTOR inhibitor
topiramate Topiramate: A sulfamate-substituted fructose analog that was originally identified as a hypoglycemic agent. It is used for the treatment of EPILEPSY and MIGRAINE DISORDERS, and may also promote weight loss.. topiramate : A hexose derivative that is 2,3:4,5-di-O-isopropylidene-beta-D-fructopyranose in which the hydroxy group has been converted to the corresponding sulfamate ester. It blocks voltage-dependent sodium channels and is used as an antiepileptic and for the prevention of migraine.	2.6	1	0	cyclic ketal; ketohexose derivative; sulfamate ester	anticonvulsant; sodium channel blocker
fenretinide Fenretinide: A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent.. 4-hydroxyphenyl retinamide : A retinoid obtained by formal condensation of the carboxy group of all-trans retinoic acid and the anilino group of 4-hydroxyaniline. Synthetic retinoid agonist. Antiproliferative, antioxidant and anticancer agent with a long half-life in vivo. Apoptotic effects appear to be mediated by a mechanism distinct from that of 'classical' retinoids.	2.08	1	0	monocarboxylic acid amide; retinoid	antineoplastic agent; antioxidant
17-(dimethylaminoethylamino)-17-demethoxygeldanamycin 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin: structure in first source. alvespimycin : A 19-membered macrocyle that is geldanamycin in which the methoxy group attached to the benzoquinone moiety has been replaced by a 2-(N,N-dimethylamino)ethylamino group.	2.47	2	0	1,4-benzoquinones; ansamycin; carbamate ester; secondary amino compound; tertiary amino compound	Hsp90 inhibitor
ter 199 [no description available]	2.08	1	0
arachidonylcyclopropylamide arachidonylcyclopropylamide: a potent and selective agonist of neuronal cannabinoid receptor; structure in first source	2.08	1	0
4-amino-5-chloro-N-[(3R,4S)-1-[3-(4-fluorophenoxy)propyl]-3-methoxy-4-piperidinyl]-2-methoxybenzamide [no description available]	2.31	1	0	benzamides
fr 173657 FR 173657: structure given in first source	2.31	1	0
fr 190997 FR 190997: structure given in first source	2.31	1	0
benzyloxycarbonyl-phe-ala-fluormethylketone cathepsin B inhibitor : A cysteine protease inhibitor which inhibits cathepsin B (EC 3.4.22.1).	2.6	1	0
ly 320135 LY 320135: cannabinoid receptor antagonist; structure in first source	2.08	1	0	benzofurans
n-(n-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester DAPT : A dipeptide consisting of alanylphenylglycine derivatised as a 3,5-difluorophenylacetamide at the amino terminal and a tert-butyl ester at the carboxy terminal. A gamma-secretase inhibitor.	2.6	1	0	carboxylic ester; difluorobenzene; dipeptide; tert-butyl ester	EC 3.4.23.46 (memapsin 2) inhibitor
pd 166285 [no description available]	2.08	1	0
kn 62 KN 62: inhibitor of Ca/calmodulin-dependent protein kinase II	2.08	1	0	piperazines
su 6656 SU 6656: a c-Src kinase inhibitor; used to probe growth signaling; structure in first source. SU6656 : A member of the class of oxindoles that is 3-methyleneoxindole in which the hydrogeh at position 5 has been replaced by a dimethylaminosulfonyl group and in which one of the hydrogens of the methylene group has been replaced by a 4,5,6,7-tetrahydro-indol-2-yl group. It is a specific inhibitor of Src family kinase.	2.08	1	0
casticin casticin: from fruit of Vitex rotundifolia; structure in second source. casticin : A tetramethoxyflavone that consists of quercetagetin in which the hydroxy groups at positions 3, 6, 7 and 4' have been replaced by methoxy groups. It has been isolated from Eremophila mitchellii.	2.6	1	0	dihydroxyflavone; tetramethoxyflavone	apoptosis inducer; plant metabolite
andrographolide [no description available]	2.31	1	0	carbobicyclic compound; gamma-lactone; labdane diterpenoid; primary alcohol; secondary alcohol	anti-HIV agent; anti-inflammatory drug; antineoplastic agent; metabolite
5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one 5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one: isolated from the Chinese herb Scutellariae radix. oroxylin A : A dihydroxy- and monomethoxy-flavone in which the hydroxy groups are positioned at C-5 and C-7 and the methoxy group is at C-6.	2.6	1	0	dihydroxyflavone; monomethoxyflavone	antineoplastic agent; EC 1.14.13.39 (nitric oxide synthase) inhibitor
(E)-2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucopyranoside: Tyrosinase inhibitor from Polygonum multiflorum; structure in first source. (E)-2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside : A stilbenoid that is trans-stilbene which has been substituted by hydroxy groups at positions 2, 3, 5, and 4', and in which the hydroxy group at positon 2 has then been converted to the corresponding the beta-D-glucoside.	2.6	1	0	beta-D-glucoside; resorcinols; stilbenoid	anti-inflammatory agent; antioxidant; apoptosis inhibitor; cardioprotective agent; cyclooxygenase 2 inhibitor; platelet aggregation inhibitor
tyrphostin ag 555 [no description available]	2.6	1	0
semaxinib semaxanib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is replaced by a 3,5-dimethylpyrrol-2-yl group.	2.08	1	0	olefinic compound; oxindoles; pyrroles	angiogenesis modulating agent; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; vascular endothelial growth factor receptor antagonist
su 11248 [no description available]	2.08	1	0	monocarboxylic acid amide; pyrroles	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; immunomodulator; neuroprotective agent; vascular endothelial growth factor receptor antagonist
palbociclib [no description available]	7.86	3	0	aminopyridine; aromatic ketone; cyclopentanes; piperidines; pyridopyrimidine; secondary amino compound; tertiary amino compound	antineoplastic agent; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
jnj-7706621 [no description available]	2.08	1	0	sulfonamide
bay 11-7082 (E)-3-tosylacrylonitrile : A nitrile that is acrylonitrile in which the hydrogen located beta,trans to the cyano group is replaced by a tosyl group. It is an inhibitor of cytokine-induced IkappaB-alpha phosphorylation in cells.	2.25	1	0	nitrile; sulfone	apoptosis inducer; EC 2.7.11.10 (IkappaB kinase) inhibitor; EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor; non-steroidal anti-inflammatory drug; platelet aggregation inhibitor
pd 151746 [no description available]	2.6	1	0
lisinopril Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.	2.6	1	0	dipeptide	EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
verteporfin (2R,2(1)S)-8-ethenyl-2(1),2(2)-bis(methoxycarbonyl)-17-(3-methoxy-3-oxopropyl)-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13-propanoic acid : The 2(1),2(2),17-trimethyl ester of (2R,2(1)S)-2(1),2(2)-dicarboxy-8-ethenyl-2,7,12,18-tetramethyl-2,2(1)-dihydrobenzo[b]porphyrin-13,17-dipropanoic acid.	2.6	1	0
batimastat batimastat: structure given in first source; a synthetic matrix metalloproteinase inhibitor. batimastat : A secondary carboxamide resulting from the formal condensation of the carboxy group of (2S,3R)-5-methyl-3-{[(2S)-1-(methylamino)-1-oxo-3-phenylpropan-2-yl]carbamoyl}-2-[(thiophen-2-ylsulfanyl)methyl]hexanoic acid with the amino group of hydroxylamine. It a broad-spectrum matrix metalloprotease inhibitor.	2.6	1	0	hydroxamic acid; L-phenylalanine derivative; organic sulfide; secondary carboxamide; thiophenes; triamide	angiogenesis inhibitor; antineoplastic agent; matrix metalloproteinase inhibitor
indinavir sulfate Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.	2.6	1	0	dicarboxylic acid diamide; N-(2-hydroxyethyl)piperazine; piperazinecarboxamide	HIV protease inhibitor
cisplatin [no description available]	2.08	1	0	diamminedichloroplatinum	antineoplastic agent; apoptosis inducer; cross-linking reagent; ferroptosis inducer; genotoxin; mutagen; nephrotoxin; photosensitizing agent
silicon Silicon: A trace element that constitutes about 27.6% of the earth's crust in the form of SILICON DIOXIDE. It does not occur free in nature. Silicon has the atomic symbol Si, atomic number 14, and atomic weight [28.084; 28.086].	2.1	1	0	carbon group element atom; metalloid atom; nonmetal atom
solanesol solanesol : A nonaprenol that is hexatriaconta-2,6,10,14,18,22,26,30,34-nonaen-1-ol substituted by 9 methyl groups at positions 3, 7, 11, 15, 19, 23, 27, 31 and 35 (the all-trans0stereoisomer).	2.6	1	0	nonaprenol; primary alcohol	plant metabolite
pepstatin pepstatin: inhibits the aspartic protease endothiapepsin	2.6	1	0	pentapeptide; secondary carboxamide	bacterial metabolite; EC 3.4.23.* (aspartic endopeptidase) inhibitor
l 685458 L 685458: a gamma-secretase inhibitor; structure in first source. L-685,458 : A peptide and carboxamide that is L-leucyl-L-phenylalaninamide, L-Leu-L-Phe-NH2, which has been acylated on the N-terminus by a Phe-Phe hydroxyethylene dipeptide isotere, 2R-benzyl-5S-tert-butoxycarbonylamino-4R-hydroxy-6-phenylhexanoic acid. Compounds based on the structure of L-685,458 are potent inhibitors of gamma-secretase, which mediates the final catalytic step that generates the amyloid beta-peptide (Abeta), which assembles into the neurotoxic aggregates in the brains of sufferers of Alzheimer's disease.	2.6	1	0	carbamate ester; monocarboxylic acid amide; peptide; secondary alcohol	EC 3.4.23.46 (memapsin 2) inhibitor; peptidomimetic
talaporfin Talaporfin: effective tumor localizer that brings about the selective degradation of tumor tissue following light exposure; structure given in first source	2.31	1	0
vx680 [no description available]	2.08	1	0	N-arylpiperazine
bms 806 BMS 806: prevents entry of HIV into cells by binding HIV envelope protein gp120; no further info available 4/2002	2.6	1	0
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone [no description available]	2.6	1	0
tulobuterol hydrochloride [no description available]	2.6	1	0	organic molecular entity
carbocyanines Carbocyanines: Compounds that contain three methine groups. They are frequently used as cationic dyes used for differential staining of biological materials.	2.31	1	0	cyanine dye; organic iodide salt	fluorochrome
salubrinal salubrinal: prevents dephosphorylation of eIF2alpha; structure in first source. salubrinal : A member of the class of quinolines that is a mixed aminal resulting from the formal condensation oftrichloroacetaldehyde with the amide nitrogen of trans-cinnamamide and the primary amino group of 1-quinolin-8-ylthiourea. It is a selective inhibitor of cellular complexes that dephosphorylate eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha).	2.6	1	0	aminal; organochlorine compound; quinolines; secondary carboxamide; thioureas
proguanil Proguanil: A biguanide compound which metabolizes in the body to form cycloguanil, an anti-malaria agent.. proguanil : A biguanide compound which has isopropyl and p-chlorophenyl substituents on the terminal N atoms. A prophylactic antimalarial drug, it works by inhibiting the enzyme dihydrofolate reductase, which is involved in the reproduction of the malaria parasites Plasmodium falciparum and P. vivax within the red blood cells.	7.41	1	0	biguanides; monochlorobenzenes	antimalarial; antiprotozoal drug; EC 1.5.1.3 (dihydrofolate reductase) inhibitor
boron oxide boron oxide: RN given refers to B2O3	2.21	1	0	boron oxide
d 4476 [no description available]	2.08	1	0	imidazoles
cyc 116 4-methyl-5-(2-(4-morpholinophenylamino)pyrimidin-4-yl)thiazol-2-amine: an aurora kinase inhibitor; structure in first source	2.08	1	0
bay 19-8004 BAY 19-8004: a PDE4 inhibitor; structure in first source	2.08	1	0
germacrone germacrone: isolated from Curcuma wenyujin	2.6	1	0	germacrane sesquiterpenoid; olefinic compound	androgen antagonist; anti-inflammatory agent; antifeedant; antifungal agent; antimicrobial agent; antineoplastic agent; antioxidant; antitussive; antiviral agent; apoptosis inducer; autophagy inducer; hepatoprotective agent; insecticide; neuroprotective agent; plant metabolite; volatile oil component
(2e,4e,6e,10e)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid (2E,4E,6E,10E)-3,7,11,15-tetramethyl-2,4,6,10,14-hexadecapentaenoic acid: an acyclic retinoid that suppresses hepatocellular carcinoma recurrence; structure in first source	2.6	1	0
lithospermic acid [no description available]	2.6	1	0
everolimus [no description available]	3.98	3	0	cyclic acetal; cyclic ketone; ether; macrolide lactam; primary alcohol; secondary alcohol	anticoronaviral agent; antineoplastic agent; geroprotector; immunosuppressive agent; mTOR inhibitor
laq824 LAQ824: Histone deacetylase inhibitor	2.6	1	0
ekb 569 EKB 569: an EGF receptor kinase inhibitor	2.6	1	0	aminoquinoline; monocarboxylic acid amide; monochlorobenzenes; nitrile	protein kinase inhibitor
axitinib [no description available]	2.08	1	0	aryl sulfide; benzamides; indazoles; pyridines	antineoplastic agent; tyrosine kinase inhibitor; vascular endothelial growth factor receptor antagonist
pai 039 tiplaxtinin: inhibitor of plasminogen activator inhibitor-1	2.08	1	0	indole-3-acetic acids
i(3)so3-galactosylceramide Sulfoglycosphingolipids: GLYCOSPHINGOLIPIDS with a sulfate group esterified to one of the sugar groups.. 1-(3-O-sulfo-beta-D-galactosyl)-N-tetracosanoylsphingosine : A D-galactosyl-N-acylsphingosine having a sulfo group at the 3-position on the galactose ring and tetracosanoyl as the N-acyl group.	2.6	1	0	galactosylceramide sulfate; N-acyl-beta-D-galactosylsphingosine
rilpivirine [no description available]	2.6	1	0	aminopyrimidine; nitrile	EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor; HIV-1 reverse transcriptase inhibitor
(1Ar,7aS,10aS,10bS)-1a,5-dimethyl-8-methylidene-2,3,6,7,7a,8,10a,10b-octahydrooxireno[9,10]cyclodeca[1,2-b]furan-9(1aH)-one [no description available]	2.6	1	0	germacranolide
4,5-di-O-caffeoylquinic acid [no description available]	2.6	1	0	quinic acid
indigo carmine 3,5-di-O-(E)-caffeoylquinic acid: from roots of Lychnophora ericoides; structure in first source. 3,5-di-O-caffeoyl quinic acid : A carboxylic ester that is the diester obtained by the condensation of the hydroxy groups at positions 3 and 5 of (-)-quinic acid with the carboxy group of trans-caffeic acid. Isolated from Brazilian propolis and Suaeda glauca, it exhibits hepatoprotective and cytotoxic activities.	2.6	1	0
tanespimycin CP 127374: analog of herbimycin A	2.1	1	0	1,4-benzoquinones; ansamycin; carbamate ester; organic heterobicyclic compound; secondary amino compound	antineoplastic agent; apoptosis inducer; Hsp90 inhibitor
gw2974 GW2974: quinazoline derivative, which is able to block the activation of both the EGFR and erbB2	2.08	1	0	pyridopyrimidine
ispinesib [no description available]	2.08	1	0	benzamides
3-hydroxy-4-methoxybenzaldehyde thiosemicarbazone 3-hydroxy-4-methoxybenzaldehyde thiosemicarbazone: inhibits cabbage butterfly larvae phenoloxidase; structure in first source	2.21	1	0
fk 866 N-(4-(1-benzoylpiperidin-4-yl)butyl)-3-(pyridin-3-yl)acrylamide: inhibits nicotinamide phosphoribosyltransferase; structure in first source	2.52	2	0	benzamides; N-acylpiperidine
artesunate artesunic acid: RN given for (3R-(3alpha,5abeta,6beta,8abeta,9alpha,10alpha,12beta,(2aR*))-isomer; succinic ester of artemether	2.6	1	0	artemisinin derivative; cyclic acetal; dicarboxylic acid monoester; hemisuccinate; semisynthetic derivative; sesquiterpenoid	antimalarial; antineoplastic agent; ferroptosis inducer
temsirolimus [no description available]	2.08	1	0	macrolide lactam
(3S,6S,9S,12R)-3-[(2S)-Butan-2-yl]-6-[(1-methoxyindol-3-yl)methyl]-9-(6-oxooctyl)-1,4,7,10-tetrazabicyclo[10.4.0]hexadecane-2,5,8,11-tetrone [no description available]	2.6	1	0	oligopeptide
pd 184352 2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide: inhibits MAP kinase kinase; structure in first source	2.08	1	0	aminobenzoic acid
bibx 1382bs BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001	2.08	1	0	substituted aniline
vildagliptin [no description available]	2.6	1	0	amino acid amide
belinostat [no description available]	2.6	1	0	hydroxamic acid; olefinic compound; sulfonamide	antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
panobinostat Panobinostat: An indole and hydroxamic acid derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used as an antineoplastic agent in combination with BORTEZOMIB and DEXAMETHASONE for the treatment of MULTIPLE MYELOMA.. panobinostat : A hydroxamic acid obtained by formal condensation of the carboxy group of (2E)-3-[4-({[2-(2-methylindol-3-yl)ethyl]amino}methyl)phenyl]prop-2-enoic acid with the amino group of hydroxylamine. A histone deacetylase inhibitor used (as its lactate salt) in combination with bortezomib and dexamethasone for the treatment of multiple myeloma.	2.94	3	0	cinnamamides; hydroxamic acid; methylindole; secondary amino compound	angiogenesis modulating agent; antineoplastic agent; EC 3.5.1.98 (histone deacetylase) inhibitor
hdac-42 HDAC-42: structure in first source	2.58	2	0	amidobenzoic acid
taxane taxane: produced by Taxomyces andreanae	5.93	2	1	diterpene; terpenoid fundamental parent
[4-[[4-(1-benzothiophen-2-yl)-2-pyrimidinyl]amino]phenyl]-[4-(1-pyrrolidinyl)-1-piperidinyl]methanone [no description available]	2.08	1	0	benzamides; N-acylpiperidine
chlorhexidine Chlorhexidine: A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.. chlorhexidine : A bisbiguanide compound with a structure consisting of two (p-chlorophenyl)guanide units linked by a hexamethylene bridge.	2.6	1	0	biguanides; monochlorobenzenes	antibacterial agent; antiinfective agent
3-aminopyridine-2-carboxaldehyde thiosemicarbazone 3-aminopyridine-2-carboxaldehyde thiosemicarbazone: a neuroprotective agent; structure given in first source	2.53	2	0
gs-7340 tenofovir alafenamide: component of Biktarvy. tenofovir alafenamide : An L-alanine derivative that is isopropyl L-alaninate in which one of the amino hydrogens is replaced by an (S)-({[(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy}methyl)(phenoxy)phosphoryl group. A prodrug for tenofovir, it is used (as the fumarate salt) in combination therapy for the treatment of HIV-1 infection.	2.6	1	0	6-aminopurines; ether; isopropyl ester; L-alanine derivative; phosphoramidate ester	antiviral drug; HIV-1 reverse transcriptase inhibitor; prodrug
iniparib [no description available]	13.4	22	0	carbonyl compound; organohalogen compound
n-(2-amino-5-fluorobenzyl)-4-(n-(pyridine-3-acrylyl)aminomethyl)benzamide [no description available]	2.6	1	0
pri-2205 [no description available]	2.6	1	0
mk 0752 [no description available]	2.58	2	0
gw 501516 GW 501516: a selective PPARdelta agonist; structure in first source. GW 501516 : An aromatic ether that is phenoxyacetic acid in which the phenyl group is substituted at position 2 by a methyl group and at position 4 by a (1,3-thiazol-5-ylmethyl)sulfanediyl group, and in which the 1,3-thiazolyl group is substituted at positions 2 and 4 by p-trifluoromethylphenyl and methyl groups, respectively.	2.08	1	0	1,3-thiazoles; aromatic ether; aryl sulfide; monocarboxylic acid; organofluorine compound	carcinogenic agent; PPARbeta/delta agonist
givinostat [no description available]	2.6	1	0	carbamate ester
av 412 [no description available]	2.08	1	0
ag-041r AG-041R: structure in first source	2.08	1	0
telatinib [no description available]	2.08	1	0
cp 547632 3-(4-bromo-2,6-difluorobenzyloxy)-5-(3-(4-pyrrolidin-1-ylbutyl)ureido)isothiazole-4-carboxylic acid amide: inhibits vascular endothelial growth factor receptor-2 tyrosine kinase; structure in first source	2.08	1	0
bms345541 4(2'-aminoethyl)amino-1,8-dimethylimidazo(1,2-a)quinoxaline: structure in first source	2.21	1	0	quinoxaline derivative
pd 144418 [no description available]	2.6	1	0
spc-839 SPC-839: an inhibitor of activator protein 1; structure in first source	2.08	1	0
bicyclol bicyclol: an antihepatitis drug, on the metabolism and hepatotoxicity of aflatoxin B1 (AFB1) in rats.	2.6	1	0
abiraterone acetate Abiraterone Acetate: An androstene derivative that inhibits STEROID 17-ALPHA-HYDROXYLASE and is used as an ANTINEOPLASTIC AGENT in the treatment of metastatic castration-resistant PROSTATE CANCER.. abiraterone acetate : A sterol ester obtained by formal condensation of the 3-hydroxy group of abiraterone with the carboxy group of acetic acid. A prodrug that is converted in vivo into abiraterone. Used for treatment of metastatic castrate-resistant prostate cancer.	8.01	2	0	pyridines; sterol ester	antineoplastic agent; EC 1.14.99.9 (steroid 17alpha-monooxygenase) inhibitor; prodrug
lenvatinib lenvatinib : A member of the class of quinolines that is the carboxamide of 4-{3-chloro-4-[(cyclopropylcarbamoyl)amino]phenoxy}-7-methoxyquinoline-6-carboxylic acid. A multi-kinase inhibitor and orphan drug used (as its mesylate salt) for the treatment of various types of thyroid cancer that do not respond to radioiodine.	3.61	2	0	aromatic amide; aromatic ether; cyclopropanes; monocarboxylic acid amide; monochlorobenzenes; phenylureas; quinolines	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist; orphan drug; vascular endothelial growth factor receptor antagonist
andarine [no description available]	2.08	1	0	acetamides; anilide
gw843682x [no description available]	2.08	1	0	(trifluoromethyl)benzenes
pd 0325901 mirdametinib: has antineoplastic activity; appears to be a MEK inhibitor. PD 0325901 : A hydroxamic acid ester that is benzhydroxamic acid (N-hydroxybenzamide) in which the hydroxamic acid group has been converted to the corresponding 2,3-dihydroxypropyl ester and in which the benzene ring has been substituted at position 2 by a (2-fluoro-4-iodophenyl)amino group and at positions 3 and 4 by fluorines (the R enantiomer).	2.08	1	0	difluorobenzene; hydroxamic acid ester; monofluorobenzenes; organoiodine compound; propane-1,2-diols; secondary amino compound	antineoplastic agent; EC 2.7.12.2 (mitogen-activated protein kinase kinase) inhibitor
midostaurin midostaurin : An organic heterooctacyclic compound that is the N-benzoyl derivative of staurosporine.	2.58	2	0	benzamides; gamma-lactam; indolocarbazole; organic heterooctacyclic compound	antineoplastic agent; EC 2.7.11.13 (protein kinase C) inhibitor
ag 14361 [no description available]	2.08	1	0	benzimidazoles
sb 265610 [no description available]	2.08	1	0
ly 450139 [no description available]	2.6	1	0	peptide
fr 148083 5Z-7-oxozeaenol : A macrolide that is the 7-oxo derivative of zeaenol (the 5Z stereoisomer). Isolated from Fungi, it exhibits cytotoxic, antibacterial and inhibitory activity against NF-kappaB.	2.08	1	0	aromatic ether; macrolide; phenols; secondary alcohol; secondary alpha-hydroxy ketone	antibacterial agent; antineoplastic agent; metabolite; NF-kappaB inhibitor
mocetinostat mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).	2.87	3	0	aminopyrimidine; benzamides; pyridines; secondary amino compound; secondary carboxamide; substituted aniline	antineoplastic agent; apoptosis inducer; autophagy inducer; cardioprotective agent; EC 3.5.1.98 (histone deacetylase) inhibitor; hepatotoxic agent
osi 930 OSI 930: inhibits both receptor tyrosine kinase Kit and kinase insert domain receptor; structure in first source	2.08	1	0	aromatic amide
ki 20227 [no description available]	2.08	1	0
scio-469 SCIO-469: a small-molecule p38 mitogen-activated protein (MAP) kinase inhibitor for potential oral therapy for inflammatory disorders; in phase lib clinical trials for rheumatoid arthritis 4/2004. talmapimod : An indolecarboxamide obtained by formal condensation of the carboxy group of 6-chloro-3-[(dimethylamino)(oxo)acetyl]-1-methylindole-5-carboxylic acid with the secondary amino group of (2S,5R)-1-[(4-fluorophenyl)methyl]-2,5-dimethylpiperazine. It is a potent inhibitor of MAPK and exhibits anti-cancer properties.	2.08	1	0	aromatic amide; aromatic ketone; chloroindole; dicarboxylic acid diamide; indolecarboxamide; monofluorobenzenes; N-acylpiperazine; N-alkylpiperazine	antineoplastic agent; apoptosis inducer; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
ssr 69071 SSR 69071: structure in first source	2.08	1	0	pyridopyrimidine
rivaroxaban Rivaroxaban: A morpholine and thiophene derivative that functions as a FACTOR XA INHIBITOR and is used in the treatment and prevention of DEEP-VEIN THROMBOSIS and PULMONARY EMBOLISM. It is also used for the prevention of STROKE and systemic embolization in patients with non-valvular ATRIAL FIBRILLATION, and for the prevention of atherothrombotic events in patients after an ACUTE CORONARY SYNDROME.. rivaroxaban : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-chlorothiophene-2-carboxylic acid with the amino group of 4-{4-[(5S)-5-(aminomethyl)-2-oxo-1,3-oxazolidin-3-yl]phenyl}morpholin-3-one. An anticoagulant used for prophylaxis of venous thromboembolism in patients with knee or hip replacement surgery.	2.6	1	0	aromatic amide; lactam; monocarboxylic acid amide; morpholines; organochlorine compound; oxazolidinone; thiophenes	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor
sb 3ct compound SB 3CT compound: a matrix metalloproteinase-2 inhibitor; structure in first source	2.6	1	0	aromatic ether
pi103 PI103: pyridofuropyrimidine antineoplastic; a potent inhibitor of class I phosphatidylinositide 3-kinases (PI3K); structure in first soruce	7.5	2	0	aromatic amine; morpholines; organic heterotricyclic compound; phenols; tertiary amino compound	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
sb 210313 [no description available]	2.08	1	0
gw 4064 [no description available]	2.08	1	0	stilbenoid
ginsenoside rb1 [no description available]	2.6	1	0	ginsenoside; glycoside; tetracyclic triterpenoid	anti-inflammatory drug; anti-obesity agent; apoptosis inhibitor; neuroprotective agent; plant metabolite; radical scavenger
sa 4503 [no description available]	2.08	1	0
ic 87114 IC 87114: structure in first source	2.08	1	0	6-aminopurines; biaryl; quinazolines	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
zibotentan ZD4054: a potent endothelin receptor A antagonist that inhibits ovarian carcinoma cell proliferation	2.08	1	0	phenylpyridine
tivozanib N-(2-chloro-4-((6,7-dimethoxy-4-quinolyl)oxy)phenyl)-N'-(5-methyl-3-isoxazolyl)urea: KNR-951 is the HCl, monohydrate salt; an antineoplastic agent; structure in first source	2.08	1	0	aromatic ether
hki 272 [no description available]	2.91	3	0	nitrile; quinolines	antineoplastic agent; tyrosine kinase inhibitor
tofacitinib tofacitinib : A pyrrolopyrimidine that is pyrrolo[2,3-d]pyrimidine substituted at position 4 by an N-methyl,N-(1-cyanoacetyl-4-methylpiperidin-3-yl)amino moiety. Used as its citrate salt to treat moderately to severely active rheumatoid arthritis.	2.08	1	0	N-acylpiperidine; nitrile; pyrrolopyrimidine; tertiary amino compound	antirheumatic drug; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
bibr 1532 [no description available]	2.08	1	0
n-(6-chloro-7-methoxy-9h-beta-carbolin-8-yl)-2-methylnicotinamide [no description available]	2.08	1	0
rucaparib AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source	11.4	66	0	azepinoindole; caprolactams; organofluorine compound; secondary amino compound	antineoplastic agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
cediranib [no description available]	13.53	27	15	aromatic ether
gw0742 GW 610742: structure in first source	2.08	1	0	monocarboxylic acid
6h-thieno[3,2-f][1,2,4]triazolo[4,3-a][1,4]diazepine-6-acetamide, 4-(4-chlorophenyl)-n-(4-hydroxyphenyl)-2,3,9-trimethyl-, (6s)- [no description available]	2.66	2	0	organonitrogen heterocyclic compound; organosulfur heterocyclic compound
3,4-dihydro-5-(4-(1-piperidinyl)butoxy)-1(2h)-isoquinolinone [no description available]	2.1	1	0
ps1145 PS1145: IkappaB kinase inhibitor; structure in first source	2.08	1	0	beta-carbolines
cetilistat cetilistat: lipase inhibitor in randomized, placebo-controlled study of weight reduction in obese patients (3/2007)	2.6	1	0	benzoxazine
bay 41-8543 BAY 41-8543: structure in first source	2.08	1	0	pyrazolopyridine
chir 99021 Chir 99021: structure in first source. CHIR 99021 : A member of the class of aminopyrimidines that is 2-aminopyrimidine substituted at positions N2, 5 and 6 by (5-cyanopyridin-2-yl)ethyl, 4-methylimidazol-2-yl and 2,4-dichlorophenyl groups respectively.	2.08	1	0	aminopyridine; aminopyrimidine; cyanopyridine; diamine; dichlorobenzene; imidazoles; secondary amino compound	EC 2.7.11.26 (tau-protein kinase) inhibitor
ym 201636 6-amino-N-(3-(4-(4-morpholinyl)pyrido(3',2'-4,5)furo(3,2-d)pyrimidin-2-yl)phenyl)-3-pyridinecarboxamide: an antiviral agent; structure in first source	2.6	1	0	aromatic amide
sb 525334 6-(2-tert-butyl-5-(6-methylpyridin-2-yl)-1H-imidazol-4-yl)quinoxaline: a TGF-betaR kinase inhibitor	2.08	1	0	quinoxaline derivative
way-362450 [no description available]	2.08	1	0	indoles
masitinib [no description available]	2.08	1	0	1,3-thiazoles; benzamides; N-alkylpiperazine; pyridines	antineoplastic agent; antirheumatic drug; tyrosine kinase inhibitor
bx795 BX795: structure in first source	2.08	1	0	ureas
linagliptin Linagliptin: A purine and quinazoline derivative that functions as an INCRETIN and DIPEPTIDYL-PEPTIDASE IV INHIBTOR. It is used as a HYPOGLYCEMIC AGENT in the treatment of TYPE II DIABETES MELLITUS.. linagliptin : A xanthine that is 7H-xanthine bearing (4-methylquinazolin-2-yl)methyl, methyl, but-2-yn-1-yl and 3-aminopiperidin-1-yl substituents at positions 1, 3, 7 and 8 respectively (the R-enantiomer). Used for treatment of type II diabetes.	2.6	1	0	aminopiperidine; quinazolines	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
pazopanib pazopanib: a protein kinase inhibitor. pazopanib : A pyrimidine that is 5-(pyrimidin-2-yl}amino-2-methylbenzenesulfonamide substituted at position 4 by a (2,3-dimethylindazol-6-yl)(methyl)amino group. Used as its hydrochloride salt for treatment of kidney cancer.	8.91	3	0	aminopyrimidine; indazoles; sulfonamide	angiogenesis modulating agent; antineoplastic agent; tyrosine kinase inhibitor; vascular endothelial growth factor receptor antagonist
sepantronium sepantronium: a survivin suppressant with antineoplastic activity. sepantronium : An organic cation that is 1-(2-methoxyethyl)-2-methyl-1H-naphtho[2,3-d]imidazole-4,9-dione in which the nitrogen at position 3 of the napthoimidazole moiety has been alkylated by a pyrazin-2-ylmethyl group.	2.08	1	0	organic cation
azd 6244 AZD 6244: a MEK inhibitor	2.58	2	0	benzimidazoles; bromobenzenes; hydroxamic acid ester; monochlorobenzenes; organofluorine compound; secondary amino compound	anticoronaviral agent; antineoplastic agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
odanacatib odanacatib: a selective inhibitor of cathepsin K for the treatment of post-menopausal osteoporosis; structure in first source	2.6	1	0
1-(2-(1-adamantyl)ethyl)-1-pentyl-3-(3-(4-pyridyl)propyl)urea 1-(2-(1-adamantyl)ethyl)-1-pentyl-3-(3-(4-pyridyl)propyl)urea: structure in first source	2.08	1	0
apilimod [no description available]	2.6	1	0
apixaban [no description available]	2.6	1	0	aromatic ether; lactam; piperidones; pyrazolopyridine	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor
bibw 2992 [no description available]	2.55	2	0	aromatic ether; enamide; furans; monochlorobenzenes; organofluorine compound; quinazolines; secondary carboxamide; tertiary amino compound	antineoplastic agent; tyrosine kinase inhibitor
N-(3-cyanophenyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide N-(3-cyanophenyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide : A member of the class of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)[1,1'-biphenyl]-4-carboxylic acid with the amino group of 3-cyanoaniline.	2.08	1	0	1,3,4-oxadiazoles; benzamides; biphenyls; nitrile	EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
ar c155858 AR C155858: an MCT1 inhibitor; structure in first source	2.08	1	0
betrixaban betrixaban: a highly potent, selective, and orally efficacious factor Xa inhibitor; structure in first source. betrixaban : A secondary carboxamide obtained by formal condensation of the carboxy group of 4-(N,N-dimethylcarbamimidoyl)benzoic acid with the amino group of 2-amino-N-(5-chloropyridin-2-yl)-5-methoxybenzamide. A synthetic anticoagulant compound that targets activated factor Xa in the coagulation cascade.	2.6	1	0	benzamides; guanidines; monochloropyridine; monomethoxybenzene; secondary carboxamide	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor
edoxaban edoxaban : A monocarboxylic acid amide that is used (as its tosylate monohydrate) for the treatment of deep vein thrombosis and pulmonary embolism.	2.6	1	0	chloropyridine; monocarboxylic acid amide; tertiary amino compound; thiazolopyridine	anticoagulant; EC 3.4.21.6 (coagulation factor Xa) inhibitor; platelet aggregation inhibitor
aee 788 AEE 788: structure in first source	2.08	1	0	6-{4-[(4-ethylpiperazin-1-yl)methyl]phenyl}-N-(1-phenylethyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amine	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; epidermal growth factor receptor antagonist; trypanocidal drug
saracatinib [no description available]	2.58	2	0	aromatic ether; benzodioxoles; diether; N-methylpiperazine; organochlorine compound; oxanes; quinazolines; secondary amino compound	anticoronaviral agent; antineoplastic agent; apoptosis inducer; autophagy inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; radiosensitizing agent
sd-208 [no description available]	2.08	1	0
n-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide boceprevir : A synthetic tripeptide consisting of N-(tert-butylcarbamoyl)-3-methyl-L-valyl, a cyclopropyl-fused prolyl and 3-amino-4-cyclobutyl-2-oxobutanamide residues joined in sequence. Used for treatment of chronic hepatitis C virus genotype 1 infection.	2.6	1	0	tripeptide; ureas	antiviral drug; hepatitis C protease inhibitor; peptidomimetic
vx 702 VX 702: a p38 MAP kinase inhibitor	2.08	1	0	phenylpyridine
ly 411575 [no description available]	2.6	1	0	dibenzoazepine; difluorobenzene; lactam; secondary alcohol	EC 3.4.23.46 (memapsin 2) inhibitor
galidesivir [no description available]	2.6	1	0
volasertib BI 6727: a polo-like kinase inhibitor with broad antitumor activity; structure in first source	2.08	1	0
PB28 PB28 : A member of the class of tetralins that is tetralin that is substituted by 3-(4-cyclohexylpiperazin-1-yl)propyl and methoxy groups at positions 1 and 5, respectively. It is a sigma 2 (sigma2) receptor agonist (Ki = 0.68 nM) and exhibits antineoplastic and anti SARS-CoV-2 activities.	2.58	2	0	aromatic ether; piperazines; tetralins	anticoronaviral agent; antineoplastic agent; apoptosis inducer; sigma-2 receptor agonist
oxadiazoles Oxadiazoles: Compounds containing five-membered heteroaromatic rings containing two carbons, two nitrogens, and one oxygen atom which exist in various regioisomeric forms.	2.11	1	0
ribose ribopyranose : The pyranose form of ribose.	6.69	8	1	D-ribose; ribopyranose
azd 7762 [no description available]	2.08	1	0	aromatic amide; thiophenes
krp-203 [no description available]	2.08	1	0
mk 0354 [no description available]	2.08	1	0
regorafenib [no description available]	2.08	1	0	(trifluoromethyl)benzenes; aromatic ether; monochlorobenzenes; monofluorobenzenes; phenylureas; pyridinecarboxamide	antineoplastic agent; hepatotoxic agent; tyrosine kinase inhibitor
acetic acid 2-[4-methyl-8-(4-morpholinylsulfonyl)-1,3-dioxo-2-pyrrolo[3,4-c]quinolinyl]ethyl ester [no description available]	2.08	1	0	pyrroloquinoline
6-[[5-fluoro-2-(3,4,5-trimethoxyanilino)-4-pyrimidinyl]amino]-2,2-dimethyl-4H-pyrido[3,2-b][1,4]oxazin-3-one [no description available]	2.08	1	0	methoxybenzenes; substituted aniline
degrasyn degrasyn: a JAK2 kinase inhibitor that induces rapid degradation of c-Myc protein in MM-1 multiple myeloma and other tumor cell lines; structure in first source	2.72	2	0
epoxomicin [no description available]	2.6	1	0	morpholines; tripeptide	proteasome inhibitor
brivanib [no description available]	2.08	1	0	aromatic ether; diether; fluoroindole; pyrrolotriazine; secondary alcohol	angiogenesis inhibitor; antineoplastic agent; apoptosis inducer; drug metabolite; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; fibroblast growth factor receptor antagonist
icg 001 [no description available]	2.08	1	0	peptide
bms 477118 [no description available]	2.6	1	0	adamantanes; azabicycloalkane; monocarboxylic acid amide; nitrile; tertiary alcohol	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
pha 680632 PHA 680632: Aurora kinase inhibitor with potent antitumoral activity; structure in first source	2.6	1	0
tmc 353121 [no description available]	2.6	1	0
amd 070 mavorixafor: a derivative of AMD3100; a CXCR4 blocker	2.6	1	0	aminoquinoline
mp470 [no description available]	2.08	1	0	N-arylpiperazine
danoprevir [no description available]	2.6	1	0
bms-626529 [no description available]	2.6	1	0
bms-663068 fostemsavir: an HIV-1 attachment inhibitor; structure in first source	2.6	1	0
nu 7441 8-dibenzothiophen-4-yl-2-morpholin-4-yl-chromen-4-one: structure in first source	3.03	4	0	dibenzothiophenes
at 7519 4-(2,6-dichlorobenzamido)-N-(piperidin-4-yl)-pyrazole-3-carboxamide : A member of the class of pryrazoles that is 4-amino-1H-pyrazole-3-carboxylic acid in which the primary amino group has been acylated by a 2,6-dichlorobenzoyl group and in which the carboxylic acid has been converted into a carboxamide by formal condensation with the primary amino group of 4-aminopiperidine.	2.08	1	0	dichlorobenzene; piperidines; pyrazoles; secondary carboxamide	antineoplastic agent; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
er-086526 eribulin: a halichondrin B derivative that suppresses microtubule growth and acts as an antimitotic agent; structure in first source. eribulin : A fully synthetic macrocyclic ketone analogue of marine sponge natural products. Inhibits growth phase of microtubules via tubulin-based antimitotic mechanism, which leads to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death after prolonged mitotic blockage	5.44	4	3	cyclic ketal; cyclic ketone; macrocycle; polycyclic ether; polyether; primary amino compound	antineoplastic agent; microtubule-destabilising agent
bi 2536 [no description available]	2.08	1	0
amenamevir ASP2151: a herpesvirus helicase-primase inhibitor, in a guinea pig model of genital herpes; structure in first source	2.6	1	0
vx 765 belnacasan: a NSAID	2.6	1	0	dipeptide
Dihydrotanshinone I dihydrotanshinone I: extracted from Radix Salviae	2.6	1	0	abietane diterpenoid	anticoronaviral agent
nutlin-3a nutlin 3: an MDM2 antagonist; structure in first source	2.13	1	0	stilbenoid
danusertib [no description available]	2.08	1	0	piperazines
alogliptin alogliptin: structure in first source. alogliptin : A piperidine that is 3-methyl-2,4-dioxo-3,4-dihydropyrimidine carrying additional 2-cyanobenzyl and 3-aminopiperidin-1-yl groups at positions 1 and 2 respectively (the R-enantiomer). Used in the form of its benzoate salt for treatment of type 2 diabetes.	2.6	1	0	nitrile; piperidines; primary amino compound; pyrimidines	EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor; hypoglycemic agent
N-[4-(2-tert-butylphenyl)sulfonylphenyl]-2,3,4-trihydroxy-5-[(2-propan-2-ylphenyl)methyl]benzamide [no description available]	2.08	1	0	benzamides
N-[5-[[5-[(4-acetyl-1-piperazinyl)-oxomethyl]-4-methoxy-2-methylphenyl]thio]-2-thiazolyl]-4-[(3,3-dimethylbutan-2-ylamino)methyl]benzamide [no description available]	2.08	1	0	benzamides
abt 869 [no description available]	2.08	1	0	aromatic amine; indazoles; phenylureas	angiogenesis inhibitor; antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
fr 180204 FR 180204: structure in first source	2.6	1	0	pyrazoles; ring assembly
nsc 725776 NSC 725776: inhibits topoisomerase I; structure in first source	2.21	1	0
dorsomorphin dorsomorphin: an AMPK inhibitor. dorsomorphin : A pyrazolopyrimidine that is pyrazolo[1,5-a]pyrimidine which is substituted at positions 3 and 6 by pyridin-4-yl and p-[2-(piperidin-1-yl)ethoxy]phenyl groups, respectively. It is a potent, selective, reversible, and ATP-competitive inhibitor of AMPK (AMP-activated protein kinase, EC 2.7.11.31) and a selective inhibitor of bone morphogenetic protein (BMP) signaling.	2.08	1	0	aromatic ether; piperidines; pyrazolopyrimidine; pyridines	bone morphogenetic protein receptor antagonist; EC 2.7.11.31 {[hydroxymethylglutaryl-CoA reductase (NADPH)] kinase} inhibitor
ac 261066 [no description available]	2.08	1	0
quisinostat [no description available]	2.6	1	0	indoles
carfilzomib [no description available]	2.58	2	0	epoxide; morpholines; tetrapeptide	antineoplastic agent; proteasome inhibitor
hcv 796 HCV 796: inhibits HCV RdRp; structure in first source	2.6	1	0
gw9508 GW9508: structure in first source	2.08	1	0	aromatic amine
jnj 26854165 [no description available]	2.08	1	0
resminostat resminostat: a histone deacetylase inhibitor; structure in first source	2.6	1	0
pf 573228 6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one: structure in first source	2.08	1	0	quinolines
gw 2580 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine: a cFMS kinase inhibitor; structure in first source	2.08	1	0
idelalisib idelalisib: an antineoplastic agent and p110delta inhibitor; structure in first source. idelalisib : A member of the class of quinazolines that is 5-fluoro-3-phenylquinazolin-4-one in which the hydrogen at position 2 is replaced by a (1S)-1-(3H-purin-6-ylamino)propyl group. used for for the treatment of refractory indolent non-Hodgkin's lymphoma and relapsed chronic lymphocytic leukemia.	2.08	1	0	aromatic amine; organofluorine compound; purines; quinazolines; secondary amino compound	antineoplastic agent; apoptosis inducer; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
crizotinib Crizotinib: A piperidine and aminopyridine derivative that acts as an inhibitor of RECEPTOR PROTEIN-TYROSINE KINASES, including ANAPLASTIC LYMPHOMA KINASE (ALK) and HEPATOCYTE GROWTH FACTOR RECEPTOR (HGFR; c-Met). It is used in the treatment of NON-SMALL CELL LUNG CANCER.. crizotinib : A 3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine that has R configuration at the chiral centre. The active enantiomer, it acts as a kinase inhibitor and is used for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC)	2.51	2	0	3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine	antineoplastic agent; biomarker; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
5-(5,6-dimethoxy-1-benzimidazolyl)-3-[(2-methylsulfonylphenyl)methoxy]-2-thiophenecarbonitrile [no description available]	2.08	1	0	benzimidazoles
4-[2-(2-chloro-4-fluoroanilino)-5-methyl-4-pyrimidinyl]-N-[(1S)-1-(3-chlorophenyl)-2-hydroxyethyl]-1H-pyrrole-2-carboxamide Vx-11e: ERK1-2 inhibitor	2.08	1	0	aromatic amide; heteroarene
osi 906 [no description available]	2.08	1	0	cyclobutanes; quinolines
ly2109761 [no description available]	2.08	1	0
chir-265 [no description available]	2.08	1	0	aromatic ether
motesanib [no description available]	2.08	1	0	pyridinecarboxamide
az-628 AZ-628: a multikinase inhibitor; structure in first source	2.08	1	0	benzamides
zk 756326 2-(2-(4-(3-phenoxybenzyl)piperazin-1-yl)ethoxy)ethanol: a CC chemokine receptor CCR8 agonist; structure in first source	2.6	1	0	aromatic ether
balapiravir balapiravir: a prodrug of R1479; structure in first source	2.6	1	0
trametinib [no description available]	2.9	3	0	acetamides; aromatic amine; cyclopropanes; organofluorine compound; organoiodine compound; pyridopyrimidine; ring assembly	anticoronaviral agent; antineoplastic agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor; geroprotector
pf-562,271 [no description available]	2.08	1	0	indoles
deoxyarbutin 4-((tetrahydro-2H-pyran-2-yl)oxy)phenol: has antineoplastic activity; structure in first source	2.6	1	0
abexinostat abexinostat: structure in first source	2.6	1	0	benzofurans
silvestrol silvestrol: isolated from the fruit and twig of Aglaia silvestris. silvestrol : An organic heterotricyclic compound that consists of a 2,3,3a,8b-tetrahydro-H-benzo[b]cyclopenta[d]furan framework substituted by hydroxy groups at positions C-1 and C-8b, a methoxycarbonyl group at C-2, a phenyl group at C-3, a 4-methoxyphenyl group at C-3a, a methoxy group at C-8 and a 1,4-dioxan-2-yloxy group at position C-6 which in turn is substituted by a methoxy group at position 3 and a 1,2-dihydroxyethyl group at position 6. Isolated from Aglaia silvestris, it exhibits antineoplastic activity.	2.6	1	0	dioxanes; ether; methyl ester; organic heterotricyclic compound	antineoplastic agent; metabolite
narlaprevir narlaprevir: an antiviral agent that inhibits hepatitis C virus NS3 protease. narlaprevir : An azabicyclohexane that is (1R,5S)-6,6-dimethyl-3-azabicyclo[3.1.0]hexane substituted by [(3S)-1-(cyclopropylamino)-1,2-dioxoheptan-3-yl]aminoacyl and N-({1-[(tert-butylsulfonyl)methyl]cyclohexyl}carbamoyl)-3-methyl-L-valyl groups at positions 2S and 3, respectively. It is a hepatitis C virus (HCV) NS3/4A serine protease inhibitor (Ki = 6 nM) that is used for the treatment of chronic hepatitis C.	2.6	1	0	azabicyclohexane; cyclopropanes; pyrrolidinecarboxamide; secondary carboxamide; sulfone; tertiary carboxamide; ureas	anticoronaviral agent; antiviral drug; EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor; hepatitis C protease inhibitor
teneligliptin [no description available]	2.6	1	0	amino acid amide
ly2603618 [no description available]	3.19	1	0	ureas
dextrothyroxine [no description available]	2.6	1	0
veliparib [no description available]	14.63	53	0	benzimidazoles	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
ku-0060648 [no description available]	2.08	1	0	dibenzothiophenes
dactolisib dactolisib: antineoplastic agent that inhibits both phosphatidylinositol 3-kinase and mTOR. dactolisib : An imidazoquinoline that is 3-methyl-2-oxo-2,3-dihydro-1H-imidazo[4,5-c]quinoline substituted at position 1 by a 4-(1-cyanoisopropyl)phenyl group and at position 8 by a quinolin-3-yl group. A dual PI3K/mTOR inhibitor used in cancer treatment.	2.8	3	0	imidazoquinoline; nitrile; quinolines; ring assembly; ureas	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor
palomid 529 [no description available]	2.08	1	0
pf 03491390 [no description available]	2.6	1	0
alloin [no description available]	2.6	1	0	anthracenes; C-glycosyl compound; cyclic ketone; phenols	laxative; metabolite
tosedostat [no description available]	2.08	1	0	carboxylic ester; hydroxamic acid; secondary carboxamide
nad NAD(1-) : An anionic form of nicotinamide adenine dinucleotide arising from deprotonation of the two OH groups of the diphosphate moiety.	4.38	6	0	organophosphate oxoanion	cofactor; human metabolite; hydrogen acceptor; Saccharomyces cerevisiae metabolite
mdv 3100 [no description available]	8.77	14	4	(trifluoromethyl)benzenes; benzamides; imidazolidinone; monofluorobenzenes; nitrile; thiocarbonyl compound	androgen antagonist; antineoplastic agent
ku 60019 [no description available]	2.08	1	0
gsk 461364 GSK 461364: an antineoplastic agent that inhibits polo-like kinase 1	2.08	1	0	(trifluoromethyl)benzenes
n-(3,4-difluoro-2-(2-fluoro-4-iodophenylamino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamide N-(3,4-difluoro-2-(2-fluoro-4-iodophenylamino)-6-methoxyphenyl)-1-(2,3-dihydroxypropyl)cyclopropane-1-sulfonamide: a MEK inhibitor; structure in first source	2.08	1	0
nvp-tae684 [no description available]	2.08	1	0	piperidines
bms-650032 asunaprevir: an NS3 protease inhibitor against hepatitis C virus	2.6	1	0	oligopeptide
4-methyl-3-(2-(2-morpholinoethylamino)quinazolin-6-yl)-n-(3-(trifluoromethyl)phenyl)benzamide 4-methyl-3-(2-(2-morpholinoethylamino)quinazolin-6-yl)-N-(3-(trifluoromethyl)phenyl)benzamide: structure in first source	2.08	1	0
gsk 269962a [no description available]	2.08	1	0
rg 7128 2'-fluoro-2'-methyl-3',5'-diisobutyryldeoxycytidine: inhibits HCV polymerase; structure in first source	2.6	1	0
ceruletide Ceruletide: A specific decapeptide obtained from the skin of Hila caerulea, an Australian amphibian. Caerulein is similar in action and composition to CHOLECYSTOKININ. It stimulates gastric, biliary, and pancreatic secretion; and certain smooth muscle. It is used in paralytic ileus and as diagnostic aid in pancreatic malfunction.. ceruletide : A decapeptide comprising 5-oxoprolyl, glutamyl, aspartyl, O-sulfotyrosyl, threonyl, glycyl, tryptopyl, methionyl, aspartyl and phenylalaninamide residues in sequence. Found in the skins of certain Australian amphibians, it is an analogue of the gastrointestinal peptide hormone cholecystokinin and stimulates gastric, biliary, and pancreatic secretion. It is used in cases of paralysis of the intestine (paralytic ileus) and as a diagnostic aid in pancreatic malfunction.	2.25	1	0	oligopeptide	diagnostic agent; gastrointestinal drug
oritavancin oritavancin : A semisynthetic glycopeptide used (as its bisphosphate salt) for the treatment of acute bacterial skin and skin structure infections caused or suspected to be caused by susceptible isolates of designated Gram-positive microorganisms including MRSA.	2.6	1	0	disaccharide derivative; glycopeptide; semisynthetic derivative	antibacterial drug; antimicrobial agent
a-83-01 A-83-01: an ALK-5 inhibitor; structure in first source	2.08	1	0
3-[(1-methyl-3-indolyl)methylidene]-1H-pyrrolo[3,2-b]pyridin-2-one [no description available]	2.08	1	0	indoles
vx-770 ivacaftor: a CFTR potentiator; structure in first source. ivacaftor : An aromatic amide obtained by formal condensation of the carboxy group of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid with the amino group of 5-amino-2,4-di-tert-butylphenol. Used for the treatment of cystic fibrosis.	2.08	1	0	aromatic amide; monocarboxylic acid amide; phenols; quinolone	CFTR potentiator; orphan drug
mk-8776 MK-8776: a checkpoint kinase 1 (CHK1) inhibitor; SCH900776 was renamed MK-8776; structure in first source	2.31	1	0	pyrazolopyrimidine
buparlisib NVP-BKM120: a pan class I PI3 kinase inhibitor with antineoplastic activity; structure in first source	11.35	12	1	aminopyridine; aminopyrimidine; morpholines; organofluorine compound	antineoplastic agent; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
azd 1480 [no description available]	2.08	1	0
chlorophyll a Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms.. chlorophyll : A family of magnesium porphyrins, defined by the presence of a fifth ring beyond the four pyrrole-like rings. The rings can have various side chains which usually include a long phytol chain.	2.31	1	0	chlorophyll; methyl ester	cofactor
pevonedistat pevonedistat: a potent and selective inhibitor of NAE (NEDD8-activating enzyme). pevonedistat : A pyrrolopyrimidine that is 7H-pyrrolo[2,3-d]pyrimidine which is substituted by a (1S)-2,3-dihydro-1H-inden-1-ylnitrilo group at position 4 and by a (1S,3S,4S)-3-hydroxy-4-[(sulfamoyloxy)methyl]cyclopentyl group at position 7. It is a potent and selective NEDD8-activating enzyme inhibitor with an IC50 of 4.7 nM, and currently under clinical investigation for the treatment of acute myeloid leukemia (AML) and myelodysplastic syndromes.	2.66	2	0	cyclopentanols; indanes; pyrrolopyrimidine; secondary amino compound; sulfamidate	antineoplastic agent; apoptosis inducer
fedratinib fedratinib: a selective small-molecule inhibitor of JAK2	2.08	1	0	sulfonamide
gsk690693 [no description available]	2.08	1	0	1,2,5-oxadiazole; acetylenic compound; aromatic amine; aromatic ether; imidazopyridine; piperidines; primary amino compound; tertiary alcohol	antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
cnf 2024 [no description available]	2.08	1	0	2-aminopurines; aromatic ether; organochlorine compound; pyridines	antineoplastic agent; Hsp90 inhibitor
ku 0063794 Ku 0063794: an mTOR inhibitor; structure in first source	2.08	1	0	benzyl alcohols; monomethoxybenzene; morpholines; pyridopyrimidine; tertiary amino compound	antineoplastic agent; mTOR inhibitor
uk 453,061 UK 453,061: a reverse transcriptase inhibitor/anti-HIV agent; structure in first source	2.6	1	0	aromatic ether
azd 7545 AZD 7545: an anilide tertiary carbinol; a pyruvate dehydrogenase kinase 2 inhibitor. AZD7545 : A sulfone that is benzene substituted by [4-(dimethylcarbamoyl)phenyl]sulfonyl, chloro and [(2R)-3,3,3-trifluoro-2-hydroxy-2-methylpropanoyl]amino groups at positions 1, 3 and 4, respectively. It is a potent and non-ATP-competitive inhibitor of pyruvate dehydrogenase kinase 2 (PDHK2) with IC50 of 6.4 nM and exhibits glucose-lowering activity. Also inhibits PDHK1 at higher levels (IC50 = 36.8 nM).	2.08	1	0	benzamides; monochlorobenzenes; organofluorine compound; secondary carboxamide; sulfone; tertiary alcohol; tertiary carboxamide	EC 2.7.11.2 - [pyruvate dehydrogenase (acetyl-transferring)] kinase inhibitor; hypoglycemic agent
nutlin-3b [no description available]	2.08	1	0	Nutlin; piperazinone	anticoronaviral agent
N-(2-aminophenyl)-2-pyrazinecarboxamide [no description available]	2.6	1	0	aromatic amide
pf 04217903 [no description available]	2.08	1	0	quinolines
gdc 0941 pictrelisib : A sulfonamide composed of indazole, morpholine, and methylsulfonyl-substituted piperazine rings bound to a thienopyrimidine ring.	2.08	1	0	indazoles; morpholines; piperazines; sulfonamide; thienopyrimidine	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
sm 164 SM 164: a bivalent Smac mimetic with antineoplastic activity; structure in first source	2.08	1	0	benzenes; organic heterobicyclic compound; secondary carboxamide; triazoles	antineoplastic agent; apoptosis inducer; radiosensitizing agent
calpain Calpain: Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC 3.4.22.4.	2.1	1	0
icotinib [no description available]	2.25	1	0
ph 797804 PH 797804: an NSAID; structure in first source. PH 797804 : A member of the class of benzamides obtained by formal condensation of the carboxy group of 3-{3-bromo-4-[(2,4-difluorobenzyl)oxy]-6-methyl-2-oxopyridin-1-yl}-4-methylbenzoic acid with the amino group of methylamine.	2.08	1	0	aromatic ether; benzamides; organobromine compound; organofluorine compound; pyridone	anti-inflammatory agent; EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
pha 408 PHA 408: an IKK-2 antagonist; structure in first source	2.08	1	0
gsk 1016790a GSK1016790A : A tertiary carboxamide that is piperazine in which one of the amino groups has undergone condensation with the carboxy group of N-[(2,4-dichlorophenyl)sulfonyl]-L-serine, while the other has undergone condensation with the carboxy group of N-(1-benzothiophen-2-ylcarbonyl)-L-leucine. It is a cell-permeable, potent and selective agonist of the TRPV4 (transient receptor potential vanilloid 4) channel.	2.08	1	0	1-benzothiophenes; aromatic primary alcohol; dichlorobenzene; N-acylpiperazine; sulfonamide; tertiary carboxamide	TRPV4 agonist
tegobuvir tegobuvir: a non-structural protein 5B polymerase inhibitor	2.6	1	0
pf-429242 PF-429242: a subtilisin kexin isozyme-1/site-1 protease inhibitor	2.6	1	0
sodium iodate sodium iodate: RN given refers to iodic acid, Na salt	2.25	1	0	organic molecular entity
srt1720 [no description available]	2.08	1	0
plx 4720 PLX 4720: a B-Raf(V600E) kinase inhibitor; structure in first source	2.08	1	0	aromatic ketone; difluorobenzene; organochlorine compound; pyrrolopyridine; sulfonamide	antineoplastic agent; B-Raf inhibitor
cx 4945 [no description available]	2.58	2	0
pci 34051 PCI 34051: an HDAC8 inhibitor	2.6	1	0	indolecarboxamide
cudc 101 7-(4-(3-ethynylphenylamino)-7-methoxyquinazolin-6-yloxy)-N-hydroxyheptanamide: a histone deacetylase inhibitor; structure in first source	2.08	1	0
mln 8237 MLN 8237: an aurora kinase A inhibitor	3.61	2	0	benzazepine
lde225 sonidegib: specific Smoothened/Smo antagonist. sonidegib : A member of the classo of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2-methyl-4'-(trifluoromethoxy)[1,1'-biphenyl]-3-carboxylic acid with the amino group of 6-(2,6-dimethylmorpholin-4-yl)pyridin-3-amine. Used (as its phosphate salt) for treatment of locally advanced basal cell carcinoma.	2.08	1	0	aminopyridine; aromatic ether; benzamides; biphenyls; morpholines; organofluorine compound; tertiary amino compound	antineoplastic agent; Hedgehog signaling pathway inhibitor; SMO receptor antagonist
gdc 0449 HhAntag691: inhibits the hedgehog pathway and ABC transporters; has antineoplastic activity	2.52	2	0	benzamides; monochlorobenzenes; pyridines; sulfone	antineoplastic agent; Hedgehog signaling pathway inhibitor; SMO receptor antagonist; teratogenic agent
sgx 523 [no description available]	2.08	1	0	aryl sulfide; biaryl; pyrazoles; quinolines; triazolopyridazine	c-Met tyrosine kinase inhibitor; nephrotoxic agent
cep-9722 CEP-9722: a prodrug of the poly(ADP-ribose) polymerase inhibitor CEP-8983	3.27	1	0
bms 777607 N-(4-(2-amino-3-chloropyridin-4-yloxy)-3-fluorophenyl)-4-ethoxy-1-(4-fluorophenyl)-2-oxo-1,2-dihydropyridine-3-carboxamide: a Met kinase inhibitor; structure in first source	2.08	1	0	aromatic amide
sgi 1776 SGI 1776: a Pim kinase inhibitor; structure in first source	2.08	1	0	imidazoles
lomibuvir lomibuvir: an antiviral agent with polymerase NS5 inhibitory activity	2.6	1	0	thiophenecarboxylic acid
delanzomib [no description available]	2.6	1	0	C-terminal boronic acid peptide; phenylpyridine; secondary alcohol; threonine derivative	antineoplastic agent; apoptosis inducer; proteasome inhibitor
pci 32765 ibrutinib: a Btk protein inhibitor. ibrutinib : A member of the class of acrylamides that is (3R)-3-[4-amino-3-(4-phenoxyphenyl)pyrazolo[3,4-d]pyrimidin-1-yl]piperidine in which the piperidine nitrogen is replaced by an acryloyl group. A selective and covalent inhibitor of the enzyme Bruton's tyrosine kinase, it is used for treatment of B-cell malignancies.	2.84	3	0	acrylamides; aromatic amine; aromatic ether; N-acylpiperidine; pyrazolopyrimidine; tertiary carboxamide	antineoplastic agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
ponatinib [no description available]	2.08	1	0	(trifluoromethyl)benzenes; acetylenic compound; benzamides; imidazopyridazine; N-methylpiperazine	antineoplastic agent; tyrosine kinase inhibitor
pitavastatin(1-) pitavastatin(1-) : A hydroxy monocarboxylic acid anion that is the conjugate base of pitavastatin, obtained by deprotonation of the carboxy group.	2.6	1	0	hydroxy monocarboxylic acid anion
amg 900 N-(4-((3-(2-amino-4-pyrimidinyl)-2-pyridinyl)oxy)phenyl)-4-(4-methyl-2-thienyl)-1-phthalazinamine: a pan-aurora kinase inhibitor; structure in first source	2.08	1	0
mk-1775 adavosertib: a Wee1 kinase inhibitor; structure in first source	4.92	9	0	piperazines
apalutamide [no description available]	2.31	1	0
bag956 BAG956: an imidazo[4,5-c]quinoline; dual PI3K/PDK-1 inhibitor, used in antileukemic therapies	2.08	1	0
quizartinib [no description available]	2.52	2	0	benzoimidazothiazole; isoxazoles; morpholines; phenylureas	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor; necroptosis inhibitor
GRL-0617 GRL-0617 : A benzamide resulting from the formal condensation of the carboxy group of 5-amino-2-methylbenzoic acid with the amino group of (1R)-1-(naphthalen-1-yl)ethan-1-amine. It is a potent noncovalent inhibitor (IC50 = 600 nM) of severe acute respiratory syndrome-coronavirus papain-like protease (SARS-CoV PLpro).	2.6	1	0	benzamides; naphthalenes; secondary carboxamide; substituted aniline	anticoronaviral agent; protease inhibitor
N-[4-[3-[[[7-(hydroxyamino)-7-oxoheptyl]amino]-oxomethyl]-5-isoxazolyl]phenyl]carbamic acid tert-butyl ester CAY10603: a HDAC6 inhibitor	2.58	2	0	carbamate ester
niraparib 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide : A member of the class of indazoles that is 2H-indazole substituted by 4-(piperidin-3-yl)phenyl and aminocarbonyl groups at positions 2 and 7, respectively. It is a potent PARP1 inhibitor with IC50 of 3.2 nM.	2.11	1	0	benzenes; indazoles; piperidines; primary carboxamide	antineoplastic agent; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
niraparib niraparib: structure in first source. niraparib : A 2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide that has S-configuration. It is a potent inhibitor of PARP1 and PARP2 (IC50 of 3.8 and 2.1 nM, respectively) and approved as a first-line maintenance treatment for women with advanced ovarian cancer after responding to platinum-based chemotherapy.	9.21	56	0	2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamide	antineoplastic agent; apoptosis inducer; EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor; radiosensitizing agent
tak 733 [no description available]	2.08	1	0
mk 2206 MK 2206: a protein kinase inhibitor and antineoplastic agent	2.51	2	0	organic heterotricyclic compound	EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
navitoclax [no description available]	2.08	1	0	aryl sulfide; monochlorobenzenes; morpholines; N-sulfonylcarboxamide; organofluorine compound; piperazines; secondary amino compound; sulfone; tertiary amino compound	antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
sns 314 SNS 314: an aurora kinase inhibitor; structure in first source	2.08	1	0	ureas
jzl 184 JZL 184: inhibits monoacylglycerol lipase; structure in first source	2.58	2	0	benzodioxoles
gsk 650394 [no description available]	2.6	1	0	phenylpyridine
4,4-difluoro-4-bora-3a,4a-diaza-s-indacene [no description available]	2.08	1	0	BODIPY compound
n-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide N-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide: a Janus kinase 1 and Janus kinase 2 inhibitor; structure in first source. momelotinib : A benzamide obtained by formal condensation of the carboxy group of 4-{2-[4-(morpholin-4-yl)anilino]pyrimidin-4-yl}benzoic acid with the primary amino group of aminoacetonitrile. It is an ATP-competitive JAK1/JAK2 inhibitor with IC50 of 11 nM and 18 nM, respectively. Used for the treatment of patients with intermediate- or high-risk myelofibrosis.	2.08	1	0	aminopyrimidine; benzamides; morpholines; nitrile; secondary amino compound; tertiary amino compound	anti-anaemic agent; antineoplastic agent; apoptosis inducer; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
dcc-2036 rebastinib: an inhibitor of Tie2 tyrosine kinase receptor and antineoplastic agent	2.08	1	0	organofluorine compound; phenylureas; pyrazoles; pyridinecarboxamide; quinolines	tyrosine kinase inhibitor
oprozomib ONX 0912: antineoplastic; an orally active proteasome inhibitor; structure in first source	2.6	1	0
az 960 [no description available]	2.6	1	0
cabozantinib cabozantinib: a multikinase inhibitor. cabozantinib : A dicarboxylic acid diamide that is N-phenyl-N'-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide in which the hydrogen at position 4 on the phenyl ring is substituted by a (6,7-dimethoxyquinolin-4-yl)oxy group. A multi-tyrosine kinase inhibitor, used (as its malate salt) for the treatment of progressive, metastatic, medullary thyroid cancer.	2.08	1	0	aromatic ether; dicarboxylic acid diamide; organofluorine compound; quinolines	antineoplastic agent; tyrosine kinase inhibitor
golgicide a golgicide A: inhibits the cis-golgi ArfGEF GBF1; structure in first source. golgicide A : A diastereoisomeric mixture comprising racemic cis- and racemic trans-goglioside A in a 10:1 ratio. It is a potent and rapidly reversible GBF1 (Golgi-specific brefeldin A-resistance guanine nucleotide exchange factor 1) inhibitor. The (3aS,4R,9bR) isomer is the most active (see Bioorg. Med. Chem. Lett., 2012, 22, 5177-5181).	2.6	1	0	diastereoisomeric mixture	cis-Golgi ArfGEF GBF inhibitor
N-(2,6-difluorophenyl)-5-[3-[2-[5-ethyl-2-methoxy-4-[4-(4-methylsulfonyl-1-piperazinyl)-1-piperidinyl]anilino]-4-pyrimidinyl]-2-imidazo[1,2-a]pyridinyl]-2-methoxybenzamide [no description available]	2.08	1	0	benzamides
incb-018424 [no description available]	2.82	3	0	nitrile; pyrazoles; pyrrolopyrimidine	antineoplastic agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
jnj-31020028 [no description available]	2.11	1	0
bix 01294 [no description available]	3.66	2	0	piperidines
cobicistat [no description available]	4.4	2	1	1,3-thiazoles; carbamate ester; monocarboxylic acid amide; morpholines; ureas	P450 inhibitor
bms-790052 daclatasvir: an HCV NS5A inhibitor. daclatasvir : A member of the class of biphenyls that is a potent inhibitor of nonstructural protein 5A and is used (as its hydrochloride salt) for treatment of hepatitis C.	2.6	1	0	biphenyls; carbamate ester; carboxamide; imidazoles; valine derivative	antiviral drug; nonstructural protein 5A inhibitor
pf 3845 PF 3845: inhibits fatty acid amide hydrolase	2.08	1	0	piperidines
gsk 2126458 omipalisib: inhibitor of mTOR protein. omipalisib : A member of the class of quinolines that is quinoline which is substituted by pyridazin-4-yl and 5-[(2,4-difluorobenzene-1-sulfonyl)amino]-6-methoxypyridin-3-yl groups at positions 4 and 6, respectively. It is a highly potent inhibitor of PI3K and mTOR developed by GlaxoSmithKline and was previously in human phase 1 clinical trials for the treatment of idiopathic pulmonary fibrosis and solid tumors.	2.08	1	0	aromatic ether; difluorobenzene; pyridazines; pyridines; quinolines; sulfonamide	anticoronaviral agent; antineoplastic agent; autophagy inducer; EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor; mTOR inhibitor; radiosensitizing agent
ixazomib ixazomib: a proteasome inhibitor with antineoplastic activity; MLN2238 is the biologically active form of MLN9708; structure in first source. ixazomib : A glycine derivative that is the amide obtained by formal condensation of the carboxy group of N-(2,5-dichlorobenzoyl)glycine with the amino group of [(1R)-1-amino-3-methylbutyl]boronic acid. The active metabolite of ixazomib citrate, it is used in combination therapy for treatment of multiple myeloma.	2.58	2	0	benzamides; boronic acids; dichlorobenzene; glycine derivative	antineoplastic agent; apoptosis inducer; drug metabolite; orphan drug; proteasome inhibitor
ldn 193189 LDN 193189: inhibits bone morphogenetic protein signaling	2.08	1	0	pyrimidines
ucph 101 2-amino-4-(4-methoxyphenyl)-7-(naphthalen-1-yl)-5-oxo-5,6,7,8-tetrahydro-4H-chromene-3-carbonitrile: structure in first source	2.6	1	0
gdc 0980 [no description available]	2.31	1	0
cx 5461 CX 5461: structure in first source	3.25	1	0	diazepine; naphthyridine derivative; organic heterotetracyclic compound; pyrazines; secondary carboxamide	antineoplastic agent; apoptosis inducer; EC 2.7.7.6 (RNA polymerase) inhibitor
plx4032 [no description available]	2.08	1	0	aromatic ketone; difluorobenzene; monochlorobenzenes; pyrrolopyridine; sulfonamide	antineoplastic agent; B-Raf inhibitor
(2S)-2-[[2-(2,3-dihydro-1H-inden-5-yloxy)-9-[(4-phenylphenyl)methyl]-6-purinyl]amino]-3-phenyl-1-propanol [no description available]	2.08	1	0	biphenyls
gsk 1363089 GSK 1363089: a multikinase inhibitor that acts on Met, RON, Axl, and VEGFR; structure in first source	2.51	2	0	aromatic ether
kin-193 [no description available]	2.08	1	0	pyridopyrimidine
5-(3-methylsulfonylphenyl)-4-[(1-methyl-5-tetrazolyl)thio]thieno[2,3-d]pyrimidine [no description available]	2.6	1	0	aryl sulfide; thienopyrimidine
bay 869766 [no description available]	2.08	1	0
baricitinib [no description available]	2.6	1	0	azetidines; nitrile; pyrazoles; pyrrolopyrimidine; sulfonamide	anti-inflammatory agent; antirheumatic drug; antiviral agent; EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor; immunosuppressive agent
4-[6-[4-(methoxycarbonylamino)phenyl]-4-(4-morpholinyl)-1-pyrazolo[3,4-d]pyrimidinyl]-1-piperidinecarboxylic acid methyl ester WYE-354: an mTOR inhibitor; structure in first source	2.08	1	0	carbamate ester
KOM70144 KOM70144 : A benzamide that is GRL-0617 in which one of the hydrogen's of the primary amino group is replaced by an acetyl group. It an inhibitor of SARS-CoV and SARS-CoV-2 papain-like protease (PLpro) with an IC50 of 2.6 muM and 5.0 muM, respectively. It also inhibits SARS-CoV and SARS-CoV-2 infection of Vero E6 cells in vitro (EC50 values are 13.1 and 21 muM, respectively).	2.6	1	0	acetamides; benzamides; naphthalenes; secondary carboxamide	anticoronaviral agent; protease inhibitor
piperidines Piperidines: A family of hexahydropyridines.	9.04	53	0
6-[(3-aminophenyl)methyl]-4-methyl-2-methylsulfinyl-5-thieno[3,4]pyrrolo[1,3-d]pyridazinone ML-265: a small molecule activator of PKM2	2.08	1	0	organic heterobicyclic compound; organonitrogen heterocyclic compound; organosulfur heterocyclic compound
e-52862 [no description available]	2.6	1	0
ly2811376 [no description available]	2.6	1	0
5-hydroxymethyl-2'-deoxyuridine 5-hydroxymethyl-2'-deoxyuridine : A pyrimidine 2'-deoxyribonucleoside composed of 2'-deoxyuridine having a 5-hydroxymethyl substituent.	2.31	1	0
iwr-1 endo IWR-1-endo : A dicarboximide having an endo bridged phthalimide structure, substituted at nitrogen by a 4-(quinolin-8-ylcarbamoyl)benzoyl group.	2.52	2	0	benzamides; bridged compound; dicarboximide; quinolines	axin stabilizer; Wnt signalling inhibitor
anagliptin anagliptin: anagliptin hydrochloride salt is the active compound	2.6	1	0	amino acid amide
3-[[4-(2,3-dihydro-1,4-benzodioxin-6-ylsulfonyl)-1,4-diazepan-1-yl]sulfonyl]aniline [no description available]	2.08	1	0	benzenes; sulfonamide
cp 466722 [no description available]	2.08	1	0	quinazolines
gardiquimod [no description available]	2.6	1	0
CAY10626 [no description available]	2.08	1	0	ureas
grazoprevir grazoprevir: has antiviral activity; component of Zepatier. grazoprevir : An azamacrocyclic compound that is a hepatitis C protease inhibitor used in combination with elbasvir (under the brand name Zepatier) for treatment of chronic HCV genotypes 1 or 4 infection in adults.	2.6	1	0	aromatic ether; azamacrocycle; carbamate ester; cyclopropanes; lactam; N-sulfonylcarboxamide; quinoxaline derivative	antiviral drug; hepatitis C protease inhibitor; hepatoprotective agent
thiopental sodium [no description available]	2.08	1	0	organochlorine compound; piperazines; pyrimidines	antineoplastic agent; tyrosine kinase inhibitor
ribociclib ribociclib: inhibits both CDK4 and CDK6	2.31	1	0
abt-450 paritaprevir: inhibits HCV NS3 protease. paritaprevir : An azamacrocycle which is used which is in combination with dasabuvir sodium hydrate, ombitasvir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0
letermovir letermovir: has antiviral activity; structure in first source	2.6	1	0
apatinib apatinib: reverses multidrug resistance by inhibiting the efflux function of multiple ATP-binding cassette transporters; structure in first source	7.6	1	0
gx 15-070 obatoclax: a pan-Bcl-2 inhibitor potentially useful in treating mantle cell lymphoma	2.1	1	0
sofosbuvir Sofosbuvir: A uridine monophosphate analog inhibitor of HEPATITIS C VIRUS (HCV) polymerase NS5B that is used as an ANTIVIRAL AGENT in the treatment of CHRONIC HEPATITIS C.. sofosbuvir : A nucleotide conjugate that is used in combination with ledipasvir (under the trade name Harvoni) for the treatment of chronic hepatitis C genotype 1 infection.	2.6	1	0	isopropyl ester; L-alanyl ester; nucleotide conjugate; organofluorine compound; phosphoramidate ester	antiviral drug; hepatitis C protease inhibitor; prodrug
5-(4-amino-1-propan-2-yl-3-pyrazolo[3,4-d]pyrimidinyl)-1,3-benzoxazol-2-amine sapanisertib: an mTOR inhibitor	2.6	1	0	benzoxazole
blz 945 [no description available]	2.6	1	0
pha 793887 [no description available]	2.08	1	0	piperidinecarboxamide
azd3839 AZD3839: a BACE1 inhibitor; structure in first source	2.6	1	0
pf 3084014 nirogacestat: an antineoplastic agent. nirogacestat : A member of the class of imidazoles that is 1H-imidazole substituted by a 1-[(2,2-dimethylpropyl)amino]-2-methylpropan-2-yl group at position 1 and a {N-[(2S)-6,8-difluoro-1,2,3,4-tetrahydronaphthalen-2-yl]-L-norvalyl}amino group at position 4. It is a gamma-secretase inhibitor whose hydrobromide salt is indicated for adult patients with progressing desmoid tumours who require systemic treatment.	2.6	1	0
unc 0638 UNC 0638: inhibits lysine methyltransferases G9a and GLP; structure in first source	2.6	1	0	quinazolines
gs-9620 [no description available]	2.6	1	0
nvp-bsk805 [no description available]	2.08	1	0
xmd 8-92 XMD8-92 : A dimethylpyrimido[4,5-b][1,4]benzodiazepin-6-one carrying at C-2 on the pyrimidine ring a [2-ethoxy-4-(4-hydroxypiperidin-1-yl)phenyl]amino substituent. It is an inhibitor of the BMK1 kinase pathway.	2.08	1	0	pyrimidobenzodiazepine	protein kinase inhibitor
n-((5-(methanesulfonyl)pyridin-2-yl)methyl)-6-methyl-5-(1-methyl-1h-pyrazol-5-yl)-2-oxo-1-(3-(trifluoromethyl)phenyl)-1,2-dihydropyridine-3-carboxamide N-((5-(methanesulfonyl)pyridin-2-yl)methyl)-6-methyl-5-(1-methyl-1H-pyrazol-5-yl)-2-oxo-1-(3-(trifluoromethyl)phenyl)-1,2-dihydropyridine-3-carboxamide: structure in first source	2.6	1	0
bms 708163 BMS 708163: structure in first source	2.6	1	0	oxadiazole; ring assembly
azd3514 AZD3514: in Phase I clinical trial in patients with castrate-resistant prostate cancer (2/2013); structure in first source	2.17	1	0
jq1 compound [no description available]	3.13	4	0	carboxylic ester; organochlorine compound; tert-butyl ester; thienotriazolodiazepine	angiogenesis inhibitor; anti-inflammatory agent; antineoplastic agent; apoptosis inducer; bromodomain-containing protein 4 inhibitor; cardioprotective agent; ferroptosis inducer
jnj38877605 [no description available]	2.08	1	0	quinolines
N-[3-(1,3-benzothiazol-2-yl)-5,6-dihydro-4H-thieno[2,3-c]pyrrol-2-yl]acetamide [no description available]	2.08	1	0	benzothiazoles
dinaciclib [no description available]	2.21	1	0	pyrazolopyrimidine
1-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanone 1-(5-((2,4-difluorophenyl)thio)-4-nitrothiophen-2-yl)ethanone: a USP7 inhibitor; structure in first source	2.6	1	0
gsk525762a molibresib: mimicks acetylated histones; structure in first source	2.93	3	0	benzodiazepine
ML240 ML240 : A member of the class of quinazolines that is quinazoline which is substituted at positions 2, 5 and 8 by 2-amino-1H-benzimidazol-1-yl, benzylnitrilo and methoxy groups, respectively. It is a ATP-competetive inhibitor of AAA ATPase p97, also known as valosin-containing protein (VCP).	2.6	1	0	aromatic amine; aromatic ether; benzimidazoles; primary amino compound; quinazolines; secondary amino compound	antineoplastic agent
birinapant birinapant: a Smac mimetic with antineoplastic activity	2.6	1	0	dipeptide
torin 1 torin 1 : A member of the class of pyridoquinolines that is 9-(quinolin-3-yl)benzo[h][1,6]naphthyridin-2-one bearing an additional 4-(4-propionylpiperazin-1-yl)-3-(trifluoromethyl)phenyl substituent at position 1. It is a potent inhibitor of mTOR and exhibits anti-cancer properties.	2.08	1	0	N-acylpiperazine; N-arylpiperazine; organofluorine compound; pyridoquinoline; quinolines	antineoplastic agent; mTOR inhibitor
ly2886721 [no description available]	2.6	1	0
nms-p118 NMS-P118: a PARP-1 inhibitor; structure in first source	2.93	3	0
abt-199 venetoclax: A BCL-2 inhibitor with antineoplastic activity that is used in the treatment of CHRONIC LYMPHOCYTIC LEUKEMIA associated with chromosome 17p deletion; structure in first source.. venetoclax : A member of the class of pyrrolopyridines that is a potent inhibitor of the antiapoptotic protein B-cell lymphoma 2. It is used for treamtment of chronic lymphocytic leukemia with 17p deletion.	2.41	1	0	aromatic ether; C-nitro compound; monochlorobenzenes; N-alkylpiperazine; N-arylpiperazine; N-sulfonylcarboxamide; oxanes; pyrrolopyridine	antineoplastic agent; apoptosis inducer; B-cell lymphoma 2 inhibitor
ly2940680 [no description available]	2.08	1	0
tubastatin a [no description available]	2.6	1	0	hydroxamic acid; pyridoindole; tertiary amino compound	EC 3.5.1.98 (histone deacetylase) inhibitor
1-[4-fluoro-3-(trifluoromethyl)phenyl]-3-(5-pyridin-4-yl-1,3,4-thiadiazol-2-yl)urea [no description available]	2.08	1	0	ureas
pracinostat pracinostat : A hydroxamic acid that is N-hydroxyacrylamide which is substituted at position 3 by a 2-butyl-1-[2-(diethylamino)ethyl]-1H-benzimidazol-5-yl group (the E isomer). An orally available pan-histone deacetylase inhibitor with demonstrated activity in the treatment of advanced solid tumours.	2.6	1	0	benzimidazole; hydroxamic acid; olefinic compound; tertiary amino compound	antimalarial; antineoplastic agent; apoptosis inducer; EC 3.5.1.98 (histone deacetylase) inhibitor
ro 4929097 [no description available]	2.08	1	0	dibenzoazepine; dicarboxylic acid diamide; lactam; organofluorine compound	EC 3.4.23.46 (memapsin 2) inhibitor
LSM-6732 [no description available]	2.41	1	0	organonitrogen heterocyclic compound; organosulfur heterocyclic compound; tert-butyl ester
gsk4112 GSK4112: a Rev-erbalpha agonist; structure in first source	2.08	1	0
ve 821 3-amino-6-(4-(methylsulfonyl)phenyl)-N-phenylpyrazine-2-carboxamide: an antineoplastic agent; structure in first source	2.57	2	0	aromatic amide
spautin-1 [no description available]	2.6	1	0
torin 2 torin 2 : A member of the class of pyridoquinolines that is benzo[h][1,6]naphthyridin-2-one carrying additional 3-(trifluoromethyl)phenyl and 6-aminopyridin-3-yl substituents at positions 1 and 9 respectively. It is a potent inhibitor of mTOR and exhibits anti-cancer properties.	2.08	1	0	aminopyridine; organofluorine compound; primary amino compound; pyridoquinoline	antineoplastic agent; mTOR inhibitor
pf-4708671 [no description available]	2.08	1	0
ldn 57444 LDN 57444: inhibitor of ubiquitin C-terminal hydrolase-L1; structure in first source	2.6	1	0
gsk1210151a GSK1210151A: inhibitor of the BET family of proteins; structure in first source	2.6	1	0	imidazoquinoline
i-bet726 [no description available]	2.6	1	0
apr-246 eprenetapopt: works in tandem with cisplatin to cause apoptosis of tumor cells; structure in first source	7.13	1	0
acy-1215 ricolinostat: an HDAC6 inhibitor; structure in first source	2.6	1	0	pyrimidinecarboxylic acid
N-[4-(1-benzoyl-4-piperidinyl)butyl]-3-(3-pyridinyl)-2-propenamide [no description available]	2.08	1	0	benzamides; N-acylpiperidine
2-methoxy-N-[3-[4-[3-methyl-4-[(6-methyl-3-pyridinyl)oxy]anilino]-6-quinazolinyl]prop-2-enyl]acetamide 2-methoxy-N-[3-[4-[3-methyl-4-[(6-methyl-3-pyridinyl)oxy]anilino]-6-quinazolinyl]prop-2-enyl]acetamide : A member of the class of quinazolines that is quinazoline substituted by {3-methyl-4-[(6-methylpyridin-3-yl)oxy]phenyl}amino and 3-(2-methoxyacetamido)prop-1-en-1-yl groups at positions 4 and 6, respectively.	2.08	1	0	aromatic ether; methylpyridines; olefinic compound; quinazolines; secondary amino compound; secondary carboxamide; toluenes
belinostat [no description available]	2.08	1	0	olefinic compound
cudc-907 [no description available]	7.76	2	0
ascorbic acid Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.	7.6	1	0	ascorbic acid; vitamin C	coenzyme; cofactor; flour treatment agent; food antioxidant; food colour retention agent; geroprotector; plant metabolite; skin lightening agent
minocycline Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.	2.31	1	0
salicylates Salicylates: The salts or esters of salicylic acids, or salicylate esters of an organic acid. Some of these have analgesic, antipyretic, and anti-inflammatory activities by inhibiting prostaglandin synthesis.. hydroxybenzoate : Any benzoate derivative carrying a single carboxylate group and at least one hydroxy substituent.. salicylates : Any salt or ester arising from reaction of the carboxy group of salicylic acid, or any ester resulting from the condensation of the phenolic hydroxy group of salicylic acid with an organic acid.. salicylate : A monohydroxybenzoate that is the conjugate base of salicylic acid.	2.31	1	0	monohydroxybenzoate	plant metabolite
mobic Meloxicam: A benzothiazine and thiazole derivative that acts as a NSAID and cyclooxygenase-2 (COX-2) inhibitor. It is used in the treatment of RHEUMATOID ARTHRITIS; OSTEOARTHRITIS; and ANKYLOSING SPONDYLITIS.. meloxicam : A benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. A non-steroidal anti-inflammatory drug and selective inhibitor of COX-2, it is used particularly for the management of rheumatoid arthritis.	2.6	1	0	1,3-thiazoles; benzothiazine; monocarboxylic acid amide	analgesic; antirheumatic drug; cyclooxygenase 2 inhibitor; non-steroidal anti-inflammatory drug
ethyl 1-benzyl-3-hydroxy-2(5h)-oxopyrrole-4-carboxylate ethyl 1-benzyl-3-hydroxy-2(5H)-oxopyrrole-4-carboxylate: RN & structure given in first source	2.08	1	0	carboxylic acid; pyrroline
warfarin Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.. warfarin : A racemate comprising equal amounts of (R)- and (S)-warfarin. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.. 4-hydroxy-3-(3-oxo-1-phenylbutyl)-1-benzopyran-2-one : A member of the class of coumarins that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenyl-3-oxo-1-butyl group.	2.11	1	0	benzenes; hydroxycoumarin; methyl ketone
tipranavir tipranavir: inhibits HIV-1 protease. tipranavir : A pyridine-2-sulfonamide substituted at C-5 by a trifluoromethyl group and at the sulfonamide nitrogen by a dihydropyrone-containing m-tolyl substituent. It is an HIV-1 protease inhibitor.	2.6	1	0	sulfonamide	antiviral drug; HIV protease inhibitor
tasquinimod tasquinimod: a lead second generation quinoline-3-carboxamide anti-angiogenic agent for the treatment of prostate cancer; structure in first source	2.6	1	0
choline salicylate choline salicylate: exists as gel or solution	2.31	1	0	hydroxybenzoic acid
a 769662 [no description available]	2.08	1	0	biphenyls
gsk1265744 [no description available]	2.6	1	0	difluorobenzene; monocarboxylic acid amide; organic heterotricyclic compound; secondary carboxamide	HIV-1 integrase inhibitor
abt-267 ombitasvir: inhibits HCV NS5A protein, component of Viekirax. ombitasvir : A dipeptide derivative which is used which is in combination with dasabuvir sodium hydrate, paritaprevir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0	aromatic amide; carbamate ester; dipeptide; pyrrolidines	antiviral drug; hepatitis C virus nonstructural protein 5A inhibitor
abt-333 dasabuvir: an antiviral agent. dasabuvir : A member of the class of pyrimidone, which is (as the monohydrate of its sodium salt) in combination with ombitasvir, paritaprevir and ritonavir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.	2.6	1	0	aromatic ether; naphthalenes; pyrimidone; sulfonamide	antiviral drug; nonnucleoside hepatitis C virus polymerase inhibitor
byl719 [no description available]	6.51	4	2	proline derivative
rgfp966 [no description available]	2.6	1	0
rg2833 RG2833: a histone deacetylase inhibitor; structure in first source	2.6	1	0
transforming growth factor beta Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.	2.66	2	0
pi-1840 PI-1840: has both antineoplastic and proteasome inhibitory activities; structure in first source	2.6	1	0
LimKi 3 LIMKi3: LIMK inhibitor. LimKi 3 : A member of the class of pyrazoles that is 1-(2,6-dichlorophenyl)-1H-pyrazole which is substituted by a difluoromethyl group at position 3 and by a 2-(isobutyrylamino)-1,3-thiazol-5-yl group at position 5. It is a a potent cell-permeable inhibitor of LIM kinase 1 and 2.	2.08	1	0	1,3-thiazoles; dichlorobenzene; organofluorine compound; pyrazoles; secondary carboxamide	LIM kinase inhibitor
1-[4-amino-7-[3-(2-methoxyethylamino)propyl]-5-(4-methylphenyl)-6-pyrrolo[2,3-d]pyrimidinyl]-2-fluoroethanone [no description available]	2.08	1	0	pyrroles
pm 01183 PM 01183: a covalent DNA minor groove binder and antineoplastic; structure in first source	5.1	2	1
2-[5-[(3,5-dimethyl-1H-pyrrol-2-yl)methylidene]-4-methoxy-2-pyrrolylidene]indole [no description available]	2.08	1	0	dipyrrins
ceritinib ceritinib: an anaplastic lymphoma kinase inhibitor. ceritinib : A member of the class of aminopyrimidines that is 2,6-diamino-5-chloropyrimidine in which the amino groups at positions 2 and 6 are respectively carrying 2-methoxy-4-(piperidin-4-yl)-5-methylphenyl and 2-(isopropylsulfonyl)phenyl substituents. Used for the treatment of ALK-positive metastatic non-small cell lung cancer.	2.41	1	0	aminopyrimidine; aromatic ether; organochlorine compound; piperidines; secondary amino compound; sulfone	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
acy-738 [no description available]	2.6	1	0
pelabresib CPI-0610: a bromodomain and extra-terminal protein inhibitor with antineoplastic activity; structure in first source	2.6	1	0	monochlorobenzenes; organic heterotricyclic compound; primary carboxamide	antineoplastic agent; bromodomain-containing protein 4 inhibitor
N-hydroxy-3-[4-[[2-(2-methyl-1H-indol-3-yl)ethylamino]methyl]phenyl]-2-propenamide [no description available]	2.08	1	0	tryptamines
3-[(5-tert-butyl-1H-imidazol-4-yl)methylidene]-6-(phenylmethylene)piperazine-2,5-dione [no description available]	2.08	1	0	pyrazines
gsk837149a GSK837149A: structure in first source	2.08	1	0
N-[4-(3-chloro-4-fluoroanilino)-7-[[(3S)-3-oxolanyl]oxy]-6-quinazolinyl]-4-(dimethylamino)-2-butenamide [no description available]	2.08	1	0	quinazolines
N-[4-(3-chloro-4-fluoroanilino)-7-methoxy-6-quinazolinyl]-4-(1-piperidinyl)-2-butenamide [no description available]	2.08	1	0	quinazolines
wnt-c59 2-(4-(2-methylpyridin-4-yl)phenyl)-N-(4-(pyridin-3-yl)phenyl)acetamide: a PORCN acyltransferase inhibitor; structure in first source	2.08	1	0
5-[1-(2-hydroxyethyl)-3-pyridin-4-yl-4-pyrazolyl]-2,3-dihydroinden-1-one oxime [no description available]	2.08	1	0	indanes
gs-5806 presatovir: a respiratory syncytial virus entry inhibitor	2.6	1	0
cc-115 1-ethyl-7-(2-methyl-6-(1H-1,2,4-triazol-3-yl)pyridin-3-yl)-3,4-dihydropyrazino(2,3-b)pyrazin-2(1H)-one: an mTOR kinase inhibitor; structure in first source	3.51	1	0
doravirine [no description available]	2.6	1	0
epz005687 EPZ005687: inhibits EZH2 protein; structure in first source	3.51	1	0	indazoles
gn6958 GN6958: inhibits SUMO-sentrin specific protease 1 (SENP1); structure in first source	2.6	1	0
epz-6438 tazemetostat: a histone methyltransferase EZH2 inhibitor with antineoplastic activity	3.51	1	0
vx-787 pimodivir: non‐nucleotide inhibitor of the polymerase basic protein 2 (PB2) subunit of the influenza A that is active against H1N1, H7N9 and H5N1, as well as influenza A strains with reduced susceptibility to NAIs	2.6	1	0
ledipasvir ledipasvir : A benzimidazole derivative that is used in combination with sofosbuvir (under the trade name Harvoni) for the treatment of chronic hepatitis C genotype 1 infection.	2.6	1	0	azaspiro compound; benzimidazole; bridged compound; carbamate ester; carboxamide; fluorenes; imidazoles; L-valine derivative; N-acylpyrrolidine; organofluorine compound	antiviral drug; hepatitis C protease inhibitor
gs-5816 velpatasvir: an NS5A inhibitor used for treating hepatitis C infections. velpatasvir : A complex organic heteropentacyclic compound that is a hepatitis C virus nonstructural protein 5A inhibitor used in combination with sofosbuvir (under the brand name Epclusa) for treatment of patients with chronic hepatitis C of all six major genotypes.	2.6	1	0	carbamate ester; ether; imidazoles; L-valine derivative; N-acylpyrrolidine; organic heteropentacyclic compound; ring assembly	antiviral drug; hepatitis C virus nonstructural protein 5A inhibitor
g007-lk G007-LK: potent and specific small-molecule tankyrase inhibitor; structure in first source	2.6	1	0
gsk-2816126 GSK-2816126: inhibits EZH2 methyltransferase; structure in first source	3.51	1	0	piperazines; pyridines
4-((1-butyl-3-phenylureido)methyl)-n-hydroxybenzamide 4-((1-butyl-3-phenylureido)methyl)-N-hydroxybenzamide: inhibits HDAC6; structure in first source	2.6	1	0
selinexor selinexor: inhibits karyopherin XPO1	8.07	3	0
verdinexor verdinexor: a selective inhibitor of nuclear export	2.6	1	0
cb-839 [no description available]	2.76	2	0
mk-8742 elbasvir: inhibits NS5A protein of hepatitis C virus. elbasvir : A complex organic heterotetracyclic compound that is a hepatitis C virus nonstructural protein 5A inhibitor used in combination with grazoprevir (under the brand name Zepatier) for treatment of chronic HCV genotypes 1 or 4 infection in adults.	2.6	1	0	carbamate ester; imidazoles; L-valine derivative; N-acylpyrrolidine; organic heterotetracyclic compound; ring assembly	antiviral drug; hepatitis C virus nonstructural protein 5A inhibitor; hepatoprotective agent
atglistatin atglistatin: inhibits adipose triglyceride lipase; structure in first source. atglistatin : A biphenyl that is 1,1'-biphenyl substituted by (dimethylcarbamoyl)amino and dimethylamino groups at positions 3 and 4', respectively. It is a potent inhibitor of adipose triglyceride lipase activity (IC50 = 700nM).	2.6	1	0
pf-06463922 lorlatinib: inhibits both anaplastic lymphoma kinase and c-ros oncogene 1 (ROS1) protein. lorlatinib : A cyclic ether that is 16,17-dihydro-2H-8,4-(metheno)pyrazolo[4,3-h][2,5,11]benzoxadiazacyclotetradecin-15(10H)-one substituted by methyl groups at positions 2 and 10R, and by cyano, amino and fluoro groups at positions 3, 7 and 12 respectively. It is a small molecule inhibitor of ALK and ROS1 kinase developed by Pfizer for the treatment of ALK-positive non-small cell lung cancer.	2.41	1	0	aminopyridine; aromatic ether; azamacrocycle; benzamides; cyclic ether; monofluorobenzenes; nitrile; organic heterotetracyclic compound; pyrazoles	antineoplastic agent; EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
etp-46464 ETP-46464: inhibits ATM and Rad3-related kinase; structure in first source	3.19	1	0
xen445 [no description available]	2.6	1	0
santacruzamate a santacruzamate A: HDAC2 inhibitor from the Panamanian marine cyanobacterium cf. Symploca sp.; structure in first source	2.6	1	0	organonitrogen compound; organooxygen compound
glutaminase [no description available]	2.59	2	0
cyclin d1 Cyclin D1: Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.	4.22	5	0
ldc4297 LDC4297: a CDK7 inhibitor with antineoplastic activity; structure in first source. LDC4297 : A pyrazolotriazine that is pyrazolo[1,5-a][1,3,5]triazine substituted by a piperidin-3-yloxy group, [2-(1H-pyrazol-1-yl)benzyl]nitrilo group and an isopropyl group at positions 2, 4 and 8 respectively. It is a potent and selective CDK7 inhibitor and exhibits antiviral activity.	2.6	1	0	aromatic ether; piperidines; pyrazoles; pyrazolotriazine; secondary amino compound	antineoplastic agent; antiviral agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
enasidenib [no description available]	2.6	1	0	1,3,5-triazines; aminopyridine; aromatic amine; organofluorine compound; secondary amino compound; tertiary alcohol	antineoplastic agent; EC 1.1.1.42 (isocitrate dehydrogenase) inhibitor
sbi-0206965 SBI-0206965: inhibits ULK1 kinase; structure in first source	2.25	1	0
nct-501 NCT-501: inhibits aldehyde dehydrogenase 1A1; structure in first source	2.25	1	0
THZ531 THZ531: inhibits both CDK12 and CDK13; structure in first source. THZ531 : A member of the class of indoles that is 5-chloro-4-(1H-indol-3-yl)-N-[(3R)-piperidin-3-yl]pyrimidin-2-amine in which the piperidine NH group is substituted by a 4-{[(2E)-4-(dimethylamino)but-2-enoyl]amino}benzoyl group. It is a first-in-class CDK12 and CDK13 covalent kinase inhibitor with IC50 of 158 nM and 69 nM, respectively.	2.41	1	0	aminopyrimidine; enamide; indoles; N-acylpiperidine; organochlorine compound; secondary amino compound; secondary carboxamide	antineoplastic agent; apoptosis inducer; EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
vitamin b 12 Vitamin B 12: A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.	2.6	1	0
s 8932 [no description available]	2.6	1	0	aromatic amine; C-nucleoside; carboxylic ester; nitrile; phosphoramidate ester; pyrrolotriazine	anticoronaviral agent; antiviral drug; prodrug
nedaplatin nedaplatin: structure given in first source	7.25	1	0
tetra(4-n-methylpyridyl)porphine tetra(4-N-methylpyridyl)porphine: structure in first source	2.31	1	0
entecavir entecavir (anhydrous) : Guanine substituted at the 9 position by a 4-hydroxy-3-(hydroxymethyl)-2-methylidenecyclopentyl group. A synthetic analogue of 2'-deoxyguanosine, it is a nucleoside reverse transcriptase inhibitor with selective antiviral activity against hepatitis B virus. Entecavir is phosphorylated intracellularly to the active triphosphate form, which competes with deoxyguanosine triphosphate, the natural substrate of hepatitis B virus reverse transcriptase, inhibiting every stage of the enzyme's activity, although it has no activity against HIV. It is used for the treatment of chronic hepatitis B.	2.6	1	0	2-aminopurines; oxopurine; primary alcohol; secondary alcohol	antiviral drug; EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
chir 258 [no description available]	2.08	1	0
acyclovir Acyclovir: A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.. acyclovir : An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9. Used in the treatment of viral infections.	2.6	1	0	2-aminopurines; oxopurine	antimetabolite; antiviral drug
osi 027 OSI 027: inhibits both mTORC1 and mTORC2; structure in first source	2.08	1	0
nu 1025 NU 1064: structure in first source	3.5	7	0	phenols; quinazolines	EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
levoleucovorin Levoleucovorin: A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.. (6S)-5-formyltetrahydrofolic acid : The pharmacologically active (6S)-stereoisomer of 5-formyltetrahydrofolic acid.	2.61	2	0	5-formyltetrahydrofolic acid	antineoplastic agent; metabolite
cyclic gmp Cyclic GMP: Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed). 3',5'-cyclic GMP : A 3',5'-cyclic purine nucleotide in which the purine nucleobase is specified as guanidine.	2.13	1	0	3',5'-cyclic purine nucleotide; guanyl ribonucleotide	Escherichia coli metabolite; human metabolite; mouse metabolite; plant metabolite; Saccharomyces cerevisiae metabolite
folic acid folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.	4.23	4	0	folic acids; N-acyl-amino acid	human metabolite; mouse metabolite; nutrient
dacarbazine (E)-dacarbazine : A dacarbazine in which the N=N double bond adopts a trans-configuration.	10.36	12	1	dacarbazine
didanosine Didanosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.. didanosine : A purine 2',3'-dideoxyribonucleoside that is inosine in which the hydroxy groups at both the 2' and the 3' positions on the sugar moiety have been replaced by hydrogen. An antiviral drug, it is used as a medication to treat HIV/AIDS.	2.6	1	0	purine 2',3'-dideoxyribonucleoside	antimetabolite; antiviral drug; EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor; geroprotector; HIV-1 reverse transcriptase inhibitor
ganciclovir [no description available]	2.6	1	0	2-aminopurines; oxopurine	antiinfective agent; antiviral drug
valacyclovir Valacyclovir: A prodrug of acyclovir that is used in the treatment of HERPES ZOSTER and HERPES SIMPLEX VIRUS INFECTION of the skin and mucous membranes, including GENITAL HERPES.	2.6	1	0	L-valyl ester	antiviral drug
penciclovir penciclovir : A member of the class of 2-aminopurines that is guanine in which the hydrogen at position 9 is substituted by a 4-hydroxy-3-(hydroxymethyl)but-1-yl group. An antiviral drug, it is administered topically for treatment of herpes labialis. A prodrug, famciclovir, is used for oral administration.	2.6	1	0	2-aminopurines; propane-1,3-diols	antiviral drug
hli 373 [no description available]	2.08	1	0
4-hydroxyquinazoline 4-oxo-3,4-dihydroquinazoline: structure in first source	2.6	1	0	quinazolines
tegaserod tegaserod: a nonbenzamide 5-hydroxytryptamine(4) agonist; used in treatment of irritable bowel syndrome; marketing suspended 2007 in US due to higher incidence of MI, stroke, and unstable angina; structure given in first source	2.6	1	0	carboxamidine; guanidines; hydrazines; indoles	gastrointestinal drug; serotonergic agonist
norclozapine norclozapine: structure given in first source. N-desmethylclozapine : A dibenzodoazepine substituted with chloro and piperazino groups which is a major metabolite of clozapine; a potent and selective 5-HT2C serotonin receptor antagonist.	2.6	1	0	dibenzodiazepine; organochlorine compound; piperazines	delta-opioid receptor agonist; metabolite; serotonergic antagonist
pemetrexed pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT).	2.88	3	0	N-acyl-L-glutamic acid; pyrrolopyrimidine	antimetabolite; antineoplastic agent; EC 1.5.1.3 (dihydrofolate reductase) inhibitor; EC 2.1.1.45 (thymidylate synthase) inhibitor; EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor
sildenafil citrate Sildenafil Citrate: A PHOSPHODIESTERASE TYPE-5 INHIBITOR; VASODILATOR AGENT and UROLOGICAL AGENT that is used in the treatment of ERECTILE DYSFUNCTION and PRIMARY PULMONARY HYPERTENSION.. sildenafil citrate : The citrate salt of sildenafil.	2.08	1	0	citrate salt	EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor; vasodilator agent
aprepitant Aprepitant: A morpholine neurokinin-1 (NK1) receptor antagonist that is used in the management of nausea and vomiting caused by DRUG THERAPY, and for the prevention of POSTOPERATIVE NAUSEA AND VOMITING.. aprepitant : A morpholine-based antiemetic, which is or the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.	2.58	2	0	(trifluoromethyl)benzenes; cyclic acetal; morpholines; triazoles	antidepressant; antiemetic; neurokinin-1 receptor antagonist; peripheral nervous system drug; substance P receptor antagonist
azilsartan azilsartan: an angiotensin type 1 receptor blocker; receptor blocker. azilsartan : A benzimidazolecarboxylic acid that is benzimidazole-7-carboxylic acid substituted at position 2 by a methoxy group and at position 1 by a 2'-[(5-oxo-4,5-dihydro-1,2,4-oxadiazol-3-yl)biphenyl-4-yl]methyl group. Used (as the prodrug, azilsartan medoxomil) for treatment of hypertension.	2.6	1	0	1,2,4-oxadiazole; aromatic ether; benzimidazolecarboxylic acid	angiotensin receptor antagonist; antihypertensive agent
xav939 XAV939: selectively inhibits beta-catenin-mediated transcription; structure in first source. XAV939 : A thiopyranopyrimidine in which a 7,8-dihydro-5H-thiopyrano[4,3-d]pyrimidine skeleton is substituted at C-4 by a hydroxy group and at C-2 by a para-(trifluoromethyl)phenyl group.	3.22	5	0	(trifluoromethyl)benzenes; thiopyranopyrimidine	tankyrase inhibitor
2-carboxyarabinitol 1-phosphate [no description available]	2.08	1	0
hesperadin [no description available]	2.6	1	0
trypan blue Trypan Blue: A diazo-naphthalene sulfonate that is widely used as a stain.. trypan blue : An organosulfonate salt that is the tetrasodium salt of 3,3'-[(3,3'-dimethylbiphenyl-4,4'-diyl)didiazene-2,1-diyl]bis(5-amino-4-hydroxynaphthalene-2,7-disulfonic acid).	2.05	1	0
nintedanib nintedanib : A member of the class of oxindoles that is a kinase inhibitor used (in the form of its ethylsulfonate salt) for the treatment of idiopathic pulmonary fibrosis and cancer.	3.63	2	0
methylnitronitrosoguanidine Methylnitronitrosoguanidine: A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties.. N-methyl-N'-nitro-N-nitrosoguanidine : An N-nitroguanidine compound having nitroso and methyl substituents at the N'-position	2.13	1	0	nitroso compound	alkylating agent
6-bromoindirubin-3'-acetoxime 6-bromoindirubin-3'-acetoxime: a synthetic derivative of a compound from the Mediterranean mollusk Hexaplex trunculus, protects cells from varicella infection	2.6	1	0
n'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide [no description available]	2.6	1	0	catechols; hydrazide; hydrazone; naphthols	EC 3.6.5.5 (dynamin GTPase) inhibitor
ver 52296 luminespib : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-(2,4-dihydroxy-5-isopropylphenyl)-4-[4-(morpholin-4-ylmethyl)phenyl]-1,2-oxazole-3-carboxylic acid with the amino group of ethylamine.	2.08	1	0	aromatic amide; isoxazoles; monocarboxylic acid amide; morpholines; resorcinols	angiogenesis inhibitor; antineoplastic agent; Hsp90 inhibitor
sb-590885 N-{5-[2-{4-[2-(dimethylamino)ethoxy]phenyl}-4-(pyridin-4-yl)-1H-imidazol-5-yl]-2,3-dihydro-1H-inden-1-ylidene}hydroxylamine : A ketoxime that is the oxime of indan-1-one in which the hydrogen at position 5 has been replaced by an imidazol-5-yl group which has itself been substituted at positions 2 and 4 by p-[2-(dimethylamino)ethoxy]phenyl and pyridin-4-yl groups, respectively.	2.08	1	0	aromatic ether; imidazoles; ketoxime; pyridines; tertiary amino compound
XL413 XL413 : A benzofuropyrimidine that is 3,4-dihydro[1]benzofuro[3,2-d]pyrimidine substituted by (2S)-pyrrolidin-2-yl, oxo and chloro groups at positions 2, 4, and 8, respectively. It is a potent ATP competitive inhibitor of Cdc7 kinase (IC50 = 3.4 nM) and exhibits anticancer properties.	2.6	1	0	benzofuropyrimidine; organochlorine compound; pyrrolidines	antineoplastic agent; EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
rvx 208 apabetalone: a bromodomain and extra-terminal domain protein (BET) inhibitor; prevents interactions between BET proteins and acetyl-lysine residues on histone tails to modify epigenetic regulation	3.51	1	0
sta 9090 [no description available]	2.25	1	0	ring assembly; triazoles
bmn 673 talazoparib: inhibits both PARP1 and PARP2; structure in first source	15.65	55	0
pf-477736 PF 00477736: a Chk1 inhibitor; structure in first source. PF-00477736 : A diazepinoindole that is 8-amino-4,5-dihydro-6H-[1,2]diazepino[4,5,6-cd]indol-6-one which is substituted at position 2 by a 1-methylpyrazol-4-yl group and in which the amino group at position 8 has undergone condensation with the carboxy group of (2R)-2-cyclohexylglycine to give the corresponding carboxamide. It is an inhibitor of checkpoint kinase 1 (Chk 1).	2.08	1	0
me0328 ME0328: inhibits ARTD3; structure in first source	7.69	2	0
fenobam fenobam: in USAN fenobam refers to monohydrate	2.08	1	0	ureas
nvp-tnks656 [no description available]	2.6	1	0
pyrimidinones Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.	3.7	8	0
phenanthrenes Phenanthrenes: POLYCYCLIC AROMATIC HYDROCARBONS composed of three fused BENZENE rings.. phenanthrenes : Any benzenoid aromatic compound that consists of a phenanthrene skeleton and its substituted derivatives thereof.	3.11	4	0

olaparib

Cross-References

Synonyms (119)

Research Excerpts

Overview

Effects

Actions

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Roles (3)

Drug Classes (4)

Pathways (1)

Protein Targets (20)

Potency Measurements

Inhibition Measurements

Activation Measurements

Biological Processes (171)

Molecular Functions (67)

Ceullar Components (41)

Bioassays (731)

Research

Studies (1,298)

Market Indicators

Research Demand Index: 87.16

Study Types

Clinical Trials (385)

Trial Overview

Trial Outcomes

Best Percent Change in Tumour Size

Change From Baseline in ECOG Performance Status: Improvement Rate

Progression-Free Survival (PFS)

The Clinical Benefit Rate (CBR)

Duration of Response to Olaparib

Confirmed Objective Tumour Response (According to RECIST Criteria)

Duration of Response

Clinical Benefit (CB)

Best Percentage Change in Tumour Size

Progression-Free Survival (PFS)

Confirmed Objective Tumour Response (According to Response Evaluation Criteria In Solid Tumors (RECIST)

Objective Response Rate (ORR)

Disease Control Rate

Progression Free Survival (PFS)

Overall Survival (OS)

Overall Duration of Response

Confirmed RECIST Response and/or CA-125 Response

Best Percentage Change in Tumour Size

Best Percentage Change From Baseline in CA-125 Levels

Progression Free Survival (PFS)

Best QoL Response for Total Functional Analysis of Cancer Therapy - Ovarian (FACT-O)

Best Quality of Life (QoL) Response for Trial Outcome Index (TOI)

Best QoL Response for FACT-O Symptom Index (FOSI)

Best Percentage Change From Baseline in Tumour Size

Disease Control Rate (DCR)

Duration of Response

Objective Response Rate (ORR) Evaluated According to Response Evaluation Criteria In Solid Tumors (RECIST) Guidelines

Progression Free Survival (PFS)

CA-125 Levels (Ovarian Cancer Patients Only)

RECIST and CA-125 Response Separately and Combined

Objective Response Rate (ORR) (According to RECIST)

Improvement Rate for Total Functional Analysis of Cancer Therapy - Ovarian (FACT-O)

Improvement Rate for FACT-O Symptom Index (FOSI)

Functional Analysis of Cancer Therapy - Ovarian (FACT-O) Time to Worsening

FACT-O Symptom Index (FOSI) Time to Worsening

Duration of Response

Best Percentage Change in Cancer Antigen 125 (CA-125) Levels

Improvement Rate for Trial Outcome Index (TOI)

Percentage Change From Baseline in Tumour Size at Week 24

Time to Earlier of CA-125 or RECIST Progression

Progression Free Survival (PFS) (According to Response Evaluation Criteria in Solid Tumours [RECIST])

Trial Outcome Index(TOI)Time to Worsening

Best Objective Response

Overall Survival (OS)

Disease Control Rate

Tumour Response

Overall Survival

Progression Free Survival