Compounds > niraparib
Page last updated: 2024-11-13

niraparib

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Description

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. [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]

niraparib: structure in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

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. [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]

Cross-References

ID SourceID
PubMed CID24958198
CHEMBL ID1098298
CHEBI ID177298
SCHEMBL ID1421952
MeSH IDM0541827
PubMed CID24958200
CHEMBL ID1094636
CHEBI ID176844
SCHEMBL ID1421875
MeSH IDM0541827

Synonyms (91)

Synonym
CHEBI:177298
2-[4-(piperidin-3-yl)phenyl]-2h-indazole-7-carboxamide
bdbm50084625
CHEMBL1098298 ,
2-(4-(piperidin-3-yl)phenyl)-2h-indazole-7-carboxamide
SCHEMBL1421952
niraparib racemate;mk4827 racemate;mk 4827 racemate
1038915-75-1
NCGC00378571-02
AS-54143
mk-4827 racemate
AKOS030624359
2-(4-piperidin-3-ylphenyl)indazole-7-carboxamide
FT-0770704
mk-4827 (racemate)
BCP04302
mk-4827; mk 4827; mk4827
mfcd26383938
SB16547
NCGC00378571-03
P17554
PB39448
SY321246
2-[4-(3-piperidyl)phenyl]-2h-indazole-7-carboxamide
HY-10619
CHEBI:176844 ,
1038915-60-4
mk-4827 ,
niraparib
jnj-64091742
mk4827
zl-2306
CHEMBL1094636 ,
bdbm50316226
(s)-2-(4-(piperidin-3-yl)phenyl)-2h-indazole-7-carboxamide
zejula (tn)
niraparib (usan)
D10140
mk 4827 (base)
unii-hmc2h89n35
hmc2h89n35 ,
niraparib [usan:inn]
mk 4827
AKOS016004869
BCP9000940
BCP0726000077
mk-4827/mk4827
NCGC00346435-01
CS-0780
S2741
c19h20n4o
2h-indazole-7-carboxamide, 2-(4-(3s)-3-piperidinylphenyl)-
niraparib [inn]
niraparib [usan]
2-{4-[(3s)-piperidin-3-yl]phenyl}-2h-indazole-7-carboxamide
niraparib [who-dd]
niraparib [mi]
SCHEMBL1421875
3jd ,
gtpl8275
compound 56 [pmid 19873981]
2-[4-[(3s)-piperidin-3-yl]phenyl]indazole-7-carboxamide
AC-28447
DTXSID50146129 ,
EX-A290
NCGC00346435-04
DB11793
mk-4827(niraparib)
AS-35248
mfcd17779309
Q25326660
2-[4-(3s)-3-piperidinylphenyl]-2h-indazole-7-carboxamide
AMY4192
(s)-2-(4-(piperidin-3-yl)phenyl)-2h-indazole-7-carboxamide;mk-4827
CCG-267709
A857972
2h-indazole-7-carboxamide, 2-[4-(3s)-3-piperidinylphenyl]
nsc754355
nsc-754355
nsc-800020
nsc800020
mk-4827 (parp-1)
2-(4-(3s)-3-piperidinylphenyl)-2h-indazole-7-carboxamide
l01xx54
compound 56 (pmid 19873981)
niraparibum
dtxcid8068620
2-(4-((3s)-piperidin-3-yl)phenyl)indazole-7-carboxamide
2-(4-((3s)-piperidin-3-yl)phenyl)-2h-indazole-7-carboxamide
EN300-7364833
2h-indazole-7-carboxamide, 2-[4-(3s)-3-piperidinylphenyl]-; 2-[4-(3s)-3-piperidinylphenyl]-2h-indazole-7-carboxamide; niraparib; zejula; mk-4827

Research Excerpts

Toxicity

The primary endpoint (incidence of grade 3 or 4 thrombocytopenia-related events within 30 days after initial niraparib administration) was justified by the incidences of a global pivotal phase 3 study and its post-hoc safety analysis. These data demonstrate the importance of appropriate dose reduction according to toxicity criteria.

ExcerptReferenceRelevance
" In the pivotal ENGOT-OV16/NOVA trial, the dose reduction rate due to treatment-emergent adverse event (TEAE) was 68."( Safety and dose modification for patients receiving niraparib.
Berek, JS; Berton-Rigaud, D; Colombo, N; Ellard, S; Ghatage, P; Gonzalez-Martin, A; Guo, W; Hazard, S; Ledermann, J; Lesoin, A; Madry, R; Mahner, S; Matulonis, UA; Mirza, MR; Peen, U; Pineda, M; Redondo, A; Reinthaller, A; Rosengarten, O; Sehouli, J; Vergote, I, 2018)		0.48
" Adverse events (AEs) of special interest were based on the known safety profile of poly(ADP-ribose) polymerase inhibitors."( Efficacy and safety of niraparib as maintenance treatment in older patients (≥ 70 years) with recurrent ovarian cancer: Results from the ENGOT-OV16/NOVA trial.
Banerjee, S; Bover, I; Dørum, A; Fabbro, M; Follana, P; Goffin, F; Harter, P; Hazard, SJ; Hellman, K; Mahner, S; Matulonis, UA; Mirza, MR; Moore, KN; Pineda, MJ; Provencher, D; Shapira-Frommer, R; Tinker, AV; Tognon, G; Vázquez, IP; Wenham, RM, 2019)		0.51
"These data demonstrate the importance of appropriate dose reduction according to toxicity criteria and support the safe long-term use of niraparib for maintenance treatment in patients with recurrent ovarian cancer."( Long-term safety in patients with recurrent ovarian cancer treated with niraparib versus placebo: Results from the phase III ENGOT-OV16/NOVA trial.
Barceló, IB; Benigno, B; Berton-Rigaud, D; Bessette, P; Buscema, J; de Jong, FA; du Bois, A; Dørum, A; Gupta, D; Herráez, AC; Herrstedt, J; Kalbacher, E; Lau, S; Ledermann, JA; Levy, T; Lorusso, D; Mahner, S; Matulonis, UA; Mirza, MR; Rimel, BJ; Vergote, I; Wang, P, 2020)		0.56
" Safety evaluations included the incidence of treatment-emergent adverse events (TEAEs), including serious TEAEs."( Phase 2 single-arm study on the efficacy and safety of niraparib in Japanese patients with heavily pretreated, homologous recombination-deficient ovarian cancer.
Aoki, D; Hamanishi, J; Harano, K; Hasegawa, K; Hirasawa, T; Hori, K; Kase, Y; Komiyama, S; Kondo, E; Matsuura, M; Nakai, H; Nakamura, H; Nakamura, T; Okamoto, A; Sakata, J; Soeda, J; Sugiyama, T; Sumino, S; Suri, A; Tabata, T; Takehara, K; Takekuma, M; Yanagida, S; Yokoyama, Y, 2021)		0.62
" The primary endpoint (incidence of grade 3 or 4 thrombocytopenia-related events within 30 days after initial niraparib administration) was justified by the incidences of a global pivotal phase 3 study and its post-hoc safety analysis on thrombocytopenia, the major hematological adverse event of niraparib."( Phase 2 single-arm study on the safety of maintenance niraparib in Japanese patients with platinum-sensitive relapsed ovarian cancer.
Hamanishi, J; Hasegawa, K; Itamochi, H; Kase, Y; Matsumoto, T; Matsuura, M; Miura, K; Nagao, S; Nakai, H; Sumino, S; Suri, A; Takehara, K; Takeshima, N; Tanaka, N; Tokunaga, H; Ushijima, K; Watari, H; Yokoyama, Y, 2021)		0.62
" The number of patients with dose-limiting toxicities in cycle 1 and number with treatment-emergent adverse events were primary endpoints."( The safety, tolerability and pharmacokinetics of niraparib in Japanese patients with solid tumours: results of a phase I dose-escalation study.
Iwasa, S; Kase, Y; Kitano, S; Kondo, S; Koyama, T; Sato, J; Shibaki, R; Shimizu, T; Shimomura, A; Sumino, S; Suri, A; Tamura, K; Yamamoto, N; Yonemori, K, 2021)		0.62
" All patients in both cohorts developed treatment-emergent adverse events."( The safety, tolerability and pharmacokinetics of niraparib in Japanese patients with solid tumours: results of a phase I dose-escalation study.
Iwasa, S; Kase, Y; Kitano, S; Kondo, S; Koyama, T; Sato, J; Shibaki, R; Shimizu, T; Shimomura, A; Sumino, S; Suri, A; Tamura, K; Yamamoto, N; Yonemori, K, 2021)		0.62
"2%) had grade 3/4 treatment-emergent adverse events, the most common being thrombocytopenia (26."( Niraparib with androgen receptor-axis-targeted therapy in patients with metastatic castration-resistant prostate cancer: safety and pharmacokinetic results from a phase 1b study (BEDIVERE).
Bradic, B; Chi, KN; De Meulder, M; Espina, BM; Francis, P; Graff, JN; Hayreh, V; Hazra, A; Lattouf, JB; Mamidi, RNVS; Posadas, EM; Rezazadeh Kalebasty, A; Saad, F; Shore, ND; Yu, A; Zhu, E, 2021)		0.62
" Grade greater than or equal to 3 adverse events occurred in 34."( Efficacy and Safety of Niraparib as Maintenance Treatment in Patients With Extensive-Stage SCLC After First-Line Chemotherapy: A Randomized, Double-Blind, Phase 3 Study.
Ai, X; Chen, G; Cui, J; Ding, C; Dong, X; Gao, B; He, J; Hu, C; Hu, X; Huang, C; Jiang, L; Li, J; Li, X; Li, Y; Liao, W; Liu, A; Liu, C; Liu, X; Liu, Z; Lu, S; Ma, Z; Pan, Y; Shi, J; Song, Y; Wang, K; Wang, M; Wang, W; Xiong, J; Yang, N; Zhang, B; Zhang, D; Zhang, H; Zhang, X; Zhang, Y; Zhao, J; Zhou, J, 2021)		0.62
" Response and adverse events (AEs) were analyzed by Response Evaluation Criteria in Solid Tumors v1."( The efficacy and safety of niraparib for ovarian cancer: a single-center observational study from China.
Chen, X; Cheng, X; Dai, Z; Gu, H; Guo, W; Ni, J; Wang, Y; Xu, X; Zhao, Q; Zhou, R, 2021)		0.62
" Leg swelling was observed as a new adverse event."( The efficacy and safety of niraparib for ovarian cancer: a single-center observational study from China.
Chen, X; Cheng, X; Dai, Z; Gu, H; Guo, W; Ni, J; Wang, Y; Xu, X; Zhao, Q; Zhou, R, 2021)		0.62
" 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
" The authors retrospectively investigated niraparib-related adverse events (AEs) through data mining of the US Food and Drug Administration Adverse Event Reporting System (FAERS)."( A real-world pharmacovigilance study of FDA adverse event reporting system (FAERS) events for niraparib.
Chen, G; Guo, M; Li, F; Li, J; Shu, Y, 2022)		0.72
" The most common adverse events typically occurred within 3 months of starting niraparib."( Real-world safety and effectiveness of maintenance niraparib for platinum-sensitive recurrent ovarian cancer: A GEICO retrospective observational study within the Spanish expanded-access programme.
Barquin, A; Churruca, C; Constenla, M; Cueva, JF; de Juan, A; Estévez, P; Fernández, I; Gallego, A; García, Y; González-Martín, A; Guerra, E; Herrero, A; Juárez, A; Legerén, M; Manso, L; Marquina, G; Martín, C; Martín, T; Martínez Bueno, A; Maximiano, C; Palacio, I; Pardo, B; Quindós, M; Sánchez, L; Santaballa, A; Yubero, A, 2023)		0.91
" This review focuses on the adverse events associated with niraparib and their management to maintain efficacy of niraparib treatment and improve quality of life for patients."( Safety and management of niraparib monotherapy in ovarian cancer clinical trials.
Buckley, L; González-Martin, A; Matulonis, UA; Mirza, MR; Monk, BJ; Moore, KN; Rimel, BJ; Wu, X, 2023)		0.91
" The most common grade ≥ 3 treatment-emergent adverse events in niraparib patients were thrombocytopenia (39."( Progression-free survival and safety at 3.5years of follow-up: results from the randomised phase 3 PRIMA/ENGOT-OV26/GOG-3012 trial of niraparib maintenance treatment in patients with newly diagnosed ovarian cancer.
Backes, F; Compton, N; Freyer, G; González-Martín, A; Graybill, W; Heitz, F; Lorusso, D; Malinowska, IA; McCormick, CC; Mirza, MR; Monk, BJ; Moore, RG; O'Cearbhaill, RE; Pothuri, B; Redondo, A; Shtessel, L; Vergote, I; Vulsteke, C, 2023)		0.91

Pharmacokinetics

Niraparib (200 or 300mg/day) was tolerable and had a favourable pharmacokinetic profile in Japanese patients with advanced solid tumours.

ExcerptReferenceRelevance
"Niraparib (200 or 300 mg/day) was tolerable and had a favourable pharmacokinetic profile in Japanese patients with advanced solid tumours."( The safety, tolerability and pharmacokinetics of niraparib in Japanese patients with solid tumours: results of a phase I dose-escalation study.
Iwasa, S; Kase, Y; Kitano, S; Kondo, S; Koyama, T; Sato, J; Shibaki, R; Shimizu, T; Shimomura, A; Sumino, S; Suri, A; Tamura, K; Yamamoto, N; Yonemori, K, 2021)		0.62

Compound-Compound Interactions

Niraparib, a PARP inhibitor, in combination with Radium-223 for the treatment of castrate-resistant prostate cancer (mCRPC) in men without known BRCA mutations.

ExcerptReferenceRelevance
" To our knowledge, no published or ongoing trial is trying to answer the question if patient can benefit from a potentially complete resection combined with PARPi maintenance in OC patients with secondary recurrence."( A phase II trial of cytoreductive surgery combined with niraparib maintenance in platinum-sensitive, secondary recurrent ovarian cancer: SGOG SOC-3 study.
Ai, Z; Bao, W; Chen, X; Feng, Y; Gao, W; Huang, H; Jia, H; Jiang, R; Jiang, W; Li, J; Li, Y; Liu, J; Luan, Y; Shi, T; Teng, Y; Wang, X; Wu, S; Yin, S; Yu, A; Zang, R; Zhang, J; Zhang, P; Zhang, W; Zhang, Y; Zhu, J; Zhu, T; Zhu, Y, 2020)		0.56
"To identify the safety of niraparib, a PARP inhibitor, in combination with Radium-223 for the treatment of metastatic castrate-resistant prostate cancer (mCRPC) in men without known BRCA mutations."( Phase I Study of Niraparib in Combination with Radium-223 for the Treatment of Metastatic Castrate-Resistant Prostate Cancer.
Choudhury, AD; Einstein, D; Kelly, WK; Knudsen, K; Leiby, B; Quinn, Z; Sartor, O; Sonpavde, G; Sweeney, C; Szmulewitz, R; Yang, ES, 2023)		0.91
" Niraparib dose was escalated in combination with standard dosing of Radium-223 using a time-to-event continual reassessment method."( Phase I Study of Niraparib in Combination with Radium-223 for the Treatment of Metastatic Castrate-Resistant Prostate Cancer.
Choudhury, AD; Einstein, D; Kelly, WK; Knudsen, K; Leiby, B; Quinn, Z; Sartor, O; Sonpavde, G; Sweeney, C; Szmulewitz, R; Yang, ES, 2023)		0.91

Bioavailability

ExcerptReferenceRelevance
"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
"The poly-(ADP-ribose) polymerase (PARP) inhibitor, MK-4827, is a novel potent, orally bioavailable PARP-1 and PARP-2 inhibitor currently in phase I clinical trials for cancer treatment."( MK-4827, a PARP-1/-2 inhibitor, strongly enhances response of human lung and breast cancer xenografts to radiation.
Ang, KK; Buchholz, T; Buser-Doepner, C; Mason, KA; Mathur, A; Milas, L; Toniatti, C; Valdecanas, D; Wang, L, 2012)		0.38
"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

Dosage Studied

Niraparib dosing was at the treating physician's discretion (300 mg/day fixed starting dose or individualised starting dose [ISD] according to baseline body weight and platelet count) Dose interruptions, dose reductions, haematological toxicities and asthenia/fatigue were less common with ISD. progression-free survival was similar irrespective of dosing strategy.

ExcerptRelevanceReference
" Efficacy analyses were additionally done in all dosed patients with measurable disease at baseline."( Niraparib monotherapy for late-line treatment of ovarian cancer (QUADRA): a multicentre, open-label, single-arm, phase 2 trial.
Azodi, M; Berek, JS; Chan, JK; Cloven, N; Cristea, M; DiSilvestro, P; Fleming, GF; Geller, MA; Li, Y; Luptakova, K; Matei, DE; Matulonis, UA; Miller, DS; Monk, BJ; Moore, KN; Oza, AM; Rimel, BJ; Secord, AA; Sun, K; Wahner Hendrickson, AE, 2019)		0.51
" 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
" Individualized niraparib dosing is effective and safe and should be considered standard practice in this setting."( Niraparib maintenance therapy in patients with platinum-sensitive recurrent ovarian cancer using an individualized starting dose (NORA): a randomized, double-blind, placebo-controlled phase III trial
Abulizi, G; An, RF; Chen, LP; Chen, QH; Cui, H; Gao, YN; Hao, M; Hou, JM; Huang, XH; Huang, Y; Kong, BH; Li, GL; Liu, JH; Liu, ZL; Lou, G; Lu, WG; Lu, X; Mirza, MR; Tian, XF; Wang, DB; Wang, J; Wang, K; Wang, L; Wen, H; Wu, LY; Wu, XH; Yan, XJ; Yang, HY; Yang, JX; Yin, RT; Zhang, C; Zhang, Y; Zhou, Q; Zhu, JQ, 2021)		0.62
" A weight- and platelet count-based individualised dosage regimen introduced during the trial (and subsequently approved) appeared to improve haematological tolerability."( Niraparib: A Review in First-Line Maintenance Therapy in Advanced Ovarian Cancer.
Lee, A, 2021)		0.62
" Starting treatment at a personalised lower dosage may also reduce the likelihood of adverse drug reactions."( Niraparib: A Review in First-Line Maintenance Therapy in Advanced Ovarian Cancer.
Lee, A, 2021)		0.62
" Niraparib dose was escalated in combination with standard dosing of Radium-223 using a time-to-event continual reassessment method."( Phase I Study of Niraparib in Combination with Radium-223 for the Treatment of Metastatic Castrate-Resistant Prostate Cancer.
Choudhury, AD; Einstein, D; Kelly, WK; Knudsen, K; Leiby, B; Quinn, Z; Sartor, O; Sonpavde, G; Sweeney, C; Szmulewitz, R; Yang, ES, 2023)		0.91
" Niraparib dosing was at the treating physician's discretion (300 mg/day fixed starting dose or individualised starting dose [ISD] according to baseline body weight and platelet count)."( Real-world safety and effectiveness of maintenance niraparib for platinum-sensitive recurrent ovarian cancer: A GEICO retrospective observational study within the Spanish expanded-access programme.
Barquin, A; Churruca, C; Constenla, M; Cueva, JF; de Juan, A; Estévez, P; Fernández, I; Gallego, A; García, Y; González-Martín, A; Guerra, E; Herrero, A; Juárez, A; Legerén, M; Manso, L; Marquina, G; Martín, C; Martín, T; Martínez Bueno, A; Maximiano, C; Palacio, I; Pardo, B; Quindós, M; Sánchez, L; Santaballa, A; Yubero, A, 2023)		0.91
" Dose interruptions, dose reductions, haematological toxicities and asthenia/fatigue were less common with ISD than fixed starting dose niraparib, but progression-free survival was similar irrespective of dosing strategy."( Real-world safety and effectiveness of maintenance niraparib for platinum-sensitive recurrent ovarian cancer: A GEICO retrospective observational study within the Spanish expanded-access programme.
Barquin, A; Churruca, C; Constenla, M; Cueva, JF; de Juan, A; Estévez, P; Fernández, I; Gallego, A; García, Y; González-Martín, A; Guerra, E; Herrero, A; Juárez, A; Legerén, M; Manso, L; Marquina, G; Martín, C; Martín, T; Martínez Bueno, A; Maximiano, C; Palacio, I; Pardo, B; Quindós, M; Sánchez, L; Santaballa, A; Yubero, A, 2023)		0.91
" Once-daily niraparib dosing may be advantageous for some patients for many reasons, including night-time dosing which may help alleviate gastrointestinal symptoms."( Safety and management of niraparib monotherapy in ovarian cancer clinical trials.
Buckley, L; González-Martin, A; Matulonis, UA; Mirza, MR; Monk, BJ; Moore, KN; Rimel, BJ; Wu, X, 2023)		0.91
" Individualized dosing is essential to minimize adverse events."( Real-world data on niraparib maintenance treatment in patients with non-gBRCA mutated platinum-sensitive recurrent ovarian cancer.
Aune, G; Bentzen, AG; Berge Nilsen, E; Bjørge, L; Dørum, A; Fallås Dahl, J; Ingebrigtsen, VA; Lindemann, K; Solheim, O; Vilming, B; Vistad, I; Zucknick, M, 2023)		0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitorAn EC 2.4.2.* (pentosyltransferase) inhibitor that interferes with the action of a NAD(+) ADP-ribosyltransferase (EC 2.4.2.30).
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitorAn EC 2.4.2.* (pentosyltransferase) inhibitor that interferes with the action of a NAD(+) ADP-ribosyltransferase (EC 2.4.2.30).
radiosensitizing agentA drug that makes increases the sensitivity of tumour cells to radiation therapy.
apoptosis inducerAny 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]

Drug Classes (5)

ClassDescription
indazoles
piperidines
benzenesAny benzenoid aromatic compound consisting of the benzene skeleton and its substituted derivatives.
primary carboxamideA carboxamide resulting from the formal condensation of a carboxylic acid with ammonia; formula RC(=O)NH2.
2-[4-(piperidin-3-yl)phenyl]-2H-indazole-7-carboxamideA 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.
[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]

Protein Targets (22)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency23.91850.01237.983543.2770AID1645841
Spike glycoproteinSevere acute respiratory syndrome-related coronavirusPotency35.48130.009610.525035.4813AID1479145
Fumarate hydrataseHomo sapiens (human)Potency11.77040.00308.794948.0869AID1347053
EWS/FLI fusion proteinHomo sapiens (human)Potency3.84070.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
cytochrome P450 2D6Homo sapiens (human)Potency23.91850.00108.379861.1304AID1645840
polyproteinZika virusPotency11.77040.00308.794948.0869AID1347053
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Poly [ADP-ribose] polymerase 1Homo sapiens (human)IC50 (µMol)0.00320.00020.81239.8100AID1205269; AID477514
Poly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)IC50 (µMol)11.31730.00190.62935.0000AID1428392; AID1895769; AID477534
Poly [ADP-ribose] polymerase 1Homo sapiens (human)IC50 (µMol)0.02780.00020.81239.8100AID1064455; AID1064607; AID1205269; AID1205300; AID1205301; AID1276413; AID1428384; AID1428386; AID1631788; AID1638254; AID1802336; AID1872299; AID1895766; AID477514; AID762672
Poly [ADP-ribose] polymerase 1Homo sapiens (human)Ki0.00320.00060.65955.0000AID1638254
5-hydroxytryptamine receptor 2ARattus norvegicus (Norway rat)IC50 (µMol)0.00210.00040.908610.0000AID1638281
5-hydroxytryptamine receptor 2ARattus norvegicus (Norway rat)Ki0.00400.00010.601710.0000AID1638281
Sodium-dependent dopamine transporterRattus norvegicus (Norway rat)IC50 (µMol)0.00210.00070.97749.7000AID1638281
Sodium-dependent dopamine transporterRattus norvegicus (Norway rat)Ki0.00400.00030.37088.1600AID1638281
D(2) dopamine receptorRattus norvegicus (Norway rat)IC50 (µMol)0.00210.00010.54948.4000AID1638281
D(2) dopamine receptorRattus norvegicus (Norway rat)Ki0.00400.00000.437510.0000AID1638281
Protein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)IC50 (µMol)29.02022.40006.40979.0000AID1428398
Protein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)IC50 (µMol)9.51891.73785.66258.9125AID1428397
Protein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)IC50 (µMol)2.61530.56234.10539.7724AID1428394; AID1428395
Protein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)IC50 (µMol)0.43670.07902.43076.6500AID1428396
Poly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)IC50 (µMol)5.12930.00210.67505.1300AID1428393
Poly [ADP-ribose] polymerase 2Homo sapiens (human)IC50 (µMol)0.23060.00010.21886.6000AID1205300; AID1205301; AID1428387; AID1638281; AID1872300; AID1895767; AID477512
Poly [ADP-ribose] polymerase 2Homo sapiens (human)Ki0.00400.00070.00480.0175AID1638281
Protein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)IC50 (µMol)0.40760.33001.68274.3900AID1428390; AID477535
Protein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)IC50 (µMol)0.37970.00351.12186.3000AID1205300; AID1205301; AID1428389; AID477511
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Cytochrome P450 1A2 Rattus norvegicus (Norway rat)EC50 (µMol)0.02400.00400.01400.0240AID477515
Poly [ADP-ribose] polymerase 1Homo sapiens (human)EC50 (µMol)0.02400.00040.18093.0000AID1205270; AID477515
Poly [ADP-ribose] polymerase 2Homo sapiens (human)EC50 (µMol)0.02400.00250.00840.0240AID1205270; AID477515
Protein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)EC50 (µMol)0.02400.00250.00840.0240AID1205270; AID477515
Cytochrome P450 1A2 Rattus norvegicus (Norway rat)EC50 (µMol)0.00400.00400.01400.0240AID477515
Poly [ADP-ribose] polymerase 1Homo sapiens (human)EC50 (µMol)7.80200.00040.18093.0000AID1205270; AID477515; AID762670; AID762671
Poly [ADP-ribose] polymerase 1Homo sapiens (human)Kd0.00100.00020.43565.3100AID1895777
Protein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)Kd5.00003.10006.06009.7000AID1895786
Protein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)Kd10.00001.00001.95002.9000AID1895790
Poly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)Kd10.00000.00421.50918.9000AID1895782
Poly [ADP-ribose] polymerase 2Homo sapiens (human)EC50 (µMol)0.00400.00250.00840.0240AID1205270; AID477515
Poly [ADP-ribose] polymerase 2Homo sapiens (human)Kd0.07800.00030.29141.4000AID1895778
Protein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)Kd0.27200.00070.20430.5030AID1895780
Protein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)EC50 (µMol)0.00400.00250.00840.0240AID1205270; AID477515
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Cytochrome P450 1A2 Rattus norvegicus (Norway rat)EC90 (µMol)0.22000.04500.13250.2200AID477515
Poly [ADP-ribose] polymerase 1Homo sapiens (human)EC90 (µMol)0.22000.04500.13250.2200AID477515
Poly [ADP-ribose] polymerase 2Homo sapiens (human)EC90 (µMol)0.22000.04500.13250.2200AID477515
Protein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)EC90 (µMol)0.22000.04500.13250.2200AID477515
Cytochrome P450 1A2 Rattus norvegicus (Norway rat)EC90 (µMol)0.04500.04500.13250.2200AID477515
Poly [ADP-ribose] polymerase 1Homo sapiens (human)EC90 (µMol)0.04500.04500.13250.2200AID477515
Poly [ADP-ribose] polymerase 1Homo sapiens (human)IC90 (µMol)0.04930.04600.04930.0520AID1205270; AID1205300; AID1205301
Poly [ADP-ribose] polymerase 2Homo sapiens (human)EC90 (µMol)0.04500.04500.13250.2200AID477515
Poly [ADP-ribose] polymerase 2Homo sapiens (human)IC90 (µMol)0.04930.04600.04930.0520AID1205270; AID1205300; AID1205301
Protein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)EC90 (µMol)0.04500.04500.13250.2200AID477515
Protein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)IC90 (µMol)0.04930.04600.04930.0520AID1205270; AID1205300; AID1205301
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (107)

Processvia Protein(s)Taxonomy
DNA damage responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrion organizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrial DNA metabolic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of protein localizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to oxidative stressPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein modification processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrial DNA repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of transcription by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
telomere maintenancePoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
double-strand break repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
apoptotic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA damage responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
response to gamma radiationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of cardiac muscle hypertrophyPoly [ADP-ribose] polymerase 1Homo sapiens (human)
carbohydrate biosynthetic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein autoprocessingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
signal transduction involved in regulation of gene expressionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
macrophage differentiationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA ADP-ribosylationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of DNA-templated transcription, elongationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to insulin stimulusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of intracellular estrogen receptor signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of transcription elongation by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to UVPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
innate immune responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of circadian sleep/wake cycle, non-REM sleepPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of innate immune responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of DNA-templated transcriptionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
decidualizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of catalytic activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of mitochondrial depolarizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of SMAD protein signal transductionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of necroptotic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein poly-ADP-ribosylationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein auto-ADP-ribosylationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein localization to chromatinPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to zinc ionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
replication fork reversalPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of cGAS/STING signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of protein localization to nucleusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of oxidative stress-induced neuron intrinsic apoptotic signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of single strand break repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
response to aldosteronePoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of adipose tissue developmentPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengtheningPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to amyloid-betaPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of myofibroblast differentiationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of base-excision repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of double-strand break repair via homologous recombinationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to nerve growth factor stimulusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
ATP generation from poly-ADP-D-ribosePoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of ATP biosynthetic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA repairPoly [ADP-ribose] polymerase 2Homo sapiens (human)
base-excision repairPoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA damage responsePoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA ADP-ribosylationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
decidualizationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
positive regulation of cell growth involved in cardiac muscle cell developmentPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein poly-ADP-ribosylationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein auto-ADP-ribosylationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
response to oxygen-glucose deprivationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
extrinsic apoptotic signaling pathwayPoly [ADP-ribose] polymerase 2Homo sapiens (human)
hippocampal neuron apoptotic processPoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA repair-dependent chromatin remodelingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
double-strand break repairPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein poly-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
telomere maintenanceProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
double-strand break repairProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
positive regulation of DNA ligationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
regulation of mitotic spindle organizationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
protein localization to site of double-strand breakProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
DNA ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
negative regulation of isotype switchingProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
protein auto-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
negative regulation of telomerase RNA reverse transcriptase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
positive regulation of double-strand break repair via nonhomologous end joiningProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
double-strand break repairProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
peptidyl-serine phosphorylationPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
peptidyl-threonine phosphorylationPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
protein polyubiquitinationPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
mitotic spindle organizationPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
protein transportPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
Wnt signaling pathwayPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
regulation of telomere maintenance via telomerasePoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
positive regulation of telomere maintenance via telomerasePoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
mRNA transportPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
spindle assemblyPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
cell divisionPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
positive regulation of telomerase activityPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
protein localization to chromosome, telomeric regionPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
protein poly-ADP-ribosylationPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
protein auto-ADP-ribosylationPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
positive regulation of canonical Wnt signaling pathwayPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
positive regulation of telomere cappingPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengtheningPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
negative regulation of telomeric DNA bindingPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
negative regulation of maintenance of mitotic sister chromatid cohesion, telomericPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
DNA damage responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrion organizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrial DNA metabolic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of protein localizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to oxidative stressPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein modification processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrial DNA repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of transcription by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
telomere maintenancePoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
double-strand break repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
apoptotic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA damage responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
response to gamma radiationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of cardiac muscle hypertrophyPoly [ADP-ribose] polymerase 1Homo sapiens (human)
carbohydrate biosynthetic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein autoprocessingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
signal transduction involved in regulation of gene expressionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
macrophage differentiationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
DNA ADP-ribosylationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of DNA-templated transcription, elongationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to insulin stimulusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of intracellular estrogen receptor signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of transcription elongation by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to UVPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
innate immune responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of circadian sleep/wake cycle, non-REM sleepPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of innate immune responsePoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of DNA-templated transcriptionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIPoly [ADP-ribose] polymerase 1Homo sapiens (human)
decidualizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of catalytic activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of mitochondrial depolarizationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of SMAD protein signal transductionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of necroptotic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein poly-ADP-ribosylationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein auto-ADP-ribosylationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein localization to chromatinPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to zinc ionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
replication fork reversalPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of cGAS/STING signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of protein localization to nucleusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of oxidative stress-induced neuron intrinsic apoptotic signaling pathwayPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of single strand break repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
response to aldosteronePoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of adipose tissue developmentPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengtheningPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to amyloid-betaPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of myofibroblast differentiationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
regulation of base-excision repairPoly [ADP-ribose] polymerase 1Homo sapiens (human)
positive regulation of double-strand break repair via homologous recombinationPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cellular response to nerve growth factor stimulusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
ATP generation from poly-ADP-D-ribosePoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of ATP biosynthetic processPoly [ADP-ribose] polymerase 1Homo sapiens (human)
negative regulation of transcription by RNA polymerase IIProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
protein poly-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
negative regulation of gene expressionProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
negative regulation of gene expressionProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
positive regulation of tyrosine phosphorylation of STAT proteinProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
negative regulation of tyrosine phosphorylation of STAT proteinProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
innate immune responseProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
negative regulation of DNA-templated transcriptionProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
negative regulation of type II interferon-mediated signaling pathwayProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
positive regulation of interleukin-4-mediated signaling pathwayProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
protein poly-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
chromatin organizationProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
negative regulation of gene expressionProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
viral protein processingProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
translesion synthesisProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
negative regulation of NF-kappaB transcription factor activityProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
NAD biosynthesis via nicotinamide riboside salvage pathwayProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
negative regulation of DNA-templated transcriptionProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
negative regulation of fibroblast proliferationProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
protein poly-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
protein auto-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
negative regulation of protein K63-linked ubiquitinationProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
viral protein processingProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
endoplasmic reticulum unfolded protein responseProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
NAD biosynthesis via nicotinamide riboside salvage pathwayProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
IRE1-mediated unfolded protein responseProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
protein auto-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
cellular response to leukemia inhibitory factorProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
negative regulation of cytoplasmic translationProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
protein auto-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
protein polyubiquitinationPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
Wnt signaling pathwayPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
positive regulation of telomere maintenance via telomerasePoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
protein localization to chromosome, telomeric regionPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
protein poly-ADP-ribosylationPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
protein auto-ADP-ribosylationPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
positive regulation of canonical Wnt signaling pathwayPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
positive regulation of telomere cappingPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
negative regulation of telomere maintenance via telomere lengtheningPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
nuclear envelope organizationProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
spermatogenesisProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
protein transportProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
cell differentiationProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
mRNA transportProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
protein auto-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
DNA repairPoly [ADP-ribose] polymerase 2Homo sapiens (human)
base-excision repairPoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA damage responsePoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA ADP-ribosylationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
decidualizationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
positive regulation of cell growth involved in cardiac muscle cell developmentPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein poly-ADP-ribosylationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein auto-ADP-ribosylationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
response to oxygen-glucose deprivationPoly [ADP-ribose] polymerase 2Homo sapiens (human)
extrinsic apoptotic signaling pathwayPoly [ADP-ribose] polymerase 2Homo sapiens (human)
hippocampal neuron apoptotic processPoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA repair-dependent chromatin remodelingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
double-strand break repairPoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA repairProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
inflammatory responseProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
DNA damage responseProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
response to xenobiotic stimulusProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
protein modification processProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
regulation of telomerase activityProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
protein poly-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
telomere maintenanceProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
double-strand break repairProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
positive regulation of DNA ligationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
regulation of mitotic spindle organizationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
protein localization to site of double-strand breakProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
DNA ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
negative regulation of isotype switchingProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
protein auto-ADP-ribosylationProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
negative regulation of telomerase RNA reverse transcriptase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
positive regulation of double-strand break repair via nonhomologous end joiningProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
double-strand break repairProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (43)

Processvia Protein(s)Taxonomy
DNA bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromatin bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
damaged DNA bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
RNA bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
zinc ion bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleotidyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
enzyme bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein kinase bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear estrogen receptor bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleosome bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
ubiquitin protein ligase bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
identical protein bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein homodimerization activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
histone deacetylase bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
R-SMAD bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription regulator activator activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-tyrosine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-histidine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-histone H2BS6 serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-histone H3S10 serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-histone H2BE35 glutamate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromatin bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
damaged DNA bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleotidyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleosome bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
poly-ADP-D-ribose bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+-protein-serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
poly-ADP-D-ribose modification-dependent protein bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
catalytic activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
protein bindingPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
zinc ion bindingPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nucleotidyltransferase activityPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
histone bindingPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
DNA bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromatin bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
damaged DNA bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
RNA bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
zinc ion bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleotidyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
enzyme bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein kinase bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear estrogen receptor bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleosome bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
ubiquitin protein ligase bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
identical protein bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein homodimerization activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
histone deacetylase bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
R-SMAD bindingPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription regulator activator activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-tyrosine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein-histidine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-histone H2BS6 serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-histone H3S10 serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-histone H2BE35 glutamate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription corepressor activityProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
NAD+ bindingProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
enzyme bindingProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
transcription corepressor activityProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
K63-linked polyubiquitin modification-dependent protein bindingProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
DNA-binding transcription factor bindingProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
transcription corepressor activityProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
kinase bindingProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
protein serine/threonine kinase activator activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
RNA bindingProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
metal ion bindingProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
NAD+- protein-cysteine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
protein bindingPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
nucleotidyltransferase activityPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
enzyme bindingPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
metal ion bindingPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
NAD+- protein-cysteine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
chromatin bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
damaged DNA bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
protein bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleotidyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleosome bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
poly-ADP-D-ribose bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+-protein-serine ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
poly-ADP-D-ribose modification-dependent protein bindingPoly [ADP-ribose] polymerase 2Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityPoly [ADP-ribose] polymerase 2Homo sapiens (human)
DNA bindingProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
enzyme bindingProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
catalytic activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+ ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
protein bindingProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
nucleotidyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD DNA ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+- protein-lysine ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+- protein-aspartate ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+-protein-glutamate ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
NAD+-protein ADP-ribosyltransferase activityProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (35)

Processvia Protein(s)Taxonomy
nucleusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cytosolPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of double-strand breakPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear replication forkPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromosome, telomeric regionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear envelopePoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleoplasmPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
membranePoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear bodyPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of double-strand breakPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromatinPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription regulator complexPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein-containing complexPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein-DNA complexPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
virion membraneSpike glycoproteinSevere acute respiratory syndrome-related coronavirus
site of DNA damagePoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleoplasmPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 2Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleoplasmProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
centrosomeProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
centrioleProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
nuclear bodyProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
site of double-strand breakProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
intercellular bridgeProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
nucleolusProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
site of double-strand breakProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
Golgi membranePoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
pericentriolar materialPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
chromosome, telomeric regionPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nucleoplasmPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
Golgi apparatusPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
cytosolPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nuclear bodyPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nuclear membranePoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
mitotic spindle polePoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nuclear porePoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
cytoplasmPoly [ADP-ribose] polymerase tankyrase-1Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
cytosolPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of double-strand breakPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear replication forkPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromosome, telomeric regionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear envelopePoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleoplasmPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
mitochondrionPoly [ADP-ribose] polymerase 1Homo sapiens (human)
membranePoly [ADP-ribose] polymerase 1Homo sapiens (human)
nuclear bodyPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of double-strand breakPoly [ADP-ribose] polymerase 1Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 1Homo sapiens (human)
chromatinPoly [ADP-ribose] polymerase 1Homo sapiens (human)
transcription regulator complexPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein-containing complexPoly [ADP-ribose] polymerase 1Homo sapiens (human)
protein-DNA complexPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 1Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP15Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
cytosolProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
plasma membraneProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
membraneProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP14Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
nucleolusProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
Golgi apparatusProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
cytosolProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP10Homo sapiens (human)
nuclear envelopeProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
endoplasmic reticulumProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
endoplasmic reticulum membraneProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
cytosolProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
membraneProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
endoplasmic reticulum tubular networkProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
nuclear envelopeProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
endoplasmic reticulum tubular networkProtein mono-ADP-ribosyltransferase PARP16Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP12Homo sapiens (human)
Golgi membranePoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
pericentriolar materialPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
chromosome, telomeric regionPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
nuclear envelopePoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
cytoplasmPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
cytosolPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
perinuclear region of cytoplasmPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
cytoplasmPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase tankyrase-2Homo sapiens (human)
nuclear envelopeProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
nucleoplasmProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
cytosolProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
nuclear bodyProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
nuclear poreProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP11Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleusPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleoplasmPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 2Homo sapiens (human)
site of DNA damagePoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleolusPoly [ADP-ribose] polymerase 2Homo sapiens (human)
nucleusProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
nucleoplasmProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
cytosolProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
spindle microtubuleProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
membraneProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
extracellular exosomeProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
ribonucleoprotein complexProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP4Homo sapiens (human)
nucleoplasmProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
cytoplasmProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
centrosomeProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
centrioleProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
nuclear bodyProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
site of double-strand breakProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
intercellular bridgeProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
nucleolusProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
site of double-strand breakProtein mono-ADP-ribosyltransferase PARP3Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (219)

Assay IDTitleYearJournalArticle
AID477529Intrinsic clearance in rat liver microsomes assessed per mg of protein up to 60 mins in presence of rat recombinant CYP1A22009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477521Oral bioavailability in rat2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477515Inhibition of PARP in hydrogen peroxide-induced human HeLa cells assessed as inhibition DNA-damage-induced PARylation2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205284Drug metabolism assessed as recombinant CYP1A1 (unknown origin)-mediated compound intrinsic clearance measured per mg of protein2015Journal 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.
AID1205276Intrinsic clearance in rat liver microsomes measured per mg of protein2015Journal 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.
AID1205269Inhibition of PARP1 (unknown origin)2015Journal 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.
AID1205270Inhibition of PARP in human HeLa cells assessed as inhibition of hydrogen peroxide-induced PARylation by cell-based assay2015Journal 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.
AID477520Plasma clearance in rat2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477518Intrinsic clearance in rat liver microsomes assessed per mg of protein up to 90 mins2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477517Antiproliferative activity against human HeLa cells expressing wild type BRCA1 after 7 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477519Intrinsic clearance in mouse liver microsomes assessed per mg of protein up to 90 mins2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477514Inhibition of human PARP1 by SPA2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477516Antiproliferative activity against BRCA1 deficient human HeLa cells after 7 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477525Selectivity index, ratio of CC50 for BRCA1 proficient human HeLa cells to CC50 for BRCA1 deficient human HeLa cells2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205277Total plasma clearance in iv dosed rat2015Journal 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.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347160Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings 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.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347159Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings 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.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347159Primary screen GU Rhodamine qHTS for Zika virus inhibitors: Unlinked NS2B-NS3 protease assay2020Proceedings 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.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347160Primary screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings 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.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings 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.
AID1347113qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347128qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347121qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347118qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347123qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347109qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347129qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347116qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347126qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347122qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347114qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347127qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347112qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347117qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347119qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347124qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347125qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347115qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347110qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for A673 cells)2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347111qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Confirmatory screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID477626Antitumor activity against human MDA-MB-436 cells expressing BRCA1 5396 + 1G>A mutant xenografted in CD1 mouse assessed as tumor regression at 50 mg/kg, po bid for 33 days2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1276413Inhibition of human PARP1 using [3H]NAD as substrate after 1 min by microplate scintillation counting analysis2016Journal 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
AID1205290Volume of distribution at steady state in dog2015Journal 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.
AID1064607Inhibition of recombinant human GST-fused PARP-1 expressed in Escherichia coli after 30 mins by fluorescence assay2014Bioorganic & medicinal chemistry, Feb-01, Volume: 22, Issue:3
7-Azaindole-1-carboxamides as a new class of PARP-1 inhibitors.
AID477624Antiproliferative activity against HMEC after 6 to 7 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1428394Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1205309Cytotoxicity against human SUM149PT cells carrying BRCA1 mutant assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1205294Stability in dog blood2015Journal 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.
AID1428386Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1683000Cytotoxicity against human MDA-MB-468 cells measured after 72 hrs by Celltiter-Glo assay2020Journal 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.
AID1276422Cytotoxicity against human MRC5 cells2016Journal 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
AID1205318Antitumor activity against human MDA-MB-436 cells harboring BRCA1 mutant xenografted in immunocompromised mouse assessed as tumor growth inhibition at 80 mg/kg, po qd for 1 to 2 weeks2015Journal 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.
AID1205301Inhibition of PARP in BRCA2-deficient human CAPAN-1 cells assessed as inhibition of hydrogen peroxide-induced PARylation by cell-based assay2015Journal 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.
AID1205305Selectivity ratio of CC50 for wild type human A549 cells to CC50 for human A549 cells transfected with BRCA2 shRNA2015Journal 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.
AID1428396Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1895780Binding affinity to PARP4 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID762669Chemopotentiation factor, ratio of EC50 for PARP1 in human Jurkat cells to EC50 for PARP1 in human Jurkat cells in presence of 100 uM of temozolomide2013Bioorganic & 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.
AID1276416Inhibition of PARP in human LoVo cells assessed as inhibition of poly(ADP)-ribose polymerization for 30 mins by fluorescence assay2016Journal 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
AID1428393Inhibition of recombinant human TNKS2 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1428384Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1179170Terminal half life in BRCA mutation carrying cancer patient with sporadic cancer2014Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19
Development of synthetic lethality anticancer therapeutics.
AID1205326Inhibition of PARP activity in tumor of immunocompromised mouse xenografted with BRCA2-deficient human Capan1 cells assessed as incorporation of [3H]NAD in PAR chains in response to nicked DNA at 50 to 100 mg/kg, po measured after 24 hrs2015Journal 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.
AID1872301Selectivity ratio of IC50 for PARP2 (unknown origin) to IC50 for PARP1 (unknown origin)2022European journal of medicinal chemistry, Feb-15, Volume: 230Recent advances in DDR (DNA damage response) inhibitors for cancer therapy.
AID1205289Oral bioavailability in dog2015Journal 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.
AID1205293Stability in human blood2015Journal 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.
AID477539Antiproliferative activity against human MDA-MB-436 cells expressing BRCA1 5396 + 1G>A mutant after 6 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1428390Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1638254Inhibition of PARP1 (unknown origin)2019European journal of medicinal chemistry, Mar-01, Volume: 165Medicinal chemistry approaches of poly ADP-Ribose polymerase 1 (PARP1) inhibitors as anticancer agents - A recent update.
AID1205307Cytotoxicity against human UWB1.289 cells expressing BRCA1 assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1205319Antitumor activity against human MDA-MB-436 cells harboring BRCA1 mutant xenografted in immunocompromised mouse assessed as tumor shrinkage at 80 mg/kg, po qd for 3 weeks2015Journal 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.
AID477519Intrinsic clearance in mouse liver microsomes assessed per mg of protein up to 90 mins2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1895783Binding affinity to PARP7 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205315Fraction unbound in human plasma2015Journal 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.
AID1895784Binding affinity to PARP8 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205299Drug metabolism in iv dosed bile cannulated rat assessed as metabolite formation2015Journal 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.
AID477510Toxicity in expressing BRCA1 5396 + 1G>A mutant xenografted CD1 mouse assessed as body weight loss at 50 mg/kg, po bid for 33 days2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477535Inhibition of human v-PARP catalytic domain by trichloroacetic acid precipitation assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1895790Binding affinity to PARP16 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205330Plasma trough concentration in human at 300 mg/day2015Journal 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.
AID477541Antiproliferative activity against human PrEC cells after 6 to 7 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205274Cytotoxicity against human HeLa cells transfected with BRCA1 shRNA assessed as reduction of cell viability after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1895767Inhibition 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 assay2021Journal 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}-
AID1895778Binding affinity to PARP2 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205323Antitumor activity against BRCA2-deficient human Capan1 cells xenografted in immunocompromised mouse assessed as tumor growth inhibition at 80 mg/kg, po qd for 2 to 4 weeks2015Journal 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.
AID1205295Drug metabolism in dog hepatocytes assessed as 2-[4-(3-piperidyl)phenyl]indazole-7-carboxamide formation by HPLC analysis2015Journal 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.
AID477627Toxicity in expressing BRCA1 5396 + 1G>A mutant xenografted CD1 mouse assessed as mouse mortality at 100 mg/kg, po qd for 33 days2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1428397Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID477516Antiproliferative activity against BRCA1 deficient human HeLa cells after 7 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477517Antiproliferative activity against human HeLa cells expressing wild type BRCA1 after 7 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205306Cytotoxicity against human UWB1.289 cells carrying BRCA1 mutant assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1205304Cytotoxicity against human A549 cells transfected with BRCA2 shRNA assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1895786Binding affinity to PARP10 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205325Inhibition of PARP activity in tumor of immunocompromised mouse xenografted with human MDA-MB-436 cells harboring BRCA1 mutant assessed as incorporation of [3H]NAD in PAR chains in response to nicked DNA at 50 to 100 mg/kg, po measured after 24 hrs2015Journal 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.
AID477625Antitumor activity against human MDA-MB-436 cells expressing BRCA1 5396 + 1G>A mutant xenografted in CD1 mouse assessed as tumor regression at 100 mg/kg, po qd for 33 days2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205322Cytotoxicity against BRCA2-deficient human Capan1 cells2015Journal 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.
AID477538Selectivity for human PARP1/2 over human TANK12009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205329Terminal half-life in human at 30 to 400 mg/day2015Journal 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.
AID1179168Toxicity in patient with sporadic cancer2014Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19
Development of synthetic lethality anticancer therapeutics.
AID1428392Inhibition of recombinant human TNKS1 ADP-ribosyltransferase domain expressed in Escherichia coli BL21(DE3) preincubated for 15 mins followed by biotinylated NAD+ addition by chemiluminescence assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1895787Binding affinity to PARP11 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1064455Inhibition of GST-tagged recombinant human PARP-1 expressed in Escherichia coli after 30 mins by fluorescence-based assay2014Bioorganic & medicinal chemistry letters, Jan-15, Volume: 24, Issue:2
Novel PARP-1 inhibitors based on a 2-propanoyl-3H-quinazolin-4-one scaffold.
AID1638281Inhibition of PARP2 (unknown origin)2019European journal of medicinal chemistry, Mar-01, Volume: 165Medicinal chemistry approaches of poly ADP-Ribose polymerase 1 (PARP1) inhibitors as anticancer agents - A recent update.
AID1428398Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1428395Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1205327Inhibition of PARP-mediated incorporation of [3H]NAD in PAR chains in response to nicked DNA in human PBMC after 24 hrs2015Journal 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.
AID477534Inhibition of human TANK1 C-terminal domain by trichloroacetic acid precipitation assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1895789Binding affinity to PARP14 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205316Cytotoxicity against human MDA-MB-436 cells carrying BRCA1 mutant assessed as inhibition of cell proliferation2015Journal 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.
AID1205321Toxicity against immunocompromised mouse xenografted with human MDA-MB-436 cells harboring BRCA1 mutant assessed as reduction in body weight at 80 mg/kg, po qd for 1 to 4 weeks2015Journal 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.
AID1205331Plasma trough concentration in human at 40 mg/day2015Journal 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.
AID1179169Cmax in BRCA mutation carrying cancer patient with sporadic cancer2014Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19
Development of synthetic lethality anticancer therapeutics.
AID477540Antiproliferative activity against human Capan1 cells expressing BRCA2 6174delT mutation and loss of wild-type allele after 13 days by cell titer-blue assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477511Inhibition of human PARP3 by trichloroacetic acid precipitation assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID477508Toxicity in expressing BRCA1 5396 + 1G>A mutant xenografted CD1 mouse assessed as mouse mortality at 50 mg/kg, po bid for 33 days2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205320Antitumor activity against human MDA-MB-436 cells harboring BRCA1 mutant xenografted in immunocompromised mouse assessed as complete and sustained tumor regression at 80 mg/kg, po qd for 4 weeks2015Journal 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.
AID762671Inhibition of PARP1 in human Jurkat cells assessed as reduction of cell viability after 96 hrs by MTS assay2013Bioorganic & 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.
AID1205273Terminal half life in rat2015Journal 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.
AID477520Plasma clearance in rat2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1895766Inhibition 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 assay2021Journal 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}-
AID1205291Terminal half life in dog2015Journal 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.
AID1205270Inhibition of PARP in human HeLa cells assessed as inhibition of hydrogen peroxide-induced PARylation by cell-based assay2015Journal 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.
AID477518Intrinsic clearance in rat liver microsomes assessed per mg of protein up to 90 mins2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1428389Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1205311Cytotoxicity against human BT20 cells assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1205297Drug metabolism in iv dosed bile cannulated dog assessed as parent compound recovery2015Journal 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.
AID1276421Cytotoxicity against BRCA1-deficient human MX1 cells2016Journal 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
AID1895791Binding affinity to PARP1 (unknown origin) assessed as residence time2021Journal 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}-
AID1895788Binding affinity to PARP12 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205300Inhibition of PARP in human A2780 cells assessed as inhibition of hydrogen peroxide-induced PARylation by cell-based assay2015Journal 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.
AID1276417Potentiation of temozolomide-induced cytotoxicity in human LoVo cells assessed as temozolomide GI50 at 0.4 uM after 5 days by Celltiter-Glo assay2016Journal 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
AID1205310Cytotoxicity against human SUM1315MO2 cells carrying BRCA1 mutant assessed as inhibition of cell proliferation after 12 days by CellTiter-Blue assay2015Journal 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.
AID1205281Drug excretion in iv dosed rat bile assessed as acylglucuronide metabolite formation2015Journal 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.
AID1428387Inhibition 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 assay2017Journal of medicinal chemistry, 02-23, Volume: 60, Issue:4
Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors.
AID1205313Plasma concentration in CD-1 mouse at 50 mg/kg, po after 24 hrs2015Journal 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.
AID477525Selectivity index, ratio of CC50 for BRCA1 proficient human HeLa cells to CC50 for BRCA1 deficient human HeLa cells2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1872300Inhibition of PARP2 (unknown origin)2022European journal of medicinal chemistry, Feb-15, Volume: 230Recent advances in DDR (DNA damage response) inhibitors for cancer therapy.
AID1895769Inhibition of human recombinant PARP5a (E1023 to T1327 amino acids) incubated for 4 hrs by fluorescence anisotropy binding assay2021Journal 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}-
AID1205302Cytotoxicity against wild type human HeLa cells assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1205284Drug metabolism assessed as recombinant CYP1A1 (unknown origin)-mediated compound intrinsic clearance measured per mg of protein2015Journal 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.
AID1205292Stability in rat blood2015Journal 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.
AID1205286Bioavailability in rat2015Journal 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.
AID477536Selectivity for human PARP1/2 over human PARP32009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205324Toxicity against immunocompromised mouse xenografted with BRCA2-deficient human CAPAN-1 cells assessed as reduction in body weight at 80 mg/kg, po qd for 2 to 4 weeks2015Journal 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.
AID1631788Inhibition of PARP1 (unknown origin)2016Bioorganic & 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.
AID477515Inhibition of PARP in hydrogen peroxide-induced human HeLa cells assessed as inhibition DNA-damage-induced PARylation2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1895768Selectivity ratio of IC50 for PARP1 (unknown origin) to IC50 for PARP2 (unknown origin )2021Journal 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}-
AID1205269Inhibition of PARP1 (unknown origin)2015Journal 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.
AID477537Selectivity for human PARP1/2 over human V-PARP2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1179167Toxicity in BRCA mutation carrying cancer patient2014Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19
Development of synthetic lethality anticancer therapeutics.
AID1179171In vivo inhibition of PARP activity in in BRCA mutation carrying cancer patient with sporadic cancer at >80 mg/day2014Journal of medicinal chemistry, Oct-09, Volume: 57, Issue:19
Development of synthetic lethality anticancer therapeutics.
AID1205279Drug excretion in iv dosed rat bile assessed as 4-(7-carbamoylindazol-2-yl)benzoic acid metabolite formation2015Journal 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.
AID1205275Selectivity for BRCA1 shRNA-transfected human HeLa cells over wild type human HeLa cells2015Journal 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.
AID477529Intrinsic clearance in rat liver microsomes assessed per mg of protein up to 60 mins in presence of rat recombinant CYP1A22009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205308Selectivity ratio of CC50 for human UWB1.289 cells expressing BRCA1 to CC50 for human UWB1.289 cells carrying BRCA1 mutant2015Journal 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.
AID1895781Binding affinity to PARP5a (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205278Drug excretion in iv dosed rat urine assessed as 4-(7-carbamoylindazol-2-yl)benzoic acid metabolite formation2015Journal 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.
AID477512Inhibition of human PARP2 by trichloroacetic acid precipitation assay2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1205280Drug excretion in iv dosed rat urine assessed as acylglucuronide metabolite formation2015Journal 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.
AID1205285Intrinsic clearance in human liver microsomes measured per mg of protein2015Journal 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.
AID1205288Plasma clearance in dog2015Journal 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.
AID1205303Cytotoxicity against wild type human A549 cells assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID1205317Antitumor activity against human MDA-MB-436 cells harboring BRCA1 mutant xenografted in immunocompromised mouse assessed as tumor growth inhibition at 50 mg/kg, po administered daily2015Journal 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.
AID477521Oral bioavailability in rat2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID762670Inhibition of PARP1 in human Jurkat cells assessed as reduction of cell viability after 96 hrs by MTS assay in presence of 100 uM of temozolomide2013Bioorganic & 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.
AID1638256Protein binding in plasma (unknown origin)2019European journal of medicinal chemistry, Mar-01, Volume: 165Medicinal chemistry approaches of poly ADP-Ribose polymerase 1 (PARP1) inhibitors as anticancer agents - A recent update.
AID1205298Drug metabolism in iv dosed bile cannulated rat assessed as parent compound recovery2015Journal 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.
AID1205312Cytotoxicity against human DoTc2-4510 cells carrying BRCA2 mutant assessed as inhibition of cell proliferation after 5 to 7 days by CellTiter-Blue assay2015Journal 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.
AID762672Inhibition of human PARP1 catalytic activity after 10 mins by ELISA2013Bioorganic & 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.
AID1205287Volume of distribution at steady state in rat2015Journal 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.
AID1895782Binding affinity to PARP5b (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1895777Binding affinity to PARP1 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1895779Binding affinity to PARP3 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1276419Cytotoxicity against BRCA2-deficient human Capan1 cells2016Journal 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
AID1205276Intrinsic clearance in rat liver microsomes measured per mg of protein2015Journal 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.
AID1205296Drug metabolism in iv dosed bile cannulated dog assessed as 2-[4-(3-piperidyl)phenyl]indazole-7-carboxamide formation2015Journal 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.
AID1895785Binding affinity to PARP9 (unknown origin) assessed as apparent dissociation constant2021Journal 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}-
AID1205277Total plasma clearance in iv dosed rat2015Journal 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.
AID1205314Fraction unbound in mouse plasma2015Journal 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.
AID477509Toxicity in expressing BRCA1 5396 + 1G>A mutant xenografted CD1 mouse assessed as body weight loss at 100 mg/kg, po qd for 33 days2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1872299Inhibition of PARP1 (unknown origin)2022European journal of medicinal chemistry, Feb-15, Volume: 230Recent advances in DDR (DNA damage response) inhibitors for cancer therapy.
AID477514Inhibition of human PARP1 by SPA2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1895770Antiproliferative activity against human DLD-1 deficient in BRCA-2 cells measured after 7 days2021Journal 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}-
AID1745854NCATS anti-infectives library activity on HEK293 viability as a counter-qHTS vs the C. elegans viability qHTS2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1347411qHTS 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) Libary2020ACS 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.
AID1745855NCATS anti-infectives library activity on the primary C. elegans qHTS viability assay2023Disease models & mechanisms, 03-01, Volume: 16, Issue:3
In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.
AID1346152Human poly(ADP-ribose) polymerase 2 (2.4.2.30 poly(ADP-ribose)polymerases)2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1346183Human poly(ADP-ribose) polymerase 1 (2.4.2.30 poly(ADP-ribose)polymerases)2009Journal of medicinal chemistry, Nov-26, Volume: 52, Issue:22
Discovery of 2-{4-[(3S)-piperidin-3-yl]phenyl}-2H-indazole-7-carboxamide (MK-4827): a novel oral poly(ADP-ribose)polymerase (PARP) inhibitor efficacious in BRCA-1 and -2 mutant tumors.
AID1802336In 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.\\2016Cell chemical biology, Dec-22, Volume: 23, Issue:12
Proteome-wide Profiling of Clinical PARP Inhibitors Reveals Compound-Specific Secondary Targets.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (211)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's0 (0.00)18.2507
2000's1 (0.47)29.6817
2010's83 (39.34)24.3611
2020's127 (60.19)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 77.66

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be very strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index77.66 (24.57)
Research Supply Index1.79 (2.92)
Research Growth Index5.08 (4.65)
Search Engine Demand Index127.50 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (77.66)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Trials46 (21.70%)5.53%
Reviews0 (0.00%)6.00%
Reviews36 (16.98%)6.00%
Case Studies0 (0.00%)4.05%
Case Studies8 (3.77%)4.05%
Observational0 (0.00%)0.25%
Observational3 (1.42%)0.25%
Other5 (100.00%)84.16%
Other119 (56.13%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (188)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Phase II Trial of Combination Niraparib and Dostarlimab Therapy for Recurrent or Persistent Uterine Serous Carcinoma [NCT05870761]Phase 235 participants (Anticipated)Interventional2023-10-17Recruiting
An Open-label, Randomized Study to Assess the Relative Bioavailability (BA) and Bioequivalence (BE) of Comparative Formulations of Niraparib and Abiraterone Acetate (AA) in Men With Prostate Cancer [NCT04577833]Phase 1136 participants (Actual)Interventional2020-11-13Active, not recruiting
A Phase 3 Randomized, Placebo-controlled, Double-blind Study of Niraparib in Combination With Abiraterone Acetate and Prednisone Versus Abiraterone Acetate and Prednisone for the Treatment of Participants With Deleterious Germline or Somatic Homologous Re [NCT04497844]Phase 3696 participants (Actual)Interventional2020-09-23Active, not recruiting
An Open-Label, Single-Arm, Phase I Clinical Trial to Evaluate the Safety and Tolerability of ZL-2306 (Niraparib) in Combination With Brivanib in Patients With Recurrent Ovarian Cancer [NCT03895788]Phase 124 participants (Anticipated)Interventional2019-01-14Recruiting
A Phase 2, Multicenter, Open-label, Single-arm Study to Evaluate the Safety and Efficacy of Niraparib in Japanese Patients With Advanced, Relapsed, High-grade Serous Epithelial Ovarian, Fallopian Tube, or Primary Peritoneal Cancer Who Have Received 3 or 4 [NCT03759600]Phase 220 participants (Actual)Interventional2018-12-26Completed
The Molecular and the Clinical Effects of Preoperative Niraparib in Patients With High-grade Endometrial Cancer: Phase 0 Exploratory Trial [NCT05289648]Early Phase 131 participants (Anticipated)Interventional2023-05-01Not yet recruiting
Phase II Study of Niraparib Single Agent in Metastatic Triple Negative Breast Cancer Patients With Homologous Recombination Deficiency [NCT05461690]Phase 250 participants (Anticipated)Interventional2022-09-01Not yet recruiting
A Phase Ib Dose Escalation Study of MK-4827 in Combination With Carboplatin, Carboplatin/Paclitaxel and Carboplatin/Liposomal Doxorubicin in Patients With Advanced Solid Tumors [NCT01110603]Phase 112 participants (Actual)Interventional2010-07-31Terminated
A Phase I Study of MK-4827 in Patients With Solid Tumor [NCT01226901]Phase 13 participants (Actual)Interventional2010-11-30Terminated
Phase 1 Study of Niraparib in Combination With Osimertinib in EGFR-Mutated Advanced Lung Cancer [NCT03891615]Phase 130 participants (Anticipated)Interventional2019-06-06Recruiting
Niraparib Maintenance Treatment in Metastatic Colorectal Cancer Patients With a Partial or Complete Response After Oxaliplatin-based Induction Therapy: Bohème Trial [NCT05412706]Phase 20 participants (Actual)Interventional2023-09-04Withdrawn(stopped due to The Principal Investigator has retired and has not been replaced has retired and a new one has not been identified Principal Investigator)
A Prospective, Multicenter, Randomized Phase II Trial on Optimal Timing of Surgery Combined With Maintenance Targeted Therapy in the Treatment of Advanced Ovarian Cancer [NCT05200260]Phase 2207 participants (Anticipated)Interventional2022-02-28Not yet recruiting
Phase 1b Dose-Finding Study of Niraparib, TSR-022, Bevacizumab, and Platinum-Based Doublet Chemotherapy in Combination With TSR-042 in Patients With Advanced or Metastatic Cancer [NCT03307785]Phase 158 participants (Actual)Interventional2017-10-12Active, not recruiting
A Phase 1, Open-label Study of Niraparib as Single Agent in Patients With Advanced Solid Tumors [NCT03497429]Phase 19 participants (Actual)Interventional2018-04-05Completed
A Phase 0 'Trigger' Trial of Niraparib in Newly-diagnosed Glioblastoma and Recurrent IDH1/2(+) ATRX Mutant Glioma [NCT05076513]Early Phase 142 participants (Anticipated)Interventional2021-10-29Recruiting
Multi-Centre Observational Study of Maintenance Niraparib in Treatment of Ovarian CanceR: UK Routine Clinical Practice Experience [NCT04295577]350 participants (Anticipated)Observational2020-02-03Recruiting
Re-VOLVE: A Phase II Clinical Trial in Women With Ovarian Cancer Progressing Post-PARP Inhibitor With Treatment Adapted to Real-time Assessment of Evolving Genomic Resistance [NCT05065021]Phase 240 participants (Anticipated)Interventional2023-02-23Recruiting
Niraparib Efficacy in Patient With Unresectable Mesothelioma: A Randomised Phase II Trial of Niraparib Versus Active Symptom Control in Patients With Previously Treated Mesothelioma [NCT05455424]Phase 284 participants (Anticipated)Interventional2022-07-11Recruiting
A Phase II Study of Niraparib and Dostarlimab With Radiation in Patients With Metastatic Pancreatic Cancer [NCT04409002]Phase 218 participants (Actual)Interventional2020-07-23Completed
A Two-part Phase I Study With the Antibody-drug Conjugate SYD985 in Combination With Niraparib to Evaluate Safety, Pharmacokinetics and Efficacy in Patients With HER2-expressing Locally Advanced or Metastatic Solid Tumors. [NCT04235101]Phase 132 participants (Actual)Interventional2020-06-22Completed
A Multicentric Randomized Phase II/III Evaluating TSR-042 (Anti-PD-1 mAb) in Combination With Niraparib (Parpi) Versus Niraparib Alone Compared to Chemotherapy in the Treatment of Metastatic or Recurrent Endometrial or Ovarian Carcinosarcoma After at Leas [NCT03651206]Phase 2/Phase 3196 participants (Anticipated)Interventional2020-07-15Active, not recruiting
PARPVAX: Parpvax: A Phase 1b/2, Open Label Study of Niraparib Plus Either Ipilimumab or Nivolumab in Patients With Advanced Pancreatic Cancer Whose Disease Has Not Progressed on Platinum-based Therapy [NCT03404960]Phase 1/Phase 2104 participants (Actual)Interventional2018-01-31Active, not recruiting
A Phase II, Single-Arm Trial Assessing Alternative Dosing Of Niraparib To Decrease Dose Interruption In First Line Maintenance Treatment For Ovarian Cancer: Dose Escalation [NCT05961124]Phase 240 participants (Anticipated)Interventional2023-08-21Recruiting
An Open-Label, Single Arm, Phase II Trial of Niraparib in Combination With Anlotinib in Patients With Platinum-Resistant Recurrent or Platinum-Refractory Clear Cell Ovarian Cancer. [NCT05130515]Phase 26 participants (Actual)Interventional2021-12-15Completed
A Phase II Study Evaluating the Efficacy and Safety of Niraparib and Tumor-Treating Fields in Recurrent Glioblastoma [NCT04221503]Phase 230 participants (Anticipated)Interventional2019-12-30Active, not recruiting
A Phase 3, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study Comparing Niraparib Plus Pembrolizumab Versus Placebo Plus Pembrolizumab as Maintenance Therapy in Participants Whose Disease Has Remained Stable or Responded to First-Line Platinu [NCT04475939]Phase 3666 participants (Actual)Interventional2020-10-26Active, not recruiting
A Phase III Randomized, Double-blinded Trial of Platinum-based Chemotherapy With or Without Atezolizumab Followed by Niraparib Maintenance With or Without Atezolizumab in Patients With Recurrent Ovarian, Tubal or Peritoneal Cancer and Platinum Treatment-f [NCT03598270]Phase 3414 participants (Anticipated)Interventional2018-11-21Active, not recruiting
Phase II Study of Niraparib for Leiomyosarcoma With Alterations in the Homologous Recombination DNA Repair Pathway [NCT05174455]Phase 20 participants (Actual)Interventional2023-12-01Withdrawn(stopped due to PI decision)
Arterial Hypertension With PARP Inhibitors in Cancer Patients: an Observational and Retrospective Study Using the WHO Pharmacovigilance Database (ArteRIB) [NCT04774406]2,336 participants (Actual)Observational2021-02-24Completed
A Phase 3 Randomized, Placebo-controlled, Double-blind Study of Niraparib in Combination With Abiraterone Acetate and Prednisone Versus Abiraterone Acetate and Prednisone in Subjects With Metastatic Prostate Cancer [NCT03748641]Phase 3765 participants (Actual)Interventional2019-01-25Active, not recruiting
A Phase Ib Study of the Oral PARP Inhibitor Niraparib With the Intravenous PI3K Inhibitor Copanlisib for Recurrent Endometrial and Recurrent Ovarian, Primary Peritoneal, or Fallopian Tube Cancer [NCT03586661]Phase 131 participants (Actual)Interventional2019-04-29Active, not recruiting
A Phase 1b-2 Study of Niraparib Combination Therapies for the Treatment of Metastatic Castration-Resistant Prostate Cancer [NCT03431350]Phase 1/Phase 2136 participants (Actual)Interventional2018-03-02Active, not recruiting
Niraparib Plus Carboplatin in Patients With Homologous Recombination Deficient Advanced Solid Tumor Malignancies [NCT03209401]Phase 123 participants (Actual)Interventional2017-10-13Active, not recruiting
Phase 1/2 Clinical Study of Niraparib in Combination With Pembrolizumab (MK-3475) in Patients With Advanced or Metastatic Triple-Negative Breast Cancer and in Patients With Recurrent Ovarian Cancer [NCT02657889]Phase 1/Phase 2122 participants (Actual)Interventional2016-04-15Completed
A Phase IV Open-label, Multicenter Study of Niraparib as Maintenance Therapy in BRCA Wild-type, Newly Diagnosed Advanced Ovarian Cancer Patients in Korea [NCT05187208]Phase 4102 participants (Anticipated)Interventional2022-01-31Not yet recruiting
Serial Measurements of Molecular and Architectural Responses to Therapy (SMMART) Trial: Adaptive Clinical Treatment (ACT) [NCT05238831]Early Phase 125 participants (Anticipated)Interventional2023-12-01Not yet recruiting
A Randomized Phase 3 Double-Blinded Study Comparing the Efficacy and Safety of Niraparib to Placebo in Participants With Either HER2-Negative BRCA-Mutated or Triple-Negative Breast Cancer With Molecular Disease Based on Presence of Circulating Tumor DNA A [NCT04915755]Phase 340 participants (Actual)Interventional2021-06-28Active, not recruiting
Combination Therapy of Niraparib and Irinotecan in Cancers With Mutations in DNA Repair Genes [NCT05694715]Phase 124 participants (Anticipated)Interventional2023-05-23Recruiting
Chemotherapy Combined With Bevacizumab Followed by Niraparib Monotherapy in Newly Diagnostic Advanced Ovarian Cancer With HRD Positive : A Perspective, Multicenter, Single-arm Phase II Trial [NCT06141265]Phase 2116 participants (Anticipated)Interventional2023-11-01Recruiting
Niraparib vs Niraparib in Combination With Bevacizumab in Patients With Carboplatinum-taxane Based Chemotherapy in Advanced Ovarian Cancer (A Multicentre Randomised Phase III Trial) [NCT05009082]Phase 3970 participants (Anticipated)Interventional2022-09-13Recruiting
Multicenter,Open-label,Phase II Clinical Trial to Evaluate the Efficacy and Safety of Niraparib + Aromatase Inhibitors for(HR)+/(HER2)-, MBC With Either Germline BRCA-mutated or Germinal BRCA-wildtype and Homologous Recombination Deficiency [NCT04240106]Phase 214 participants (Actual)Interventional2020-06-15Completed
Phase 1 Trial of CB-839 in Combination With Niraparib in Platinum Resistant BRCA-wild-type Ovarian Cancer Patients [NCT03944902]Phase 11 participants (Actual)Interventional2021-09-01Terminated(stopped due to will not resume. company choosing not to continue with drug. one participant now off study.)
A Phase I Study of MK-4827 in Combination With Temozolomide in Patients With Advanced Cancer [NCT01294735]Phase 119 participants (Actual)Interventional2011-02-28Completed
A Phase II Study of Combination of Niraparib And Sintilimab In Recurrent/Metastatic Nasopharyngeal Carcinoma [NCT05162872]Phase 299 participants (Anticipated)Interventional2021-08-05Recruiting
A Phase Ib Dose Escalation Study of MK-4827 in Combination With Pegylated Liposomal Doxorubicin (Doxil™ or Caelyx™) in Patients With Advanced Solid Tumors With a Cohort Expansion in Patients With Platinum Resistant/Refractory High Grade Serous Ovarian Can [NCT01227941]Phase 16 participants (Actual)Interventional2010-11-30Terminated
An Open-Label, Non-Randomized, Multicenter Study to Determine the Pharmacokinetics and Safety of Niraparib Following a Single Oral Dose in Patients With Advanced Solid Tumors and Either Normal Hepatic Function or Moderate Hepatic Impairment [NCT03359850]Phase 117 participants (Actual)Interventional2018-02-20Completed
An Open Label Phase II Basket Trial Exploring the Efficacy and Safety of the Combination of Niraparib and Dostarlimab in Patients With DNA Repair-deficient or Platinum-sensitive Solid Tumors [NCT04779151]Phase 2112 participants (Anticipated)Interventional2021-04-07Recruiting
A Feasibility Study of Niraparib for Advanced, BRCA1-like, HER2-negative Breast Cancer Patients: the ABC Study [NCT02826512]Phase 29 participants (Actual)Interventional2018-05-15Terminated(stopped due to Not enough eligble patient can be found, too many screen failures)
A Phase II, Randomized, Trial of Niraparib Versus Best Supportive Care as Maintenance Treatment In Patients With Locally Advanced Or Metastatic Urothelial Cancer Whose Disease Did Not Progress After First-line Platinum-based Chemotherapy [NCT03945084]Phase 258 participants (Actual)Interventional2019-08-27Completed
Absorption, Metabolism, Excretion, and the Determination of Absolute Bioavailability of Niraparib in Subjects With Cancer [NCT02476552]Phase 112 participants (Actual)Interventional2015-02-28Completed
A Randomized, Double-blind, Phase 3 Comparison of Platinum-based Therapy With TSR-042 and Niraparib Versus Standard of Care Platinum-based Therapy as First-line Treatment of Stage III or IV Nonmucinous Epithelial Ovarian Cancer [NCT03602859]Phase 31,402 participants (Actual)Interventional2018-10-11Active, not recruiting
Efficacy and Safety of Niraparib in Combination With Anlotinib Based on CA 125 Level in Newly Diagnosed Ovarian Cancer: A Open-label, Single Arm, Prospective Phase II Trial [NCT05311579]Phase 236 participants (Anticipated)Interventional2022-03-27Recruiting
A Phase II, Open-Label, Single Arm, Prospective, Multicenter Study of Niraparib Plus Dostarlimab in Patients With Advanced NSCLC and/or MPM, and Positive for PD-L1 Expression and Germline or Somatic Mutations in the HRR Genes [NCT04940637]Phase 270 participants (Anticipated)Interventional2020-12-23Recruiting
A Phase I/IIa, Open-label, Multi-centre Study to Assess the Safety, Tolerability, Pharmacokinetics and Preliminary Efficacy of the DNA Polymerase Theta Inhibitor ART4215 Administered Orally as Monotherapy and in Combination to Patients With Advanced or Me [NCT04991480]Phase 1/Phase 2390 participants (Anticipated)Interventional2021-09-13Active, not recruiting
A PHASE 1, MULTICENTRE, OPEN-LABEL, DOSE-ESCALATION AND COHORT EXPANSION STUDY OF NIRAPARIB AND DOSTARLIMAB IN PAEDIATRIC PATIENTS WITH RECURRENT OR REFRACTORY SOLID TUMOURS [NCT04544995]Phase 1116 participants (Anticipated)Interventional2020-10-06Suspended(stopped due to The study was paused for enrolment to further assess clinical data)
Phase II Trial of Niraparib in Combination With Dostarlimab in Patients With Recurrent or Progressive Cervix Cancer (OU-SCC-STAR) [NCT04068753]Phase 266 participants (Anticipated)Interventional2020-02-26Recruiting
A Phase Ib/II, Open-Label, Multicenter, Randomized Umbrella Study Evaluating the Efficacy and Safety of Multiple Immunotherapy-Based Treatments and Combinations in Patients With Urothelial Carcinoma (MORPHEUS-UC) [NCT03869190]Phase 1/Phase 2645 participants (Anticipated)Interventional2019-06-01Recruiting
A Phase 2 Efficacy and Safety Study of Niraparib in Men With Metastatic Castration-Resistant Prostate Cancer and DNA-Repair Anomalies [NCT02854436]Phase 2289 participants (Actual)Interventional2016-08-31Completed
Phase Ib/II Non-randomized Non-comparative Two-cohort Study of Niraparib and Dostarlimab Plus (Chemo)RadIotherapy in Locally-Advanced Head and Neck Squamous Cell Carcinoma [NCT05784012]Phase 1/Phase 234 participants (Anticipated)Interventional2023-11-08Recruiting
Niraparib Maintenance in Patients With Advanced Ovarian Cancer at Neoadjuvant Setting - a Phase 2, Single-arm Trial (NEOPRIMA Trial) [NCT04284852]Phase 220 participants (Actual)Interventional2020-05-01Completed
An Open-Label,Single-Arm,Phase I Clinical Trial to Evaluate the Pharmacokinetics,Safety and Tolerability of ZL-2306 (Niraparib) in Patients With Ovarian Cancer,Fallopian Tube Cancer and Primary Peritoneal Cancer (Collectively Termed as Ovarian Cancer) [NCT03551171]Phase 142 participants (Actual)Interventional2017-12-19Completed
Real-life Use of Niraparib in a Patient Access Program in Norway [NCT04785716]106 participants (Actual)Observational2017-07-31Completed
Niraparib (PARP Inhibitor) Plus Dostarlimab (Anti-PD1) for Small Cell Lung Cancer (SCLC) and Other High-Grade Neuroendocrine Carcinomas (NEC) [NCT04701307]Phase 248 participants (Anticipated)Interventional2021-02-01Active, not recruiting
A Single-arm Phase II Trial of the Addition of Niraparib to Anti-PD-L1 Antibody Maintenance in Patients With SLFN11-positive, Extensive-disease Small Cell Lung Cancer. [NCT05718323]Phase 244 participants (Anticipated)Interventional2023-12-01Not yet recruiting
Molecular Targeted Maintenance Therapy Versus Standard of Care in Advanced Biliary Cancer: an International, Randomised, Controlled, Open-label, Platform Phase 3 Trial [NCT05615818]Phase 3800 participants (Anticipated)Interventional2024-01-31Not yet recruiting
A Phase 1/1b Clinical Trial of Niraparib and Neratinib in Advanced Solid Tumors With an Expansion Cohort in Platinum-resistant Ovarian Cancer [NCT04502602]Phase 145 participants (Anticipated)Interventional2020-08-24Recruiting
Radiotherapy Combined With Niraparib and Toripalimab in Patients With Recurrent Small Cell Lung Cancer (CREATE): A Open-label, Single-arm, Phase II Study [NCT05162196]Phase 257 participants (Anticipated)Interventional2022-06-30Not yet recruiting
A Multicentric, Single Arm, Phase II Trial Assessing the Efficacy of Niraparib as First Line Therapy for Patients With Metastatic Homologous Repair-deficient Pancreatic Cancer [NCT05442749]Phase 228 participants (Anticipated)Interventional2022-10-28Recruiting
A Single Arm, Prospective, Multicenter, Phase II Study to Evaluate the Efficacy and Safety of Niraparib Combined With Oral Etoposide in Platinum Resistant/ Refractory Recurrent Ovarian Cancer [NCT04217798]Phase 236 participants (Anticipated)Interventional2020-05-21Recruiting
Study of the Relationship(s) Between Clinical, Biological and Pharmacokinetic Metrics and Toxicities When Niraparib is Used as Maintenance Treatment (300mg or 200 mg/Day) for Ovarian Cancer Patients. [NCT04861181]Phase 442 participants (Anticipated)Interventional2021-05-05Recruiting
A Phase 2 Open-Label, Single-Arm Study to Evaluate the Efficacy and Safety of the Combination of Niraparib and Dostarlimab (TSR-042) in Patients With Platinum-Resistant Ovarian Cancer (MOONSTONE) [NCT03955471]Phase 241 participants (Actual)Interventional2019-10-03Terminated(stopped due to The study will not resume based on the results of a planned interim analysis that showed futility)
A Phase 1b/2 Trial of Preoperative Niraparib, Dostarlimab, and Hypofractionated Radiotherapy for the Treatment of Locally-advanced Rectal Cancers. [NCT04926324]Phase 1/Phase 238 participants (Anticipated)Interventional2022-07-07Recruiting
Phase II Study to Assess the Efficacy of Niraparib Rechallenge After Surgery in Ovarian Cancer Patients With Oligometastatic Progression (The ANALLISA Study) [NCT06180356]Phase 230 participants (Anticipated)Interventional2023-12-31Not yet recruiting
An Open Label, Multicenter Extension Study in Patients Previously Enrolled in a Genentech and/or F. Hoffmann-La Roche Ltd Sponsored Atezolizumab Study (IMbrella B) [NCT03768063]Phase 31,000 participants (Anticipated)Interventional2019-02-28Recruiting
A Phase 2, Multicenter, Open-label, Single-arm Study to Evaluate the Safety of Niraparib in Japanese Patients With Platinum-sensitive, Relapsed Ovarian, Fallopian Tube, or Primary Peritoneal Cancer Who Achieved CR or PR in the Last Chemotherapy Containing [NCT03759587]Phase 219 participants (Actual)Interventional2018-12-28Completed
A Phase 2 Study of the Combination Dostarlimab With Niraparib In Patients With Penile Carcinoma Who Have Progressed Following Chemotherapy [NCT05526989]Phase 225 participants (Anticipated)Interventional2022-12-28Recruiting
Reirradiation (Re-RT) and Niraparib (NIRA) in Patients With Recurrent Glioblastoma (rGBM) [NCT05666349]Phase 115 participants (Anticipated)Interventional2023-01-01Not yet recruiting
Niraparib Monotherapy as Maintain and Recurrent Treatment of Endometrial Serous Carcinoma: A Multi-center, Open-label, Prospective Clinical Study [NCT04716686]Phase 283 participants (Anticipated)Interventional2021-02-01Recruiting
A Phase 2, Single-arm, Open-label Study to Evaluate the Safety and Efficacy of Niraparib Combined With Bevacizumab as Maintenance Treatment in Patients With Advanced Ovarian Cancer, Fallopian Tube Cancer, or Primary Peritoneal Cancer Following Front-line [NCT03326193]Phase 2105 participants (Actual)Interventional2017-12-12Active, not recruiting
PLATPARP: A Phase II Single-Arm Trial of Niraparib in Platinum-Sensitive Castration-Resistant Prostate Cancer With DNA Repair Defects [NCT04288687]Phase 218 participants (Anticipated)Interventional2020-10-19Recruiting
Phase II Trial of the PARP Inhibitor Niraparib and PD-1 Inhibitor Dostarlimab in Patients With Advanced Cancers With Active Progressing Brain Metastases (STARLET) [NCT05700721]Phase 2120 participants (Anticipated)Interventional2023-06-02Recruiting
A Phase I Study of MK-4827 in Patients With Advanced Solid Tumors or Hematologic Malignancies [NCT00749502]Phase 1113 participants (Actual)Interventional2008-09-30Completed
A Phase II Efficacy Study of MK-4827 in Patients With Mantle Cell Lymphoma [NCT01244009]Phase 20 participants (Actual)Interventional2010-12-31Withdrawn(stopped due to Sponsor decision)
Cohort A: PARP Inhibitor-Naïve Platinum-Resistant Ovarian Cancer Treatment Cohort With TSR-042, Bevacizumab, and Niraparib [NCT05751629]Phase 241 participants (Actual)Interventional2018-11-15Completed
Mesothelioma Stratified Therapy (MiST): A Stratified Multi-arm Phase IIa Clinical Trial to Enable Accelerated Evaluation of Targeted Therapies for Relapsed Malignant Mesothelioma [NCT03654833]Phase 2186 participants (Actual)Interventional2019-01-28Active, not recruiting
Phase II Clinical Trial Aiming at Investigating the Effect of a PARP-inhibitor on Advanced Metastatic Breast Cancer in Germline PALB2 Mutations Carriers [NCT05232006]Phase 212 participants (Anticipated)Interventional2022-05-31Not yet recruiting
A Phase 1/2 First-Time-in-Human, Open-label, Multicenter, Dose Escalation and Expansion Study of the Oral DNA Polymerase Theta Inhibitor (POLQi) GSK4524101 and the PARP Inhibitor (PARPi) Niraparib in Adult Participants With Solid Tumors [NCT06077877]Phase 1/Phase 2135 participants (Anticipated)Interventional2023-10-24Recruiting
Randomized Phase II Study of Platinum-Taxane-Cetrelimab Induction Followed by Niraparib Plus or Minus Cetrelimab Maintenance in Men With Aggressive Variant Prostate Cancers [NCT04592237]Phase 2120 participants (Anticipated)Interventional2020-12-29Recruiting
An Open-label Phase 1b Study to Determine the Maximum Tolerated and/or Recommended Phase 2 Dose of the ATR Inhibitor Elimusertib (BAY 1895344) in Combination With PARP Inhibitor Niraparib, in Participants With Recurrent Advanced Solid Tumors and Ovarian C [NCT04267939]Phase 114 participants (Actual)Interventional2020-02-26Terminated(stopped due to There was no anticipated benefit of the experimental combination as tested over available standard therapies; therefore Sponsor has decided to terminate the investigation.)
Phase II Study of Niraparib in Soft Tissue Sarcoma Patients With Altered DNA Damage Repair [NCT05515575]Phase 28 participants (Actual)Interventional2022-08-23Active, not recruiting
ESP1/SARC025 Global Collaboration: A Phase I Study of a Combination of the PARP Inhibitor, Niraparib and Temozolomide and/or Irinotecan in Patients With Previously Treated,Incurable Ewing Sarcoma [NCT02044120]Phase 134 participants (Actual)Interventional2014-05-31Completed
An Open-label, Phase II Clinical Trial of of a Chinese Patent Medicine Yangzhengxiaoji Capsule to Improve the Adverse Reactions Nausea of Niraparib in in the First-line Maintenance Treatment in Advanced Epithelial Ovarian Cancer (EOC) Patients [NCT05641506]Phase 250 participants (Anticipated)Interventional2022-12-31Not yet recruiting
Genomically Guided Phase II Study to Evaluate the Clinical Benefit of Niraparib in Tumors Metastatic to the CNS [NCT04992013]Phase 220 participants (Anticipated)Interventional2022-04-05Recruiting
A Single-arm, Prospective, Open-label, Phase II Study to Evaluate the Efficacy and Safety of Niraparib Combined With Bevacizumab in Platinum Refractory/Resistant Recurrent Ovarian, Fallopian Tube or Peritoneal Cancer [NCT04556071]Phase 232 participants (Anticipated)Interventional2020-11-06Recruiting
Phase II Trial of Niraparib in Patients With Recurrent Glioma [NCT05297864]Phase 245 participants (Anticipated)Interventional2022-06-09Recruiting
A Dose-escalation Study of the Safety and Pharmacology of DAN-222 in Subjects With Metastatic Breast Cancer [NCT05261269]Phase 130 participants (Actual)Interventional2022-02-02Completed
A Retrospective, Multicenter Study of Niraparib as Maintenance Therapy in Patients With Platinum Sensitive Recurrent Ovarian Cancer Who Have Received Niraparib Within the Expanded Access Program (EAP) in Spain [NCT04546373]316 participants (Actual)Observational2020-09-30Completed
Trial of Maintenance With Niraparib in Patients With Stage III, Stage IV or Platinum-sensitive Recurrent Uterine Serous Carcinoma [NCT04080284]Phase 245 participants (Anticipated)Interventional2019-12-30Recruiting
Randomized Phase II Trial of Niraparib With Standard Combination Radiotherapy and Androgen Deprivation Therapy (ADT) in High Risk Prostate Cancer (With Initial Phase I) [NCT04037254]Phase 2180 participants (Anticipated)Interventional2019-06-03Suspended(stopped due to Protocol specified toxicity analysis)
Phase I/II Trial of Niraparib/Selenium Combination Treatment in Patients With BRCA1/2-Wild Type Recurrent Platinum-Resistant Ovarian Cancer [NCT05672095]Phase 1/Phase 20 participants (Actual)Interventional2023-08-18Withdrawn(stopped due to Abandoned)
Randomized Study of Paclitaxel-carboplatin Followed by Niraparib Compared to Paclitaxel-carboplatin-bevacizumab Followed by Niraparib+Bevacizumab in Patients With Advanced Ovarian Cancer, Following a Front-line Complete Surgery [NCT05183984]Phase 2390 participants (Anticipated)Interventional2022-02-01Recruiting
ProBio: An Outcome-adaptive and Randomized Multi-arm Biomarker Driven Study in Patients With Metastatic Prostate Cancer [NCT03903835]Phase 3750 participants (Anticipated)Interventional2019-02-01Recruiting
Randomized Phase III Trial on NIraparib-TSR-042 (Dostarlimab) vs Physician's Choice CHEmotherapy in Recurrent, Ovarian, Fallopian Tube or Primary Peritoneal Cancer Patients Not Candidate for Platinum Retreatment: NItCHE Trial (MITO 33) [NCT04679064]Phase 3427 participants (Anticipated)Interventional2020-12-01Recruiting
An Open-label, Single-arm, Phase II Study to Investigate the Efficacy and Safety of Niraparib Combined With Anlotinib Maintenance Retreatment in PSR Ovarian Cancer Patients, Who Have Previously Received PARPi Maintenance Treatment. [NCT05385068]Phase 235 participants (Anticipated)Interventional2022-06-30Not yet recruiting
An Open-Label, Multicenter, Long-term Treatment Extension Study in Subjects Who Have Completed a Prior GlaxoSmithKline/TESARO-Sponsored Niraparib Study and Are Judged by the Investigator to Benefit From Continued Treatment With Niraparib [NCT04641247]Phase 226 participants (Actual)Interventional2021-04-16Active, not recruiting
A Phase I-II Study to Evaluate the Efficacy and Safety of Niraparib in Combination With Cabozantinib (XL184) in Patients With Advanced Urothelial Cancer After Failure to First-line Platinum-based Chemotherapy [NCT03425201]Phase 1/Phase 220 participants (Anticipated)Interventional2019-10-14Active, not recruiting
Efficacy and Safety of Huaier Granule in Combination With Nilaparil in First-line Maintenance Therapy in Postoperative Patients With Stage III/IV BRCA Wild-type Ovarian Cancer: a Single-center Prospective, Single-arm Study [NCT05749211]59 participants (Anticipated)Interventional2023-05-31Not yet recruiting
A Single-Arm Phase-II Study of Niraparib in Locally Advanced or Metastatic Solid Tumor Patients With PALB2 Mutations [NCT05169437]Phase 222 participants (Actual)Interventional2022-03-15Active, not recruiting
A Phase II Study Evaluating Safety and Efficacy of Niraparib in Patients With Previously Treated Homologous Recombination (HR) Defective or Loss of Heterozygosity (LOH) High Metastatic Esophageal/Gastroesophageal Junction/Proximal Gastric Adenocarcinoma [NCT03840967]Phase 243 participants (Anticipated)Interventional2019-07-09Active, not recruiting
A Phase I Dose Escalation Study of ATR Inhibitor M4344 in Combination With Niraparib in Participants With Advanced Solid Tumors Followed by Phase II Cohort Expansion in Participants With Breast Cancer With DNA Damage Response (DDR) Mutations [NCT04655183]Phase 1/Phase 20 participants (Actual)Interventional2020-12-01Withdrawn(stopped due to Trial withdrawn based on portfolio prioritization; oral ATRi M1774 in combination with niraparib is under investigation in DDRiver Solid Tumor 301)
Phase 2, Multi-Arm Study of Niraparib Administered Alone and in Combination With a PD-1 Inhibitor in Patients With Non-Small Cell Lung Cancer [NCT03308942]Phase 253 participants (Actual)Interventional2017-09-29Completed
An Open-label, Multicenter Trial of the Safety, Tolerability, and Pharmacokinetic/Pharmacodynamic Profile of M1774 in Participants With Metastatic or Locally Advanced Unresectable Solid Tumors (DDRiver Solid Tumors 301) [NCT04170153]Phase 1204 participants (Anticipated)Interventional2019-12-20Recruiting
A Safety and Pharmacokinetics Study of Niraparib Plus Androgen Receptor-Targeted Therapy (Apalutamide or Abiraterone Acetate Plus Prednisone) in Men With Metastatic Castration-Resistant Prostate Cancer [NCT02924766]Phase 134 participants (Actual)Interventional2016-10-03Completed
The Real World Efficacy and Safety of Niraparib in Korean Women With Primary and Recurrent Epithelial Ovarian Cancer [NCT06086665]850 participants (Actual)Observational2019-12-01Completed
A Phase II Study of Niraparib With Dostarlimab Therapy as Neoadjuvant Treatment for Patients With BRCA-mutated Breast Cancer [NCT04584255]Phase 262 participants (Anticipated)Interventional2020-12-18Recruiting
ENGOT-OV42 / NSGO-AVATAR: A Three-arm Randomized Study to Evaluate the Efficacy of Niraparib-bevacizumab-dostarlimab Triplet Combination Against Niraparib-bevacizumab Doublet Combination and Against Standard of Care Therapy in Women With Relapsed Ovarian [NCT03806049]Phase 30 participants (Actual)Interventional2019-12-31Withdrawn(stopped due to Lack of financial support)
A Phase 1/2a, Open-label, Multicenter Study to Assess the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics, and Preliminary Anti-tumor Activity of PEN-866 in Patients With Advanced Solid Malignancies [NCT03221400]Phase 1/Phase 2340 participants (Anticipated)Interventional2017-08-29Recruiting
An Open-label, Single Arm, Phase II Trial of Niraparib in Combination With Anlotinib in Patients With Platinum-resistant Recurrent Ovarian Cancer, Fallopian Tube Cancer, and Primary Peritoneal Cancer (Ovarian Cancer) [NCT04376073]Phase 240 participants (Anticipated)Interventional2020-05-22Recruiting
LCI-BRE-MTN-NIR-001: A Phase I Study of Niraparib in Combination With Standard Chemotherapy in Metastatic Triple-Negative Breast Cancer [NCT04762901]Phase 10 participants (Actual)Interventional2021-04-01Withdrawn(stopped due to Funding was terminated.)
A Phase 0 Clinical Trial to Evaluate Drug Concentrations and Pharmacodynamic Parameters of Niraparib in Tumor Tissue of Patients With Surgically Accessible Recurrent IDH 1/2 Gliomas [NCT05406700]Early Phase 116 participants (Anticipated)Interventional2023-05-18Recruiting
Efficacy and Safety of Niraparib Combined With Radiotherapy in Patients With Recurrent Glioblastoma [NCT04715620]Phase 230 participants (Anticipated)Interventional2021-01-31Recruiting
Genomic Biomarker-Selected Umbrella Neoadjuvant Study for High Risk Localized Prostate Cancer [NCT04812366]Phase 2315 participants (Anticipated)Interventional2021-09-21Recruiting
"Zedula Special Drug Use Observational Study Ovarian Cancer" [NCT05021562]300 participants (Anticipated)Observational2021-09-13Recruiting
Canadian Multi-arm Multi-stage Randomized Controlled Trial Assessing Front Line Treatment in Serous or p53 Mutant Endometrial Cancer [NCT04159155]Phase 2/Phase 3120 participants (Anticipated)Interventional2020-11-17Suspended(stopped due to Low accrual, protocol amendment in progress , to be re-opened soon.)
A Pilot Study of Personalized Biomarker-based Treatment Strategy or Immunotherapy in Patients With Recurrent/Metastatic Squamous Cell Carcinoma of the Head and Neck [NCT03088059]Phase 2340 participants (Anticipated)Interventional2017-11-16Active, not recruiting
Niraparib for the Neoadjuvant Treatment of Unresectable Ovarian Cancer [NCT04507841]Phase 253 participants (Anticipated)Interventional2020-07-01Recruiting
A Single-arm Phase II Study of Niraparib and Bevacizumab Maintenance Therapy in Platinum-sensitive Recurrent Ovarian Cancer Patients Previously Treated With a PARP Inhibitor [NCT04734665]Phase 244 participants (Anticipated)Interventional2021-07-05Recruiting
ProTarget - A Danish Nationwide Clinical Trial on Targeted Cancer Treatment Based on Genomic Profiling [NCT04341181]Phase 2300 participants (Anticipated)Interventional2020-08-24Recruiting
An Open-Label Phase 1b Dose-Finding Trial Evaluating the Safety of Niraparib and Temozolomide and Atezolizumab in Participants With Advanced Solid Tumors and Expansion to a Phase 2 Trial Comparing the Effects of Niraparib and Temozolomide Plus Atezolizuma [NCT03830918]Phase 1/Phase 274 participants (Anticipated)Interventional2019-03-06Recruiting
Trial of M4344 and Niraparib in Patients With PARP Resistant Recurrent Ovarian Cancer [NCT04149145]Phase 10 participants (Actual)Interventional2023-05-31Withdrawn(stopped due to never opened)
Real-world Data From a Multi-center Study: Insights to the Effectiveness and Safety in Patients With Ovarian Cancer Receiving Niraparib as First-line Maintenance Therapy [NCT05734911]199 participants (Actual)Observational [Patient Registry]2019-01-01Completed
An Observational, Non-interventional Study of Niraparib Maintenance Treatment in Patients With Ovarian Cancer After Frontline Platinum-based Chemotherapy [NCT04986371]300 participants (Anticipated)Observational2021-08-10Not yet recruiting
Niraparib in Metastatic Pancreatic Cancer After Previous Chemotherapy (NIRA-PANC): a Phase 2 Trial [NCT03553004]Phase 218 participants (Anticipated)Interventional2019-01-22Active, not recruiting
Phase 2, Single Arm Clinical Trial to Evaluate the Safety and Activity of Oregovomab and Niraparib as a Combinatorial Immune Priming Strategy in Subjects With Platinum Sensitive Recurrent Ovarian Cancer [NCT05335993]Phase 210 participants (Actual)Interventional2022-07-25Active, not recruiting
Pre-Approval Access Single Patient Request for Niraparib / Abiraterone Acetate Combination (Nira/AA Combination) [NCT05401214]0 participants Expanded AccessApproved for marketing
A Phase 1b/2 Trial Evaluating Safety and Efficacy of CAPecitabine in Combination With Ni-rapaRIb in HER2-negative Advanced Breast canCEr [NCT05519670]Phase 1/Phase 272 participants (Anticipated)Interventional2023-03-31Not yet recruiting
A Multicenter, Open-label, Single-arm, Phase Ib Dose Escalation and Multi-cohort Expansion Clinical Study to Assess the Safety and Antitumor Activity of Niraparib in Combination With MGD013 in Patients With Advanced or Metastatic Solid Tumor Who Failed Pr [NCT04178460]Phase 160 participants (Actual)Interventional2020-02-03Terminated(stopped due to This termination decision is a business decision and is not due to any safety concerns.)
Molecularly Driven, Immune-Based, Maintenance Niraparib and Dostarlimab in Advanced Stage Cholangiocarcinoma [NCT04895046]Phase 20 participants (Actual)Interventional2021-10-11Withdrawn(stopped due to Funder decision)
Induction and Maintenance Treatment With PARP Inhibitor and Immunotherapy in HPV-negative Head and Neck Squamous Cell Carcinoma (HNSCC) [NCT04681469]Phase 249 participants (Anticipated)Interventional2021-02-08Recruiting
An Open-label, Phase II Study Evaluating the Efficacy of Niraparib and Dostarlimab (TSR-042) in Recurrent/Metastatic Head and Neck Squamous Cell Carcinoma Patients [NCT04313504]Phase 223 participants (Anticipated)Interventional2020-11-04Active, not recruiting
An Open-Label, Single-arm Pilot Study Evaluating the Antitumor Activity and Safety of Niraparib as Neoadjuvant Treatment in Localized, HER2-negative, BRCA-mutant Breast Cancer Patients [NCT03329937]Phase 121 participants (Actual)Interventional2018-04-12Completed
A Phase 2, Open-Label, Single-Arm Study to Evaluate the Safety and Efficacy of Niraparib in Patients With Advanced, Relapsed, High-Grade Serous Epithelial Ovarian, Fallopian Tube, or Primary Peritoneal Cancer Who Have Received Three or Four Previous Chemo [NCT02354586]Phase 2463 participants (Actual)Interventional2015-03-23Completed
A Multicenter, Open-label Phase II Trial of a New Customized Dosing (RADAR Dosing) of Niraparib as Maintenance Therapy in Platinum Sensitive Ovarian, Fallopian Tube or Primary Peritoneal Recurrent Cancer Patients [NCT03891576]Phase 2105 participants (Anticipated)Interventional2019-11-13Recruiting
A Multicentre, Open-label, Three-arm Randomised Phase II Trial Assessing the Safety and Efficacy of the HSP90 Inhibitor Ganetespib in Combination With Carboplatin Followed by Maintenance Treatment With Niraparib Versus Ganetespib Plus Carboplatin Followed [NCT03783949]Phase 2122 participants (Actual)Interventional2018-11-30Completed
A Phase II, Open Label Study of the Poly(ADP-ribose) Polymerase Inhibitor Niraparib in Monotherapy or in Combination With Anti-PD1 Inhibitor TSR-042 in Recurrent Endometrial Cancer [NCT03016338]Phase 251 participants (Actual)Interventional2017-11-06Active, not recruiting
A Phase 1B/2 Multicohort Umbrella Study to Evaluate the Safety and Efficacy of Novel Treatments And/Or Combinations of Treatments in Participants With Ovarian Cancer (OPAL) [NCT03574779]Phase 1/Phase 2125 participants (Anticipated)Interventional2018-11-15Recruiting
Part 1: AVANOVA1 - A Phase I Study to Evaluate the Safety and Tolerability of Bevacizumab-niraparib Combination Therapy and Determine the Recommended Phase 2 Dose (RP2D) in Women With Platinum-sensitive Epithelial Ovarian, Fallopian Tube, or Peritoneal Ca [NCT02354131]Phase 1/Phase 2108 participants (Actual)Interventional2015-02-15Completed
Phase II Study of Niraparib and TSR-042 in Patients With Germline or Somatic BRCA1/2 and PALB2-Related Pancreatic Cancer [NCT04493060]Phase 222 participants (Actual)Interventional2020-12-28Active, not recruiting
A Phase 1/2 Dose-Escalation and Dose-Expansion Study of ZN-c3 in Combination With Niraparib in Subjects With Platinum-Resistant Ovarian Cancer [NCT05198804]Phase 1/Phase 2138 participants (Anticipated)Interventional2022-01-27Recruiting
A Phase 2, Open-Label, Single-Arm Study to Evaluate the Safety and Efficacy of Niraparib in Patients With Advanced and Relapsed Ovarian Cancer After 3 or 4 Previous Chemotherapies [NCT04392102]Phase 215 participants (Actual)Interventional2020-08-04Completed
Pancytopenia Related to PARP Inhibitors in Cancer Patients : an Observational and Retrospective Study Using the WHO's Pharmacovigilance Database (PancytoRIB) [NCT04774627]200 participants (Actual)Observational2021-02-07Completed
Phase l Study of a BET Inhibitor, ZEN003694, Combined With a PARP Inhibitor, Niraparib in Patients With Metastatic or Recurrent Solid Tumors [NCT06161493]Phase 126 participants (Anticipated)Interventional2023-12-31Not yet recruiting
A Single Arm, Single Center, Phase I Trial of Niraparib Plus Anlotinib in Advanced Solid Tumors With Homologous Recombination Repair (HRR) Gene Mutations [NCT04764084]Phase 152 participants (Anticipated)Interventional2021-04-01Not yet recruiting
A Phase II Study of Niraparib in Combination With EGFR Inhibitor Panitumumab in Patients With Advanced Colorectal Cancer [NCT03983993]Phase 240 participants (Anticipated)Interventional2019-10-15Active, not recruiting
A Clinical Proof-of-concept Study Evaluating Efficacy and Safety of ZL-2306 (Niraparib) Combined With Brivanib or Toripalimab in Patients With Metastatic, Recurrent, and Persistent Cervical Cancer [NCT04395612]Phase 238 participants (Anticipated)Interventional2020-05-08Recruiting
A Phase II, Randomized Study of Cytoreductive Surgery Combined With Niraparib Maintenance in Platinum-sensitive, Secondary Recurrent Ovarian Cancer [NCT03983226]Phase 2167 participants (Anticipated)Interventional2019-10-18Recruiting
Combined Targeting of the Androgen Receptor in Metastatic Castrate-Resistant Prostate Cancer With Enzalutamide and the Poly (ADP- Ribose) Polymerase (PARP) Inhibitor Niraparib: Hoosier Cancer Research Network GU14-202 [NCT02500901]Phase 12 participants (Actual)Interventional2016-03-31Terminated(stopped due to Suspended by funder)
Phase II Trial of PARP Inhibitor Niraparib for Men With High Risk Prostate Cancer and DNA Damage Response Defects [NCT04030559]Phase 230 participants (Anticipated)Interventional2020-02-25Recruiting
A Phase 3, Randomized, Double-blind, Multicenter Study of Dostarlimab (TSR-042) Plus Carboplatin-paclitaxel Versus Placebo Plus Carboplatin-paclitaxel in Patients With Recurrent or Primary Advanced Endometrial Cancer (RUBY) [NCT03981796]Phase 3787 participants (Actual)Interventional2019-07-18Active, not recruiting
A Phase 3, Randomized, Double-Blind, Placebo-Controlled, Multicenter Study of Niraparib Maintenance Treatment in Patients With Advanced Ovarian Cancer Following Response on Front-Line Platinum-Based Chemotherapy [NCT02655016]Phase 3733 participants (Actual)Interventional2016-07-07Active, not 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 226 participants (Anticipated)Interventional2020-10-05Recruiting
Phase 2 Proof-of-Concept Trial Testing the PARP Inhibitor Niraparib in Patients With Pancreatic Cancer Harboring Deficiencies in Homologous Recombination DNA Repair [NCT03601923]Phase 232 participants (Actual)Interventional2018-08-22Active, not recruiting
An Open-label, Single Arm, Phase II Trial of Niraparib in Combination With Anti-PD1 Antibody in Recurrent/ Advanced Stage Endometrial Cancer Patients [NCT04885413]Phase 237 participants (Anticipated)Interventional2021-07-01Recruiting
Phase 1b/2 Study of ATR InhibiTor RP-3500 and PARP Inhibitor Combinations in Patients With Molecularly Selected Cancers (ATTACC) [NCT04972110]Phase 1/Phase 2196 participants (Anticipated)Interventional2021-07-21Recruiting
A Phase 1 Study of Abemaciclib and Niraparib as Neoadjuvant Therapy in Hormone Receptor Positive (HR+) HER2 Negative (HER2-) Breast Cancer [NCT04481113]Phase 18 participants (Actual)Interventional2021-06-07Active, not recruiting
A Phase Ib Study of Cobimetinib Administered in Combination With Niraparib, With or Without Atezolizumab, To Patients With Advanced Platinum-sensitive Ovarian Cancer [NCT03695380]Phase 177 participants (Actual)Interventional2019-01-09Completed
Expanded Access Protocol for Niraparib in Patients With Recurrent Ovarian Cancer [NCT03025867]0 participants Expanded AccessApproved for marketing
A Phase II Study of Niraparib in Patients With Advanced Melanoma With Genetic Homologous Recombination (HR) Mutation / Alteration [NCT03925350]Phase 241 participants (Anticipated)Interventional2019-03-20Recruiting
A Phase II Trial of the PARP Inhibitor, Niraparib, in BAP1 and Other DNA Damage Response (DDR) Pathway Deficient Neoplasms (UF-STO-ETI-001) [NCT03207347]Phase 237 participants (Actual)Interventional2018-08-13Completed
A Phase II Study of NirAparib, Dostarlimab and Radiotherapy in Metastatic, PD-L1 Negative or Immunotherapy-Refractory Triple-Negative Breast Cancer (NADiR) [NCT04837209]Phase 232 participants (Anticipated)Interventional2021-07-21Recruiting
A Phase 1 Evaluation of the Safety and Tolerability of Niraparib in Combination With Everolimus in Advanced Gynecologic Malignancies and Breast Cancer [NCT03154281]Phase 124 participants (Anticipated)Interventional2017-07-17Active, not recruiting
A Multi-Center Trial of Androgen Suppression With Abiraterone aCetate, LEuprolide, PARP Inhibition and Stereotactic Body Radiotherapy (ASCLEPIuS): A Phase I/2 Trial in High Risk and Node Positive Prostate Cancer [NCT04194554]Phase 1/Phase 2100 participants (Anticipated)Interventional2020-11-06Recruiting
An Open-Label, Randomized-Sequence, Multicenter, Single-Crossover Study to Assess the Relative Bioavailability and Bioequivalence of Niraparib Tablet Formulation Compared to Niraparib Capsule Formulation in Patients With Advanced Solid Tumors [NCT03329001]Phase 1236 participants (Actual)Interventional2017-11-29Active, not recruiting
SOPRANO: Stereotactic Radiotherapy Alone or Followed by Niraparib for Oligometastases or Oligoprogression in Ovarian Cancer Following PARP Inhibitor Therapy [NCT05990192]Phase 242 participants (Anticipated)Interventional2024-01-31Not yet recruiting
Phase 2 Trial of Niraparib or Niraparib and Bevacizumab Combination in Patients With Recurrent Endometrial Cancer and/or Ovarian Cancer With ARID1A Mutation (OU-SCC-ARID1A) [NCT05523440]Phase 292 participants (Anticipated)Interventional2023-02-15Recruiting
Platform Study of Genotyping Guided Precision Medicine for Rare Tumors in China [NCT04423185]Phase 2770 participants (Anticipated)Interventional2020-08-15Not yet recruiting
A Phase I Study of Niraparib Administered Concurrently With Postoperative RT in Triple Negative Breast Cancer Patients (UNITY) [NCT03945721]Phase 120 participants (Anticipated)Interventional2019-07-11Recruiting
A Liquid-biopsy Informed Platform Trial to Evaluate Treatment in CDK4/6-inhibitor Resistant ER+/HER2- Metastatic Breast Cancer [NCT05601440]Phase 2484 participants (Anticipated)Interventional2023-06-13Recruiting
A Pilot Study to Estimate Efficacy of Combining Dostarlimab and Niraparib in Patients With Relapsed EOC After Treatment With PARPi [NCT05126342]Phase 2100 participants (Anticipated)Interventional2023-07-01Not yet recruiting
Combination of HX008 And Niraparib in GErm-line-mutAted Metastatic Breast Cancer: a muLti-centEr Phase II Study [NCT04508803]Phase 237 participants (Anticipated)Interventional2020-09-14Recruiting
Phase 2 Study of CJNJ-67652000 (Niraparib/Abiraterone Acetate Fixed-Dose Combination) and Prednisone for Metastatic Castration-Resistant Prostate Cancer Associated With SPOP Mutation With or Without Homologous Recombination Deficiency [NCT05689021]Phase 230 participants (Anticipated)Interventional2023-07-07Recruiting
Phase II Trial of Primary Radiotherapy With Androgen Ablation With or Without Adjuvant Niraparib for Selected High-Risk Locoregional Prostate Cancer [NCT04947254]Phase 2200 participants (Anticipated)Interventional2021-08-05Recruiting
A Phase 1b/2 Study of the PARP Inhibitor Niraparib in Combination With Trastuzumab in Patients With Metastatic HER2+ Breast Cancer [NCT03368729]Phase 1/Phase 240 participants (Anticipated)Interventional2019-09-06Recruiting
A Phase 3 Randomized Double-blind Trial of Maintenance With Niraparib Versus Placebo in Patients With Platinum Sensitive Ovarian Cancer. [NCT01847274]Phase 3596 participants (Actual)Interventional2013-06-21Completed
Longitudinal Study Evaluating in Real Life the Tolerability of Niraparib in Maintenance After Platine-based Chemotherapy for Patients With Ovarian Cancer Late Relapse : the French GINECO - NiQoLe Study [NCT03752216]Phase 4141 participants (Actual)Interventional2019-04-03Completed
Phase IB Trial of Niraparib and TSR-042 in Patients With BRCA-Mutated Breast, Pancreas or Ovary Cancer [NCT04673448]Phase 118 participants (Anticipated)Interventional2021-10-18Recruiting
Phase IB Trial of Radium-223 and Niraparib in Patients With Castrate Resistant Prostate Cancer (NiraRad) [NCT03076203]Phase 114 participants (Actual)Interventional2017-09-22Completed
A Phase III, Randomized, Open Label, Multicenter, Controlled Trial of Niraparib Versus Physician's Choice in Previously-treated, HER2 Negative, Germline BRCA Mutation-positive Breast Cancer Patients [NCT01905592]Phase 3216 participants (Actual)Interventional2014-02-25Terminated(stopped due to The study was terminated due to futility.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Cycle 6
NCT01847274 (49) [back to overview]Change From Baseline in European Quality of Life Scale, 5-Dimensions (EQ-5D-5L) in Cohort With Germline BRCA at Cycle 2
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Cycle 2
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Cycle 4
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Cycle 6
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Post-progression
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Cycle 2
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Cycle 4
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Cycle 6
NCT01847274 (49) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Post-progression
NCT01847274 (49) [back to overview]Chemotherapy-Free Interval in Cohort With Germline BRCA Mutation (gBRCA)
NCT01847274 (49) [back to overview]Overall Survival in Cohort With No Germline BRCA Mutation
NCT01847274 (49) [back to overview]Overall Survival in Cohort With Germline BRCA Mutation (gBRCA)
NCT01847274 (49) [back to overview]Chemotherapy-Free Interval in Cohort With No Germline BRCA Mutation
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Post-progression
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Cycle 6
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Cycle 4
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With Germline BRCA at Post-progression
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With Germline BRCA at Cycle 6
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With Germline BRCA at Cycle 4
NCT01847274 (49) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 to the Last Quantifiable Concentration (AUC[0-last]) Following Administration of Niraparib (FE Sub-study)
NCT01847274 (49) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 Extrapolated to Infinity (AUC[0-infinity]) Following Administration of Niraparib (FE Sub-study)
NCT01847274 (49) [back to overview]Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Cycle 2
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Post-progression
NCT01847274 (49) [back to overview]Maximum Observed Plasma Concentration (Cmax) Following Administration of Niraparib (FE Sub-study)
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Cycle 4
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Cycle 2
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Baseline
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Post-progression
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Cycle 6
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Cycle 4
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Cycle 2
NCT01847274 (49) [back to overview]Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Baseline
NCT01847274 (49) [back to overview]Number of Participants With Non-serious AEs and SAEs in QTc Sub-study
NCT01847274 (49) [back to overview]Number of Participants With Non-serious AEs and SAEs in FE Sub-study
NCT01847274 (49) [back to overview]Number of Participants With Non-serious AEs and SAEs (Post-study Unblinding)
NCT01847274 (49) [back to overview]Number of Participants With Non-serious Adverse Events (AEs) and Serious AEs (SAEs)
NCT01847274 (49) [back to overview]Number of Participants With Maximum Post-Baseline QT Interval Corrected by Fridericia's Formula (QTcF) Greater Than Pre-specified Thresholds
NCT01847274 (49) [back to overview]Time to Second Subsequent Therapy in Cohort With No Germline BRCA Mutation
NCT01847274 (49) [back to overview]Time to Second Subsequent Therapy in Cohort With Germline BRCA Mutation (gBRCA)
NCT01847274 (49) [back to overview]Time to Reach Maximum (Tmax) Following Administration of Niraparib (FE Sub-study)
NCT01847274 (49) [back to overview]Time to First Subsequent Therapy in Cohort With No Germline BRCA Mutation
NCT01847274 (49) [back to overview]Time to First Subsequent Therapy in Cohort With Germline BRCA Mutation (gBRCA)
NCT01847274 (49) [back to overview]Terminal Elimination Half-life (t1/2) Following Administration of Niraparib (FE Sub-study)
NCT01847274 (49) [back to overview]Progression-Free Survival 2 in Cohort With No Germline BRCA Mutation
NCT01847274 (49) [back to overview]Progression-Free Survival 2 in Cohort With Germline BRCA Mutation (gBRCA)
NCT01847274 (49) [back to overview]Progression-Free Survival (PFS) in Cohort With No Germline BRCA Mutation
NCT01847274 (49) [back to overview]Progression-Free Survival (PFS) in Cohort With No Germline BCRA With Homologous Recombination Deficiency-positive (HRD+) Tumors (Non-gBRCAmut HRD+)
NCT01847274 (49) [back to overview]Progression-Free Survival (PFS) in Cohort With Germline BReast CAncer Gene (BRCA) Mutation (gBRCA)
NCT01905592 (10) [back to overview]Number of Participants With Subsequent Anticancer Therapies
NCT01905592 (10) [back to overview]Number of Participants With Serious Adverse Events (SAE) and Non-serious Adverse Events (Non-SAE)
NCT01905592 (10) [back to overview]Number of Participants With Central BRCA Mutation Status
NCT01905592 (10) [back to overview]Time to Treatment Failure
NCT01905592 (10) [back to overview]Progression Free Survival (PFS) - Investigator Assessment
NCT01905592 (10) [back to overview]Progression Free Survival (PFS) - Central Review Assessment
NCT01905592 (10) [back to overview]Overall Survival
NCT01905592 (10) [back to overview]Overall Response Rate (ORR)
NCT01905592 (10) [back to overview]Number of Participants With Serious Adverse Events Related to New Malignancy
NCT01905592 (10) [back to overview]Duration of Response (DOR)
NCT02354586 (8) [back to overview]ORR by HRD Status and Breast Cancer Gene (BRCA) Status
NCT02354586 (8) [back to overview]Number of Participants With Any Non-serious Adverse Event (Non-SAE) and Any Serious Adverse Event (SAE)
NCT02354586 (8) [back to overview]Time to First Subsequent Therapy (TFST)
NCT02354586 (8) [back to overview]Overall Survival
NCT02354586 (8) [back to overview]Objective Response Rate (ORR)
NCT02354586 (8) [back to overview]Duration of Response (DoR)
NCT02354586 (8) [back to overview]Disease Control Rate (DCR)
NCT02354586 (8) [back to overview]Progression Free Survival
NCT02655016 (12) [back to overview]Overall Survival
NCT02655016 (12) [back to overview]Change From Baseline in PRO: European Quality of Life Scale, 5-dimensions, 5-levels of Severity (EQ-5D-5L) Utility Score
NCT02655016 (12) [back to overview]Change From Baseline in Participant Reported Outcome (PRO): Functional Assessment of Cancer Therapy-Ovarian Symptom Index (FOSI)
NCT02655016 (12) [back to overview]Change From Baseline in Global Health Status/QoL of EORTC-QLQ-C30
NCT02655016 (12) [back to overview]Number of Participants With Any Non-serious Adverse Event (Non-SAE) or Any SAE
NCT02655016 (12) [back to overview]Change From Baseline in Symptoms Scales and Symptoms Items (Dyspnea, Appetite Loss, Insomnia, Constipation, Diarrhea and Financial Difficulty) of EORTC-QLQ-C30
NCT02655016 (12) [back to overview]Change From Baseline in Symptoms Scale of EORTC-QLQ-OV28
NCT02655016 (12) [back to overview]Change From Baseline in Functional Scales of European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire Ovarian Cancer Module (EORTC-QLQ-OV28)
NCT02655016 (12) [back to overview]Change From Baseline in Functional Scales of European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire C30 (EORTC-QLQ-C30)
NCT02655016 (12) [back to overview]Time to First Subsequent Therapy (TFST)
NCT02655016 (12) [back to overview]Progression-Free Survival-2 (PFS2)
NCT02655016 (12) [back to overview]Progression Free Survival
NCT02657889 (22) [back to overview]Phase 1: Minimum Observed Plasma Concentration (Cmin) and Maximum Observed Plasma Concentration (Cmax) of Niraparib
NCT02657889 (22) [back to overview]Phase 1: Minimum Observed Plasma Concentration at Steady State (Cmin,ss) and Maximum Observed Plasma Concentration at Steady State (Cmax,ss) of Niraparib
NCT02657889 (22) [back to overview]Phase 1: Cmin,ss and Cmax,ss of Major Metabolite of Niraparib (M1)
NCT02657889 (22) [back to overview]Phase 1: Cmin and Cmax of Major Metabolite of Niraparib (M1)
NCT02657889 (22) [back to overview]Phase 2: Progression Free Survival (PFS) as Measured by RECIST v1.1
NCT02657889 (22) [back to overview]Phase 2: Overall Survival (OS)
NCT02657889 (22) [back to overview]Phase 2: Objective Response Rate (ORR) as Measured by Response Evaluation Criteria in Solid Tumors (RECIST) Version (v) 1.1
NCT02657889 (22) [back to overview]Phase 2: Number of Participants With TEAEs
NCT02657889 (22) [back to overview]Phase 2: Duration of Response (DOR) as Measured by RECIST v1.1
NCT02657889 (22) [back to overview]Phase 1: Number of Participants Reporting Dose-Limiting Toxicities (DLTs)
NCT02657889 (22) [back to overview]Phase 2: Disease Control Rate (DCR) as Measured by RECIST v1.1
NCT02657889 (22) [back to overview]Phase 1: Volume of Distribution (Vz/F) of Niraparib
NCT02657889 (22) [back to overview]Phase 2: Plasma Concentrations of Major Metabolite of Niraparib (M1)
NCT02657889 (22) [back to overview]Phase 1: Volume of Distribution (Vz/F) of Major Metabolite of Niraparib (M1)
NCT02657889 (22) [back to overview]Phase 1: Number of Participants With Treatment Emergent Adverse Events (TEAEs)
NCT02657889 (22) [back to overview]Phase 2: Plasma Concentrations of Niraparib
NCT02657889 (22) [back to overview]Phase 1: Apparent Oral Clearance (CL/F) of Major Metabolite of Niraparib (M1)
NCT02657889 (22) [back to overview]Phase 1: Apparent Oral Clearance (CL/F) of Niraparib
NCT02657889 (22) [back to overview]Phase 1: Area Under the Plasma Concentration-time Curve From Time 0 (Predose) to 24 Hours Post Dose (AUC [0-24]) of Niraparib
NCT02657889 (22) [back to overview]Phase 1: AUC (0-24) of Major Metabolite of Niraparib (M1)
NCT02657889 (22) [back to overview]Phase 1: AUC at Steady State (AUC,ss) of Niraparib
NCT02657889 (22) [back to overview]Phase 1: AUC,ss of Major Metabolite of Niraparib (M1)
NCT02854436 (11) [back to overview]Overall Survival (OS)
NCT02854436 (11) [back to overview]Radiographic Progression-Free Survival (rPFS)
NCT02854436 (11) [back to overview]Time to Prostate-Specific Antigen (PSA) Progression
NCT02854436 (11) [back to overview]Time to Radiographic Progression
NCT02854436 (11) [back to overview]Time to Symptomatic Skeletal Event (SSE)
NCT02854436 (11) [back to overview]Number of Participants With Adverse Events (AEs)
NCT02854436 (11) [back to overview]Objective Response Rate (ORR) for Participants With Measurable Metastatic Castration-resistant Prostate Cancer (mCRPC) and Breast Cancer Gene (BRCA) Mutation
NCT02854436 (11) [back to overview]Objective Response Rate for Participants With Measurable Metastatic Castration-resistant Prostate Cancer (mCRPC) and Non-Breast Cancer Gene (BRCA) Mutation
NCT02854436 (11) [back to overview]Circulating Tumor Cells (CTC) Response Rate
NCT02854436 (11) [back to overview]Duration of Objective Response
NCT02854436 (11) [back to overview]Number of Participants With Worst Toxicity Grades for Clinical Laboratory Tests Based on National Cancer Institute - Common Terminology Criteria for Adverse Events (NCI-CTCAE)
NCT03207347 (5) [back to overview]Progression-Free Survival Rate at 6 Months
NCT03207347 (5) [back to overview]Progression-Free Survival Rate at 3 Months
NCT03207347 (5) [back to overview]Progression-Free Survival
NCT03207347 (5) [back to overview]Overall Survival
NCT03207347 (5) [back to overview]Objective Response Rate (ORR)
NCT03307785 (158) [back to overview]Part A: Number of Participants With Non-serious Treatment-emergent Adverse Events (TEAEs), Serious TEAEs (STEAEs) and Adverse Events of Special Interest (AESIs)
NCT03307785 (158) [back to overview]Part A: Tmax at Steady State (Tmax,ss) of Niraparib
NCT03307785 (158) [back to overview]Part A: Tmax at Steady State (Tmax,ss) of Niraparib
NCT03307785 (158) [back to overview]Part A: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part A: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part A: Volume of Distribution After Intravenous Administration (Vss) of of TSR-042
NCT03307785 (158) [back to overview]Part A: Area Under the Plasma Concentration From Time Zero to Infinity (AUC[0-infinity]) of Niraparib
NCT03307785 (158) [back to overview]Part A: AUC at Steady State (AUCss) of Niraparib
NCT03307785 (158) [back to overview]Part A: AUC(0-infinity) of TSR-042
NCT03307785 (158) [back to overview]Part A: Cmax of TSR-042
NCT03307785 (158) [back to overview]Part A: Ctau of TSR-042
NCT03307785 (158) [back to overview]Part A: Disease Control Rate
NCT03307785 (158) [back to overview]Part A: Duration of Response
NCT03307785 (158) [back to overview]Part A: Maximum Observed Plasma (Cmax) of Niraparib
NCT03307785 (158) [back to overview]Part A: Number of Participants With Dose-limiting Toxicity (DLT)
NCT03307785 (158) [back to overview]Part A: Number of Participants With Positive Anti-TSR-042 Antibodies
NCT03307785 (158) [back to overview]Part A: Objective Response Rate
NCT03307785 (158) [back to overview]Part A: Observed Concentration at the End of the Dosing Interval (Ctau) of Niraparib
NCT03307785 (158) [back to overview]Part A: Progression-free Survival
NCT03307785 (158) [back to overview]Part A: Time to Reach Maximum Plasma Concentration (Tmax) of Niraparib
NCT03307785 (158) [back to overview]Part A: Tmax of TSR-042
NCT03307785 (158) [back to overview]Part B: AUC(0-infinity) of TSR-042
NCT03307785 (158) [back to overview]Part B: Cmax of TSR-042
NCT03307785 (158) [back to overview]Part B: Ctau of TSR-042
NCT03307785 (158) [back to overview]Part B: Disease Control Rate
NCT03307785 (158) [back to overview]Part B: Number of Participants With DLT
NCT03307785 (158) [back to overview]Part B: Number of Participants With Positive Anti-TSR-042 Antibodies
NCT03307785 (158) [back to overview]Part B: Objective Response Rate
NCT03307785 (158) [back to overview]Part B: Progression-free Survival
NCT03307785 (158) [back to overview]Part B: Tmax of TSR-042
NCT03307785 (158) [back to overview]Part C: AUC(0-infinity) of Niraparib
NCT03307785 (158) [back to overview]Part C: AUC(0-infinity) of TSR-042
NCT03307785 (158) [back to overview]Part C: AUCss of Niraparib
NCT03307785 (158) [back to overview]Part C: Cmax of Niraparib
NCT03307785 (158) [back to overview]Part C: Cmax of TSR-042
NCT03307785 (158) [back to overview]Part C: Ctau of Niraparib
NCT03307785 (158) [back to overview]Part C: Ctau of TSR-042
NCT03307785 (158) [back to overview]Part C: Disease Control Rate
NCT03307785 (158) [back to overview]Part C: Number of Participants With DLT
NCT03307785 (158) [back to overview]Part C: Number of Participants With Positive Anti-TSR-042 Antibodies
NCT03307785 (158) [back to overview]Part C: Objective Response Rate
NCT03307785 (158) [back to overview]Part C: Progression-free Survival
NCT03307785 (158) [back to overview]Part C: Tmax of Niraparib
NCT03307785 (158) [back to overview]Part C: Tmax of TSR-042
NCT03307785 (158) [back to overview]Part D: AUC(0-infinity) of TSR-042
NCT03307785 (158) [back to overview]Part D: Cmax of TSR-042
NCT03307785 (158) [back to overview]Part D: Ctau of TSR-042
NCT03307785 (158) [back to overview]Part D: Disease Control Rate
NCT03307785 (158) [back to overview]Part D: Number of Participants With Positive Anti-TSR-042 Antibodies
NCT03307785 (158) [back to overview]Part D: Objective Response Rate
NCT03307785 (158) [back to overview]Part D: Progression-free Survival
NCT03307785 (158) [back to overview]Part D: Tmax of TSR-042
NCT03307785 (158) [back to overview]Part E: AUC(0-infinity) of TSR-042
NCT03307785 (158) [back to overview]Part E: AUC0-t of TSR-042
NCT03307785 (158) [back to overview]Part E: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part E: CL of TSR-042
NCT03307785 (158) [back to overview]Part E: Cmax of TSR-042
NCT03307785 (158) [back to overview]Part E: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part E: Ctau of TSR-042
NCT03307785 (158) [back to overview]Part E: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part E: Disease Control Rate
NCT03307785 (158) [back to overview]Part E: Duration of Response
NCT03307785 (158) [back to overview]Part E: Number of Participants With DLT
NCT03307785 (158) [back to overview]Part E: Number of Participants With Positive Anti-TSR-042 Antibodies
NCT03307785 (158) [back to overview]Part E: Objective Response Rate
NCT03307785 (158) [back to overview]Part E: Progression-free Survival
NCT03307785 (158) [back to overview]Part E: Tmax of TSR-042
NCT03307785 (158) [back to overview]Part E: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part E: Vss of TSR-042
NCT03307785 (158) [back to overview]Part E: Vz of TSR-042
NCT03307785 (158) [back to overview]Part F: AUC(0-infinity) of TSR-022
NCT03307785 (158) [back to overview]Part F: AUC(0-infinity) of TSR-042
NCT03307785 (158) [back to overview]Part F: AUC0-t of TSR-022
NCT03307785 (158) [back to overview]Part F: AUC0-t of TSR-042
NCT03307785 (158) [back to overview]Part F: AUCss of TSR-022
NCT03307785 (158) [back to overview]Part F: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part F: CL of TSR-022
NCT03307785 (158) [back to overview]Part F: CL of TSR-042
NCT03307785 (158) [back to overview]Part F: Cmax of TSR-022
NCT03307785 (158) [back to overview]Part F: Cmax of TSR-042
NCT03307785 (158) [back to overview]Part F: Cmax,ss of TSR-022
NCT03307785 (158) [back to overview]Part F: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part F: Ctau of TSR-022
NCT03307785 (158) [back to overview]Part F: Ctau of TSR-042
NCT03307785 (158) [back to overview]Part F: Ctau,ss of TSR-022
NCT03307785 (158) [back to overview]Part F: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part F: Disease Control Rate
NCT03307785 (158) [back to overview]Part F: Duration of Response
NCT03307785 (158) [back to overview]Part F: Number of Participants With DLT
NCT03307785 (158) [back to overview]Part F: Number of Participants With Positive Anti-TSR-022 Antibodies
NCT03307785 (158) [back to overview]Part F: Number of Participants With Positive Anti-TSR-042 Antibodies
NCT03307785 (158) [back to overview]Part F: Objective Response Rate
NCT03307785 (158) [back to overview]Part F: Progression-free Survival
NCT03307785 (158) [back to overview]Part F: Tmax of TSR-022
NCT03307785 (158) [back to overview]Part F: Tmax of TSR-042
NCT03307785 (158) [back to overview]Part F: Tmax,ss of TSR-022
NCT03307785 (158) [back to overview]Part F: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part F: Vss of TSR-022
NCT03307785 (158) [back to overview]Part F: Vss of TSR-042
NCT03307785 (158) [back to overview]Part F: Vz of TSR-022
NCT03307785 (158) [back to overview]Part A: Volume of Distribution After Intravenous Administration (Vss) of of TSR-042
NCT03307785 (158) [back to overview]Part A: Area Under the Plasma Concentration From Time Zero to t (AUC[0-t]) of Niraparib
NCT03307785 (158) [back to overview]Part A: AUC(0-t) of TSR-042
NCT03307785 (158) [back to overview]Part A: AUC(0-t) of TSR-042
NCT03307785 (158) [back to overview]Part A: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part A: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part A: Clearance After Intravenous Administration (CL) of TSR-042
NCT03307785 (158) [back to overview]Part A: Clearance After Intravenous Administration (CL) of TSR-042
NCT03307785 (158) [back to overview]Part A: Clearance After Oral Administration (CL/F) of Niraparib
NCT03307785 (158) [back to overview]Part A: Volume of Distribution After Intravenous Administration (Vz) of of TSR-042
NCT03307785 (158) [back to overview]Part A: Volume of Distribution After Intravenous Administration (Vz) of of TSR-042
NCT03307785 (158) [back to overview]Part A: Volume of Distribution After Oral Administration (Vz/F) of Niraparib
NCT03307785 (158) [back to overview]Part A: Volume of Distribution After Oral Administration (Vz/F) of Niraparib
NCT03307785 (158) [back to overview]Part B: AUC0-t of TSR-042
NCT03307785 (158) [back to overview]Part B: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part B: CL of TSR-042
NCT03307785 (158) [back to overview]Part B: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part B: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part B: Number of Participants With Non-serious TEAEs, STEAEs and AESIs
NCT03307785 (158) [back to overview]Part B: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part B: Vss of TSR-042
NCT03307785 (158) [back to overview]Part B: Vz of TSR-042
NCT03307785 (158) [back to overview]Part C: AUC0-t of Niraparib
NCT03307785 (158) [back to overview]Part C: AUC0-t of TSR-042
NCT03307785 (158) [back to overview]Part C: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part C: CL of TSR-042
NCT03307785 (158) [back to overview]Part C: CL/F of Niraparib
NCT03307785 (158) [back to overview]Part C: Cmax,ss of Niraparib
NCT03307785 (158) [back to overview]Part C: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part C: Ctau,ss of Niraparib
NCT03307785 (158) [back to overview]Part C: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part C: Number of Participants With Non-serious TEAEs, STEAEs and AESIs
NCT03307785 (158) [back to overview]Part C: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part C: Vss of TSR-042
NCT03307785 (158) [back to overview]Part C: Vz of TSR-042
NCT03307785 (158) [back to overview]Part C: Vz/F of Niraparib
NCT03307785 (158) [back to overview]Part D: AUC0-t of TSR-042
NCT03307785 (158) [back to overview]Part D: AUCss of TSR-042
NCT03307785 (158) [back to overview]Part D: CL of TSR-042
NCT03307785 (158) [back to overview]Part D: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part D: Number of Participants With Non-serious TEAEs, STEAEs and AESIs
NCT03307785 (158) [back to overview]Part D: Tmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part D: Vss of TSR-042
NCT03307785 (158) [back to overview]Part D: Vz of TSR-042
NCT03307785 (158) [back to overview]Part E: Number of Participants With Non-serious TEAEs, STEAEs and AESIs
NCT03307785 (158) [back to overview]Part F: Vz of TSR-042
NCT03307785 (158) [back to overview]Part F: Number of Participants With Non-serious TEAEs, STEAEs and AESIs
NCT03307785 (158) [back to overview]Part D: Number of Participants With DLT
NCT03307785 (158) [back to overview]Part A: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part A: Ctau at Steady State (Ctau,ss) of Niraparib
NCT03307785 (158) [back to overview]Part A: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part D: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part A: Ctau,ss of TSR-042
NCT03307785 (158) [back to overview]Part C: Tmax,ss of Niraparib
NCT03307785 (158) [back to overview]Part A: Cmax,ss of TSR-042
NCT03307785 (158) [back to overview]Part A: Cmax at Steady State (Cmax,ss) of Niraparib
NCT03307785 (158) [back to overview]Part A: Cmax at Steady State (Cmax,ss) of Niraparib
NCT03307785 (158) [back to overview]Part A: Clearance After Oral Administration (CL/F) of Niraparib
NCT03308942 (27) [back to overview]Stage 1 : Cohort 2: Progression-free Survival
NCT03308942 (27) [back to overview]Stage 1 : Cohort 3: Disease Control Rate
NCT03308942 (27) [back to overview]Stage 1 : Cohort 3: Progression-free Survival
NCT03308942 (27) [back to overview]Stage 1: Cohort 1: Duration of Response
NCT03308942 (27) [back to overview]Stage 1: Cohort 1: Number of Participants Discontinuing the Study Due to AEs
NCT03308942 (27) [back to overview]Stage 1: Cohort 1: Objective Response Rate (ORR)
NCT03308942 (27) [back to overview]Stage 1: Cohort 2: Duration of Response
NCT03308942 (27) [back to overview]Stage 1: Cohort 2: Objective Response Rate
NCT03308942 (27) [back to overview]Stage 1: Cohort 3: Number of Participants Discontinuing the Study Due to AEs
NCT03308942 (27) [back to overview]Stage 1: Cohort 3: Objective Response Rate
NCT03308942 (27) [back to overview]Stage 2: Cohort 1A and Cohort 2A: Objective Response Rate
NCT03308942 (27) [back to overview]Stage 2: Cohorts 1A and 2A: Disease Control Rate
NCT03308942 (27) [back to overview]Stage 2: Cohorts 1A and 2A: Duration of Response
NCT03308942 (27) [back to overview]Stage 2: Cohorts 1A and 2A: Number of Participants Discontinuing the Study Due to AEs
NCT03308942 (27) [back to overview]Stage 2: Cohorts 1A and 2A: Progression-free Survival
NCT03308942 (27) [back to overview]Stage 1: Cohort 1: Number of Participants With Non-serious Adverse Events (Non-SAEs) and Serious Adverse Events (SAEs)
NCT03308942 (27) [back to overview]Stage 1: Cohort 1: Plasma Concentration of Niraparib Following Combination Therapy of Niraparib and Pembrolizumab
NCT03308942 (27) [back to overview]Stage 1: Cohort 2: Number of Participants With Non-SAEs and SAEs
NCT03308942 (27) [back to overview]Stage 1: Cohort 2: Plasma Concentration of Niraparib Following Combination Therapy of Niraparib and Pembrolizumab
NCT03308942 (27) [back to overview]Stage 1: Cohort 3: Number of Participants With Non-SAEs and SAEs
NCT03308942 (27) [back to overview]Stage 1: Cohort 3: Plasma Concentration of Niraparib Following Niraparib Monotherapy
NCT03308942 (27) [back to overview]Stage 2: Cohorts 1A and 2A: Number of Participants With Non-SAEs and SAEs
NCT03308942 (27) [back to overview]Stage 2: Cohorts 1A and 2A: Plasma Concentration of Niraparib Following Combination Therapy of Niraparib and TSR-042 (Dostarlimab)
NCT03308942 (27) [back to overview]Stage 1: Cohort 2: Number of Participants Discontinuing the Study Due to AEs
NCT03308942 (27) [back to overview]Stage 1 : Cohort 1: Disease Control Rate
NCT03308942 (27) [back to overview]Stage 1 : Cohort 1: Progression-free Survival
NCT03308942 (27) [back to overview]Stage 1 : Cohort 2: Disease Control Rate
NCT03326193 (4) [back to overview]Number of Participants With TEAEs Leading to Niraparib Dose Reductions
NCT03326193 (4) [back to overview]Number of Participants With TEAEs Leading to Niraparib Treatment Discontinuation
NCT03326193 (4) [back to overview]Number of Participants With Non-serious Treatment-emergent Adverse Events (TEAEs)
NCT03326193 (4) [back to overview]Progression Free Survival (PFS) Rate
NCT03329937 (6) [back to overview]Percent Change From Baseline in Tumor Volume Measured by MRI
NCT03329937 (6) [back to overview]Percent Change From Baseline in Tumor Volume Measured by Ultrasound
NCT03329937 (6) [back to overview]Percentage of Participants With Pathological Complete Response (pCR)
NCT03329937 (6) [back to overview]Percentage of Participants With Tumor Response as Measured by Breast Ultrasound
NCT03329937 (6) [back to overview]Percentage of Participants With Tumor Response Measured by Breast MRI
NCT03329937 (6) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), Treatment Discontinuations and Dose Reductions Due to Adverse Events (AEs)
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Amylase During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Amylase During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Bilirubin and Creatinine During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Bilirubin and Creatinine During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Bilirubin and Creatinine During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Protein and Albumin During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Alkaline Phosphatase, Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and Lactate Dehydrogenase (LDH) During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Protein and Albumin During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Protein and Albumin During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Hb During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Hb During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Hemoglobin (Hb) During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Platelets, Neutrophils, Monocytes, Lymphocytes and Leukocyte During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Platelets, Neutrophils, Monocytes, Lymphocytes and Leukocytes During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Platelets, Neutrophils, Monocytes, Lymphocytes and Leukocytes During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Pulse Rate During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Pulse Rate During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Pulse Rate During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in SBP and DBP During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in SBP and DBP During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Temperature During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Temperature During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Weight During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Weight During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Weight During PK Phase
NCT03359850 (41) [back to overview]Number of Participants With TEAE Including Non-SAEs, SAEs and Discontinuations Due to AEs During Extension Phase
NCT03359850 (41) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAE) Including Non-serious Adverse Events (Non-SAEs), Serious Adverse Events (SAEs) and Discontinuations Due to AEs During PK Phase
NCT03359850 (41) [back to overview]Time to Maximum Concentration (Tmax) of Niraparib and M1 During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Amylase During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Chemistry Parameters: Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Alkaline Phosphatase, ALT, AST and LDH During Extension Phase
NCT03359850 (41) [back to overview]Change From Baseline in Clinical Chemistry Parameter of Alkaline Phosphatase, ALT, AST and LDH During Extension Phase
NCT03359850 (41) [back to overview]Apparent Total Body Clearance (CL/F) of Niraparib and M1 During PK Phase
NCT03359850 (41) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 Extrapolated to Infinity (AUC 0-infinity) of Niraparib and M1 During PK Phase
NCT03359850 (41) [back to overview]Area Under the Plasma Concentration-time Curve From Time 0 to the Time of the Last Quantifiable Concentration (AUClast) of Niraparib and Its Major Metabolite (M1) During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Body Temperature During PK Phase
NCT03359850 (41) [back to overview]Terminal Half-life (t½) of Niraparib and M1 During PK Phase
NCT03359850 (41) [back to overview]Observed Maximum Plasma Concentration (Cmax) of Niraparib and M1 During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Chemistry Parameters: Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and Blood Urea Nitrogen (BUN) During PK Phase
NCT03359850 (41) [back to overview]Change From Baseline in Chemistry Parameters: Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN During Extension Phase
NCT03404960 (1) [back to overview]Rate of Progression-free Survival at 6 Months (PFS6)
NCT03431350 (11) [back to overview]Combination 1: Part 1: Number of Participants With Specified Toxicity
NCT03431350 (11) [back to overview]Combination 2: Composite Response Rate (RR)
NCT03431350 (11) [back to overview]Combination 3: Maximum Observed Plasma Concentration (Cmax) of Niraparib Normalized by the Dose(Niraparib) (Cmax/Dose) of Niraparib Administered With AA After a Single Dose
NCT03431350 (11) [back to overview]Combination 1: Part 2: Objective Response Rate (ORR)
NCT03431350 (11) [back to overview]Combination 3: Maximum Observed Plasma Concentration (Cmax) of Niraparib and Abiraterone Acetate After a Single Dose
NCT03431350 (11) [back to overview]Combination 3: Area Under the Plasma Concentration-Time Curve From Time Zero to 168 Hours (AUC [0-168hr]) of Niraparib Administered With AA After a Single Dose
NCT03431350 (11) [back to overview]Combination 3: Area Under the Plasma Concentration-Time Curve for Niraparib From Time Zero to 168 Hours (AUC [0-168 Hours]/Dose) of Niraparib Administered With AA After a Single Dose
NCT03431350 (11) [back to overview]Combination 2: Number of Participants With Adverse Events (AEs) of Grade >=3 Severity
NCT03431350 (11) [back to overview]Combination 2: Number of Participants With Adverse Events (AEs)
NCT03431350 (11) [back to overview]Combination 1: Part 2: Number of Participants With Adverse Events (AEs) of Grade >=3 Severity
NCT03431350 (11) [back to overview]Combination 1: Part 2: Number of Participants With Adverse Events (AEs)
NCT03497429 (8) [back to overview]Number of Participants With Dose Limiting Toxicities (DLTs)
NCT03497429 (8) [back to overview]Cmax: Maximum Observed Plasma Concentration for Niraparib
NCT03497429 (8) [back to overview]Tmax: Time to Reach the Maximum Plasma Concentration (Cmax) for Niraparib
NCT03497429 (8) [back to overview]Number of Participants With Serious TEAEs
NCT03497429 (8) [back to overview]Number of Participants With Grade 3 or Higher TEAEs
NCT03497429 (8) [back to overview]Number of Participants Who Discontinued Study Drug Due to TEAEs
NCT03497429 (8) [back to overview]AUC24：Area Under the Plasma Concentration-time Curve From Time 0 to 24 Hours for Niraparib
NCT03497429 (8) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT03748641 (1) [back to overview]Cohort 1: Radiographic Progression-Free Survival (rPFS) as Assessed by Blinded Independent Central Review (BICR)
NCT03759587 (10) [back to overview]Progression Free Survival (PFS)
NCT03759587 (10) [back to overview]Overall Survival (OS)
NCT03759587 (10) [back to overview]Overall Response Rate (ORR)
NCT03759587 (10) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT03759587 (10) [back to overview]Number of Participants With TEAEs Leading to Drug Discontinuation
NCT03759587 (10) [back to overview]Number of Participants With Grade 3 or 4 Thrombocytopenia Occurring Within 30 Days After Initial Administration of Niraparib
NCT03759587 (10) [back to overview]Number of Participants With TEAEs Leading to Dose Interruption
NCT03759587 (10) [back to overview]Number of Participants With TEAEs Leading to Dose Reduction
NCT03759587 (10) [back to overview]Number of Participants With Serious Adverse Events (SAEs)
NCT03759587 (10) [back to overview]Number of Participants With Grade 3 or Higher TEAEs
NCT03759600 (11) [back to overview]Number of Participants With Grade 3 or Higher TEAEs
NCT03759600 (11) [back to overview]Duration of Response (DOR)
NCT03759600 (11) [back to overview]Number of Participants With TEAEs Leading to Dose Interruption
NCT03759600 (11) [back to overview]Disease Control Rate (DCR)
NCT03759600 (11) [back to overview]Progression Free Survival (PFS)
NCT03759600 (11) [back to overview]Overall Survival (OS)
NCT03759600 (11) [back to overview]Objective Response Rate (ORR)
NCT03759600 (11) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT03759600 (11) [back to overview]Number of Participants With TEAEs Leading to Drug Discontinuation
NCT03759600 (11) [back to overview]Number of Participants With TEAEs Leading to Dose Reduction
NCT03759600 (11) [back to overview]Number of Participants With Serious TEAEs
NCT03955471 (19) [back to overview]PFS in Participants With PROC Who Have PD-L 1 Positive Status
NCT03955471 (19) [back to overview]Objective Response Rate (ORR) in Participants With Platinum-resistant Ovarian Cancer (PROC)
NCT03955471 (19) [back to overview]Duration of Response (DOR) in Participants With PROC
NCT03955471 (19) [back to overview]DCR in Participants With PROC Who Have PD-L 1 Positive Status
NCT03955471 (19) [back to overview]Disease Control Rate (DCR) in Participants With PROC
NCT03955471 (19) [back to overview]Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs), Treatment-emergent Adverse Events (TEAEs) and Adverse Event of Special Interest (AESI)
NCT03955471 (19) [back to overview]DOR in Participants With PROC Who Have PD-L 1 Positive Status
NCT03955471 (19) [back to overview]Number of Participants With Grade Shift From Baseline in Plasma Chemistry
NCT03955471 (19) [back to overview]Number of Participants With Grade Shift From Baseline in Hematology
NCT03955471 (19) [back to overview]Change in Baseline in Activated Partial Thromboplastin Time
NCT03955471 (19) [back to overview]Change From Baseline in Thyrotropin
NCT03955471 (19) [back to overview]Change From Baseline in Temperature
NCT03955471 (19) [back to overview]Change From Baseline in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)
NCT03955471 (19) [back to overview]Change From Baseline in Pulse Rate
NCT03955471 (19) [back to overview]Change From Baseline in Prothrombin International Normalized Ratio
NCT03955471 (19) [back to overview]Progression-free Survival (PFS) in Participants With PROC
NCT03955471 (19) [back to overview]Overall Survival (OS) in Participants With PROC
NCT03955471 (19) [back to overview]OS in Participants With PROC Who Have PD-L 1 Positive Status
NCT03955471 (19) [back to overview]ORR in Participants With PROC Who Have Programmed Cell Death-ligand 1 (PD-L 1) Positive Status
NCT04409002 (5) [back to overview]Disease Control Rate With irRECIST Criteria
NCT04409002 (5) [back to overview]Disease Control Rate With RECIST 1.1 Criteria
NCT04409002 (5) [back to overview]Overall Survival
NCT04409002 (5) [back to overview]Progression-free Survival
NCT04409002 (5) [back to overview]Number of Treatment-Related Adverse Events Per CTCAE v5.0
NCT05751629 (11) [back to overview]Disease Control Rate (DCR) Per RECIST Version 1.1 by Investigator Assessment
NCT05751629 (11) [back to overview]Number of Participants With Eastern Cooperative Oncology Group (ECOG) Performance Status at Baseline and End of Treatment
NCT05751629 (11) [back to overview]Absolute Values in Urinalysis Parameter - Specific Gravity (Ratio)
NCT05751629 (11) [back to overview]Change From Baseline in Cancer Antigen 125 (CA-125) at End of Treatment
NCT05751629 (11) [back to overview]Change From Baseline in Vital Signs (Weight) at End of Treatment
NCT05751629 (11) [back to overview]Confirmed Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1 by Investigator Assessment
NCT05751629 (11) [back to overview]Overall Survival (OS)
NCT05751629 (11) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs)
NCT05751629 (11) [back to overview]Number of Participants With Clinically Significant Changes in Clinical Laboratory Parameters - Chemistry, Coagulation, Hematology and Thyroid
NCT05751629 (11) [back to overview]Duration of Response (DOR) Per RECIST Version 1.1 by Investigator Assessment
NCT05751629 (11) [back to overview]Progression Free Survival (PFS) Per RECIST Version 1.1 by Investigator Assessment

Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Cycle 6

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: At Cycle 6 (Each cycle was of 28 days)

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
Non-gBRCA Niraparib43293018568301393
Non-gBRCA Placebo161011952910650

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Change From Baseline in European Quality of Life Scale, 5-Dimensions (EQ-5D-5L) in Cohort With Germline BRCA at Cycle 2

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 2 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
gBRCA Niraparib-0.008
gBRCA Placebo-0.008

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Cycle 2

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (pre-dose on Day 1) and at Cycle 2 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
gBRCA Niraparib-0.8
gBRCA Placebo-0.3

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Cycle 4

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 4 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
gBRCA Niraparib-0.1
gBRCA Placebo-0.3

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Cycle 6

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (pre-dose on Day 1) and at Cycle 6 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
gBRCA Niraparib0.5
gBRCA Placebo-0.5

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With Germline BRCA at Post-progression

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Cycle 1 Day 1, Each cycle was of 28 days) and up to 7 years, 7 months and 4 days

InterventionScores on a scale (Mean)
gBRCA Niraparib-0.751
gBRCA Placebo-1.324

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Cycle 2

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 2 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-1.0
Non-gBRCA Placebo-0.3

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Cycle 4

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 4 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-0.7
Non-gBRCA Placebo-0.9

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Cycle 6

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 6 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-0.2
Non-gBRCA Placebo-0.9

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Change From Baseline in Functional Assessment of Cancer Therapy-Ovarian Symptom Index in Cohort With no Germline BRCA at Post-progression

"Functional Assessment of Cancer Therapy-Ovarian Symptom Index is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants respond to their symptom experience over the past 7 days using a 5-point Likert scale score from not at all (0) to very much (4). The total score was calculated by multiplying the sum of all items scored by 8 and dividing the result by the number of responses. The total symptom index was calculated as the total of the 8 scores, ranging from 0 (severely symptomatic) to 32 (asymptomatic). A positive change from Baseline indicates improvement. Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and up to 7 years, 7 months and 4 days

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-2.595
Non-gBRCA Placebo-1.801

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Chemotherapy-Free Interval in Cohort With Germline BRCA Mutation (gBRCA)

Chemotherapy-Free Interval was defined as the time from the last platinum therapy prior to randomization to the initiation of the next anti-cancer therapy after maintenance treatment (NCT01847274)
Timeframe: From date of last platinum therapy prior to randomization to the initiation of the next anti-cancer therapy after maintenance treatment, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
gBRCA Niraparib20.0
gBRCA Placebo9.4

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Overall Survival in Cohort With No Germline BRCA Mutation

Overall survival was defined as the date of randomization to the date of death by any cause. (NCT01847274)
Timeframe: From treatment randomization to date of death by any cause, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
Non-gBRCA Niraparib31.0
Non-gBRCA Placebo34.8

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Overall Survival in Cohort With Germline BRCA Mutation (gBRCA)

Overall survival was defined as the date of randomization to the date of death by any cause. (NCT01847274)
Timeframe: From treatment randomization to date of death by any cause, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
gBRCA Niraparib40.9
gBRCA Placebo38.1

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Chemotherapy-Free Interval in Cohort With No Germline BRCA Mutation

Chemotherapy-Free Interval was defined as the time from the last platinum therapy prior to randomization to the initiation of the next anti-cancer therapy after maintenance treatment (NCT01847274)
Timeframe: From date of last platinum therapy prior to randomization to the initiation of the next anti-cancer therapy after maintenance treatment, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
Non-gBRCA Niraparib13.4
Non-gBRCA Placebo8.7

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Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Post-progression

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and up to 7 years, 7 months and 4 days

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-0.047
Non-gBRCA Placebo-0.050

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Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Cycle 6

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 6 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib0.005
Non-gBRCA Placebo-0.011

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Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Cycle 4

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 4 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-0.004
Non-gBRCA Placebo-0.014

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Change From Baseline in EQ-5D-5L in Cohort With Germline BRCA at Post-progression

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and up to 7 years, 7 months and 4 days

InterventionScores on a scale (Mean)
gBRCA Niraparib-0.041
gBRCA Placebo-0.013

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Change From Baseline in EQ-5D-5L in Cohort With Germline BRCA at Cycle 6

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 6 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
gBRCA Niraparib0.002
gBRCA Placebo-0.004

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Change From Baseline in EQ-5D-5L in Cohort With Germline BRCA at Cycle 4

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 4 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
gBRCA Niraparib-0.010
gBRCA Placebo-0.035

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Area Under the Plasma Concentration-time Curve From Time 0 to the Last Quantifiable Concentration (AUC[0-last]) Following Administration of Niraparib (FE Sub-study)

Blood samples were collected at indicated time points to analyze the AUC(0-last) of niraparib. (NCT01847274)
Timeframe: Pre-dose (Day -1) and at 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72, 96, 120 hours post dose

InterventionNanograms*hour per milliliter (Mean)
FE Niraparib Fasted28638.1
FE Niraparib Fed27186.4

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Area Under the Plasma Concentration-time Curve From Time 0 Extrapolated to Infinity (AUC[0-infinity]) Following Administration of Niraparib (FE Sub-study)

Blood samples were collected at indicated time points to analyze AUC(0-infinity) of niraparib. (NCT01847274)
Timeframe: Pre-dose and at 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72, 96, 120 hours post dose

InterventionNanograms*hour per milliliter (Mean)
FE Niraparib Fasted29016.1
FE Niraparib Fed31194

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Change From Baseline in EQ-5D-5L in Cohort With no Germline BRCA at Cycle 2

"EQ-5D-5L is a well-validated, general preference-based, health-related Quality of Life (QoL) instrument. The EQ-5D-5L encompasses 5 domains, asking participants to rate their perceived health state today on the following dimensions: Mobility, Self-Care, Usual Activities, Pain/Discomfort, and Anxiety/Depression. Each domain has 5 possible levels: no problems (Level 1), slight problems (Level 2), moderate problems (Level 3), severe problems (Level 4), and extreme problems (Level 5). Responses for 5 dimensions together formed a 5-figure description of health state (e.g.11111 indicates no problems in all 5 dimensions). Baseline was latest non-missing pre-dose assessment on or before randomization date. Change from Baseline was calculated by subtracting the Baseline value from the post-dose visit value." (NCT01847274)
Timeframe: Baseline (Pre-dose on Day 1) and at Cycle 2 (Each cycle was of 28 days)

InterventionScores on a scale (Mean)
Non-gBRCA Niraparib-0.007
Non-gBRCA Placebo-0.011

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Post-progression

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: Up to 7 years, 7 months and 4 days

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
Non-gBRCA Niraparib57452319588351373
Non-gBRCA Placebo32121616848159101

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Maximum Observed Plasma Concentration (Cmax) Following Administration of Niraparib (FE Sub-study)

Blood samples were collected at indicated time points to analyze the maximum observed plasma concentration of niraparib. (NCT01847274)
Timeframe: Pre-dose (Day -1) and at 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72, 96, 120 hours post dose

InterventionNanograms per milliliter (Mean)
FE Niraparib Fasted803.7
FE Niraparib Fed582.1

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Cycle 4

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: At Cycle 4 (Each cycle was of 28 days)

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
Non-gBRCA Niraparib543734209892914146
Non-gBRCA Placebo31161711543211031

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Cycle 2

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: At Cycle 2 (Each cycle was of 28 days)

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
Non-gBRCA Niraparib6939303491003820174
Non-gBRCA Placebo32171218844241953

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With no Germline BRCA at Baseline

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit). Baseline was latest non-missing pre-dose assessment on or before randomization date." (NCT01847274)
Timeframe: At Baseline

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
Non-gBRCA Niraparib71583743181205628158
Non-gBRCA Placebo402616219483712112

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Post-progression

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: Up to 7 years, 7 months and 4 days

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
gBRCA Niraparib312071574418873
gBRCA Placebo159373264340

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Cycle 6

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: At Cycle 6 (Each cycle was of 28 days)

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
gBRCA Niraparib44171315954251062
gBRCA Placebo175752218421

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Cycle 4

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: At Cycle 4 (Each cycle was of 28 days)

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
gBRCA Niraparib47222015670181642
gBRCA Placebo206782296341

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Cycle 2

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit)." (NCT01847274)
Timeframe: At Cycle 2 (Each cycle was of 28 days)

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
gBRCA Niraparib48221720873191373
gBRCA Placebo255151033116622

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Number of Participants With Response to Neuropathy Questionnaire in Cohort With Germline BRCA at Baseline

"A Neuropathy Questionnaire measures the participant's symptom experience over the past 7 days using a 5-point Likert scale of not at all (0) to very much (4). There are 2 items that ask if the participant's feet (item 1) or hands (item 2) feel numb or have prickling/tingling feelings. The Neuropathy Questionnaire was used to determine the chemotherapy-induced peripheral neuropathy (CIPN) status of each participant as well as provide an anchor for interpreting the impact of CIPN on participant's QoL. Two thresholds were used. For the first, a participant was determined to have CIPN if a score greater than 0 (not at all) was recorded for either item. For the second, CIPN was assigned if a participant recorded a score greater than 1 (a little bit). Baseline was latest non-missing pre-dose assessment on or before randomization date." (NCT01847274)
Timeframe: At Baseline

,
InterventionParticipants (Count of Participants)
Feet, 0-Not at allFeet, 1-A little bitFeet, 2-SomewhatFeet, 3-Quite a bitFeet, 4-Very muchHands, 0-Not at allHands, 1-A little bitHands, 2-SomewhatHands, 3-Quite a bitHands, 4-Very much
gBRCA Niraparib47322421980288143
gBRCA Placebo261291063713652

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Number of Participants With Non-serious AEs and SAEs in QTc Sub-study

An AE is any untoward medical occurrence that occurs in a participants or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that at any dose which results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not serious adverse events were considered as non serious adverse events. (NCT01847274)
Timeframe: Up to 5 years 10 months and 22 days

InterventionParticipants (Count of Participants)
Non-serious AEsSAEs
QTc Sub-study: Niraparib2412

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Number of Participants With Non-serious AEs and SAEs in FE Sub-study

An AE is any untoward medical occurrence that occurs in a participants or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that at any dose which results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not serious adverse events were considered as non serious adverse events. (NCT01847274)
Timeframe: Up to 2 years, 3 months and 11 days

,
InterventionParticipants (Count of Participants)
Non-serious AEsSAEs
FE Niraparib Fasted41
FE Niraparib Fed60

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Number of Participants With Non-serious AEs and SAEs (Post-study Unblinding)

An AE is any untoward medical occurrence that occurs in a participants or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that at any dose which results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not serious adverse events were considered as non serious adverse events. The data is presented for post-study unblinding duration 01-Apr-2021 to 26-Dec-2021 (NCT01847274)
Timeframe: Up to 8 months, 26 days

,,,
InterventionParticipants (Count of Participants)
Non-serious AEsSAEs
gBRCA Niraparib (PSU)00
gBRCA Placebo (PSU)00
Non-gBRCA Niraparib (PSU)00
Non-gBRCA Placebo (PSU)00

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

An AE is any untoward medical occurrence that occurs in a participants or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that at any dose which results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not serious adverse events were considered as non serious adverse events. Data presented for this outcome measure is based on the data cut-off date of 31-March-2021, which aligns with the time of the study unblinding. (NCT01847274)
Timeframe: Up to 7 years, 7 months and 6 days

,,,
InterventionParticipants (Count of Participants)
Non-serious AEsSAEs
gBRCA Niraparib13651
gBRCA Placebo629
Non-gBRCA Niraparib23176
Non-gBRCA Placebo11020

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Number of Participants With Maximum Post-Baseline QT Interval Corrected by Fridericia's Formula (QTcF) Greater Than Pre-specified Thresholds

12-lead electrocardiogram was obtained at indicated time points using an automated electrocardiogram machine that measured QTcF interval. The number of participants with maximum post-Baseline ECG value exceeding the following limits have been reported: QTcF interval >450 and <= 480 milliseconds (msec) and >500 msec. (NCT01847274)
Timeframe: At Baseline (Cycle 1 Day 1, each cycle was of 28 days)

InterventionParticipants (Count of Participants)
>450 msec>480 msec>500 msec
QTc Sub-study: Niraparib200

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Time to Second Subsequent Therapy in Cohort With No Germline BRCA Mutation

TSST was defined as the date of randomization to the earlier of the start date of second follow-up anti-cancer treatment or death. (NCT01847274)
Timeframe: From the date of randomization to the start date of the second subsequent anti-cancer therapy, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
Non-gBRCA Niraparib20.3
Non-gBRCA Placebo16.7

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Time to Second Subsequent Therapy in Cohort With Germline BRCA Mutation (gBRCA)

TSST was defined as the date of randomization to the earlier of the start date of second follow-up anti-cancer treatment or death. (NCT01847274)
Timeframe: From the date of randomization to the start date of the second subsequent anti-cancer therapy, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
gBRCA Niraparib29.7
gBRCA Placebo19.6

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Time to Reach Maximum (Tmax) Following Administration of Niraparib (FE Sub-study)

Blood samples were collected at indicated time points to analyze the tmax of niraparib. (NCT01847274)
Timeframe: Pre-dose (Day -1) and at 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72, 96, 120 hours post dose

InterventionHour (Median)
FE Niraparib Fasted3.1
FE Niraparib Fed6.1

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Time to First Subsequent Therapy in Cohort With No Germline BRCA Mutation

The TFST was defined as the time from the date of randomization to the start date of the first subsequent anti-cancer therapy or death (NCT01847274)
Timeframe: From date of randomization to the earliest date of first subsequent therapy or death, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
Non-gBRCA Niraparib12.4
Non-gBRCA Placebo7.4

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Time to First Subsequent Therapy in Cohort With Germline BRCA Mutation (gBRCA)

The TFST was defined as the time from the date of randomization to the start date of the first subsequent anti-cancer therapy or death. (NCT01847274)
Timeframe: From date of randomization to the earliest date of first subsequent therapy or death, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
gBRCA Niraparib19.1
gBRCA Placebo8.6

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Terminal Elimination Half-life (t1/2) Following Administration of Niraparib (FE Sub-study)

Blood samples were collected at indicated time points to analyze the t1/2 of niraparib. (NCT01847274)
Timeframe: Pre-dose (Day -1) and at 1, 1.5, 2, 3, 4, 6, 8, 12, 24, 48, 72, 96, 120 hours post dose

InterventionHour (Mean)
FE Niraparib Fasted50.5
FE Niraparib Fed47.9

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Progression-Free Survival 2 in Cohort With No Germline BRCA Mutation

Progression-Free Survival 2 was defined as the date of randomization in the current study to the earlier date of assessment of progression on the next anti-cancer therapy following study treatment or death due to any cause. Progression was determined by the investigator via clinical and radiographic assessment using the same criteria as used in the current study. (NCT01847274)
Timeframe: From treatment randomization to the earlier of the date of disease progression on the next anti-cancer therapy following study treatment or death due to any cause, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
Non-gBRCA Niraparib19.5
Non-gBRCA Placebo16.1

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Progression-Free Survival 2 in Cohort With Germline BRCA Mutation (gBRCA)

Progression-Free Survival 2 was defined as the date of randomization in the current study to the earlier date of assessment of progression on the next anti-cancer therapy following study treatment or death due to any cause. Progression was determined by the investigator via clinical and radiographic assessment using the same criteria as used in the current study. (NCT01847274)
Timeframe: From treatment randomization to the earlier of the date of disease progression on the next anti-cancer therapy following study treatment or death due to any cause, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
gBRCA Niraparib29.9
gBRCA Placebo22.7

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Progression-Free Survival (PFS) in Cohort With No Germline BRCA Mutation

PFS was defined as the time between randomization and disease progression or death from any cause. Computed tomography or magnetic resonance imaging to assess disease progression was performed at baseline, every 8 weeks through cycle 14, and then every 12 weeks until treatment discontinuation. The objective assessment of disease progression was determined by means of central radiologic and clinical review, according to Response Evaluation Criteria in Solid Tumors (RECIST),version 1.1, which was performed in a blinded fashion.PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT01847274)
Timeframe: From date of randomization to the earliest date of disease progression or death from any cause, up to 7 years, 7 months and 4 days

InterventionMonths (Median)
Non-gBRCA Niraparib9.3
Non-gBRCA Placebo3.9

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Progression-Free Survival (PFS) in Cohort With No Germline BCRA With Homologous Recombination Deficiency-positive (HRD+) Tumors (Non-gBRCAmut HRD+)

PFS was defined as the time between randomization and disease progression or death from any cause. Computed tomography or magnetic resonance imaging to assess disease progression was performed at baseline, every 8 weeks through cycle 14, and then every 12 weeks until treatment discontinuation. The objective assessment of disease progression was determined by means of central radiologic and clinical review, according to Response Evaluation Criteria in Solid Tumors (RECIST),version 1.1, which was performed in a blinded fashion. PD was defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT01847274)
Timeframe: From date of randomization to the earliest date of disease progression or death from any cause, up to 7 years, 7 months and 4 days

Interventionmonths (Median)
Non-gBRCAmut HRD+ Niraparib12.9
Non-gBRCAmut HRD+ Placebo3.8

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Progression-Free Survival (PFS) in Cohort With Germline BReast CAncer Gene (BRCA) Mutation (gBRCA)

PFS was defined as the time between randomization and disease progression or death from any cause. Computed tomography or magnetic resonance imaging to assess disease progression was performed at baseline, every 8 weeks through cycle 14, and then every 12 weeks until treatment discontinuation. The objective assessment of disease progression was determined by means of central radiologic and clinical review, according to Response Evaluation Criteria in Solid Tumors (RECIST),version 1.1, which was performed in a blinded fashion. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT01847274)
Timeframe: From date of randomization to the earliest date of disease progression or death from any cause, up to 7 years 7 months and 4 days

Interventionmonths (Median)
gBRCA Niraparib21
gBRCA Placebo5.5

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Number of Participants With Subsequent Anticancer Therapies

The number of participants with subsequent anticancer therapies were evaluated. Data has been reported as per following categories: any new anitumoral therapy, any chemotherapy, any radiotherapy, any surgery, any hormonal therapy, any targeted agents, and any other treatment. Participants may have received more than one subsequent therapies. (NCT01905592)
Timeframe: Up to 7 years

,
InterventionParticipants (Count of Participants)
Any new antitumoral therapyAny chemotherapyAny radiotherapyAny surgeryAny hormonal therapyAny targeted agent therapyAny other treatment
Niraparib108964813272217
Physician's Choice554822513198

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Number of Participants With Serious Adverse Events (SAE) and Non-serious Adverse Events (Non-SAE)

An adverse event (AE) is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. An SAE is defined as any untoward medical occurrence or effect in a participant, whether or not considered related to the protocol treatment, at any dose that results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing participant hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an medically important event or reaction as per medical and scientific judgment. Adverse events which were not serious adverse events were considered as non serious adverse events. (NCT01905592)
Timeframe: Up to 7 years

,
InterventionParticipants (Count of Participants)
SAENon-SAE
Niraparib33134
Physician's Choice462

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Number of Participants With Central BRCA Mutation Status

Blood samples were collected to evaluate central BRCA mutation status of participants. Baseline was defined as the most recent non-missing measurement prior to or on the first administration of study drug. Number of participants with central BRCA mutation status as BRCA1 positive only, BRCA2 positive only, Rearrangement only, BRCA1 and BRCA2 positive, BRCA1 positive and rearrangement, and BRCA2 positive and rearrangement were reported. (NCT01905592)
Timeframe: At Baseline (Cycle 1 Day1) (Cycle duration was 21 days)

,
InterventionParticipants (Count of Participants)
BRCA1 positive onlyBRCA2 positive onlyRearrangement onlyBRCA1 and BRCA2 positiveBRCA1 positive and rearrangementBRCA2 positive and rearrangement
Niraparib66577311
Physician's Choice38283110

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Time to Treatment Failure

Time to treatment failure was defined from the date of randomization to progression or discontinuation of treatment for any reason, including but not restricted to disease progression, treatment toxicity and death. (NCT01905592)
Timeframe: Date of randomization to discontinuation of treatment for any reason, up to 4 years

InterventionMonths (Median)
Physician's Choice2.6
Niraparib4.3

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Progression Free Survival (PFS) - Investigator Assessment

PFS is defined as the date of randomization to the date of disease progression or death due to any cause, whichever occurs earlier as per RECIST version 1.1 as determined by Investigator assessment. Progressive Disease is defined as at least a 20 % increase in the sum of diameters of measured lesions taking as references the smallest sum of diameters recorded on study (including Baseline) and an absolute increase of >= 5 mm. (NCT01905592)
Timeframe: Assessed up to 4 years

InterventionMonths (Median)
Physician's Choice3.1
Niraparib5.0

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Progression Free Survival (PFS) - Central Review Assessment

The primary objective of this study is to compare progression-free survival (PFS), as assessed by blinded central review, of participants with advanced/metastatic human epidermal growth factor receptor 2 (HER2)-negative gBRCA mutation breast cancer when treated with niraparib as compared to those treated with physician's choice single agent chemotherapy standards (eribulin, vinorelbine, gemcitabine or capecitabine). PFS is defined as the date of randomization to the date of disease progression or death due to any cause, whichever occurs earlier as per Response evaluation criteria in solid tumors (RECIST) version (v)1.1 as determined by central review assessment. Progressive Disease is defined as at least a 20 percent (%) increase in the sum of diameters of measured lesions taking as references the smallest sum of diameters recorded on study (including Baseline) and an absolute increase of >= 5 millimeter (mm). (NCT01905592)
Timeframe: From the date of randomization to the date of disease progression or death due to any cause, whichever occurs earlier, up to 4 years

InterventionMonths (Median)
Physician's Choice3.1
Niraparib4.1

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Overall Survival

Overall Survival (OS) was defined as the time from randomization to the date of death of any causes. (NCT01905592)
Timeframe: From treatment randomization to date of death of any cause, up to 4 years

InterventionMonths (Median)
Physician's Choice15.8
Niraparib14.5

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Overall Response Rate (ORR)

ORR was defined as the percentage of the participants who achieved a complete response (CR) or partial response (PR) to treatment evaluated using Response Evaluation Criteria in Solid Tumors (RECIST) v1.1. Complete Response (CR)=disappearance of all target and non-target lesions and normalization of tumor markers. Pathological lymph nodes must have short axis measures <10 mm. Partial Response (PR)= at least a 30% decrease in the sum of measures (longest diameter for tumor lesions and short axis measure for nodes) of target lesions, taking as reference the Baseline sum of diameters. Percentage values are rounded off up to 1 decimal. (NCT01905592)
Timeframe: Up to 4 years

InterventionPercentage of participants (Number)
Physician's Choice12.5
Niraparib21.4

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Duration of Response (DOR)

Duration of response was defined as the time from first documentation of response (confirmed CR or PR) until the time of first documentation of disease progression by RECIST v1.1 or death by any cause. (NCT01905592)
Timeframe: Up to 4 years

InterventionMonths (Median)
Physician's Choice5.65
Niraparib4.14

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ORR by HRD Status and Breast Cancer Gene (BRCA) Status

The ORR was defined as the percentage of participants achieving CR or PR as assessed by the Investigator per RECIST (version1.1), where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. ORR was evaluated for participants with following characteristics: HRD status (positive, negative and unknown) and BRCA status (mutation positive, wild-type and unknown). (NCT02354586)
Timeframe: Up to 3 years

InterventionPercentage of participants (Number)
HRD positive, n=221HRD negative, n=195HRD unknown, n=45BRCA mutation positive, n=87BRCA wild-type, n=317BRCA unknown, n=57
Niraparib 300 mg14.02.66.723.05.05.3

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Number of Participants With Any Non-serious Adverse Event (Non-SAE) and Any Serious Adverse Event (SAE)

An adverse event is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with study treatment. Any untoward event resulting in death, life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, congenital anomaly or birth defect or any other situation according to medical or scientific judgment was categorized as SAE. Adverse events which were not serious were considered as Non-serious adverse events. (NCT02354586)
Timeframe: Up to a maximum of 71.56 months

InterventionParticipants (Count of Participants)
Any non-SAEAny SAE
Niraparib 300 mg461200

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Time to First Subsequent Therapy (TFST)

Time to first subsequent therapy (TFST) was defined as the time from the date of first dose to the date of first subsequent therapy or death, whichever occurs first. It was calculated as (Earlier of [First dose of first subsequent therapy or death] minus First dose date plus 1) divided by 30.4375. (NCT02354586)
Timeframe: Up to 3 years

InterventionMonths (Median)
Niraparib 300 mg6.8

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Overall Survival

Overall Survival was defined as the time from the date of the first dose to the date of death by any cause. It was calculated as (Date of Death minus First dose date plus 1) divided by 30.4375. (NCT02354586)
Timeframe: Up to 3 years

InterventionMonths (Median)
Niraparib 300 mg17.2

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Objective Response Rate (ORR)

The ORR was defined as the percentage of participants achieving complete response (CR) or partial response (PR) as assessed by the Investigator per Response Evaluation Criteria in Solid Tumors (RECIST) (version1.1), where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 millimeters (mm) in the short axis, PR=At least a 30 percent (%) decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Primary Analysis Population comprised of participants who received 3 or 4 prior lines of therapy (LOT), had homologous recombination deficiency positive (HRDpos) tumors, had platinum-sensitive disease, and were poly(adenosine 5'-diphosphate [ADP]-ribose) polymerase inhibitors (PARPi) naïve. (NCT02354586)
Timeframe: Up to 3 years

InterventionPercentage of participants (Number)
Niraparib 300 mg27.66

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Duration of Response (DoR)

DoR was defined as the time from first documentation of CR or PR until the time of first documentation of disease progression (PD) as assessed by the Investigator per RECIST (version1.1). DoR was analyzed using Kaplan-Meier (KM) method. (NCT02354586)
Timeframe: Up to 3 years

InterventionMonths (Median)
Niraparib 300 mg9.4

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Disease Control Rate (DCR)

Disease control rate was defined as the percentage of participants achieving CR, PR, or stable disease (SD) as assessed by the Investigator per RECIST (version1.1). The exact (Clopper-Pearson) method was used to calculate 95% confidence interval. (NCT02354586)
Timeframe: Up to 3 years

InterventionPercentage of participants (Number)
Niraparib 300 mg49.02

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Progression Free Survival

Progression-free survival was defined as the time from the date of first dose to the earlier date of assessment of progression or death by any cause in the absence of progression as assessed by the Investigator per RECIST (version 1.1) or clinical criteria. Progression is defined using RECIST version1.1 as at least a 20% increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions or the appearance of one or more new lesions. (NCT02354586)
Timeframe: Up to 3 years

InterventionMonths (Median)
Niraparib 300 mg3.5

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Overall Survival

Overall survival was defined as the time from the date of randomization to the date of death by any cause. Median and 95% CI are presented for overall survival interim analysis. (NCT02655016)
Timeframe: Up to 34 months

InterventionMonths (Median)
PlaceboNA
Niraparib30.3

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Change From Baseline in PRO: European Quality of Life Scale, 5-dimensions, 5-levels of Severity (EQ-5D-5L) Utility Score

The EQ-5D-5L is a well-validated general preference-based, health-related QoL instrument. The five-item measure has 1 question assessing each of 5 dimensions: mobility, self-care, usual activities, pain/discomfort, and anxiety/depression and 5 levels for each dimension including 1=no problems, 2=slight problems, 3=moderate problems, 4=severe problems and 5=extreme problems. The health state is defined by combining the levels of answers from each of the 5 questions. Each health state is referred to in terms of a 5 digit code. Health state 5 digit code is translated into utility score, which is valued up to 1 (perfect health) with lower values meaning worse state. EQ-5D-5L utility score ranges from -0.281 to 1. Higher scores indicate better health. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose). (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to Week 24

InterventionScores on a scale (Least Squares Mean)
Placebo0.005
Niraparib0.016

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Change From Baseline in Participant Reported Outcome (PRO): Functional Assessment of Cancer Therapy-Ovarian Symptom Index (FOSI)

"FOSI is a validated, 8-item measure of symptom response to treatment for ovarian cancer. Participants responded to their symptom experience over the past 7 days using a 5-point Likert scale scored from not at all (0) to very much (4). FOSI score was calculated as (sum of item scores)*8 divided by (number of items answered). The FOSI score ranged from 0 (severely symptomatic) to 32 (asymptomatic). A higher score indicated a better quality of life (QoL). Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose)." (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to Week 24

InterventionScores on a scale (Least Squares Mean)
Placebo-0.3
Niraparib-0.4

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Change From Baseline in Global Health Status/QoL of EORTC-QLQ-C30

"EORTC-QLQ-C30 incorporates 5 functional scales (physical, role, cognitive, emotional, and social), 3 symptom scales (fatigue, pain, and nausea/vomiting), a global health status/QoL scale (global health status, QoL), and 6 single items (dyspnea, appetite loss, insomnia, constipation, diarrhea, and financial difficulty) assessing additional symptoms commonly reported by participants with cancer. A global health status/QoL scale had total 2 items. Each global health status/QoL scales score was calculated by averaging scores of all scale items and transforming average scores linearly ([average score minus 1] divided by 6*100). The global health status/QoL scales range in score from 0 to 100. Higher score represents a higher (better) level of health status/QoL. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose)." (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to Week 24

InterventionScores on a scale (Least Squares Mean)
Placebo1.177
Niraparib1.009

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Number of Participants With Any Non-serious Adverse Event (Non-SAE) or Any SAE

An adverse event is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with study treatment. Any untoward event resulting in death, life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, congenital anomaly or birth defect or any other situation according to medical or scientific judgment was categorized as SAE. (NCT02655016)
Timeframe: Up to 34 months

,
InterventionParticipants (Count of Participants)
Any non-SAEAny SAE
Niraparib478156
Placebo22332

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Change From Baseline in Symptoms Scales and Symptoms Items (Dyspnea, Appetite Loss, Insomnia, Constipation, Diarrhea and Financial Difficulty) of EORTC-QLQ-C30

"EORTC-QLQ-C30 incorporates 5 functional scales (physical, role, cognitive, emotional, and social), 3 symptom scales (fatigue, pain, and nausea/vomiting), a global health status/QoL scale, and 6 single items (dyspnea, appetite loss, insomnia, constipation, diarrhea, and financial difficulty) assessing additional symptoms commonly reported by participants with cancer. Symptom scale had total 7 items (fatigue-3, pain-2, nausea/vomiting-2). Each symptoms scales and 6 single additional symptoms items score was calculated by averaging scores of all scale items and transforming average scores linearly ([average score minus 1] divided by 3*100). All of the symptoms scales and 6 single additional symptoms scales range in score from 0 to 100. Higher score represents a higher (worse) level of symptoms. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose)." (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to Week 24

,
InterventionScores on a scale (Least Squares Mean)
Fatigue, n=243,479Nausea/Vomiting, n=244,479Pain, n=244,480Dyspnea, n=244,479Insomnia, n=244,479Appetite Loss, n=8,30Constipation, n=244,478Diarrhea, n=8,30Financial Difficulties, n=243,475
Niraparib0.0853.1150.7651.3473.478-0.3956.356-3.340-3.356
Placebo-0.0821.673-0.1950.6442.195-0.827-1.1479.335-5.058

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Change From Baseline in Symptoms Scale of EORTC-QLQ-OV28

"EORTC-QLQ-OV28 is supplement to EORTC-QLQ-C30. It includes 3 functional scales (body image, sexuality, attitude to disease/treatment) and 5 symptom scales/items (abdominal/GI symptoms, peripheral neuropathy, hormonal/menopausal symptoms, other chemotherapy side-effects, and hair loss). Symptoms scales score was calculated by averaging scores of all scale items and transforming average scores linearly ([average score minus 1] divided by 3*100). All of the symptoms scales range in score from 0 to 100. Higher score represents a higher (worse) level of symptoms. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose)." (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to 34 months

,
InterventionScores on a scale (Least Squares Mean)
Abdominal/GI, n=244,481Peripheral Neuropathy, n=244,480Hormonal/Menopausal Symptoms, n=244,480Other Chemotherapy Side Effects, n=244,480Hair Loss, n=242,477
Niraparib2.185-8.2171.501-2.219-23.363
Placebo0.832-9.629-2.521-3.023-20.743

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Change From Baseline in Functional Scales of European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire Ovarian Cancer Module (EORTC-QLQ-OV28)

"EORTC-QLQ-OV28 is supplement to EORTC-QLQ-C30. It includes 3 functional scales (body image, sexuality, attitude to disease/treatment) and 5 symptom scales/items (abdominal/gastrointestinal [GI] symptoms, peripheral neuropathy, hormonal/menopausal symptoms, other chemotherapy side-effects, and hair loss). Functional scales score (body Image and attitude to disease/treatment) was calculated by averaging scores of all scale items and transforming average scores linearly (1 minus [average score minus 1] divided by 3*100). Functional scales score (sexuality) was calculated by averaging scores of all scale items and transforming average scores linearly ([average score minus 1] divided by 3*100). All of the functional scales range in score from 0 to 100. Higher score represents a higher (better) level of functioning. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose)." (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to 34 months

,
InterventionScores on a scale (Least Squares Mean)
Body Image, n=244,475Sexuality, n=240,471Attitude to disease/Treatment, n=244,475
Niraparib8.4883.62513.660
Placebo10.0693.25712.216

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Change From Baseline in Functional Scales of European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire C30 (EORTC-QLQ-C30)

"EORTC-QLQ-C30 incorporates 5 functional scales (physical, role, cognitive, emotional, and social), 3 symptom scales (fatigue, pain, and nausea/vomiting), a global health status/QoL scale (global health status, QoL), and 6 single items (dyspnea, appetite loss, insomnia, constipation, diarrhea, and financial difficulty) assessing additional symptoms commonly reported by participants with cancer. Five functional scales had total 15 items (physical-5, role-2, cognitive-4, emotional-2, and social-2). Each functional scales score was calculated by averaging scores of all scale items and transforming average scores linearly (1 minus [average score minus 1] divided by 3*100). All of the functional scales range in score from 0 to 100. Higher score represents a higher (better) level of functioning. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. Baseline was defined as the latest pre-dose assessment (Day 1 pre-dose)." (NCT02655016)
Timeframe: Baseline (Day 1, Pre-dose) and Up to Week 24

,
InterventionScores on a scale (Least Squares Mean)
Physical Functioning, n=244,479Role Functioning, n=244,479Emotional Functioning, n=243,478Cognitive Functioning, n=243,478Social Functioning, n=243,478
Niraparib2.0131.590-0.870-0.8424.445
Placebo2.1192.341-0.011-0.0205.557

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Time to First Subsequent Therapy (TFST)

Time to first subsequent therapy was defined as the time from the date of randomization to the date of the first subsequent anti-cancer therapy or death, whichever occurs first. Median and 95% CI are presented. (NCT02655016)
Timeframe: Up to 34 months

InterventionMonths (Median)
Placebo12.0
Niraparib18.6

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Progression-Free Survival-2 (PFS2)

PFS2 was defined as the time from the date of randomization to the date of progression on the next anti-cancer therapy following study treatment or death by any cause, whichever occurs first. Median and 95% CI are presented. (NCT02655016)
Timeframe: Up to 34 months

InterventionMonths (Median)
PlaceboNA
Niraparib27.2

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Progression Free Survival

Progression free survival was defined as the time from the date of treatment randomization to the date of first documentation of disease progression or death due to any cause in the absence of documented progression, whichever occurs first. It was assessed by the blinded independent central review (BICR). Median and 95% confidence interval (CI) are presented. (NCT02655016)
Timeframe: Up to 34 months

InterventionMonths (Median)
Placebo8.2
Niraparib13.8

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Phase 1: Minimum Observed Plasma Concentration (Cmin) and Maximum Observed Plasma Concentration (Cmax) of Niraparib

Blood samples were collected at indicated time points. Pharmacokinetic analysis of Niraparib was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

,
InterventionNanogram per milliliter (Mean)
CminCmax
Phase 1: Niraparib 200 mg + Pembrolizumab174.00546.0
Phase 1: Niraparib 300 mg + Pembrolizumab205.63711.3

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Phase 1: Minimum Observed Plasma Concentration at Steady State (Cmin,ss) and Maximum Observed Plasma Concentration at Steady State (Cmax,ss) of Niraparib

Blood samples were collected at indicated time points. Pharmacokinetic analysis of Niraparib was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 2 Day 1 (each cycle of 21 days)

,
InterventionNanograms per milliliter (Mean)
Cmin,ssCmax,ss
Phase 1: Niraparib 200 mg + Pembrolizumab878.751585.5
Phase 1: Niraparib 300 mg + Pembrolizumab849.001606.7

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Phase 1: Cmin,ss and Cmax,ss of Major Metabolite of Niraparib (M1)

Blood samples were collected at indicated time points. Pharmacokinetic analysis of major metabolite of Niraparib (M1) was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 2 Day 1(each cycle of 21 days)

,
InterventionNanograms per milliliter (Mean)
Cmin,ssCmax,ss
Phase 1: Niraparib 200 mg + Pembrolizumab1410.0002177.50
Phase 1: Niraparib 300 mg + Pembrolizumab3280.0004213.33

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Phase 1: Cmin and Cmax of Major Metabolite of Niraparib (M1)

Blood samples were collected at indicated time points. Pharmacokinetic analysis of major metabolite of Niraparib (M1) was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

,
InterventionNanogram per milliliter (Mean)
CminCmax
Phase 1: Niraparib 200 mg + Pembrolizumab42.114340.14
Phase 1: Niraparib 300 mg + Pembrolizumab46.677491.66

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Phase 2: Progression Free Survival (PFS) as Measured by RECIST v1.1

PFS is defined as the time from first dose of study treatment to the earlier date of assessment of progression or death by any cause in the absence of progression based on the time of first documentation of disease progression per RECIST v1.1. Progression is defined using RECIST v1.1 as a 20% increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions or the appearance of one or more new lesions. (NCT02657889)
Timeframe: Up to a maximum of 54 months

InterventionMonths (Median)
Phase 2 OC: Niraparib 200 mg + Pembrolizumab3.4
Phase 2 TNBC: Niraparib 200 mg + Pembrolizumab2.5

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Phase 2: Overall Survival (OS)

OS is defined as the time from date of first dose of study treatment to the date of death by any cause. (NCT02657889)
Timeframe: Up to a maximum of 54 months

InterventionMonths (Median)
Phase 2 OC: Niraparib 200 mg + Pembrolizumab17.1
Phase 2 TNBC: Niraparib 200mg + Pembrolizumab9.4

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Phase 2: Objective Response Rate (ORR) as Measured by Response Evaluation Criteria in Solid Tumors (RECIST) Version (v) 1.1

ORR is defined as the percentage of participants with a confirmed best overall response of Complete Response (CR) or Partial Response (PR), RECIST v1.1 for target lesions as assessed by the Investigator. CR is defined as disappearance of all target lesions, Any pathological lymph nodes must be <10 millimeters (mm) in the short axis; PR is defined as at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the Baseline sum diameters. (NCT02657889)
Timeframe: Up to 40 weeks

InterventionPercentage of participants (Number)
Phase 2 OC: Niraparib 200mg + Pembrolizumab15.1
Phase 2 TNBC: Niraparib 200mg + Pembrolizumab18.2

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Phase 2: Number of Participants With TEAEs

An adverse event was any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. TEAEs were any new AE that begins, or any pre-existing condition that worsens in severity, after at least 1 dose of study treatment has been administered. (NCT02657889)
Timeframe: Up to a maximum of 54 months

InterventionParticipants (Count of Participants)
Phase 2 OC: Niraparib 200 mg + Pembrolizumab53
Phase 2 TNBC: Niraparib 200 mg + Pembrolizumab54

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Phase 2: Duration of Response (DOR) as Measured by RECIST v1.1

DoR per RECIST v1.1 was defined as the time from first documented evidence of CR or PR until first documented disease progression per RECIST v1.1 based upon investigator assessment or death due to any cause, whichever occurs first, among participants who demonstrated CR or PR as the best overall response per RECIST v1.1. CR is defined as disappearance of all target lesions. Any pathological lymph nodes must be <10 millimeters (mm) in the short axis. PR is defined as at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the Baseline sum diameters. (NCT02657889)
Timeframe: Up to a maximum of 54 months

InterventionMonths (Median)
Phase 2 OC: Niraparib 200 mg + Pembrolizumab14.4
Phase 2 TNBC: Niraparib 200 mg + Pembrolizumab21.5

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Phase 1: Number of Participants Reporting Dose-Limiting Toxicities (DLTs)

DLTs are defined as: Any treatment-related Grade >=3 non-hematologic clinical (non-laboratory) adverse event (AE); Any treatment-related Grade 3 or Grade 4 non-hematologic laboratory (lab) abnormality if Medical intervention is required to treat the participant or the abnormality leads to hospitalization or the abnormality persists for >=7 days; Any treatment-related hematologic toxicity specifically defined as: Thrombocytopenia Grade 4 for >=7 days, or Grade 3 or 4 associated with bleeding or requiring platelet transfusion, Neutropenia Grade 4 for >=7 days, or Grade 3 or 4 associated with infection or febrile neutropenia, Anemia Grade 4, or Grade 3 or 4 requiring blood transfusion; Any treatment-related AE leading to niraparib dose interruption per the following criteria: A dose interruption for a non-DLT lab abnormality lasting >=14 days, A dose in interruption per dose modification rules for non-hematologic AE leading to <80 percent (%) of an intended dose being administered. (NCT02657889)
Timeframe: During Cycle 1, ie, during the first 21 days of treatment

InterventionParticipants (Count of Participants)
Phase 1: Niraparib 200 mg + Pembrolizumab1
Phase 1: Niraparib 300 mg + Pembrolizumab1

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Phase 2: Disease Control Rate (DCR) as Measured by RECIST v1.1

DCR is defined as the percentage of participants who achieved a CR or PR or stable disease (SD) using RECIST (v1.1) as assessed by the investigator. (NCT02657889)
Timeframe: Up to 40 weeks

InterventionPercentage of participants (Number)
Phase 2 OC: Niraparib 200mg + Pembrolizumab58.5
Phase 2 TNBC: Niraparib 200mg + Pembrolizumab41.8

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Phase 1: Volume of Distribution (Vz/F) of Niraparib

Blood samples were planned to be collected for to determine Vz/F of Niraparib. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

InterventionLiters (Mean)
Phase 1: Niraparib 200 mg + PembrolizumabNA
Phase 1: Niraparib 300 mg + PembrolizumabNA

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Phase 2: Plasma Concentrations of Major Metabolite of Niraparib (M1)

Blood samples were collected by sparse PK sampling to analyze plasma concentration of major metabolite of Niraparib (M1). (NCT02657889)
Timeframe: Pre-dose and 2 Hours post-dose on Cycle 1 Day 1; Pre-dose and 2 Hours post-dose on Cycle 2 Day 1 (each cycle of 21 days)

,
InterventionNanograms per milliliter (Median)
Cycle 1 Day 1; PredoseCycle 1 Day1; 2 hours post doseCycle 2 Day 1; PredoseCycle 2 Day 1; 2 hours post dose
Phase 2 OC: Niraparib 200 mg + Pembrolizumab0.000116.6661278.9261500.143
Phase 2 TNBC: Niraparib 200mg + Pembrolizumab0.00084.8751070.9231205.444

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Phase 1: Volume of Distribution (Vz/F) of Major Metabolite of Niraparib (M1)

Blood samples were planned to be collected for to determine Vz/F of major metabolite (M1) of Niraparib. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

InterventionLiters (Mean)
Phase 1: Niraparib 200 mg + PembrolizumabNA
Phase 1: Niraparib 300 mg + PembrolizumabNA

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Phase 1: Number of Participants With Treatment Emergent Adverse Events (TEAEs)

An adverse event was any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. TEAEs were any new AE that begins, or any pre-existing condition that worsens in severity, after at least 1 dose of study treatment has been administered. (NCT02657889)
Timeframe: Up to a maximum of 22 months

InterventionParticipants (Count of Participants)
Phase 1: Niraparib 200 mg + Pembrolizumab7
Phase 1: Niraparib 300 mg + Pembrolizumab7

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Phase 2: Plasma Concentrations of Niraparib

Blood samples were collected by sparse PK sampling to analyze plasma concentration of Niraparib. (NCT02657889)
Timeframe: Pre-dose and 2 Hours post-dose on Cycle 1 Day 1; Pre-dose and 2 Hours post-dose on Cycle 2 Day 1(each cycle of 21 days)

,
InterventionNanograms per milliliter (Median)
Cycle 1 Day 1: PredoseCycle 1 Day 1; 2 hours post doseCycle 2 Day 1; PredoseCycle 2; Day 1; 2 hours post dose
Phase 2 OC: Niraparib 200 mg + Pembrolizumab0.000315.979441.978764.500
Phase 2 TNBC: Niraparib 200mg + Pembrolizumab0.000302.642510.154884.185

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Phase 1: Apparent Oral Clearance (CL/F) of Major Metabolite of Niraparib (M1)

Blood samples were planned to be collected for to determine CL/F of major metabolite (M1) of Niraparib. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

InterventionLiters per hour (Mean)
Phase 1: Niraparib 200 mg + PembrolizumabNA
Phase 1: Niraparib 300 mg + PembrolizumabNA

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Phase 1: Apparent Oral Clearance (CL/F) of Niraparib

Blood samples were planned to be collected for to determine CL/F of Niraparib. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

InterventionLiters per hour (Mean)
Phase 1: Niraparib 200 mg + PembrolizumabNA
Phase 1: Niraparib 300 mg + PembrolizumabNA

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Phase 1: Area Under the Plasma Concentration-time Curve From Time 0 (Predose) to 24 Hours Post Dose (AUC [0-24]) of Niraparib

Blood samples were collected at indicated time points. Pharmacokinetic (PK) analysis of Niraparib was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

InterventionHour*nanogram per milliliter (Mean)
Phase 1: Niraparib 200 mg + Pembrolizumab6524.035
Phase 1: Niraparib 300 mg + Pembrolizumab8855.687

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Phase 1: AUC (0-24) of Major Metabolite of Niraparib (M1)

Blood samples were collected at indicated time points. Pharmacokinetic analysis of major metabolite of Niraparib (M1) was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 1 Day 1 (each cycle of 21 days)

InterventionHour*nanogram per milliliter (Mean)
Phase 1: Niraparib 200 mg + Pembrolizumab4886.115
Phase 1: Niraparib 300 mg + Pembrolizumab11076.538

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Phase 1: AUC at Steady State (AUC,ss) of Niraparib

Blood samples were collected at indicated time points. Pharmacokinetic analysis of Niraparib was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 2 Day 1 (each cycle of 21 days)

InterventionHour*nanograms per milliliter (Mean)
Phase 1: Niraparib 200 mg + Pembrolizumab27396.910
Phase 1: Niraparib 300 mg + Pembrolizumab30799.742

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Phase 1: AUC,ss of Major Metabolite of Niraparib (M1)

Blood samples were collected at indicated time points. Pharmacokinetic analysis of major metabolite of Niraparib (M1) was conducted using standard non-compartmental analysis. (NCT02657889)
Timeframe: Pre-dose and 1, 2, 4, 6, 8, 24 Hours post-dose on Cycle 2 Day 1 (each cycle of 21 days)

InterventionHour*nanograms per milliliter (Mean)
Phase 1: Niraparib 200 mg + Pembrolizumab32878.205
Phase 1: Niraparib 300 mg + Pembrolizumab127430.14

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Overall Survival (OS)

OS is defined as time from enrollment to death from any cause. (NCT02854436)
Timeframe: Up to 52 months

Interventionmonths (Median)
BRCANon-BRCA
Niraparib13.019.63

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Radiographic Progression-Free Survival (rPFS)

rPFS was defined as time from enrollment to radiographic progression or death from any cause, whichever occurred first. Radiographic progression was evaluated per RECIST 1.1 criteria for soft tissue disease and per PCWG3 criteria for bone disease. (NCT02854436)
Timeframe: Up to 52 months

Interventionmonths (Median)
BRCANon-BRCA
Niraparib8.083.71

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Time to Prostate-Specific Antigen (PSA) Progression

Time to PSA progression was defined as time from enrollment to the first date of documented PSA progression based on PCWG3 criteria. A participant was considered to have a PSA progression if the PSA level had a 25 percent (%) or greater increase from nadir and an absolute increase of 2 nanograms per milliliter (ng/mL) or more, which is confirmed by a second value obtained in 3 or more weeks. (NCT02854436)
Timeframe: Up to 52 months

Interventionmonths (Median)
BRCANon-BRCA
Niraparib5.133.65

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Time to Radiographic Progression

Time to radiographic progression is defined as time from enrollment to radiographic progression or death due to disease progression, whichever occurs first. Disease progression is defined as at least a 20 percent (%) increase in the sum of 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. The appearance of one or more new lesions is also considered progression. (NCT02854436)
Timeframe: Up to 52 months

Interventionmonths (Median)
BRCANon-BRCA
Niraparib8.083.78

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Time to Symptomatic Skeletal Event (SSE)

Time to SSE was defined as the time from enrollment to first occurrence of one of the following symptomatic skeletal events: tumor-related spinal cord compression, radiation to bone to relieve skeletal symptoms, surgery to bone or need for tumor-related orthopedic surgical intervention, symptomatic or pathologic fracture. (NCT02854436)
Timeframe: Up to 52 months

Interventionmonths (Median)
BRCANon-BRCA
Niraparib13.8010.35

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Number of Participants With Adverse Events (AEs)

An AE is any untoward medical occurrence in a participant participating in a clinical study that does not necessarily have a causal relationship with the pharmaceutical/ biological agent under study. (NCT02854436)
Timeframe: Up to 52 months

InterventionParticipants (Count of Participants)
Niraparib288

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Objective Response Rate (ORR) for Participants With Measurable Metastatic Castration-resistant Prostate Cancer (mCRPC) and Breast Cancer Gene (BRCA) Mutation

ORR defined as percentage of participants with BRCA DNA-repair anomalies and measurable disease whose best response is either complete response (CR) or partial response (PR) per Response Evaluation Criteria in Solid Tumors (RECIST 1.1) and with no evidence of bone progression per Prostate Cancer Working Group 3 (PCWG3) criteria. (NCT02854436)
Timeframe: Up to 52 months

Interventionpercentage of participants (Number)
Niraparib34.2

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Objective Response Rate for Participants With Measurable Metastatic Castration-resistant Prostate Cancer (mCRPC) and Non-Breast Cancer Gene (BRCA) Mutation

ORR defined as percentage of participants with BRCA deoxyribonucleic acid (DNA)-repair anomalies and measurable disease whose best response is either CR or PR per RECIST 1.1 and with no evidence of bone progression per PCWG3 criteria. (NCT02854436)
Timeframe: Up to 52 months

Interventionpercentage of participants (Number)
Niraparib10.6

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Circulating Tumor Cells (CTC) Response Rate

CTC response rate was defined as the percentage of participants with CTC equals to (=) 0 per 7.5 milliliter (mL) blood at 8 weeks post-baseline in participants with baseline CTC greater than (>) 0. (NCT02854436)
Timeframe: At 8 weeks post-baseline

Interventionpercentage of participants (Number)
BRCANon-BRCA
Niraparib23.78.5

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Duration of Objective Response

Duration of objective response is defined as time from CR or PR to radiographic progression of disease, unequivocal clinical progression or death, whichever occurs first. Unequivocal clinical progression defined as one or more of following: 1) deterioration in Eastern Cooperative Oncology Group Performance Status (ECOG PS) to Grade 3 or higher; 2) need to initiate any of following because of tumor progression (even in absence of radiographic evidence of disease): alternative anticancer therapy for prostate cancer, radiation therapy, surgical interventions for complications due to tumor progression. (NCT02854436)
Timeframe: Up to 52 months

Interventionmonths (Median)
BRCAnon-BRCA
Niraparib5.555.16

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Number of Participants With Worst Toxicity Grades for Clinical Laboratory Tests Based on National Cancer Institute - Common Terminology Criteria for Adverse Events (NCI-CTCAE)

Number of participants with worst toxicity grades for clinical laboratory tests (chemistry and hematology) based on NCI-CTCAE were reported. The chemistry laboratory parameters were: alanine aminotransferase (ALT) increased, alkaline phosphatase increased, aspartate aminotransferase (AST) increased, blood bilirubin increased, creatinine increased, gamma glutamyl transferase (GGT) increased and the hematology parameters were: hemoglobin increased, lymphocyte count increased. Grading was done as: Grade 1 (=mild), Grade 2 (=moderate), Grade 3 (=severe) and Grade 4 (=potentially life-threatening). (NCT02854436)
Timeframe: Up to 52 months

InterventionParticipants (Count of Participants)
ALT increased (Grade 1 or 2)ALT increased (Grade 3 or 4)Alkaline phosphatase increased (Grade 1 or 2)Alkaline phosphatase increased (Grade 3 or 4)AST increased (Grade 1 or 2)AST increased (Grade 3 or 4)Blood bilirubin increased (Grade 1 or 2)Blood bilirubin increased (Grade 3 or 4)Creatinine increased (Grade 1 or 2)Creatinine increased (Grade 3 or 4)GGT increased (Grade 1 or 2)GGT increased (Grade 3 or 4)Hemoglobin increased (Grade 1 or 2)Hemoglobin increased (Grade 3 or 4)Lymphocyte count increased (Grade 1 or 2)Lymphocyte count increased (Grade 3 or 4)
Niraparib674102770492452105140020

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Progression-Free Survival Rate at 6 Months

Determine the progression-free survival rate at 6 months after study entry in each cohort. This is the percentage of subjects that both have not had disease progression and are alive 6 months after study entry. Progression is defined by RECIST v1.1 criteria and is defined as an increase of at least 20% in the sum of the largest diameters of target lesions and/or the appearance of new lesions. (NCT03207347)
Timeframe: 6 months

Interventionpercentage of subjects (Number)
Cohort A39
Cohort B57

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Progression-Free Survival Rate at 3 Months

Determine the progression-free survival rate at 3 months after study entry in each cohort. This is the percentage of subjects that both have not had disease progression and are alive 3 months after study entry. Disease progression is defined by RECIST v1.1 criteria and is defined as an increase of at least 20% in the sum of the largest diameters of target lesions and/or the appearance of new lesions. (NCT03207347)
Timeframe: 3 months

Interventionpercentage of subjects (Number)
Cohort A43
Cohort B64

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Progression-Free Survival

Determine the median progression-free survival. Progression-free survival is defined as the duration of time from study entry to time of progression or death or the date of last contact, whichever occurs first. Progression is defined by RECIST v1.1 criteria and is defined as an increase of at least 20% in the sum of the largest diameters of target lesions and/or the appearance of new lesions. (NCT03207347)
Timeframe: 8 months

Interventionmonths (Median)
Cohort A2.1
Cohort B7.2

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Overall Survival

Estimate the median overall survival. Overall survival is defined as the duration of time from date of study entry until date of death or date of last contact. (NCT03207347)
Timeframe: 10 months

Interventionmonths (Median)
Cohort A9.1
Cohort B7.2

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Objective Response Rate (ORR)

Determine the objective response rate (ORR), which is defined as the percentage of subjects achieving a best overall response of partial or complete response (according to RECIST v1.1 criteria) from the start of the treatment until disease progression/recurrence or 30 days after the end of treatment, whichever occurs first. Per RECIST v1.1 criteria, a partial response is defined as a 30% or more decrease in the sum of the largest diameters of the target lesions. Per RECIST v1.1 criteria, a complete response is defined as the disappearance of target lesions (lymph nodes identified as lesions must have reduction in short axis to <10 mm). (NCT03207347)
Timeframe: 1 year

Interventionpercentage of subjects (Number)
Cohort A5.6
Cohort B0

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Part A: Number of Participants With Non-serious Treatment-emergent Adverse Events (TEAEs), Serious TEAEs (STEAEs) and Adverse Events of Special Interest (AESIs)

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose; results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgement. TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs, SAEs and AESIs are reported. (NCT03307785)
Timeframe: Up to 28.5 months

,
InterventionParticipants (Count of Participants)
Non-serious TEAEsSTEAEsAESIs
Part A: TSR-042 and Niraparib 200 mg QD16111
Part A: TSR-042 and Niraparib 300 mg QD641

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Part A: Tmax at Steady State (Tmax,ss) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Cycle 2, n=10,3
Part A: TSR-042 and Niraparib 300 mg QD2.250

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Part A: Tmax at Steady State (Tmax,ss) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Cycle 2, n=10,3Cycle 5, n=7,0Cycle 11, n=2,0
Part A: TSR-042 and Niraparib 200 mg QD4.0082.0001.817

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Part A: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Cycle 4, n=9,4Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD1.3002.783

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Part A: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Cycle 4, n=9,4Cycle 5, n=8,1Cycle 11, n=5,0
Part A: TSR-042 and Niraparib 200 mg QD1.5000.6250.567

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Part A: Volume of Distribution After Intravenous Administration (Vss) of of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=5,2Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD9.86805.9659

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Part A: Area Under the Plasma Concentration From Time Zero to Infinity (AUC[0-infinity]) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part A: TSR-042 and Niraparib 200 mg QDNA
Part A: TSR-042 and Niraparib 300 mg QDNA

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Part A: AUC at Steady State (AUCss) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part A: TSR-042 and Niraparib 200 mg QD16.3481
Part A: TSR-042 and Niraparib 300 mg QD29.4312

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Part A: AUC(0-infinity) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part A: TSR-042 and Niraparib 200 mg QDNA
Part A: TSR-042 and Niraparib 300 mg QDNA

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Part A: Cmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part A: TSR-042 and Niraparib 200 mg QD158.6875
Part A: TSR-042 and Niraparib 300 mg QD138.9167

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Part A: Ctau of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part A: TSR-042 and Niraparib 200 mg QD33.6000
Part A: TSR-042 and Niraparib 300 mg QD29.8000

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Part A: Disease Control Rate

Disease Control Rate is defined as the percentage of participants who had achieved CR, PR, or stable disease (SD) per RECIST version 1.1. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionPercentage of participants (Number)
Part A: TSR-042 and Niraparib 200 mg QD43.8
Part A: TSR-042 and Niraparib 300 mg QD33.3

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Part A: Duration of Response

Duration of response is defined as the time from first documentation of response (CR or PR) until the time of first documentation of disease progression by RECIST version 1.1 or death by any cause. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionMonths (Median)
Part A: TSR-042 and Niraparib 200 mg QD7.59
Part A: TSR-042 and Niraparib 300 mg QDNA

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Part A: Maximum Observed Plasma (Cmax) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part A: TSR-042 and Niraparib 200 mg QD0.460600
Part A: TSR-042 and Niraparib 300 mg QD0.625667

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Part A: Number of Participants With Dose-limiting Toxicity (DLT)

An event was considered a DLT if it occurred within the first 21 days of treatment, and met one of following DLT criteria:hematologic toxicity- Grade4 thrombocytopenia persists for >=7 days from the time of adverse event(AE) onset, Grade 4 neutropenia, Grade 4 or Grade 3 febrile neutropenia persists for >=7 days, Grade4 or Grade3 anemia requiring blood transfusion, Grade 3 thrombocytopenia associated with clinically significant bleeding, Grade 3 neutropenia associated with infection as described in Common Terminology Criteria for Adverse Events (CTCAE) version 4.0, drug related Grade 3 or 4 non-hematologic toxicity, drug related Grade 3 or 4 nonhematologic laboratory abnormality if any of the following also occur: abnormality leads to hospitalization and abnormality persists for >=7 days from the time of AE onset; drug related toxicity leading to prolonged delay (>2 weeks) in initiating Cycle 2. DLTs were collected during first cycle to establish recommended phase 2 dose (RP2D). (NCT03307785)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
Part A: TSR-042 and Niraparib 200 mg QD2
Part A: TSR-042 and Niraparib 300 mg QD0

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Part A: Number of Participants With Positive Anti-TSR-042 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-042. The presence of anti-TSR-042 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). Anti-drug Antibody Population consisted of all participants who received at least 1 dose of study treatment and had provided a pre-dose blood sample and at least 1 post-dose blood sample at or after 96 hours. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionParticipants (Count of Participants)
Part A: TSR-042 and Niraparib 200 mg QD0
Part A: TSR-042 and Niraparib 300 mg QD0

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Part A: Objective Response Rate

Objective Response Rate is defined as the percentage of participants who achieved confirmed complete response (CR) or partial response (PR), evaluated using Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1 based on Investigator assessment; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 millimeters (mm) in the short axis. PR=At least a 30 percent (%) decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionPercentage of participants (Number)
Part A: TSR-042 and Niraparib 200 mg QD25.0
Part A: TSR-042 and Niraparib 300 mg QD0

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Part A: Observed Concentration at the End of the Dosing Interval (Ctau) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part A: TSR-042 and Niraparib 200 mg QD0.191953
Part A: TSR-042 and Niraparib 300 mg QD0.342333

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Part A: Progression-free Survival

Progression-free Survival is defined as the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. Progressive Disease (PD) is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionMonths (Median)
Part A: TSR-042 and Niraparib 200 mg QD6.2
Part A: TSR-042 and Niraparib 300 mg QD2.8

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Part A: Time to Reach Maximum Plasma Concentration (Tmax) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part A: TSR-042 and Niraparib 200 mg QD2.250
Part A: TSR-042 and Niraparib 300 mg QD4.083

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Part A: Tmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part A: TSR-042 and Niraparib 200 mg QD0.817
Part A: TSR-042 and Niraparib 300 mg QD1.750

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Part B: AUC(0-infinity) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part B: TSR-042 and Carboplatin-paclitaxelNA

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Part B: Cmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part B: TSR-042 and Carboplatin-paclitaxel148.2000

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Part B: Ctau of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part B: TSR-042 and Carboplatin-paclitaxel33.9778

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Part B: Disease Control Rate

Disease Control Rate is defined as the percentage of participants who had achieved CR, PR, or SD per RECIST version 1.1. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionPercentage of participants (Number)
Part B: TSR-042 and Carboplatin-paclitaxel57.1

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Part B: Number of Participants With DLT

An event was considered a DLT if it occurred within the first 21 days of treatment, and met one of following DLT criteria:hematologic toxicity- Grade4 thrombocytopenia persists for >=7 days from the time of AE onset, Grade 4 neutropenia, Grade 4 or Grade 3 febrile neutropenia persists for >=7 days, Grade4 or Grade3 anemia requiring blood transfusion, Grade 3 thrombocytopenia associated with clinically significant bleeding, Grade 3 neutropenia associated with infection as described in CTCAE version 4.0, drug related Grade 3 or 4 non-hematologic toxicity, drug related Grade 3 or 4 nonhematologic laboratory abnormality if any of the following also occur: abnormality leads to hospitalization and abnormality persists for >=7 days from the time of AE onset; drug related toxicity leading to prolonged delay (>2 weeks) in initiating Cycle 2. DLTs were collected during first cycle to establish RP2D. (NCT03307785)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
Part B: TSR-042 and Carboplatin-paclitaxel1

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Part B: Number of Participants With Positive Anti-TSR-042 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-042. The presence of anti-TSR-042 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). (NCT03307785)
Timeframe: Up to 28.5 months

InterventionParticipants (Count of Participants)
Part B: TSR-042 and Carboplatin-paclitaxel4

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Part B: Objective Response Rate

Objective Response Rate is defined as the percentage of participants who achieved confirmed CR or PR, evaluated using RECIST version 1.1 based on Investigator assessment; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionPercentage of participants (Number)
Part B: TSR-042 and Carboplatin-paclitaxel42.9

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Part B: Progression-free Survival

Progression-free Survival is defined as the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionMonths (Median)
Part B: TSR-042 and Carboplatin-paclitaxel17.6

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Part B: Tmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part B: TSR-042 and Carboplatin-paclitaxel1.000

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Part C: AUC(0-infinity) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part C: TSR-042, Niraparib 200 mg QD and BevacizumabNA
Part C: TSR-042, Niraparib 300 mg QD and BevacizumabNA

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Part C: AUC(0-infinity) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part C: TSR-042, Niraparib 200 mg QD and BevacizumabNA
Part C: TSR-042, Niraparib 300 mg QD and BevacizumabNA

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Part C: AUCss of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab21.4926
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab26.5006

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Part C: Cmax of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab0.243667
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab0.891571

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Part C: Cmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab138.6667
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab158.4857

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Part C: Ctau of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab0.161233
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab0.478714

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Part C: Ctau of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab37.2750
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab28.7500

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Part C: Disease Control Rate

Disease Control Rate is defined as the percentage of participants who had achieved CR, PR, or SD per RECIST version 1.1. (NCT03307785)
Timeframe: Up to 22.5 months

InterventionPercentage of participants (Number)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab83.3
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab85.7

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Part C: Number of Participants With DLT

An event was considered a DLT if it occurred within the first 21 days of treatment, and met one of following DLT criteria:hematologic toxicity- Grade4 thrombocytopenia persists for >=7 days from the time of AE onset, Grade 4 neutropenia, Grade 4 or Grade 3 febrile neutropenia persists for >=7 days, Grade4 or Grade3 anemia requiring blood transfusion, Grade 3 thrombocytopenia associated with clinically significant bleeding, Grade 3 neutropenia associated with infection as described in CTCAE version 4.0, drug related Grade 3 or 4 non-hematologic toxicity, drug related Grade 3 or 4 nonhematologic laboratory abnormality if any of the following also occur: abnormality leads to hospitalization and abnormality persists for >=7 days from the time of AE onset; drug related toxicity leading to prolonged delay (>2 weeks) in initiating Cycle 2. DLTs were collected during first cycle to establish RP2D. (NCT03307785)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab1
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab1

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Part C: Number of Participants With Positive Anti-TSR-042 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-042. The presence of anti-TSR-042 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). (NCT03307785)
Timeframe: Up to 22.5 months

InterventionParticipants (Count of Participants)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab0
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab0

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Part C: Objective Response Rate

Objective Response Rate is defined as the percentage of participants who achieved confirmed CR or PR, evaluated using RECIST version 1.1 based on Investigator assessment; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03307785)
Timeframe: Up to 22.5 months

InterventionPercentage of participants (Number)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab50.0
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab14.3

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Part C: Progression-free Survival

Progression-free Survival is defined as the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT03307785)
Timeframe: Up to 22.5 months

InterventionMonths (Median)
Part C: TSR-042, Niraparib 200 mg QD and BevacizumabNA
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab9.1

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Part C: Tmax of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab3.975
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab4.050

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Part C: Tmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab1.200
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab0.583

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Part D: AUC(0-infinity) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part D: TSR-042, Carboplatin-paclitaxel and BevacizumabNA

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Part D: Cmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab188.5000

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Part D: Ctau of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab36.5250

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Part D: Disease Control Rate

Disease Control Rate is defined as the percentage of participants who had achieved CR, PR, or SD per RECIST version 1.1. (NCT03307785)
Timeframe: Up to 9.5 months

InterventionPercentage of participants (Number)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab83.3

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Part D: Number of Participants With Positive Anti-TSR-042 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-042. The presence of anti-TSR-042 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). (NCT03307785)
Timeframe: Up to 9.5 months

InterventionParticipants (Count of Participants)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab0

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Part D: Objective Response Rate

Objective Response Rate is defined as the percentage of participants who achieved confirmed CR or PR, evaluated using RECIST version 1.1 based on Investigator assessment; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03307785)
Timeframe: Up to 9.5 months

InterventionPercentage of participants (Number)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab50.0

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Part D: Progression-free Survival

Progression-free Survival is defined as the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT03307785)
Timeframe: Up to 9.5 months

InterventionMonths (Median)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab7.6

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Part D: Tmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab1.250

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Part E: AUC(0-infinity) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: AUC0-t of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: CL of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Cmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Ctau of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

[back to top]

Part E: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Disease Control Rate

Disease Control Rate is defined as the percentage of participants who had achieved CR, PR, or SD per RECIST version 1.1. (NCT03307785)
Timeframe: Up to 4.4 months

InterventionPercentage of participants (Number)
Part E: TSR-042 and Carboplatin-pemetrexed0

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Part E: Duration of Response

Duration of response is defined as the time from first documentation of response (CR or PR) until the time of first documentation of disease progression by RECIST version 1.1 or death by any cause. (NCT03307785)
Timeframe: Up to 4.4 months

InterventionMonths (Median)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Number of Participants With DLT

An event was considered a DLT if it occurred within the first 21 days of treatment, and met one of following DLT criteria:hematologic toxicity- Grade4 thrombocytopenia persists for >=7 days from the time of AE onset, Grade 4 neutropenia, Grade 4 or Grade 3 febrile neutropenia persists for >=7 days, Grade4 or Grade3 anemia requiring blood transfusion, Grade 3 thrombocytopenia associated with clinically significant bleeding, Grade 3 neutropenia associated with infection as described in CTCAE version 4.0, drug related Grade 3 or 4 non-hematologic toxicity, drug related Grade 3 or 4 nonhematologic laboratory abnormality if any of the following also occur: abnormality leads to hospitalization and abnormality persists for >=7 days from the time of AE onset; drug related toxicity leading to prolonged delay (>2 weeks) in initiating Cycle 2. DLTs were collected during first cycle to establish RP2D. (NCT03307785)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
Part E: TSR-042 and Carboplatin-pemetrexed0

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Part E: Number of Participants With Positive Anti-TSR-042 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-042. The presence of anti-TSR-042 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). (NCT03307785)
Timeframe: Up to 4.4 months

InterventionParticipants (Count of Participants)
Part E: TSR-042 and Carboplatin-pemetrexed0

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Part E: Objective Response Rate

Objective Response Rate is defined as the percentage of participants who achieved confirmed CR or PR, evaluated using RECIST version 1.1 based on Investigator assessment; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03307785)
Timeframe: Up to 4.4 months

InterventionPercentage of participants (Number)
Part E: TSR-042 and Carboplatin-pemetrexed0

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Part E: Progression-free Survival

Progression-free Survival is defined as the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT03307785)
Timeframe: Up to 4.4 months

InterventionMonths (Median)
Part E: TSR-042 and Carboplatin-pemetrexedNA

[back to top]

Part E: Tmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose (each cycle was 21 days)

InterventionHours (Median)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Vss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose (each cycle was 21 days)

InterventionLiter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part E: Vz of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose (each cycle was 21 days)

InterventionLiter (Mean)
Part E: TSR-042 and Carboplatin-pemetrexedNA

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Part F: AUC(0-infinity) of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168 and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168 and 336 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

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Part F: AUC(0-infinity) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Geometric Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: AUC0-t of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168 and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: AUC0-t of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168 and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: AUCss of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: CL of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: CL of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Cmax of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168 and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Cmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Cmax,ss of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Ctau of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Ctau of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Ctau,ss of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Disease Control Rate

Disease Control Rate is defined as the percentage of participants who had achieved CR, PR, or SD per RECIST version 1.1. (NCT03307785)
Timeframe: Up to 3.5 months

InterventionPercentage of participants (Number)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexed100

[back to top]

Part F: Duration of Response

Duration of response is defined as the time from first documentation of response (CR or PR) until the time of first documentation of disease progression by RECIST version 1.1 or death by any cause. (NCT03307785)
Timeframe: Up to 3.5 months

InterventionMonths (Median)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Number of Participants With DLT

An event was considered a DLT if it occurred within the first 21 days of treatment, and met one of following DLT criteria:hematologic toxicity- Grade4 thrombocytopenia persists for >=7 days from the time of AE onset, Grade 4 neutropenia, Grade 4 or Grade 3 febrile neutropenia persists for >=7 days, Grade4 or Grade3 anemia requiring blood transfusion, Grade 3 thrombocytopenia associated with clinically significant bleeding, Grade 3 neutropenia associated with infection as described in CTCAE version 4.0, drug related Grade 3 or 4 non-hematologic toxicity, drug related Grade 3 or 4 nonhematologic laboratory abnormality if any of the following also occur: abnormality leads to hospitalization and abnormality persists for >=7 days from the time of AE onset; drug related toxicity leading to prolonged delay (>2 weeks) in initiating Cycle 2. DLTs were collected during first cycle to establish RP2D. (NCT03307785)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexed0

[back to top]

Part F: Number of Participants With Positive Anti-TSR-022 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-022. The presence of anti-TSR-022 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). (NCT03307785)
Timeframe: Up to 3.5 months

InterventionParticipants (Count of Participants)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Number of Participants With Positive Anti-TSR-042 Antibodies

Serum samples were collected at indicated time points and tested for the presence of antibodies that bind to TSR-042. The presence of anti-TSR-042 antibodies were assessed using a tiered approach using electrochemiluminescence (that is, screening, confirmation, titer, and neutralizing antibody assay). (NCT03307785)
Timeframe: Up to 3.5 months

InterventionParticipants (Count of Participants)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Objective Response Rate

Objective Response Rate is defined as the percentage of participants who achieved confirmed CR or PR, evaluated using RECIST version 1.1 based on Investigator assessment; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03307785)
Timeframe: Up to 3.5 months

InterventionPercentage of participants (Number)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexed0

[back to top]

Part F: Progression-free Survival

Progression-free Survival is defined as the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. PD is defined as at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. (NCT03307785)
Timeframe: Up to 3.5 months

InterventionMonths (Median)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Tmax of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Tmax of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Tmax,ss of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Vss of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Vss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

[back to top]

Part F: Vz of TSR-022

Blood samples were collected at indicated time points. PK parameters of TSR-022 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

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Part A: Volume of Distribution After Intravenous Administration (Vss) of of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=5,2Cycle 5, n=8,1Cycle 11, n=4,0
Part A: TSR-042 and Niraparib 200 mg QD5.56476.65807.3107

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Part A: Area Under the Plasma Concentration From Time Zero to t (AUC[0-t]) of Niraparib

Blood samples were collected at indicated time points. Pharmacokinetic (PK) parameters of niraparib were calculated using non-compartmental methods. PK population consisted of all participants who received at least 1 dose of study treatment and had at least 1 PK sample. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

,
InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=15,6Cycle 2, n=10,3
Part A: TSR-042 and Niraparib 200 mg QD6.043014.9172
Part A: TSR-042 and Niraparib 300 mg QD7.834129.3024

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Part A: AUC(0-t) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=16,6Cycle 4, n=9,4Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD29420.834729311.8182141328.9288

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Part A: AUC(0-t) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=16,6Cycle 4, n=9,4Cycle 5, n=8,1Cycle 11, n=5,0
Part A: TSR-042 and Niraparib 200 mg QD26827.770355408.3992137108.2574139591.8834

[back to top]

Part A: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 4, n=7,2Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD46122.3924141306.3782

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Part A: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 4, n=7,2Cycle 5, n=8,1Cycle 11, n=4,0
Part A: TSR-042 and Niraparib 200 mg QD58598.5076135171.2753151575.3645

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Part A: Clearance After Intravenous Administration (CL) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Cycle 4, n=7,2Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD0.01100.0071

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Part A: Clearance After Intravenous Administration (CL) of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Cycle 4, n=7,2Cycle 5, n=8,1Cycle 11, n=4,0
Part A: TSR-042 and Niraparib 200 mg QD0.00900.00810.0072

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Part A: Clearance After Oral Administration (CL/F) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Cycle 2, n=8,2
Part A: TSR-042 and Niraparib 300 mg QD10.2833

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Part A: Volume of Distribution After Intravenous Administration (Vz) of of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=5,2Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD10.39846.3070

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Part A: Volume of Distribution After Intravenous Administration (Vz) of of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=5,2Cycle 5, n=8,1Cycle 11, n=4,0
Part A: TSR-042 and Niraparib 200 mg QD5.69256.88117.4795

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Part A: Volume of Distribution After Oral Administration (Vz/F) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 2, n=8,2
Part A: TSR-042 and Niraparib 300 mg QD487.8826

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Part A: Volume of Distribution After Oral Administration (Vz/F) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 1, n=1,0Cycle 2, n=8,2
Part A: TSR-042 and Niraparib 200 mg QD380.1478716.1418

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Part B: AUC0-t of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=14Cycle 4, n=10Cycle 5, n=9Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel28097.984654730.0053124309.5455117030.4081

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Part B: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 4, n=10Cycle 5, n=8Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel55073.0926130694.9752117033.3612

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Part B: CL of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Cycle 4, n=10Cycle 5, n=8Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel0.00980.00820.0092

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Part B: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=10Cycle 5, n=9Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel225.8000421.1111446.6667

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Part B: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=9Cycle 5, n=8Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel67.244459.300057.4833

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Part B: Number of Participants With Non-serious TEAEs, STEAEs and AESIs

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose; results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgement. TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs, SAEs and AESIs are reported. (NCT03307785)
Timeframe: Up to 28.5 months

InterventionParticipants (Count of Participants)
Non-Serious TEAEsSTEAEsAESIs
Part B: TSR-042 and Carboplatin-paclitaxel1490

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Part B: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Cycle 4, n=10Cycle 5, n=9Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel0.5751.5000.542

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Part B: Vss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=10Cycle 5, n=8Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel5.18936.77017.4351

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Part B: Vz of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=10Cycle 5, n=8Cycle 11, n=6
Part B: TSR-042 and Carboplatin-paclitaxel5.36617.26278.0529

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Part C: AUC0-t of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

,
InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=6,7Cycle 2, n=4,4
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab3.451314.7473
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab11.360124.9691

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Part C: AUC0-t of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=6,7Cycle 4, n=5,7Cycle 5, n=5,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab29830.654254268.1379137777.3188143070.3093
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab26311.178949198.8237131281.9046119161.8795

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Part C: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionHours*microgram per milliliter (Mean)
Cycle 4, n=5,5Cycle 5, n=5,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab55974.4268137399.5881147907.5379
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab50924.1510131288.0291119189.5905

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Part C: CL of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionLiter per hour (Mean)
Cycle 4, n=5,5Cycle 5, n=5,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab0.01000.00820.0079
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab0.01040.00820.0086

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Part C: CL/F of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

,
InterventionLiter per hour (Mean)
Cycle 2, n=2,4
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab10.3777
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab14.4947

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Part C: Cmax,ss of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

,
InterventionMicrogram per milliliter (Mean)
Cycle 2, n=4,4Cycle 5, n=4,3Cycle 11, n=3,1
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab0.8545000.7097500.468333
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab1.4047501.0736670.638000

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Part C: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionMicrogram per milliliter (Mean)
Cycle 4, n=5,7Cycle 5, n=5,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab234.4000325.2000349.7500
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab227.1429417.3333321.0000

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Part C: Ctau,ss of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

,
InterventionMicrogram per milliliter (Mean)
Cycle 2, n=5,4
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab0.484000
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab1.094250

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Part C: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionMicrogram per milliliter (Mean)
Cycle 4, n=4,6Cycle 5, n=5,6Cycle 11, n=3,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab70.425082.9800105.4667
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab64.266753.150060.9500

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Part C: Number of Participants With Non-serious TEAEs, STEAEs and AESIs

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose; results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgement. TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs, SAEs and AESIs are reported. (NCT03307785)
Timeframe: Up to 22.5 months

,
InterventionParticipants (Count of Participants)
Non-serious TEAEsSTEAEsAESIs
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab530
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab730

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Part C: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionHours (Median)
Cycle 4, n=5,7Cycle 5, n=5,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab1.5172.0832.000
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab0.6170.8252.417

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Part C: Vss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionLiter (Mean)
Cycle 4, n=5,5Cycle 5, n=4,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab6.45676.24058.9478
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab5.51774.80357.7750

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Part C: Vz of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

,
InterventionLiter (Mean)
Cycle 4, n=5,5Cycle 5, n=4,6Cycle 11, n=4,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab6.64626.16989.6347
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab5.89225.20668.5098

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Part C: Vz/F of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

,
InterventionLiter (Mean)
Cycle 2, n=2,2
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab551.4003
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab559.3634

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Part D: AUC0-t of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 1, n=6Cycle 4, n=5Cycle 5, n=5Cycle 11, n=4
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab32819.540152409.0255119847.099977794.6422

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Part D: AUCss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours*microgram per milliliter (Mean)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=3
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab51140.4410118845.392896800.1534

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Part D: CL of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=3
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab0.01020.00870.0104

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Part D: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=4
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab256.8000416.0000429.7500

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Part D: Number of Participants With Non-serious TEAEs, STEAEs and AESIs

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose; results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgement. TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs, SAEs and AESIs are reported. (NCT03307785)
Timeframe: Up to 9.5 months

InterventionParticipants (Count of Participants)
Non-serious TEAEsSTEAEsAESIs
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab630

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Part D: Tmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionHours (Median)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=4
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab0.5000.5500.500

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Part D: Vss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=3
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab5.14935.63998.0614

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Part D: Vz of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=3
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab5.49556.15429.8356

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Part E: Number of Participants With Non-serious TEAEs, STEAEs and AESIs

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose; results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgement. TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs, SAEs and AESIs are reported. (NCT03307785)
Timeframe: Up to 4.4 months

InterventionParticipants (Count of Participants)
Non-serious TEAEsSTEAEsAESIs
Part E: TSR-042 and Carboplatin-pemetrexed220

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Part F: Vz of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 1: Pre-dose, 0.5, 1, 2, 3, 24, 48, 96, 168, and 336 hours post-dose; Cycle 2: Pre-dose; Cycle 5: Pre-dose, 0.5, 2, 24, 48, 96, 168, and 336 hours post-dose (each cycle was 21 days)

InterventionLiter (Mean)
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexedNA

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Part F: Number of Participants With Non-serious TEAEs, STEAEs and AESIs

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose; results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgement. TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs, SAEs and AESIs are reported. (NCT03307785)
Timeframe: Up to 3.5 months

InterventionParticipants (Count of Participants)
Non-serious TEAEsSTEAEsAESIs
Part F: TSR-042, TSR-022, and Carboplatin-pemetrexed100

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Part D: Number of Participants With DLT

An event was considered a DLT if it occurred within the first 21 days of treatment, and met one of following DLT criteria:hematologic toxicity- Grade4 thrombocytopenia persists for >=7 days from the time of AE onset, Grade 4 neutropenia, Grade 4 or Grade 3 febrile neutropenia persists for >=7 days, Grade4 or Grade3 anemia requiring blood transfusion, Grade 3 thrombocytopenia associated with clinically significant bleeding, Grade 3 neutropenia associated with infection as described in CTCAE version 4.0, drug related Grade 3 or 4 non-hematologic toxicity, drug related Grade 3 or 4 nonhematologic laboratory abnormality if any of the following also occur: abnormality leads to hospitalization and abnormality persists for >=7 days from the time of AE onset; drug related toxicity leading to prolonged delay (>2 weeks) in initiating Cycle 2. DLTs were collected during first cycle to establish RP2D. (NCT03307785)
Timeframe: 21 days

InterventionParticipants (Count of Participants)
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab0

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Part A: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=9,4Cycle 5, n=8,1Cycle 11, n=5,0
Part A: TSR-042 and Niraparib 200 mg QD222.5556393.8750405.4000

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Part A: Ctau at Steady State (Ctau,ss) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

,
InterventionMicrogram per milliliter (Mean)
Cycle 2, n=11,6
Part A: TSR-042 and Niraparib 200 mg QD0.507900
Part A: TSR-042 and Niraparib 300 mg QD0.622000

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Part A: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=8,1Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD63.300071.2000

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Part D: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=5Cycle 5, n=5Cycle 11, n=3
Part D: TSR-042, Carboplatin-paclitaxel and Bevacizumab53.520048.080043.3000

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Part A: Ctau,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=8,1Cycle 5, n=8,1Cycle 11, n=4,0
Part A: TSR-042 and Niraparib 200 mg QD77.362568.550093.8000

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Part C: Tmax,ss of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

,
InterventionHours (Median)
Cycle 2, n=4,4Cycle 5, n=4,3Cycle 11, n=3,1
Part C: TSR-042, Niraparib 200 mg QD and Bevacizumab4.9502.1582.000
Part C: TSR-042, Niraparib 300 mg QD and Bevacizumab3.9581.9672.083

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Part A: Cmax,ss of TSR-042

Blood samples were collected at indicated time points. PK parameters of TSR-042 were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 4: Pre-dose, 0.5, 2, 24, 96, 168, 336 and 504 hours post-dose; Cycles 5 and 11: Pre-dose, 0.5, 2, 24, 96, 168, 336, 504 and 1008 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 4, n=9,4Cycle 5, n=8,1
Part A: TSR-042 and Niraparib 300 mg QD178.5000319.0000

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Part A: Cmax at Steady State (Cmax,ss) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 2, n=10,3Cycle 5, n=7,0Cycle 11, n=2,0
Part A: TSR-042 and Niraparib 200 mg QD0.9259000.8390710.768000

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Part A: Cmax at Steady State (Cmax,ss) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycle 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose; Cycles 5 and 11: Pre-dose, 2 hours post-dose (each cycle was 21 days)

InterventionMicrogram per milliliter (Mean)
Cycle 2, n=10,3
Part A: TSR-042 and Niraparib 300 mg QD1.706667

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Part A: Clearance After Oral Administration (CL/F) of Niraparib

Blood samples were collected at indicated time points. PK parameters of niraparib were calculated using non-compartmental methods. (NCT03307785)
Timeframe: Cycles 1 and 2: Pre-dose, 1, 2, 4, 6, 8 and 24 hours post-dose (each cycle was 21 days)

InterventionLiter per hour (Mean)
Cycle 1, n=1,0Cycle 2, n=8,2
Part A: TSR-042 and Niraparib 200 mg QD28.563816.6295

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Stage 1 : Cohort 2: Progression-free Survival

Progression-free survival was defined as the time from the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. Progression was defined using RECIST v1.1 as a 20% increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions or the appearance of one or more new lesions. (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionMonths (Median)
Stage 1 (Cohort 2): Niraparib + Pembrolizumab4.2

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Stage 1 : Cohort 3: Disease Control Rate

Disease Control Rate was defined as the percentage of participants with a best overall response of CR, PR or SD per RECIST v1.1; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 6 months

InterventionPercentage of participants (Number)
Stage 1 (Cohort 3): Niraparib50.0

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Stage 1 : Cohort 3: Progression-free Survival

Progression-free survival was defined as the time from the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. Progression was defined using RECIST v1.1 as a 20% increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions or the appearance of one or more new lesions. (NCT03308942)
Timeframe: Up to a maximum of 6 months

InterventionMonths (Median)
Stage 1 (Cohort 3): Niraparib4.0

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Stage 1: Cohort 1: Duration of Response

Duration of Response was defined as the time from first documented CR or PR until the subsequently documented disease progression by RECIST v1.1 or death, whichever occurs earlier; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 millimeter (mm) in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03308942)
Timeframe: Up to a maximum of 45 months

InterventionMonths (Median)
Stage 1 (Cohort 1): Niraparib + Pembrolizumab22.8

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Stage 1: Cohort 1: Number of Participants Discontinuing the Study Due to AEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. Number of participants discontinuing the study due to AEs have been summarized. (NCT03308942)
Timeframe: Up to a maximum of 45 months

InterventionParticipants (Count of Participants)
Stage 1 (Cohort 1): Niraparib + Pembrolizumab10

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Stage 1: Cohort 1: Objective Response Rate (ORR)

ORR is the percentage of participants with a confirmed best overall response (BOR) of complete response (CR) or partial response (PR) in the analysis population where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 millimeters (mm) in the short axis. PR=At least a 30 percent (%) decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Tumor assessment was done by the Investigator per Response Evaluation Criteria in Solid Tumors (RECIST) version (v)1.1. Data has been presented for participants with NSCLC whose tumors have high PD-L1 expression (TPS>=50%). Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 29 months

InterventionPercentage of participants (Number)
Stage 1 (Cohort 1): Niraparib + Pembrolizumab56.3

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Stage 1: Cohort 2: Duration of Response

Duration of Response was defined as the time from first documented CR or PR until the subsequently documented disease progression by RECIST v1.1 or death, whichever occurs earlier; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionMonths (Median)
Stage 1 (Cohort 2): Niraparib + Pembrolizumab9.4

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Stage 1: Cohort 2: Objective Response Rate

ORR is the percentage of participants with a confirmed BOR of CR or PR in the analysis population where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Tumor assessment was done by the Investigator per RECIST v1.1. Data has been presented for participants with NSCLC having PD-L1 expression in tumors (TPS: 1 to 49%). Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionPercentage of participants (Number)
Stage 1 (Cohort 2): Niraparib + Pembrolizumab20.0

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Stage 1: Cohort 3: Number of Participants Discontinuing the Study Due to AEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. Number of participants discontinuing the study due to AEs have been summarized. (NCT03308942)
Timeframe: Up to a maximum of 6 months

InterventionParticipants (Count of Participants)
Stage 1 (Cohort 3): Niraparib1

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Stage 1: Cohort 3: Objective Response Rate

ORR is the percentage of participants with a confirmed BOR of CR or PR in the analysis population where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Tumor assessment was done by the Investigator per RECIST v1.1. Data is presented for participants with locally advanced and metastatic squamous NSCLC. Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 6 months

InterventionPercentage of participants (Number)
Stage 1 (Cohort 3): Niraparib0

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Stage 2: Cohort 1A and Cohort 2A: Objective Response Rate

ORR is the percentage of participants with a confirmed BOR of CR or PR in the analysis population where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Tumor assessment was done by the Investigator per RECIST v1.1. Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionPercentage of participants (Number)
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)9.1

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Stage 2: Cohorts 1A and 2A: Disease Control Rate

Disease Control Rate was defined as the percentage of participants with a best overall response of CR, PR or SD per RECIST v1.1; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 29 months

InterventionPercentage of participants (Number)
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)54.5

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Stage 2: Cohorts 1A and 2A: Duration of Response

Duration of Response was defined as the time from first documented CR or PR until the subsequently documented disease progression by RECIST v1.1 or death, whichever occurs earlier; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. (NCT03308942)
Timeframe: Up to a maximum of 29 months

InterventionMonths (Median)
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)21.5

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Stage 2: Cohorts 1A and 2A: Number of Participants Discontinuing the Study Due to AEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. Number of participants discontinuing the study due to AEs have been summarized. (NCT03308942)
Timeframe: Up to maximum 29 months

InterventionParticipants (Count of Participants)
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)2

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Stage 2: Cohorts 1A and 2A: Progression-free Survival

Progression-free survival was defined as the time from the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. Progression was defined using RECIST v1.1 as a 20% increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions or the appearance of one or more new lesions. (NCT03308942)
Timeframe: Up to a maximum of 29 months

InterventionMonths (Median)
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)4.4

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Stage 1: Cohort 1: Number of Participants With Non-serious Adverse Events (Non-SAEs) and Serious Adverse Events (SAEs)

An adverse event (AE) is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that, at any dose that results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not Serious Adverse Events were considered as Non-Serious adverse events (NCT03308942)
Timeframe: Up to a maximum of 45 months

InterventionParticipants (Count of Participants)
Any SAEAny non-SAE
Stage 1 (Cohort 1): Niraparib + Pembrolizumab1117

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Stage 1: Cohort 1: Plasma Concentration of Niraparib Following Combination Therapy of Niraparib and Pembrolizumab

Blood samples were collected at indicated time points. (NCT03308942)
Timeframe: Cycle 1 Day 1(Pre-dose and 30 Minutes, 1 Hour, 2 Hours, 4 Hours, 8 Hours, 96 Hours, 168 Hours Post-dose); Cycles 2, 4, 8 (Pre-dose and 4 Hours Post-dose) (each cycle of 21 days)

InterventionNanograms per milliliter (Mean)
Cycle 1 Day 1; Pre-doseCycle 1 Day 1; 30 Minutes Post-doseCycle 1 Day 1; 1 Hour Post-doseCycle 1 Day 1; 2 Hours Post-doseCycle 1 Day 1; 4 Hours Post-doseCycle 1 Day 1; 8 Hours Post-doseCycle 1 Day 1; 96 Hours Post-doseCycle 1 Day 1; 168 Hours Post-doseCycle 2; Pre-doseCycle 2; 4 Hours Post-doseCycle 4; Pre-doseCycle 4; 4 Hours Post-doseCycle 8; Pre-doseCycle 8; 4 Hours Post-dose
Stage 1 (Cohort 1): Niraparib + Pembrolizumab28.420150073333535314001440360959600794460727

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Stage 1: Cohort 2: Number of Participants With Non-SAEs and SAEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that, at any dose that results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not Serious Adverse Events were considered as Non-Serious adverse events (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionParticipants (Count of Participants)
Any SAEAny non-SAE
Stage 1 (Cohort 2): Niraparib + Pembrolizumab1420

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Stage 1: Cohort 2: Plasma Concentration of Niraparib Following Combination Therapy of Niraparib and Pembrolizumab

Blood samples were collected at indicated time points. (NCT03308942)
Timeframe: Cycle 1 Day 1 (Pre-dose and 30 Minutes, 1, 2, 4, 8, 24, 168, 336 Hours Post-dose), Cycles 2, 8 (Pre-dose and 4 Hours Post-dose), Cycle 4 (Pre-dose and 30 Minutes, 1, 2, 4, 8, 24, 96, 168, 336 Hours Post-dose) (each cycle of 21 days)

InterventionNanograms per milliliter (Mean)
Cycle 1 Day 1; Pre-doseCycle 1 Day 1; 30 Minutes Post-doseCycle 1 Day 1; 1 Hour Post-doseCycle 1 Day 1; 2 Hours Post-doseCycle 1 Day 1; 4 Hours Post-doseCycle 1 Day 1; 8 Hours Post-doseCycle 1 Day 1; 24 Hours Post-doseCycle 1 Day 1; 168 Hours Post-doseCycle 1 Day 1; 336 Hours Post-doseCycle 2; Pre-doseCycle 2; 4 Hours Post-doseCycle 4; Pre-doseCycle 4; 30 Minutes Post-doseCycle 4; 1 Hour Post-doseCycle 4; 2 Hours Post-doseCycle 4; 4 Hours Post-doseCycle 4; 8 Hours, Post-doseCycle 4; 24 Hours Post-doseCycle 4; 96 HoursCycle 4; 168 HoursCycle 4; 336 HoursCycle 8; Pre-doseCycle 8; 4 Hours post-dose
Stage 1 (Cohort 2): Niraparib + PembrolizumabNA24.51892643452383187598087671170805841126012901040978660773767924342602

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Stage 1: Cohort 3: Number of Participants With Non-SAEs and SAEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that, at any dose that results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not Serious Adverse Events were considered as Non-Serious adverse events (NCT03308942)
Timeframe: Up to a maximum of 6 months

InterventionParticipants (Count of Participants)
Any SAEAny non-SAE
Stage 1 (Cohort 3): Niraparib13

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Stage 1: Cohort 3: Plasma Concentration of Niraparib Following Niraparib Monotherapy

Blood samples were collected at indicated time points. (NCT03308942)
Timeframe: Cycle 1 Day 1 (Pre-dose and 4 Hours Post-dose), Cycles 2, 4 and 8 (Pre-dose and 4 Hours Post-dose) (each cycle of 21 days)

InterventionNanograms per milliliter (Mean)
Cycle 1 Day 1; Pre-doseCycle 1 Day 1; 4 Hours Post-doseCycle 2; Pre-doseCycle 2; 4 Hours Post-doseCycle 4; Pre-doseCycle 4; 4 Hours Post-doseCycle 8; Pre-doseCycle 8; 4 Hours Post-dose
Stage 1 (Cohort 3): NiraparibNA279469717615871478913

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Stage 2: Cohorts 1A and 2A: Number of Participants With Non-SAEs and SAEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. A SAE is defined as any untoward medical occurrence that, at any dose that results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability or incapacity, is a congenital anomaly or birth defect, is an important medical event(s) as per medical and scientific judgment. Adverse events which were not Serious Adverse Events were considered as Non-Serious adverse events. (NCT03308942)
Timeframe: Up to a maximum of 29 months

InterventionParticipants (Count of Participants)
Any SAEAny non-SAE
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)712

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Stage 2: Cohorts 1A and 2A: Plasma Concentration of Niraparib Following Combination Therapy of Niraparib and TSR-042 (Dostarlimab)

Blood samples were collected at indicated time points. (NCT03308942)
Timeframe: Cycle 1 Day 1 (Pre-dose and 4 Hours Post-dose), Cycles 2, 4 and 9 (Pre-dose and 4 Hours Post-dose) (each cycle of 21 days)

InterventionNanograms per milliliter (Mean)
Cycle 1 Day 1; Pre-doseCycle 1 Day 1; 4 Hours Post-doseCycle 2; Pre-doseCycle 2; 4 Hours Post-doseCycle 4; Pre-doseCycle 4; 4 Hours Post-doseCycle 9; Pre-doseCycle 9; 4 Hours Post-dose
Stage 2 (Cohort 1A): Niraparib + TSR-042 (Dostarlimab)NA328669967486795456766

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Stage 1: Cohort 2: Number of Participants Discontinuing the Study Due to AEs

An AE is any untoward medical occurrence that occurs in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. Number of participants discontinuing the study due to AEs have been summarized. (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionParticipants (Count of Participants)
Stage 1 (Cohort 2): Niraparib + Pembrolizumab9

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Stage 1 : Cohort 1: Disease Control Rate

Disease Control Rate was defined as the percentage of participants with a best overall response of CR, PR or SD per RECIST v1.1; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 45 months

InterventionPercentage of participants (Number)
Stage 1 (Cohort 1): Niraparib + Pembrolizumab87.5

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Stage 1 : Cohort 1: Progression-free Survival

Progression-free survival was defined as the time from the date of first dose to the date of disease progression or death due to any cause, whichever occurs earlier. Progression was defined using RECIST v1.1 as a 20% increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions or the appearance of one or more new lesions. (NCT03308942)
Timeframe: Up to a maximum of 45 months

InterventionMonths (Median)
Stage 1 (Cohort 1): Niraparib + Pembrolizumab8.4

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Stage 1 : Cohort 2: Disease Control Rate

Disease Control Rate was defined as the percentage of participants with a best overall response of CR, PR or SD per RECIST v1.1; where CR=Disappearance of all target lesions. Any pathological lymph nodes must be <10 mm in the short axis. PR=At least a 30% decrease in the sum of the diameters of target lesions, taking as a reference, the Baseline sum of the diameters. Confidence interval was calculated using binomial exact method. (NCT03308942)
Timeframe: Up to a maximum of 17 months

InterventionPercentage of participants (Number)
Stage 1 (Cohort 2): Niraparib + Pembrolizumab70.0

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Number of Participants With TEAEs Leading to Niraparib Dose Reductions

TEAE is defined as any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAES leading to Niraparib dose reductions are reported. (NCT03326193)
Timeframe: Up to a maximum of 33.68 months

InterventionParticipants (Count of Participants)
Niraparib + Bevacizumab81

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Number of Participants With TEAEs Leading to Niraparib Treatment Discontinuation

TEAE is defined as any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with TEAEs leading to Niraparib treatment discontinuation are reported. (NCT03326193)
Timeframe: Up to a maximum of 33.68 months

InterventionParticipants (Count of Participants)
Niraparib + Bevacizumab30

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Number of Participants With Non-serious Treatment-emergent Adverse Events (TEAEs)

TEAE is defined as any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. Number of participants with non-serious TEAEs with 5% threshold are reported. (NCT03326193)
Timeframe: Up to a maximum of 33.68 months

InterventionParticipants (Count of Participants)
Niraparib + Bevacizumab105

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Progression Free Survival (PFS) Rate

PFS rate at 18 months is defined as the percentage of participants who have not progressed or died within 18 months after niraparib combined with bevacizumab treatment initiation. Progression was assessed by response evaluation criteria in solid tumors (RECIST) version (v) 1.1 criteria per Investigator assessment and defined as a 20 percent (%) increase in the sum of the diameter of target lesions or unequivocal progression of existing non-target lesions. Survival rate is the percentage of participants without progression assessed by RECIST v1.1 or death by the landmark timepoint. Confidence intervals was constructed using exact method. (NCT03326193)
Timeframe: At 18 months

InterventionPercentage of participants (Number)
Niraparib + Bevacizumab62

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Percent Change From Baseline in Tumor Volume Measured by MRI

Percentage change in tumor volume from Baseline after 2 months of niraparib treatment was measured using MRI. Baseline was defined as the most recent measurement prior to the first administration of niraparib. Tumor volume was calculated as (length × width × height × π)/6. The percentage reduction in tumor volume was set as 99% if the tumor becomes too small to measure at the post-baseline visit. Percent change from Baseline was defined as value of post Baseline minus Baseline value and multiplied by 100. (NCT03329937)
Timeframe: Baseline and at 2 months

InterventionPercent change (Mean)
Niraparib 200 mg-77.0

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Percent Change From Baseline in Tumor Volume Measured by Ultrasound

Percentage change in tumor volume from Baseline was measured using ultrasound. Baseline was defined as the most recent measurement prior to the first administration of niraparib. Tumor volume was calculated as (length × width × height × π)/6. The percentage reduction in tumor volume was set as 99% if the tumor becomes too small to measure at the post-baseline visit. Percent change from Baseline was defined as greatest change in volume, derived from all available cycles of niraparib (range from cycle 2 to 6) and multiplied by 100. (NCT03329937)
Timeframe: Baseline and up to 6 months

InterventionPercent change (Mean)
Niraparib 200 mg-83.4

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Percentage of Participants With Pathological Complete Response (pCR)

pCR is defined as ypT0/Tis ypN0 by receipt of pre-operative chemotherapy (Yes versus No). Following neoadjuvant therapy, pathological staging is recorded using the 'yp' designation. ypT0/Tis ypN0 is the absence of invasive cancer in the breast and axillary nodes. pCR is defined as the absence of residual invasive cancer on hematoxylin and eosin evaluation of the complete resected breast specimen and all sampled regional lymph nodes following completion of neoadjuvant systemic therapy (i.e., ypT0/Tis ypN0 in the current American Joint Committee on Cancer [AJCC] staging system). Percentage of participants with pCR rate its 95 percent CI has been presented. CI was based on binomial exact CI. (NCT03329937)
Timeframe: Up to 1 year

InterventionPercentage of participants (Number)
Niraparib 200 mg38.1

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Percentage of Participants With Tumor Response as Measured by Breast Ultrasound

Tumor response rate was based on the change in tumor volume as measured by breast ultrasound; a response was considered >=30 percent reduction of tumor volume from Baseline without any new lesion development. Tumor volume was calculated as (length × width × height × π)/6. Percentage of participants with tumor response and its 95 percent CI has been presented. CI was based on binomial exact CI. (NCT03329937)
Timeframe: Up to 6 months

InterventionPercentage of participants (Number)
Niraparib 200 mg95.2

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Percentage of Participants With Tumor Response Measured by Breast MRI

Tumor response measured by breast MRI is defined as >=30 percent (%) reduction of tumor volume from Baseline based on primary lesion after niraparib treatment without any new lesion development. Tumor volume was calculated as (length × width × height × pi [π])/6. Responses were assessed as Clinical complete response (CR): A complete disappearance of all tumor signs in the breast as assessed by imaging test. Clinical partial response (PR): A reduction in the tumor volume of the primary tumor size by >=30% assessed by palpation or imaging test. Clinical stable disease (SD): No significant change in tumor volume during treatment. Clinical progressive disease (cPD): The development of new, previously undetected lesions, or an estimated increase in the size of the primary lesion by greater than 20%. Percentage of participants with tumor response and its 95 percent confidence interval (CI) has been presented. The 95% CI was the binomial exact CI based on Clopper-Pearson method. (NCT03329937)
Timeframe: At 2 months

InterventionPercentage of participants (Number)
Niraparib 200 mg90.5

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Number of Participants With Treatment Emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), Treatment Discontinuations and Dose Reductions Due to Adverse Events (AEs)

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study treatment, whether or not considered related to the study treatment. An SAE is defined as any untoward medical occurrence that, at any dose results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect, or an important medical event. A TEAE is any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. (NCT03329937)
Timeframe: Up to 1 year

InterventionParticipants (Count of Participants)
Any TEAEAny SAEAny TEAEs leading to nirapirib reductionAny TEAEs leading to niraparib discontinuation
Niraparib 200 mg21240

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Change From Baseline in Clinical Chemistry Parameter of Amylase During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter: Amylase. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionUnits per Liter (Mean)
Cycle 2 Day 1, n=4, 2Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-2.5-4.0

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Change From Baseline in Clinical Chemistry Parameter of Amylase During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter: Amylase. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionUnits per Liter (Mean)
Cycle 2 Day 1, n=4, 2Cycle 3 Day 1, n=3, 1Cycle 4 Day 1, n=3, 0Cycle 5 Day 1, n=3, 0Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function-1.0-7.0-2.33.0-2.5

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Change From Baseline in Clinical Chemistry Parameter of Bilirubin and Creatinine During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter: Bilirubin and Creatinine. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionMicromoles per liter (Mean)
Bilirubin, Cycle 2 Day 1, n=6, 2Bilirubin, Cycle 3 Day 1, n=3, 1Bilirubin, Cycle 4 Day 1, n=3, 0Bilirubin, Cycle 5 Day 1, n=3, 0Bilirubin, Cycle 6 Day1, n=2, 0Creatinine, Cycle 2 Day 1, n=6, 2Creatinine, Cycle 3 Day 1, n=3, 1Creatinine, Cycle 4 Day 1, n=3, 0Creatinine, Cycle 5 Day 1, n=3, 0Creatinine, Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function0.90.60.62.9-0.97.513.00.95.65.7

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Change From Baseline in Clinical Chemistry Parameter of Bilirubin and Creatinine During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter: Bilirubin and Creatinine. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionMicromoles per liter (Mean)
Bilirubin, Cycle 2 Day 1, n=6, 2Bilirubin, Cycle 3 Day 1, n=3, 1Creatinine, Cycle 2 Day 1, n=6, 2Creatinine, Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-6.01.718.10.0

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Change From Baseline in Clinical Chemistry Parameter of Bilirubin and Creatinine During PK Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameters: Bilirubin and Creatinine. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and Day 8

,
InterventionMicromoles per liter (Mean)
BilirubinCreatinine
Participants With Impaired Hepatic Function8.3-0.7
Participants With Normal Hepatic Function0.6-1.9

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Change From Baseline in Clinical Chemistry Parameter of Protein and Albumin During Extension Phase

Blood samples were collected to analyze clinical chemistry parameters: protein and albumin. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionGrams per liter (Mean)
Protein, Cycle 2 Day 1, n=6, 2Protein, Cycle 3 Day 1, n=3, 1Protein, Cycle 4 Day 1, n=3, 0Protein, Cycle 5 Day 1, n=3, 0Protein, Cycle 6 Day1, n=2, 0Albumin, Cycle 2 Day 1, n=6, 2Albumin, Cycle 3 Day 1, n=3, 1Albumin, Cycle 4 Day 1, n=3, 0Albumin, Cycle 5 Day 1, n=3, 0Albumin, Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function-1.0-2.01.04.00.00.31.02.74.717.0

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Change From Baseline in Clinical Chemistry Parameter of Alkaline Phosphatase, Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and Lactate Dehydrogenase (LDH) During PK Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameters: alkaline phosphatase, ALT, AST and LDH. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and Day 8

,
InterventionInternational units per Liter (Mean)
Alkaline phosphataseASTALTLDH
Participants With Impaired Hepatic Function-32.6-6.4-4.4-58.5
Participants With Normal Hepatic Function26.334.624.336.0

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Change From Baseline in Clinical Chemistry Parameter of Protein and Albumin During Extension Phase

Blood samples were collected to analyze clinical chemistry parameters: protein and albumin. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionGrams per liter (Mean)
Protein, Cycle 2 Day 1, n=6, 2Protein, Cycle 3 Day 1, n=3, 1Albumin, Cycle 2 Day 1, n=6, 2Albumin, Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-2.0-5.0-1.0-1.0

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Change From Baseline in Clinical Chemistry Parameter of Protein and Albumin During PK Phase

Blood samples were collected to analyze clinical chemistry parameters: protein and albumin. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and Day 8

,
InterventionGrams per liter (Mean)
ProteinAlbumin
Participants With Impaired Hepatic Function-3.5-2.3
Participants With Normal Hepatic Function-1.0-0.9

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Change From Baseline in Hb During Extension Phase

Blood samples were collected from participants for evaluation of Hb. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 1 (Days 8, 15, 21), Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1, and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionGrams per liter (Mean)
Cycle 1 Day 8, n=8, 5Cycle 1 Day 15, n=8, 4Cycle 1 Day 21, n=7, 4Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function1.0-8.3-22.3-15.0-10.0

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Change From Baseline in Hb During Extension Phase

Blood samples were collected from participants for evaluation of Hb. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 1 (Days 8, 15, 21), Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1, and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionGrams per liter (Mean)
Cycle 1 Day 8, n=8, 5Cycle 1 Day 15, n=8, 4Cycle 1 Day 21, n=7, 4Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1Cycle 4 Day 1, n=3, 0Cycle 5 Day 1, n=3, 0Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function4.3-0.5-2.6-8.0-16.7-10.7-3.73.0

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Change From Baseline in Hemoglobin (Hb) During PK Phase

Blood samples were collected from participants for evaluation of Hb. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and at Day 8

InterventionGrams per liter (Mean)
Participants With Normal Hepatic Function-0.5
Participants With Impaired Hepatic Function0.6

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Change From Baseline in Platelets, Neutrophils, Monocytes, Lymphocytes and Leukocyte During PK Phase

Blood samples were collected to analyze hematology parameters:Leukocyte, Lymphocytes, Monocytes, Neutrophils and Platelets. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and Day 8

,
Intervention10^9 cells per liter (Mean)
LymphocytesMonocytesNeutrophilsPlateletsLeukocyte
Participants With Impaired Hepatic Function-0.1-0.1-0.7-23.4-0.8
Participants With Normal Hepatic Function0.20.1-0.5-18.4-0.2

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Change From Baseline in Platelets, Neutrophils, Monocytes, Lymphocytes and Leukocytes During Extension Phase

Blood samples were collected to analyze hematology parameters: Lymphocytes, Leukocytes, Monocytes, Neutrophils and Platelets. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 1 (Days 8, 15, 21), Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1, and Cycle 6 Day 1 (each cycle was of 28 days)

Intervention10^9 cells per liter (Mean)
Lymphocytes, Cycle 1 Day 8, n=7, 5Lymphocytes, Cycle 1 Day 15, n=8, 4Lymphocytes, Cycle 1 Day 21, n=7, 4Lymphocytes, Cycle 2 Day 1, n=6, 2Lymphocytes, Cycle 3 Day 1, n=3, 1Monocytes, Cycle 1 Day 8, n=7, 5Monocytes, Cycle 1 Day 15, n=8, 4Monocytes, Cycle 1 Day 21, n=7, 4Monocytes, Cycle 2 Day 1, n=6, 2Monocytes, Cycle 3 Day 1, n=3, 1Neutrophils, Cycle 1 Day 8, n=7, 5Neutrophils, Cycle 1 Day 15, n=8, 4Neutrophils, Cycle 1 Day 21, n=7, 4Neutrophils, Cycle 2 Day 1, n=6, 2Neutrophils, Cycle 3 Day 1, n=3, 1Platelets, Cycle 1 Day 8, n=8, 5Platelets, Cycle 1 Day 15, n=8, 4Platelets, Cycle 1 Day 21, n=7, 4Platelets, Cycle 2 Day 1, n=6, 2Platelets, Cycle 3 Day 1, n=3, 1Leukocytes, Cycle 1 Day 8, n=8, 5Leukocytes, Cycle 1 Day 15, n=8, 4Leukocytes, Cycle 1 Day 21, n=7, 4Leukocytes, Cycle 2 Day 1, n=6, 2Leukocytes, Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-0.1-0.0-0.20.10.20.0-0.1-0.1-0.10.00.40.5-0.2-1.8-0.5-0.8-8.3-19.3-102.559.00.30.4-0.5-1.9-0.2

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Change From Baseline in Platelets, Neutrophils, Monocytes, Lymphocytes and Leukocytes During Extension Phase

Blood samples were collected to analyze hematology parameters: Lymphocytes, Leukocytes, Monocytes, Neutrophils and Platelets. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 1 (Days 8, 15, 21), Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1, and Cycle 6 Day 1 (each cycle was of 28 days)

Intervention10^9 cells per liter (Mean)
Lymphocytes, Cycle 1 Day 8, n=7, 5Lymphocytes, Cycle 1 Day 15, n=8, 4Lymphocytes, Cycle 1 Day 21, n=7, 4Lymphocytes, Cycle 2 Day 1, n=6, 2Lymphocytes, Cycle 3 Day 1, n=3, 1Lymphocytes, Cycle 4 Day 1, n=3, 0Lymphocytes, Cycle 5 Day 1, n=3, 0Lymphocytes, Cycle 6 Day1, n=2, 0Monocytes, Cycle 1 Day 8, n=7, 5Monocytes, Cycle 1 Day 15, n=8, 4Monocytes, Cycle 1 Day 21, n=7, 4Monocytes, Cycle 2 Day 1, n=6, 2Monocytes, Cycle 3 Day 1, n=3, 1Monocytes, Cycle 4 Day 1, n=3, 0Monocytes, Cycle 5 Day 1, n=3, 0Monocytes, Cycle 6 Day1, n=2, 0Neutrophils, Cycle 1 Day 8, n=7, 5Neutrophils, Cycle 1 Day 15, n=8, 4Neutrophils, Cycle 1 Day 21, n=7, 4Neutrophils, Cycle 2 Day 1, n=6, 2Neutrophils, Cycle 3 Day 1, n=3, 1Neutrophils, Cycle 4 Day 1, n=3, 0Neutrophils, Cycle 5 Day 1, n=3, 0Neutrophils, Cycle 6 Day1, n=2, 0Platelets, Cycle 1 Day 8, n=8, 5Platelets, Cycle 1 Day 15, n=8, 4Platelets, Cycle 1 Day 21, n=7, 4Platelets, Cycle 2 Day 1, n=6, 2Platelets, Cycle 3 Day 1, n=3, 1Platelets, Cycle 4 Day 1, n=3, 0Platelets, Cycle 5 Day 1, n=3, 0Platelets, Cycle 6 Day1, n=2, 0Leukocytes, Cycle 1 Day 8, n=8, 5Leukocytes, Cycle 1 Day 15, n=8, 4Leukocytes, Cycle 1 Day 21, n=7, 4Leukocytes, Cycle 2 Day 1, n=6, 2Leukocytes, Cycle 3 Day 1, n=3, 1Leukocytes, Cycle 4 Day 1, n=3, 0Leukocytes, Cycle 5 Day 1, n=3, 0Leukocytes, Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function-0.2-0.1-0.1-0.1-0.30.00.3-0.0-0.1-0.2-0.2-0.1-0.2-0.0-0.1-0.10.40.3-0.60.6-0.0-0.40.5-0.112.0-58.1-81.955.3-46.334.045.734.00.4-0.1-1.00.5-0.5-0.40.9-0.3

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Change From Baseline in Pulse Rate During Extension Phase

Vital sign including pulse rate was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionBeats per minute (Mean)
Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function9.04.0

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Change From Baseline in Pulse Rate During Extension Phase

Vital sign including pulse rate was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionBeats per minute (Mean)
Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1Cycle 4 Day 1, n=3, 0Cycle 5 Day 1, n=3, 0Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function17.223.015.39.316.5

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Change From Baseline in Pulse Rate During PK Phase

Vital sign including pulse rate was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline, Day 2 and Day 8

,
InterventionBeats per minute (Mean)
Day 2, n=9, 7Day 8, n=9, 8
Participants With Impaired Hepatic Function1.3-2.3
Participants With Normal Hepatic Function8.92.8

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Change From Baseline in SBP and DBP During Extension Phase

Vital signs including SBP and DBP were measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionMillimeters of mercury (Mean)
DBP, Cycle 2 Day 1, n=6, 2DBP, Cycle 3 Day 1, n=3, 1DBP, Cycle 4 Day 1, n=3, 0DBP, Cycle 5 Day 1, n=3, 0DBP, Cycle 6 Day1, n=2, 0SBP, Cycle 2 Day 1, n=6, 2SBP, Cycle 3 Day 1, n=3, 1SBP, Cycle 4 Day 1, n=3, 0SBP, Cycle 5 Day 1, n=3, 0SBP, Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function-0.28.7-0.312.36.5-1.26.7-2.35.713.0

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Change From Baseline in SBP and DBP During Extension Phase

Vital signs including SBP and DBP were measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionMillimeters of mercury (Mean)
DBP, Cycle 2 Day 1, n=6, 2DBP, Cycle 3 Day 1, n=3, 1SBP, Cycle 2 Day 1, n=6, 2SBP, Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-12.0-9.0-2.5-6.0

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Change From Baseline in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP) During PK Phase

Vital signs including SBP and DBP were measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline, Day 2 and Day 8

,
InterventionMillimeters of mercury (Mean)
SBP, Day 2, n=9, 7SBP, Day 8, n=9, 8DBP, Day 2, n=9, 7DBP, Day 8, n=9, 8
Participants With Impaired Hepatic Function5.70.32.7-0.1
Participants With Normal Hepatic Function5.90.93.62.4

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Change From Baseline in Temperature During Extension Phase

Vital sign including temperature was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionDegrees Celsius (Mean)
Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function0.10.0

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Change From Baseline in Temperature During Extension Phase

Vital sign including temperature was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionDegrees Celsius (Mean)
Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1Cycle 4 Day 1, n=3, 0Cycle 5 Day 1, n=3, 0Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function-0.3-0.1-0.0-0.1-0.3

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Change From Baseline in Weight During Extension Phase

Weight was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionKilograms (Mean)
Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-4.6-4.5

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Change From Baseline in Weight During Extension Phase

Weight was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionKilograms (Mean)
Cycle 2 Day 1, n=6, 2Cycle 3 Day 1, n=3, 1Cycle 4 Day 1, n=3, 0Cycle 5 Day 1, n=3, 0Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function-1.6-0.3-2.3-3.3-0.4

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Change From Baseline in Weight During PK Phase

Weight was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline, Day 2 and Day 8

,
InterventionKilograms (Mean)
Day 2, n=8, 6Day 8, n=9, 8
Participants With Impaired Hepatic Function0.80.3
Participants With Normal Hepatic Function-0.0-0.0

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Number of Participants With TEAE Including Non-SAEs, SAEs and Discontinuations Due to AEs During Extension Phase

An AE is any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. SAE is defined as any untoward medical occurrence that, at any dose: results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent disability/incapacity; is a congenital anomaly/birth defect; or is an important medical event(s) requiring medical or scientific judgment. Treatment-emergent are any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. (NCT03359850)
Timeframe: Up to 28 months

,
InterventionParticipants (Count of Participants)
Any Non-SAEsAny SAEAny Discontinuations due to AE
Participants With Impaired Hepatic Function721
Participants With Normal Hepatic Function830

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Number of Participants With Treatment-Emergent Adverse Events (TEAE) Including Non-serious Adverse Events (Non-SAEs), Serious Adverse Events (SAEs) and Discontinuations Due to AEs During PK Phase

An AE is any untoward medical occurrence in a participant or clinical investigation participant administered a pharmaceutical product, and which does not necessarily have to have a causal relationship with this treatment. SAE is defined as any untoward medical occurrence that, at any dose: results in death; is life-threatening; requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent disability/incapacity; is a congenital anomaly/birth defect; or is an important medical event(s) requiring medical or scientific judgment. Treatment-emergent are any event that was not present prior to the initiation of study treatment or any event already present that worsens in either intensity or frequency following exposure to study treatment. (NCT03359850)
Timeframe: Up to Day 8

,
InterventionParticipants (Count of Participants)
Any Non -SAEsAny SAEAny Discontinuations due to AE
Participants With Impaired Hepatic Function300
Participants With Normal Hepatic Function511

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Time to Maximum Concentration (Tmax) of Niraparib and M1 During PK Phase

Blood samples were collected at indicated time points to evaluate tmax of niraparib and M1. PK parameters were calculated by standard non-compartmental analysis. (NCT03359850)
Timeframe: Pre-dose, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 120, 168 hours post dose Day 1

,
InterventionHour (Median)
NiraparibM1
Participants With Impaired Hepatic Function4.0917.73
Participants With Normal Hepatic Function4.006.00

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Change From Baseline in Clinical Chemistry Parameter of Amylase During PK Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter: Amylase. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and Day 8

InterventionUnits per Liter (Mean)
Participants With Normal Hepatic Function74.4
Participants With Impaired Hepatic Function0.3

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Change From Baseline in Chemistry Parameters: Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter:Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionMillimoles per liter (Mean)
Glucose, Cycle 2 Day 1, n=6, 2Glucose, Cycle 3 Day 1, n=3, 1Glucose, Cycle 4 Day 1, n=3, 0Glucose, Cycle 5 Day 1, n=3, 0Glucose, Cycle 6 Day1, n=2, 0Calcium, Cycle 2 Day 1, n=6, 2Calcium, Cycle 3 Day 1, n=3, 1Calcium, Cycle 4 Day 1, n=3, 0Calcium, Cycle 5 Day 1, n=3, 0Calcium, Cycle 6 Day1, n=2, 0Chloride, Cycle 2 Day 1, n=6, 2Chloride, Cycle 3 Day 1, n=3, 1Chloride, Cycle 4 Day 1, n=3, 0Chloride, Cycle 5 Day 1, n=3, 0Chloride, Cycle 6 Day1, n=2, 0Phosphate, Cycle 2 Day 1, n=5, 2Phosphate, Cycle 3 Day 1, n=3, 1Phosphate, Cycle 4 Day 1, n=3, 0Phosphate, Cycle 5 Day 1, n=3, 0Phosphate, Cycle 6 Day1, n=2, 0Potassium, Cycle 2 Day 1, n=6, 2Potassium, Cycle 3 Day 1, n=3, 1Potassium, Cycle 4 Day 1, n=3, 0Potassium, Cycle 5 Day 1, n=3, 0Potassium, Cycle 6 Day1, n=2, 0Sodium, Cycle 2 Day 1, n=6, 2Sodium, Cycle 3 Day 1, n=3, 1Sodium, Cycle 4 Day 1, n=3, 0Sodium, Cycle 5 Day 1, n=3, 0Sodium, Cycle 6 Day1, n=2, 0BUN, Cycle 2 Day 1, n=6, 2BUN, Cycle 3 Day 1, n=3, 1BUN, Cycle 4 Day 1, n=3, 0BUN, Cycle 5 Day 1, n=3, 0BUN, Cycle 6 Day1, n=2, 0Magnesium, Cycle 2 Day 1, n=5, 2Magnesium, Cycle 3 Day 1, n=3, 1Magnesium, Cycle 4 Day 1, n=2, 0Magnesium, Cycle 5 Day 1, n=2, 0Magnesium, Cycle 6 Day1, n=1, 0
Participants With Normal Hepatic Function-0.00.7-0.4-0.7-0.8-0.00.00.00.1-0.0-1.7-2.0-0.7-1.7-2.5-0.20.0-0.10.00.0-0.20.10.00.10.1-1.8-3.0-1.0-1.7-1.50.30.7-1.0-0.5-0.5-0.0-0.00.00.10.0

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Change From Baseline in Clinical Chemistry Parameter of Alkaline Phosphatase, ALT, AST and LDH During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameters: alkaline phosphatase, ALT, AST and LDH. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionInternational units per Liter (Mean)
Alkaline Phosphatase, Cycle 2 Day 1, n=6, 2Alkaline Phosphatase, Cycle 3 Day 1, n=3, 1Alkaline Phosphatase, Cycle 4 Day 1, n=3, 0Alkaline Phosphatase, Cycle 5 Day 1, n=3, 0Alkaline Phosphatase, Cycle 6 Day1, n=2, 0ALT, Cycle 2 Day 1, n=6, 2ALT, Cycle 3 Day 1, n=3, 1ALT, Cycle 4 Day 1, n=3, 0ALT, Cycle 5 Day 1, n=3, 0ALT, Cycle 6 Day1, n=2, 0AST, Cycle 2 Day 1, n=6, 2AST, Cycle 3 Day 1, n=3, 1AST, Cycle 4 Day 1, n=3, 0AST, Cycle 5 Day 1, n=3, 0AST, Cycle 6 Day1, n=2, 0LDH, Cycle 2 Day 1, n=3, 2LDH, Cycle 3 Day 1, n=3, 1LDH, Cycle 4 Day 1, n=3, 0LDH, Cycle 5 Day 1, n=3, 0LDH, Cycle 6 Day1, n=2, 0
Participants With Normal Hepatic Function23.319.720.012.01.511.84.72.05.32.04.82.04.35.35.511.76.7-11.7-5.319.0

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Change From Baseline in Clinical Chemistry Parameter of Alkaline Phosphatase, ALT, AST and LDH During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameters: alkaline phosphatase, ALT, AST and LDH. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionInternational units per Liter (Mean)
Alkaline Phosphatase, Cycle 2 Day 1, n=6, 2Alkaline Phosphatase, Cycle 3 Day 1, n=3, 1ALT, Cycle 2 Day 1, n=6, 2ALT, Cycle 3 Day 1, n=3, 1AST, Cycle 2 Day 1, n=6, 2AST, Cycle 3 Day 1, n=3, 1LDH, Cycle 2 Day 1, n=3, 2LDH, Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function-53.557.0-6.54.0-25.04.0-625.0-9.0

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Apparent Total Body Clearance (CL/F) of Niraparib and M1 During PK Phase

CL/F is calculated as Dose/(AUC 0-inf). Blood samples were collected at indicated time points to evaluate CL/F of niraparib and M1. PK parameters were calculated by standard non-compartmental analysis. Not applicable (NA) indicates that CL/F could not be measured for M1 since the dose of metabolite is unknown and only known dose is that of parent niraparib. (NCT03359850)
Timeframe: Pre-dose, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 120, 168 hours post dose Day 1

,
InterventionLiters per hour (Geometric Mean)
NiraparibM1
Participants With Impaired Hepatic Function9.74NA
Participants With Normal Hepatic Function15.2NA

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Area Under the Plasma Concentration-time Curve From Time 0 Extrapolated to Infinity (AUC 0-infinity) of Niraparib and M1 During PK Phase

Blood samples were collected at indicated time points to evaluate AUC (0-infinity) of niraparib and M1. PK parameters were calculated by standard non-compartmental analysis. (NCT03359850)
Timeframe: Pre-dose, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 120, 168 hours post dose Day 1

,
InterventionHour*nanogram per milliliter (hr*ng/mL) (Geometric Mean)
Niraparib, n= 9, 7M1, n=9, 3
Participants With Impaired Hepatic Function3080021500
Participants With Normal Hepatic Function1970020700

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Area Under the Plasma Concentration-time Curve From Time 0 to the Time of the Last Quantifiable Concentration (AUClast) of Niraparib and Its Major Metabolite (M1) During PK Phase

Blood samples were collected at indicated time points to evaluate AUC (last) of niraparib and M1. PK parameters were calculated by standard non-compartmental analysis. (NCT03359850)
Timeframe: Pre-dose, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 120, 168 hours post dose Day 1

,
InterventionHour*nanogram per milliliter (hr*ng/mL) (Geometric Mean)
NiraparibM1
Participants With Impaired Hepatic Function2680012400
Participants With Normal Hepatic Function1850019000

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Change From Baseline in Body Temperature During PK Phase

Vital sign including body temperature was measured at indicated time-points. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline, Day 2 and Day 8

,
InterventionDegrees Celsius (Mean)
Day 2, n=9, 7Day 8, n=9, 8
Participants With Impaired Hepatic Function0.10.1
Participants With Normal Hepatic Function-0.00.1

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Terminal Half-life (t½) of Niraparib and M1 During PK Phase

Blood samples were collected at indicated time points to evaluate t1/2 of niraparib and M1. PK parameters were calculated by standard non-compartmental analysis. (NCT03359850)
Timeframe: Pre-dose, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 120, 168 hours post dose Day 1

,
InterventionHour (Geometric Mean)
Niraparib, n=9, 7M1, n=9, 3
Participants With Impaired Hepatic Function54.843.7
Participants With Normal Hepatic Function43.947.9

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Observed Maximum Plasma Concentration (Cmax) of Niraparib and M1 During PK Phase

Blood samples were collected at indicated time points to evaluate Cmax of niraparib and M1. PK parameters were calculated by standard non-compartmental analysis. (NCT03359850)
Timeframe: Pre-dose, 1, 2, 3, 4, 6, 8, 12, 24, 48, 72, 120, 168 hours post dose Day 1

,
InterventionNanogram per milliliter (Geometric Mean)
NiraparibM1
Participants With Impaired Hepatic Function553151
Participants With Normal Hepatic Function594398

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Change From Baseline in Chemistry Parameters: Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and Blood Urea Nitrogen (BUN) During PK Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter:Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN. Baseline is defined as the most recent measurement prior to the first administration of study drug in PK phase. Change from Baseline was calculated as post dose value minus Baseline value. (NCT03359850)
Timeframe: Baseline and Day 8

,
InterventionMillimoles per liter (Mean)
Glucose, n=8, 8Calcium, n=8, 8Chloride, n=8, 8Phosphate, n=8, 8Potassium, n=8, 8Sodium, n=8, 8BUN, n=8, 8Magnesium, n=8, 7
Participants With Impaired Hepatic Function-0.5-0.1-0.3-0.1-0.2-0.5-0.10.0
Participants With Normal Hepatic Function-0.80.01.80.1-0.21.6-0.4-0.0

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Change From Baseline in Chemistry Parameters: Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN During Extension Phase

Blood samples were collected at indicated time-points for analysis of clinical chemistry parameter:Glucose, Calcium, Chloride, Phosphate, Potassium, Sodium, Magnesium and BUN. Baseline is defined as the most recent measurement prior to the first administration of study drug in extension phase. Change from Baseline was calculated as post dose value minus Baseline value. NA indicates standard deviation could not be calculated as a single participant was analyzed. (NCT03359850)
Timeframe: Baseline and Cycle 2 Day 1, Cycle 3 Day 1, Cycle 4 Day 1, Cycle 5 Day 1 and Cycle 6 Day 1 (each cycle was of 28 days)

InterventionMillimoles per liter (Mean)
Glucose, Cycle 2 Day 1, n=6, 2Glucose, Cycle 3 Day 1, n=3, 1Calcium, Cycle 2 Day 1, n=6, 2Calcium, Cycle 3 Day 1, n=3, 1Chloride, Cycle 2 Day 1, n=6, 2Chloride, Cycle 3 Day 1, n=3, 1Phosphate, Cycle 2 Day 1, n=5, 2Phosphate, Cycle 3 Day 1, n=3, 1Potassium, Cycle 2 Day 1, n=6, 2Potassium, Cycle 3 Day 1, n=3, 1Sodium, Cycle 2 Day 1, n=6, 2Sodium, Cycle 3 Day 1, n=3, 1BUN, Cycle 2 Day 1, n=6, 2BUN, Cycle 3 Day 1, n=3, 1Magnesium, Cycle 2 Day 1, n=5, 2Magnesium, Cycle 3 Day 1, n=3, 1
Participants With Impaired Hepatic Function1.6-2.30.00.0-3.50.00.3-0.10.10.4-1.51.01.81.40.00.1

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Rate of Progression-free Survival at 6 Months (PFS6)

"The PFS6 rate will be estimated using the Kaplan-Meier method, and the 95% confidence interval will be estimated from the Kaplan-Meier curve. The null hypothesis is that the PFS6 rate in this population of subjects is 44%.~Progressive disease is defined as at least a 20% increase in the sum of all the longest diameter (LD) 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 5mm. The appearance of one or more new lesions is also considered progression.~Target lesions assessed according to RECIST v1.1." (NCT03404960)
Timeframe: 6 months after initiation of study therapy

Interventionpercentage of participants with PFS (Number)
Niraparib + Nivolumab (Arm A)20.6
Niraparib + Ipilimumab (Arm B)59.6

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Combination 1: Part 1: Number of Participants With Specified Toxicity

Number of participants with specified toxicity during Cycle 1 was reported. Only toxicities that occurred during safety evaluation period(defined as first 28 days of treatment-Cycle 1 of Part 1) was used for analysis of specified toxicities and for dose reduction decisions. Toxicities were graded for severity as per NCI-CTCAE, version 4.03. Safety evaluation criteria were: Any Grade(G) >=3 non-hematological toxicity without anorexia, or constipation, fatigue improved to G<=2 in <7 days, vomiting and diarrhea resolved in <=3 days, laboratory abnormalities with hospitalization, tumor flare improved to G<=2 in <=7 days, elevation in AST/ALT for <=7 days and G3 hypertension controlled by medical therapy; any treatment-related(TR)G4 or G>=3 thrombocytopenia required platelet transfusion; Any TR G4 neutropenia >=7 days or G3 or 4 neutropenia with infection/fever >38.5 degrees Celsius; Any TR SAE or intolerable toxicity. (NCT03431350)
Timeframe: Cycle 1 (28 days)

InterventionParticipants (Count of Participants)
Combination 1: Part 1 (Dose Seletion): Niraparib 200 mg + Cetrelimab 240 mg0
Combination 1: Part 1 (Dose Selection): Niraparib 200 mg + Cetrelimab 480 mg0

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Combination 2: Composite Response Rate (RR)

Composite response rate was defined as the percentage of participants who had a composite response which is defined as one of the following PCWG3 criteria: Objective response (percentage of participants with measurable disease who achieved a best response of either CR or PR as assessed by RECIST 1.1 with no evidence of bone progression according to PCWG3 criteria) (confirmed per RECIST 1.1), or; circulating tumor cells (CTC) response: defined as CTC=0 per 7.5 milliliters (mL) of blood at 8 weeks for participants who had CTC greater than or equal to (>=) 1 at baseline or CTC less than (<) 5 per 7.5 mL with CTC >=5 at baseline, confirmed by a second consecutive value obtained 4 or more weeks later, or prostate-specific antigen (PSA) declined of >=50 percentage (%), measured twice 3 to 4 weeks apart. This outcome measure was analyzed for specified arms only as pre-planned in the protocol. (NCT03431350)
Timeframe: Up to 31 months

InterventionPercentage of participants (Number)
Combination 2: Cohort 2A: Niraparib+Abiraterone Acetate+Prednisone75.0
Combination 2: Cohort 2C: Niraparib+Abiraterone Acetate+Prednisone55.6
Combination 2: Cohort 2D: Niraparib+Abiraterone Acetate+Prednisone33.3

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Combination 3: Maximum Observed Plasma Concentration (Cmax) of Niraparib Normalized by the Dose(Niraparib) (Cmax/Dose) of Niraparib Administered With AA After a Single Dose

Cmax/dose of niraparib was defined as maximum observed plasma concentration of niraparib Cmax normalized by the dose of niraparib administered with AA after a single dose. (NCT03431350)
Timeframe: Pre-dose, 30 min, 1 hour (hr), 1.5 hr, 2hr, 3 hr, 4 hr, 6 hr, 8 hr, 10 hr, 24 hr, 48 hr, 72 hr, and 168 hr post dose on Day 1

Interventionnanograms per milliliter per milligram (Mean)
Combination 3: Cohort 1A: Niraparib + Abiraterone Acetate, SA2.14
Combination 3: Cohort 1B: Niraparib + Abiraterone Acetate, FDC1-RS (G010)1.99
Combination 3: Cohort 2: Niraparib + Abiraterone Acetate, FDC2-RS (G012)2.09

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Combination 1: Part 2: Objective Response Rate (ORR)

ORR of soft tissue (visceral or nodal disease) was defined as percentage of participants with measurable disease who achieved a best response of either complete response (CR) or partial response (PR) as assessed by Response Evaluation Criteria in Solid Tumors (RECIST) 1.1 with no evidence of bone progression according to prostate cancer working group 3 (PCWG3) criteria. (NCT03431350)
Timeframe: Up to 37 months

InterventionPercentage of participants (Number)
Combination 1: Part 2 (Dose Expansion): Cohort 1A: BM+: Niraparib 200 mg + Cetrelimab 480 mg23.8
Combination 1: Part 2 (Dose Expansion): Cohort 1B: BM-: Niraparib 200 mg + Cetrelimab 480 mg9.1

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Combination 3: Maximum Observed Plasma Concentration (Cmax) of Niraparib and Abiraterone Acetate After a Single Dose

Cmax is defined as maximum observed plasma concentration of niraparib and abiraterone acetate (AA) after a single dose. (NCT03431350)
Timeframe: Pre-dose, 30 min, 1 hour (hr), 1.5 hr, 2hr, 3 hr, 4 hr, 6 hr, 8 hr, 10 hr, 24 hr, 48 hr, 72 hr, and 168 hr post dose on Day 1

InterventionNanograms per milliliter (ng/mL) (Mean)
Combination 3: Cohort 1A: Niraparib + Abiraterone Acetate, SA428
Combination 3: Cohort 1B: Niraparib + Abiraterone Acetate, FDC1-RS (G010)398
Combination 3: Cohort 2: Niraparib + Abiraterone Acetate, FDC2-RS (G012)417

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Combination 3: Area Under the Plasma Concentration-Time Curve From Time Zero to 168 Hours (AUC [0-168hr]) of Niraparib Administered With AA After a Single Dose

AUC(0-168 hours) was defined as area under the plasma concentration-time curve from time zero to 168 hours of Niraparib administered with AA After a single dose. (NCT03431350)
Timeframe: Pre-dose, 30 min, 1 hour (hr), 1.5 hr, 2hr, 3 hr, 4 hr, 6 hr, 8 hr, 10 hr, 24 hr, 48 hr, 72 hr, and 168 hr post dose on Day 1

InterventionNanograms*hour per milliliter (ng*h/mL) (Mean)
Combination 3: Cohort 1A: Niraparib + Abiraterone Acetate, SA14672
Combination 3: Cohort 1B: Niraparib + Abiraterone Acetate, FDC1-RS (G010)11862
Combination 3: Cohort 2: Niraparib + Abiraterone Acetate, FDC2-RS (G012)13321

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Combination 3: Area Under the Plasma Concentration-Time Curve for Niraparib From Time Zero to 168 Hours (AUC [0-168 Hours]/Dose) of Niraparib Administered With AA After a Single Dose

AUC0(168 hours)/dose was defined as area under the plasma concentration-time curve for niraparib from time 0 to 168 hours of niraparib administered with AA after a single dose. (NCT03431350)
Timeframe: Pre-dose, 30 min, 1 hour (hr), 1.5 hr, 2hr, 3 hr, 4 hr, 6 hr, 8 hr, 10 hr, 24 hr, 48 hr, 72 hr, and 168 hr post dose on Day 1

Interventionnanogram*hour/milliliter/milligram (Mean)
Combination 3: Cohort 1A: Niraparib + Abiraterone Acetate, SA73.36
Combination 3: Cohort 1B: Niraparib + Abiraterone Acetate, FDC1-RS (G010)59.31
Combination 3: Cohort 2: Niraparib + Abiraterone Acetate, FDC2-RS (G012)66.61

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Combination 2: Number of Participants With Adverse Events (AEs) of Grade >=3 Severity

AE was defined as an any untoward medical occurrence in a clinical study subject administered a pharmaceutical (investigational or non-investigational) product. An AE does not necessarily have a causal relationship with the treatment. An assessment of severity grade was made using the NCI-CTCAE as Grade 1 (mild): awareness of symptoms that are easily tolerated, causing minimal discomfort and not interfering with everyday activities; Grade 2 (moderate): sufficient discomfort is present to cause interference with normal activity; Grade 3 (severe): extreme distress, causing significant impairment of functioning or incapacitation, prevents normal everyday activities; Grade 4 (Life-threatening): urgent intervention indicated; and Grade 5 (death). (NCT03431350)
Timeframe: Up to 31 months

InterventionParticipants (Count of Participants)
Combination 2: Cohort 2A: Niraparib+Abiraterone Acetate+Prednisone6
Combination 2: Cohort 2C: Niraparib+Abiraterone Acetate+Prednisone7
Combination 2: Cohort 2D: Niraparib+Abiraterone Acetate+Prednisone4
Combination 2: Cohort 2C: HRR Negative: Niraparib + Abiraterone Acetate + Prednisone1

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Combination 2: Number of Participants With Adverse Events (AEs)

AE was defined as an any untoward medical occurrence in a clinical study subject administered a pharmaceutical (investigational or non-investigational) product. An AE does not necessarily have a causal relationship with the treatment. (NCT03431350)
Timeframe: Up to 31 months

InterventionParticipants (Count of Participants)
Combination 2: Cohort 2A: Niraparib+Abiraterone Acetate+Prednisone8
Combination 2: Cohort 2C: Niraparib+Abiraterone Acetate+Prednisone9
Combination 2: Cohort 2D: Niraparib+Abiraterone Acetate+Prednisone5
Combination 2: Cohort 2C: HRR Negative: Niraparib + Abiraterone Acetate + Prednisone1

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Combination 1: Part 2: Number of Participants With Adverse Events (AEs) of Grade >=3 Severity

AE was defined as an any untoward medical occurrence in a clinical study subject administered a pharmaceutical (investigational or non-investigational) product. An AE does not necessarily have a causal relationship with the treatment. An assessment of severity grade was made using the National Cancer Institute - Common Terminology Criteria for Adverse Events (NCI-CTCAE) as Grade 1 (mild): awareness of symptoms that are easily tolerated, causing minimal discomfort and not interfering with everyday activities; Grade 2 (moderate): sufficient discomfort is present to cause interference with normal activity; Grade 3 (severe): extreme distress, causing significant impairment of functioning or incapacitation, prevents normal everyday activities; Grade 4 (Life-threatening): urgent intervention indicated; and Grade 5 (death). (NCT03431350)
Timeframe: Up to 37 months

InterventionParticipants (Count of Participants)
Combination 1: Part 2 (Dose Expansion): Cohort 1A: BM+: Niraparib 200 mg + Cetrelimab 480 mg14
Combination 1: Part 2 (Dose Expansion): Cohort 1B: BM-: Niraparib 200 mg + Cetrelimab 480 mg8

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Combination 1: Part 2: Number of Participants With Adverse Events (AEs)

AE was defined as an any untoward medical occurrence in a clinical study subject administered a pharmaceutical (investigational or non-investigational) product. An AE does not necessarily have a causal relationship with the treatment. (NCT03431350)
Timeframe: Up to 37 months

InterventionParticipants (Count of Participants)
Combination 1: Part 2 (Dose Expansion): Cohort 1A: BM+: Niraparib 200 mg + Cetrelimab 480 mg21
Combination 1: Part 2 (Dose Expansion): Cohort 1B: BM-: Niraparib 200 mg + Cetrelimab 480 mg11

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Number of Participants With Dose Limiting Toxicities (DLTs)

DLT was evaluated as per National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE), v4.03 and defined as any of the following events occurring during Cycle 1 that were considered by investigator to be related with niraparib: Any Grade 5 or 4 hematologic toxicity, except Grade 4 neutropenia less than (<) 7 days; Grade 3 or 4 neutropenia with fever greater than (>) 38.5 degree Celsius and/or infection requiring antibiotic/anti-fungal treatment; Any Grade 3, 4,or 5 non-hematologic toxicity except: Grade 3 nausea, vomiting, diarrhea/dehydration occurring in setting of inadequate compliance with supportive care and lasting <48 hours, Inadequately treated hypersensitivity reactions, Grade 3 acidosis/alkalosis that responded to intervention by improving to less than or equal to (<=) Grade 2 within 48 hours, Isolated asymptomatic Grade 3 amylase elevation, hypercholesterolemia and hypertriglyceridemia; Any TEAE leading to an interruption of niraparib for >14 days. (NCT03497429)
Timeframe: Baseline up to Day 21 in Cycle 1 (Cycle length=21 days)

InterventionParticipants (Count of Participants)
Cohort 1: Niraparib 200 mg0
Cohort 2: Niraparib 300 mg1

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Cmax: Maximum Observed Plasma Concentration for Niraparib

(NCT03497429)
Timeframe: Cycle 1 Days 1 and 21: pre-dose and at multiple time points (up to 24 hours) post-dose (Cycle length =21 days)

,
Interventionnanogram per milliliter (ng/mL) (Geometric Mean)
Cycle 1 Day 1Cycle 1 Day 21
Cohort 1: Niraparib 200 mg442.9729.2
Cohort 2: Niraparib 300 mg529.61167

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Tmax: Time to Reach the Maximum Plasma Concentration (Cmax) for Niraparib

(NCT03497429)
Timeframe: Cycle 1 Days 1 and 21: pre-dose and at multiple time points (up to 24 hours) post-dose (Cycle length =21 days)

,
Interventionhours (Median)
Cycle 1 Day 1Cycle 1 Day 21
Cohort 1: Niraparib 200 mg4.0003.950
Cohort 2: Niraparib 300 mg4.0352.890

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Number of Participants With Serious TEAEs

(NCT03497429)
Timeframe: From the first dose of the study drug up to 28 days after the last dose of the study drug (up to Cycle 22 Day 49) (Cycle length =21 days)

InterventionParticipants (Count of Participants)
Cohort 1: Niraparib 200 mg0
Cohort 2: Niraparib 300 mg1

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Number of Participants With Grade 3 or Higher TEAEs

TEAEs were graded as per the NCI-CTCAE version 4.03. As per the NCI-CTCAE, Grade 1 (mild, asymptomatic or mild symptoms); Grade 2 (moderate, minimal, local or noninvasive intervention indicated); Grade 3 (severe or medically significant but not immediately life-threatening, hospitalization or prolongation of hospitalization indicated); Grade 4 (life-threatening consequences, urgent intervention indicated); Grade 5 (death related to adverse event [AE]). (NCT03497429)
Timeframe: From the first dose of the study drug up to 28 days after the last dose of the study drug (up to Cycle 22 Day 49) (Cycle length =21 days)

InterventionParticipants (Count of Participants)
Cohort 1: Niraparib 200 mg1
Cohort 2: Niraparib 300 mg6

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Number of Participants Who Discontinued Study Drug Due to TEAEs

(NCT03497429)
Timeframe: From the first dose of the study drug up to 28 days after the last dose of the study drug (up to Cycle 22 Day 49) (Cycle length =21 days)

InterventionParticipants (Count of Participants)
Cohort 1: Niraparib 200 mg0
Cohort 2: Niraparib 300 mg2

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AUC24：Area Under the Plasma Concentration-time Curve From Time 0 to 24 Hours for Niraparib

(NCT03497429)
Timeframe: Cycle 1 Days 1 and 21: pre-dose and at multiple time points (up to 24 hours) post-dose (Cycle length =21 days)

,
Interventionhour*nanogram per milliliter (h*ng/mL) (Geometric Mean)
Cycle 1 Day 1Cycle 1 Day 21
Cohort 1: Niraparib 200 mg493113040
Cohort 2: Niraparib 300 mg627019540

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Number of Participants With Treatment-emergent Adverse Events (TEAEs)

(NCT03497429)
Timeframe: From the first dose of the study drug up to 28 days after the last dose of the study drug (up to Cycle 22 Day 49) (Cycle length =21 days)

InterventionParticipants (Count of Participants)
Cohort 1: Niraparib 200 mg3
Cohort 2: Niraparib 300 mg6

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Cohort 1: Radiographic Progression-Free Survival (rPFS) as Assessed by Blinded Independent Central Review (BICR)

As per BICR, rPFS is time interval from the date of randomization to radiographic progression or death, whichever occurs first. Radiographic progression was determined by: 1) progression of soft tissue lesions measured by computerized tomography (CT) or magnetic resonance imaging (MRI) as per response evaluation criteria in solid tumors (RECIST) 1.1; 2) Progression of bone lesions observed by bone scan based on prostate cancer working group 3 (PCWG3) criteria. PCWG3 criteria: bone progression was confirmed by subsequent scan greater than or equal to (>=) 6 weeks later. Week 8 scan was baseline to which all subsequent scans were compared to determine progression. Confirmatory scan >=2 new lesions indicate progression; scan does not show >= 2 new lesions means no progression. If Week 8 scan less than (<) 2 new bone lesions compared to baseline, the initial scan >=2 new lesions compared to Week 8 scan indicates progression if confirmed by subsequent scan >=6 weeks later. (NCT03748641)
Timeframe: Up to 32 months

InterventionMonths (Median)
Cohort 1: Niraparib 200 mg + Abiraterone Acetate 1000 mg + Prednisone 10 mg16.46
Cohort 1: Placebo + Abiraterone Acetate 1000 mg + Prednisone 10 mg13.70

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Progression Free Survival (PFS)

PFS is defined as the time in months from the date of first study drug administration to the date of first documentation of progressive disease (PD) or death as assessed by the Investigator per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. Per RECIST 1.1, PD is defined as at least a 20% increase in the SoD (Sum of Diameters) of target lesions, taking as a reference the smallest (nadir) SoD since (and including) baseline. In addition to the relative increase of 20%, the SoD must also demonstrate an absolute increase of at least 5 mm. (NCT03759587)
Timeframe: From first study drug administration until disease progression or death (up to 48 months)

Interventionmonths (Median)
Niraparib 300 mg18

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Overall Survival (OS)

OS is defined as the time from the study enrollment to death due to any cause. (NCT03759587)
Timeframe: Up to 48 months

Interventionmonths (Median)
Niraparib 300 mgNA

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Overall Response Rate (ORR)

ORR is defined as the proportion of participants achieving Complete Response (CR) or Partial Response (PR) as assessed by the investigator per RECIST (v.1.1). Per RECIST 1.1, CR is defined as disappearance of all target lesions; PR is defined as atleast 30% decrease in sum of diameters (SoD) of target lesions. (NCT03759587)
Timeframe: Up to 48 months

Interventionpercentage of participants (Number)
Niraparib 300 mg0

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs)

An AE is defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE is defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759587)
Timeframe: From the day of signing the informed consent form (ICF) until 30 days after last dose of study drug administration or beginning of subsequent anticancer therapy, whichever comes first (up to 48 months).

InterventionParticipants (Count of Participants)
Niraparib 300 mg19

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Number of Participants With TEAEs Leading to Drug Discontinuation

An AE is defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE is defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759587)
Timeframe: From the day of signing the ICF until 30 days after last dose of study drug administration or beginning of subsequent anticancer therapy, whichever comes first (up to 48 months).

InterventionParticipants (Count of Participants)
Niraparib 300 mg5

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Number of Participants With Grade 3 or 4 Thrombocytopenia Occurring Within 30 Days After Initial Administration of Niraparib

An adverse event of 'thrombocytopenia' was collected and graded as per the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) Version 4.03.As per the NCI-CTCAE, Grade 1 scales as Mild; Grade 2 scales as Moderate; Grade 3 scales as severe or medically significant but not immediately life threatening; Grade 4 scales as life-threatening consequences; and Grade 5 scales as death related to Adverse Events (AE). (NCT03759587)
Timeframe: Up to 30 days after the first dose

InterventionParticipants (Count of Participants)
Niraparib 300 mg6

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Number of Participants With TEAEs Leading to Dose Interruption

An AE is defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE is defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759587)
Timeframe: From the day of signing the ICF until 30 days after last dose of study drug administration or beginning of subsequent anticancer therapy, whichever comes first (up to 48 months).

InterventionParticipants (Count of Participants)
Niraparib 300 mg16

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Number of Participants With TEAEs Leading to Dose Reduction

An AE is defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE is defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759587)
Timeframe: From the day of signing the ICF until 30 days after last dose of study drug administration or beginning of subsequent anticancer therapy, whichever comes first (up to 48 months).

InterventionParticipants (Count of Participants)
Niraparib 300 mg16

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Number of Participants With Serious Adverse Events (SAEs)

An SAE is any AE that results in death, is life-threatening, requires inpatient hospitalization or prolongation of an existing hospitalization, results in significant disability or incapacity, is a congenital anomaly/birth defect or is a medically important event. (NCT03759587)
Timeframe: From the day of signing the ICF until 30 days after last dose of study drug administration or beginning of subsequent anticancer therapy, whichever comes first (up to 48 months).

InterventionParticipants (Count of Participants)
Niraparib 300 mg4

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Number of Participants With Grade 3 or Higher TEAEs

An AE is defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE is defined as an adverse event with an onset that occurs after receiving study drug. A severity grade is defined by the NCI-CTCAE Version 4.03. As per NCI-CTCAE, Grade 1 scales as Mild; Grade 2 scales as Moderate; Grade 3 scales as severe or medically significant but not immediately life threatening; Grade 4 scales as life-threatening consequences; and Grade 5 scales as death related to AE. (NCT03759587)
Timeframe: From the day of signing the ICF until 30 days after last dose of study drug administration or beginning of subsequent anticancer therapy, whichever comes first (up to 48 months).

InterventionParticipants (Count of Participants)
Niraparib 300 mg14

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Number of Participants With Grade 3 or Higher TEAEs

An AE was defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A treatment-emergent adverse event (TEAE) was defined as an adverse event with an onset that occurs after receiving study drug. A severity grade was defined by the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE) Version 4.03. As per NCI-CTCAE, Grade 1 scales as Mild; Grade 2 scales as Moderate; Grade 3 scales as severe or medically significant but not immediately life threatening; Grade 4 scales as life-threatening consequences; and Grade 5 scales as death related to AE. (NCT03759600)
Timeframe: Up to 30 days after the last dose (Approximately 6 months)

InterventionParticipants (Count of Participants)
Niraparib 300 mg15

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Duration of Response (DOR)

DOR was defined as the time from the first documented CR or PR per RECIST v. 1.1 to disease recurrence or objective disease progression whichever occurs first. CR was defined as disappearance of all target lesions and PR was defined as at least a 30% decrease in sum of diameters (SoD) of target lesions, taking as a reference the Baseline SoD. (NCT03759600)
Timeframe: Until disease progression, death or data cut-off (Up to approximately 5 months)

Interventionmonths (Median)
Niraparib 300 mgNA

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Number of Participants With TEAEs Leading to Dose Interruption

An AE was defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE was defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759600)
Timeframe: Up to 30 days after the last dose (Approximately 6 months)

InterventionParticipants (Count of Participants)
Niraparib 300 mg15

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Disease Control Rate (DCR)

DCR was defined as the percentage of participants achieving CR, PR or Stable Disease (SD) as assessed by the Investigator per RECIST v. 1.1. CR was defined as disappearance of all target lesions and PR was defined as at least a 30% decrease in sum of diameters (SoD) of target lesions, taking as a reference the Baseline SoD. SD was defined as neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for progressive disease (PD). PD was defined as at least a 20% increase in the SoD of target lesions, taking as a reference the smallest (nadir) SoD since (and including) Baseline. (NCT03759600)
Timeframe: Until disease progression, death or data cut-off (Up to approximately 5 months)

Interventionpercentage of participants (Number)
Niraparib 300 mg90.0

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Progression Free Survival (PFS)

PFS was defined as the time in months from the date of first study drug administration to the date of first documentation of progressive disease (PD) or death as assessed by the RECIST version 1.1. Per RECIST 1.1, PD was defined as at least a 20% increase in the SoD (Sum of Diameters) of target lesions, taking as a reference the smallest (nadir) SoD since (and including) Baseline. (NCT03759600)
Timeframe: Until disease progression, death or data cut-off (Up to approximately 5 months)

Interventionmonths (Median)
Niraparib 300 mg4.3

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Overall Survival (OS)

OS was defined as the time in months from the study enrollment to death due to any cause. (NCT03759600)
Timeframe: Up to data cut-off approximately 6 months

Interventionmonths (Median)
Niraparib 300 mgNA

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Objective Response Rate (ORR)

ORR was defined as the percentage of participants achieving complete response (CR) or partial response (PR) as assessed by the Investigator per Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. CR was defined as disappearance of all target lesions and PR was defined as at least a 30% decrease in sum of diameters (SoD) of target lesions, taking as a reference the Baseline SoD. (NCT03759600)
Timeframe: Until disease progression, death or data cut-off (Up to approximately 5 months)

Interventionpercentage of participants (Number)
Niraparib 300 mg35.0

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs)

An adverse event (AE) was defined as any untoward medical occurrence in a clinical investigation participant administered a drug; it does not necessarily have to have a causal relationship with this treatment. An AE can therefore be any unfavorable and unintended sign (eg, a clinically significant abnormal laboratory finding), symptom, or disease temporally associated with the use of a drug, whether or not it is considered related to the drug. A treatment-emergent adverse event (TEAE) was defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759600)
Timeframe: Up to 30 days after the last dose (Approximately 6 months)

InterventionParticipants (Count of Participants)
Niraparib 300 mg20

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Number of Participants With TEAEs Leading to Drug Discontinuation

An AE was defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE was defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759600)
Timeframe: Up to 30 days after the last dose (Approximately 6 months)

InterventionParticipants (Count of Participants)
Niraparib 300 mg1

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Number of Participants With TEAEs Leading to Dose Reduction

An AE was defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. A TEAE was defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759600)
Timeframe: Up to 30 days after the last dose (Approximately 6 months)

InterventionParticipants (Count of Participants)
Niraparib 300 mg14

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Number of Participants With Serious TEAEs

An AE was defined as any untoward medical occurrence in a participant who has enrolled in a study; it does not necessarily have a causal relationship with this treatment. An SAE was any AE that results in death, is life-threatening, requires inpatient hospitalization or prolongation of an existing hospitalization, results in significant disability or incapacity, is a congenital anomaly/birth defect or is a medically important event. TEAE was defined as an adverse event with an onset that occurs after receiving study drug. (NCT03759600)
Timeframe: Up to 30 days after the last dose (Approximately 6 months)

InterventionParticipants (Count of Participants)
Niraparib 300 mg4

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PFS in Participants With PROC Who Have PD-L 1 Positive Status

PFS is defined as the time from the date of the first dose of study treatment to the earlier date of assessment of progression or death by any cause in the absence of progression by RECIST v.1.1 based on Investigator assessment. PD-L1 is a ligand that binds to PD-L1 protein on tumor infiltrating T cells and renders the T cells inactive. Any PD-L1 positive tissue sample with a vCPS >=5% was used as specified cut-point for the assessment of PD-L1 positive patient subset with PROC. vCPS was defined as the percentage of tumor cells and immune cells staining positive within the total tumor area. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionMonths (Median)
Niraparib+Dostarlimab (TSR-042)2.22

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Objective Response Rate (ORR) in Participants With Platinum-resistant Ovarian Cancer (PROC)

ORR is defined as the percentage of participants who have achieved confirmed complete response (CR) or partial response (PR), as determined by Response Evaluation Criteria in Solid Tumors Version 1.1 (RECIST v1.1) criteria based on Investigator assessment and computed tomography (CT) scans were commonly used for tumor imaging. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionPercentage of Participants (Number)
Niraparib+Dostarlimab (TSR-042)7.3

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Duration of Response (DOR) in Participants With PROC

DOR is defined as the time from first documentation of response (CR or PR) until the time of first documentation of disease progression or death by any cause in the absence of progression by RECIST v.1.1 based on Investigator assessment. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionMonths (Median)
Niraparib+Dostarlimab (TSR-042)3.8

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DCR in Participants With PROC Who Have PD-L 1 Positive Status

DCR is defined as the percentage of participants who have achieved BOR of CR, PR, or SD per RECIST v.1.1 based on the investigator's assessment. PD-L1 is a ligand that binds to PD-L1 protein on tumor infiltrating T cells and renders the T cells inactive. Any PD-L1 positive tissue sample with vCPS >=5% was used as specified cut-point for the assessment of PD-L1 positive patient subset with PROC. vCPS was defined as the percentage of tumor cells and immune cells staining positive within the total tumor area. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionPercentage of Participants (Number)
Niraparib+Dostarlimab (TSR-042)38.5

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Disease Control Rate (DCR) in Participants With PROC

DCR is defined as the percentage of participants who have achieved best overall response (BOR) of CR, PR, or stable disease (SD) per RECIST v.1.1 based on the investigator's assessment. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionPercentage of Participants (Number)
Niraparib+Dostarlimab (TSR-042)29.3

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Number of Participants With Adverse Events (AEs), Serious Adverse Events (SAEs), Treatment-emergent Adverse Events (TEAEs) and Adverse Event of Special Interest (AESI)

An AE is any untoward medical occurrence in a patient administered with a medicinal product and that does which may or may not have a causal relationship with this treatment. A SAE is any untoward medical occurrence that, at any dose results in death, is life-threatening, requires inpatient hospitalization or prolongation of existing hospitalization, results in persistent disability/incapacity, is a congenital anomaly/birth defect or any other situation according to medical or scientific judgment. TEAEs are any event that occurred between first dose of study drug up to 22 months, which were absent before treatment or that had worsened relative to pretreatment state. AESI were any AE (serious or non-serious) that is of scientific and medical concern specific to the study treatment, for which ongoing monitoring and rapid communication by the Investigator to the Sponsor was done. (NCT03955471)
Timeframe: Up to approximately 27 months

InterventionParticipants (Count of Participants)
AEsSAEsTEAEAESIs
Niraparib+Dostarlimab (TSR-042)4123412

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DOR in Participants With PROC Who Have PD-L 1 Positive Status

DOR is defined as the time from first documentation of response (CR or PR) until the time of first documentation of disease progression or death by any cause in the absence of progression by RECIST v.1.1 based on Investigator assessment. PD-L1 is a ligand that binds to PD-L1 protein on tumor infiltrating T cells and renders the T cells inactive. Any PD-L1 positive tissue sample with vCPS >=5% was used as specified cut-point for the assessment of PD-L1 patient subset with PROC. vCPS was defined as the percentage of tumor cells and immune cells staining positive within the total tumor area. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionMonths (Median)
Niraparib+Dostarlimab (TSR-042)NA

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Number of Participants With Grade Shift From Baseline in Plasma Chemistry

Blood samples were collected and the clinical chemistry parameters assessed were Albumin (Alb), alanine aminotransferase (ALT), amylase, aspartate aminotransferase (AST), alkaline phosphatase (ALP), sodium, total bilirubin (TB), creatinine, glucose, magnesium and potassium. The Grade shift post baseline data of each parameter from Grade 0 through Grade 4 was based on the CTCAE version 4.03, grading scale, as per intensity, namely Grade 0: Normal, Grade 1: mild; Grade 2: moderate; Grade 3: severe or medically significant; Grade 4: life-threatening consequences. Baseline was defined as the most recent measurement prior to the first administration of study treatment. Data has been presented for the number of participants with plasma chemistry grade shifts from baseline grade to grade 3 and 4 for each parameter. (NCT03955471)
Timeframe: Up to approximately 27 months

InterventionParticipants (Count of Participants)
ALT, Grade 0 to Grade 3ALT, Grade 1 to Grade 3ALT, Grade 2 to Grade 3ALT, Grade 3 to Grade 3ALT, Grade 4 to Grade 3ALT, Grade 0 to Grade 4ALT, Grade 1 to Grade 4ALT, Grade 2 to Grade 4ALT, Grade 3 to Grade 4ALT, Grade 4 to Grade 4Alb, Grade 0 to Grade 3Alb, Grade 1 to Grade 3Alb, Grade 2 to Grade 3Alb, Grade 3 to Grade 3Alb, Grade 4 to Grade 3Alb, Grade 0 to Grade 4Alb, Grade 1 to Grade 4Alb, Grade 2 to Grade 4Alb, Grade 3 to Grade 4Alb, Grade 4 to Grade 4ALP, Grade 0 to Grade 3ALP, Grade 1 to Grade 3ALP, Grade 2 to Grade 3ALP, Grade 3 to Grade 3ALP, Grade 4 to Grade 3ALP, Grade 0 to Grade 4ALP, Grade 1 to Grade 4ALP, Grade 2 to Grade 4ALP, Grade 3 to Grade 4ALP, Grade 4 to Grade 4Amylase, Grade 0 to Grade 3Amylase, Grade 1 to Grade 3Amylase, Grade 2 to Grade 3Amylase, Grade 3 to Grade 3Amylase, Grade 4 to Grade 3Amylase, Grade 0 to Grade 4Amylase, Grade 1 to Grade 4Amylase, Grade 2 to Grade 4Amylase, Grade 3 to Grade 4Amylase, Grade 4 to Grade 4AST, Grade 0 to Grade 3AST, Grade 1 to Grade 3AST, Grade 2 to Grade 3AST, Grade 3 to Grade 3AST, Grade 4 to Grade 3AST, Grade 0 to Grade 4AST, Grade 1 to Grade 4AST, Grade 2 to Grade 4AST, Grade 3 to Grade 4AST, Grade 4 to Grade 4TB, Grade 0 to Grade 3TB, Grade 1 to Grade 3TB, Grade 2 to Grade 3TB, Grade 3 to Grade 3TB, Grade 4 to Grade 3TB, Grade 0 to Grade 4TB, Grade 1 to Grade 4TB, Grade 2 to Grade 4TB, Grade 3 to Grade 4TB, Grade 4 to Grade 4Creatinine, Grade 0 to Grade 3Creatinine, Grade 1 to Grade 3Creatinine, Grade 2 to Grade 3Creatinine, Grade 3 to Grade 3Creatinine, Grade 4 to Grade 3Creatinine, Grade 0 to Grade 4Creatinine, Grade 1 to Grade 4Creatinine, Grade 2 to Grade 4Creatinine, Grade 3 to Grade 4Creatinine, Grade 4 to Grade 4Glucose high, Grade 0 to Grade 3Glucose high, Grade 1 to Grade 3Glucose high, Grade 2 to Grade 3Glucose high, Grade 3 to Grade 3Glucose high, Grade 4 to Grade 3Glucose high, Grade 0 to Grade 4Glucose high, Grade 1 to Grade 4Glucose high, Grade 2 to Grade 4Glucose high, Grade 3 to Grade 4Glucose high, Grade 4 to Grade 4Glucose low, Grade 0 to Grade 3Glucose low, Grade 1 to Grade 3Glucose low, Grade 2 to Grade 3Glucose low, Grade 3 to Grade 3Glucose low, Grade 4 to Grade 3Glucose low, Grade 0 to Grade 4Glucose low, Grade 1 to Grade 4Glucose low, Grade 2 to Grade 4Glucose low, Grade 3 to Grade 4Glucose low, Grade 4 to Grade 4Magnesium high, Grade 0 to Grade 3Magnesium high, Grade 1 to Grade 3Magnesium high, Grade 2 to Grade 3Magnesium high, Grade 3 to Grade 3Magnesium high, Grade 4 to Grade 3Magnesium high, Grade 0 to Grade 4Magnesium high, Grade 1 to Grade 4Magnesium high, Grade 2 to Grade 4Magnesium high, Grade 3 to Grade 4Magnesium high, Grade 4 to Grade 4Magnesium low, Grade 0 to Grade 3Magnesium low, Grade 1 to Grade 3Magnesium low, Grade 2 to Grade 3Magnesium low, Grade 3 to Grade 3Magnesium low, Grade 4 to Grade 3Magnesium low, Grade 0 to Grade 4Magnesium low, Grade 1 to Grade 4Magnesium low, Grade 2 to Grade 4Magnesium low, Grade 3 to Grade 4Magnesium low, Grade 4 to Grade 4Potassium high, Grade 0 to Grade 3Potassium high, Grade 1 to Grade 3Potassium high, Grade 2 to Grade 3Potassium high, Grade 3 to Grade 3Potassium high, Grade 4 to Grade 3Potassium high, Grade 0 to Grade 4Potassium high, Grade 1 to Grade 4Potassium high, Grade 2 to Grade 4Potassium high, Grade 3 to Grade 4Potassium high, Grade 4 to Grade 4Potassium low, Grade 0 to Grade 3Potassium low, Grade 1 to Grade 3Potassium low, Grade 2 to Grade 3Potassium low, Grade 3 to Grade 3Potassium low, Grade 4 to Grade 3Potassium low, Grade 0 to Grade 4Potassium low, Grade 1 to Grade 4Potassium low, Grade 2 to Grade 4Potassium low, Grade 3 to Grade 4Potassium low, Grade 4 to Grade 4Sodium high, Grade 0 to Grade 3Sodium high, Grade 1 to Grade 3Sodium high, Grade 2 to Grade 3Sodium high, Grade 3 to Grade 3Sodium high, Grade 4 to Grade 3Sodium high, Grade 0 to Grade 4Sodium high, Grade 1 to Grade 4Sodium high, Grade 2 to Grade 4Sodium high, Grade 3 to Grade 4Sodium high, Grade 4 to Grade 4Sodium low, Grade 0 to Grade 3Sodium low, Grade 1 to Grade 3Sodium low, Grade 2 to Grade 3Sodium low, Grade 3 to Grade 3Sodium low, Grade 4 to Grade 3Sodium low, Grade 0 to Grade 4Sodium low, Grade 1 to Grade 4Sodium low, Grade 2 to Grade 4Sodium low, Grade 3 to Grade 4Sodium low, Grade 4 to Grade 4
Niraparib+Dostarlimab (TSR-042)300001000010000000003110001000000000000041000000001000010000100000000003010000000000000000100000000000010000000000000000310000000000000000004700000000

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Number of Participants With Grade Shift From Baseline in Hematology

Blood samples were collected for the analysis of hematology parameters and each parameter was graded according to National Cancer Institute (NCI)-Common Terminology Criteria for Adverse Events (CTCAE) version 4.3. Grade 0: Normal, Grade 1: mild; Grade 2: moderate; Grade 3: severe or medically significant; Grade 4: life-threatening consequences. Baseline was defined as the most recent measurement prior to the first administration of study treatment. Data has been presented for the number of participants with hematology grade shifts from baseline grade to grade 3 and 4 for each parameter. (NCT03955471)
Timeframe: Up to approximately 27 months

InterventionParticipants (Count of Participants)
Hemoglobin, Grade 0 to Grade 3Hemoglobin, Grade 1 to Grade 3Hemoglobin, Grade 2 to Grade 3Hemoglobin, Grade 3 to Grade 3Hemoglobin, Grade 4 to Grade 3Hemoglobin, Grade 0 to Grade 4Hemoglobin, Grade 1 to Grade 4Hemoglobin, Grade 2 to Grade 4Hemoglobin, Grade 3 to Grade 4Hemoglobin, Grade 4 to Grade 4Leukocytes, Grade 0 to Grade 3Leukocytes, Grade 1 to Grade 3Leukocytes, Grade 2 to Grade 3Leukocytes, Grade 3 to Grade 3Leukocytes, Grade 4 to Grade 3Leukocytes, Grade 0 to Grade 4Leukocytes, Grade 1 to Grade 4Leukocytes, Grade 2 to Grade 4Leukocytes, Grade 3 to Grade 4Leukocytes, Grade 4 to Grade 4Lymphocytes, Grade 0 to Grade 3Lymphocytes, Grade 1 to Grade 3Lymphocytes, Grade 2 to Grade 3Lymphocytes, Grade 3 to Grade 3Lymphocytes, Grade 4 to Grade 3Lymphocytes, Grade 0 to Grade 4Lymphocytes, Grade 1 to Grade 4Lymphocytes, Grade 2 to Grade 4Lymphocytes, Grade 3 to Grade 4Lymphocytes, Grade 4 to Grade 4Neutrophil Count, Grade 0 to Grade 3Neutrophil Count, Grade 1 to Grade 3Neutrophil Count, Grade 2 to Grade 3Neutrophil Count, Grade 3 to Grade 3Neutrophil Count, Grade 4 to Grade 3Neutrophil Count, Grade 0 to Grade 4Neutrophil Count, Grade 1 to Grade 4Neutrophil Count, Grade 2 to Grade 4Neutrophil Count, Grade 3 to Grade 4Neutrophil Count, Grade 4 to Grade 4Platelets, Grade 0 to Grade 3Platelets, Grade 1 to Grade 3Platelets, Grade 2 to Grade 3Platelets, Grade 3 to Grade 3Platelets, Grade 4 to Grade 3Platelets, Grade 0 to Grade 4Platelets, Grade 1 to Grade 4Platelets, Grade 2 to Grade 4Platelets, Grade 3 to Grade 4Platelets, Grade 4 to Grade 4
Niraparib+Dostarlimab (TSR-042)35100000000000000000533001000010000100004100040000

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Change in Baseline in Activated Partial Thromboplastin Time

Blood samples were planned to be collected to evaluate activated partial thromboplastin time (APTT). Baseline was defined as the most recent measurement prior to the first administration of study treatment. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. (NCT03955471)
Timeframe: Baseline and up to approximately 27 months

InterventionSecond (Mean)
Day 2Day 41
Niraparib+Dostarlimab (TSR-042)116.9

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Change From Baseline in Thyrotropin

Blood samples were collected to evaluate thyrotropin at indicated time points. Baseline was defined as the most recent measurement prior to the first administration of study treatment. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. (NCT03955471)
Timeframe: Baseline and up to approximately 27 months

InterventionMilliunits per liter (mU/L) (Mean)
Cycle 5 Day 1Cycle 7 Day 1Cycle 9 Day 1Cycle 11 Day 1
Niraparib+Dostarlimab (TSR-042)8.07412.792.5962.517

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Change From Baseline in Temperature

Baseline was defined as the most recent measurement prior to the first administration of study treatment. The change from baseline was calculated by subtracting the baseline values from the individual post-randomization values. The minimum (min) and maximum (max) change from baseline values have been reported. (NCT03955471)
Timeframe: Up to approximately 27 months

InterventionDegrees Celsius (Mean)
max change post baselinemin change post baseline
Niraparib+Dostarlimab (TSR-042)0.31-0.35

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Change From Baseline in Systolic Blood Pressure (SBP) and Diastolic Blood Pressure (DBP)

Baseline was defined as the most recent measurement prior to the first administration of study treatment. The change from baseline was calculated by subtracting the baseline values from the individual post-randomization values. The minimum (min) and maximum (max) change from baseline values have been reported. (NCT03955471)
Timeframe: Up to approximately 27 months

InterventionMillimeters of mercury (Mean)
DBP, max change post baselineDBP, min change post baselineSBP, max change post baselineSBP, min change post baseline
Niraparib+Dostarlimab (TSR-042)10.6-5.816.5-12.5

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Change From Baseline in Pulse Rate

Baseline was defined as the most recent measurement prior to the first administration of study treatment. The change from baseline was calculated by subtracting the baseline values from the individual post-randomization values. The minimum (min) and maximum (max) change from baseline values have been reported. (NCT03955471)
Timeframe: Up to approximately 27 months

InterventionBeats per minute (Mean)
max change post baselinemin change post baseline
Niraparib+Dostarlimab (TSR-042)20.51

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Change From Baseline in Prothrombin International Normalized Ratio

Blood samples were collected to evaluate Prothrombin International Normalized Ratio (INR). Baseline was defined as the most recent measurement prior to the first administration of study treatment. Change from Baseline was calculated by subtracting Baseline value from the post-dose visit value. (NCT03955471)
Timeframe: Baseline and up to approximately 27 months

InterventionRatio (Mean)
Day 2Day 41Day 52
Niraparib+Dostarlimab (TSR-042)0.20.30.7

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Progression-free Survival (PFS) in Participants With PROC

PFS is defined as the time from the date of the first dose of study treatment to the earlier date of assessment of progression or death by any cause in the absence of progression by RECIST v.1.1 based on Investigator assessment. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionMonths (Median)
Niraparib+Dostarlimab (TSR-042)2.1

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Overall Survival (OS) in Participants With PROC

OS is defined as the time from the date of the first dose of study treatment to the date of death by any cause. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionMonths (Median)
Niraparib+Dostarlimab (TSR-042)10.61

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OS in Participants With PROC Who Have PD-L 1 Positive Status

OS is defined as the time from the date of the first dose of study treatment to the date of death by any cause. PD-L1 is a ligand that binds to PD-L1 protein on tumor infiltrating T cells and renders the T cells inactive. Any PD-L1 positive tissue sample with vCPS >=5% was used as specified cut-point for the assessment of PD-L1 positive patient subset with PROC. vCPS was defined as the percentage of tumor cells and immune cells staining positive within the total tumor area. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionMonths (Median)
Niraparib+Dostarlimab (TSR-042)NA

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ORR in Participants With PROC Who Have Programmed Cell Death-ligand 1 (PD-L 1) Positive Status

ORR is defined as the percentage of participants who have achieved confirmed CR or PR, as determined by RECIST v1.1 criteria based on Investigator assessment and CT scans were commonly used for tumor imaging. PD-L1 is a ligand that binds to PD-L1 protein on tumor infiltrating T cells and renders the T cells inactive. Any PD-L1 positive tissue sample with combined positive score (vCPS) >=5% was used as specified cut-point for the assessment of PD-L1 positive patient subset with PROC. vCPS was defined as the percentage of tumor cells and immune cells staining positive within the total tumor area. (NCT03955471)
Timeframe: Up to approximately 22 months

InterventionPercentage of Participants (Number)
Niraparib+Dostarlimab (TSR-042)7.7

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Disease Control Rate With irRECIST Criteria

"Disease control rate (DCR) is the percentage of participants who experienced a immune-related complete response (irCR), partial response (irPR), or stable disease (irSD) assessed by the Immune-Related Response Evaluation Criteria In Solid Tumors (irRECIST) criteria below.~irCR = Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~irPR = At least 30% decrease in the sum of longest diameters of target lesions, compared to baseline.~irSD = Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, compared to baseline.~Immune-related Progressive Disease (irPD) = At least 20% increase in the sum of longest diameters of target lesions AND at least 5mm absolute increase, compared to baseline. Appearance of one or more new lesions is also considered progression. Confirmation scan required at least 4 weeks later." (NCT04409002)
Timeframe: up to 17 months

InterventionParticipants (Count of Participants)
Niraparib+Dostarlimab + Radiation0

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Disease Control Rate With RECIST 1.1 Criteria

"Disease control rate (DCR) is the percentage of participants who experienced a complete response (CR), partial response (PR), or stable disease (SD) assessed by the Response Evaluation Criteria In Solid Tumors (RECIST) v1.1 criteria below.~CR = Disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to <10 mm.~PR = At least 30% decrease in the sum of longest diameters of target lesions, taking as reference the baseline sum diameters.~SD = Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the baseline sum diameters while on study.~Progressive Disease (PD) = At least 20% increase in the sum of longest diameters of target lesions, taking as reference the baseline sum diameters while on study. Appearance of one or more new lesions is also considered progression." (NCT04409002)
Timeframe: up to 17 months

InterventionParticipants (Count of Participants)
Niraparib+Dostarlimab + Radiation0

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Overall Survival

Overall survival (OS) is defined as the time duration from the first day of protocol treatment to the date of death due to any cause, and will be censored at the date of last follow-up for patients still alive. (NCT04409002)
Timeframe: up to 17 months

Interventionmonths (Median)
Niraparib+Dostarlimab + Radiation3.1

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Progression-free Survival

Progression-free survival (PFS) is defined as the time duration from the first day of protocol treatment to the earlier date of disease progression or death due to any cause. PFS time will be censored at the date of last follow-up for surviving patients with disease control. (NCT04409002)
Timeframe: up to 17 months

Interventionmonths (Median)
Niraparib+Dostarlimab + Radiation1.6

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Disease Control Rate (DCR) Per RECIST Version 1.1 by Investigator Assessment

DCR was defined as the percentage of participants who have achieved best overall response of CR, PR, or stable disease (SD) per RECIST version 1.1 based on Investigator's assessment. Partial response is defined as at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. Complete response is defined as the disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to less than (<)10 millimeters (mm). Stable disease is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionPercentage of participants (Number)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)76.9

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Number of Participants With Eastern Cooperative Oncology Group (ECOG) Performance Status at Baseline and End of Treatment

Performance status assessments were based on 5-grade ECOG scale (from 0 to 4), where 0=fully active, able to carry on all pre-disease performance without restriction; 1=restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature (e.g., light house work, office work); 2=ambulatory and capable of all self-care but unable to carry out any work activities, up and about more than 50% of waking hours; 3=capable of only limited self-care, confined to bed or chair more than 50% of waking hours; 4=completely disabled, cannot carry on any self-care, totally confined to bed or chair. Baseline is defined as the most recent non-missing measurement prior to or on the first administration of study drug. (NCT05751629)
Timeframe: Baseline (Day 1) and end of treatment (Up to approximately 32 months)

InterventionParticipants (Count of Participants)
Baseline72299130End of Treatment72299130
Grade 4Grade 0Grade 1Grade 2Grade 3
Cohort A (Dostarlimab + Bevacizumab + Niraparib)18
Cohort A (Dostarlimab + Bevacizumab + Niraparib)22
Cohort A (Dostarlimab + Bevacizumab + Niraparib)0
Cohort A (Dostarlimab + Bevacizumab + Niraparib)9
Cohort A (Dostarlimab + Bevacizumab + Niraparib)20
Cohort A (Dostarlimab + Bevacizumab + Niraparib)7
Cohort A (Dostarlimab + Bevacizumab + Niraparib)1

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Absolute Values in Urinalysis Parameter - Specific Gravity (Ratio)

Urine samples were collected at indicated time points for the assessment of specific gravity. Baseline is defined as the most recent non-missing measurement prior to or on the first administration of study drug. (NCT05751629)
Timeframe: Baseline (Day 1) and end of treatment (Up to approximately 32 months)

InterventionRatio (Mean)
BaselineEnd of treatment
Cohort A (Dostarlimab + Bevacizumab + Niraparib)1.01491.0162

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Change From Baseline in Cancer Antigen 125 (CA-125) at End of Treatment

Blood samples were collected for the analysis of CA-125. Baseline is defined as the most recent non-missing measurement prior to or on the first administration of study drug. (NCT05751629)
Timeframe: Baseline (Day 1) and end of treatment (Up to approximately 32 months)

InterventionUnits per milliliter (U/mL) (Mean)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)246.86

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Change From Baseline in Vital Signs (Weight) at End of Treatment

Weight was measured in ordinary indoor clothing (without shoes) and was recorded at specified study visit. Baseline is defined as the most recent non-missing measurement prior to or on the first administration of study drug. (NCT05751629)
Timeframe: Baseline (Day 1) and end of treatment (Up to approximately 32 months)

Interventionkilogram (Mean)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)-5.07

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Confirmed Objective Response Rate (ORR) Per Response Evaluation Criteria in Solid Tumors (RECIST) Version 1.1 by Investigator Assessment

ORR was defined as percentage of participants with a confirmed investigator-assessed Best Overall Response (BOR) of confirmed complete response (CR) or partial response (PR), evaluated using Response Evaluation Criteria in Solid Tumors (RECIST) version (v) 1.1. PR is defined as at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. CR is defined as the disappearance of all target lesions and any pathological lymph nodes (whether target or non-target) must have reduction in short axis to less than (<)10 millimeters (mm). (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionPercentage of participants (Number)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)17.9

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Overall Survival (OS)

OS was defined as the time from the date of the first dose of study treatment to the date of death due to any cause. Median and 95% CI are presented. (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionMonths (Median)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)22.05

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Number of Participants With Treatment-emergent Adverse Events (TEAEs)

An AE is any untoward medical occurrence in a clinical study participant, temporally associated with the use of a study intervention, whether or not considered related to the study intervention. (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionParticipants (Count of Participants)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)41

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Number of Participants With Clinically Significant Changes in Clinical Laboratory Parameters - Chemistry, Coagulation, Hematology and Thyroid

Blood samples were collected for the analysis of clinical laboratory parameters - chemistry, coagulation, hematology and thyroid. (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionParticipants (Count of Participants)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)0

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Duration of Response (DOR) Per RECIST Version 1.1 by Investigator Assessment

DOR was defined as the time from first documentation of response (CR or PR) until the time of first documentation of disease progression by RECIST version 1.1 based on Investigator's assessment or death by any cause. Partial response is defined as at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. Complete response is defined as the disappearance of all target lesions. Any pathological lymph nodes (whether target or non-target) must have reduction in short axis to less than (<)10 millimeters (mm). (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionMonths (Median)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)11.76

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Progression Free Survival (PFS) Per RECIST Version 1.1 by Investigator Assessment

PFS was defined as the time from the date of the first dose of study treatment to the earliest date of assessment of disease progression or death by any cause in the absence of progression by RECIST v1.1. Disease Progression is defined using RECIST v1.1 as 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. (NCT05751629)
Timeframe: Up to approximately 38 Months

InterventionMonths (Median)
Cohort A (Dostarlimab + Bevacizumab + Niraparib)7.92

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SubstanceRelationship StrengthStudiesTrialsClassesRoles
rucaparib
AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source		2.1110azepinoindole;
caprolactams;
organofluorine compound;
secondary amino compound		antineoplastic agent;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
olaparib
[no description available]		2.1110cyclopropanes;
monofluorobenzenes;
N-acylpiperazine;
phthalazines		antineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
bmn 673
talazoparib: inhibits both PARP1 and PARP2; structure in first source		2.1110
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.		2.6104-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
benzene
[no description available]		4.811aromatic annulene;
benzenes;
volatile organic compound		carcinogenic agent;
environmental contaminant;
non-polar solvent
coumarin
2H-chromen-2-one: coumarin derivative		2.610coumarinsfluorescent 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).		2.610monohydroxybenzoic acidalgal metabolite;
antifungal agent;
antiinfective agent;
EC 1.11.1.11 (L-ascorbate peroxidase) inhibitor;
keratolytic drug;
plant hormone;
plant 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.		2.610dithiolanes;
heterocyclic fatty acid;
thia fatty acid		fundamental metabolite;
geroprotector
nickel
Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme UREASE.. nickel ion : A nickel atom having a net electric charge.. nickel atom : Chemical element (nickel group element atom) with atomic number 28.		4.811metal allergen;
nickel group element atom		epitope;
micronutrient
nitroxyl
nitroxyl: hydroxamic acid oxidized to nitroxyl free radical. nitroxyl : A nitrogen oxoacid consisting of an oxygen atom double-bonded to an NH group.		4.811nitrogen oxoacid
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.		2.610pyridinemonocarboxylic acidhuman metabolite;
MALDI matrix material
succinic acid
Succinic Acid: A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851). succinic acid : An alpha,omega-dicarboxylic acid resulting from the formal oxidation of each of the terminal methyl groups of butane to the corresponding carboxy group. It is an intermediate metabolite in the citric acid cycle.		4.811alpha,omega-dicarboxylic acid;
C4-dicarboxylic acid		anti-ulcer drug;
fundamental metabolite;
micronutrient;
nutraceutical;
radiation protective agent
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.		2.610primary alcohol;
vitamin B1		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
toluene
methylbenzene : Any alkylbenzene that is benzene substituted with one or more methyl groups.		4.811methylbenzene;
toluenes;
volatile organic compound		cholinergic antagonist;
fuel additive;
neurotoxin;
non-polar solvent
uric acid
Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.. uric acid : An oxopurine that is the final oxidation product of purine metabolism.. 6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.. 7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.		4.811uric acidEscherichia 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.		4.811isourea;
monocarboxylic acid amide;
one-carbon compound		Daphnia magna metabolite;
Escherichia coli metabolite;
fertilizer;
flour treatment agent;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
3-aminobenzamide
[no description available]		3.8220benzamides;
substituted aniline		EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
pleconaril
WIN 63843: structure given in first source		2.610
4-(2-aminoethyl)benzenesulfonylfluoride
[no description available]		2.610
phenytoin
[no description available]		2.610imidazolidine-2,4-dioneanticonvulsant;
drug allergen;
sodium channel blocker;
teratogenic agent
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)		2.610monocarboxylic acid amide;
sulfonamide;
thiadiazoles		anticonvulsant;
diuretic;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
albendazole
[no description available]		4.811aryl sulfide;
benzimidazoles;
benzimidazolylcarbamate fungicide;
carbamate ester		anthelminthic drug;
microtubule-destabilising agent;
tubulin modulator
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.		2.610secondary 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		2.610adamantanes;
primary aliphatic amine		analgesic;
antiparkinson drug;
antiviral drug;
dopaminergic agent;
NMDA receptor antagonist;
non-narcotic analgesic
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.		2.6101,3-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.		2.610aminoquinoline;
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
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.		2.610benzoic 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]		2.610amino 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.		2.610benzamides
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.		2.610benzoate 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]		2.610bornane 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.		2.610benzimidazolecarboxylic acid;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
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.		2.610pyridinium ion
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.		5.6741aminoquinoline;
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.		2.610monochlorobenzenes;
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.		2.610organochlorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
phenothiazine antipsychotic drug
ciprofibrate
[no description available]		2.610cyclopropanes;
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.		2.610dibenzoazepineanticoronaviral agent;
antidepressant;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
serotonergic antagonist;
serotonergic drug;
serotonin uptake inhibitor
danthron
danthron: structure. chrysazin : A dihydroxyanthraquinone that is anthracene-9,10-dione substituted by hydroxy groups at positions 1 and 8.		2.610dihydroxyanthraquinoneapoptosis 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.		2.6104-pyridonesiron chelator;
protective agent
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.		2.610piperidines;
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]		2.610organic 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.		2.6920branched-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.		2.610aromatic 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.		2.610benzoselenazoleanti-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.		2.6101,1-bis(phosphonic acid)antineoplastic agent;
bone density conservation agent;
chelator
2-hexyloxybenzamide
2-hexyloxybenzamide: structure		2.610aromatic ether;
benzamides		antifungal agent
brl 42810
[no description available]		2.6102-aminopurines;
acetate ester		antiviral drug;
prodrug
fluphenazine
[no description available]		2.610N-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.		2.610nucleobase analogue;
organofluorine compound		antimetabolite;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
radiosensitizing agent;
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.		2.610benzoate 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.		2.610dialdehydecross-linking reagent;
disinfectant;
fixative
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.		2.610isoquinolines;
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.		2.610aromatic 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.		2.610phosphocholines;
phospholipid		anti-inflammatory agent;
anticoronaviral agent;
antifungal agent;
antineoplastic agent;
antiprotozoal drug;
apoptosis inducer;
immunomodulator;
protein kinase inhibitor
hexylresorcinol
[no description available]		2.610resorcinols
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.		2.610cyclic 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.		2.610thioxanthenesmutagen;
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.		2.610benzothiadiazine;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
hydroxyurea
[no description available]		2.610one-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		2.610monocarboxylic acidantipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
radical scavenger;
xenobiotic
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.		2.610aromatic 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.		2.610azaspiro compound;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
itraconazole
[no description available]		2.610piperazines
kojic acid
[no description available]		2.6104-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.		2.610
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.		2.610monocarboxylic 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.		2.610benzocycloheptapyridine;
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		2.610biphenylyltetrazole;
imidazoles		angiotensin receptor antagonist;
anti-arrhythmia drug;
antihypertensive agent;
endothelin receptor antagonist
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.		2.610benzamides;
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.		2.610aromatic 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.		4.811guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
methazolamide
Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.		2.610sulfonamide;
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.		2.610aromatic ether;
carbamate ester;
secondary alcohol
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.		2.610dihydroxyanthraquinoneanalgesic;
antineoplastic agent
entinostat
[no description available]		2.610benzamides;
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.		2.610maleimidesanticoronaviral 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.		2.610methoxynaphthalene;
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		2.610benzoic 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.		2.610cyclopropanes;
dipyridodiazepine		antiviral drug;
HIV-1 reverse transcriptase inhibitor
ofloxacin
Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.		4.8113-oxo monocarboxylic acid;
N-arylpiperazine;
N-methylpiperazine;
organofluorine compound;
oxazinoquinoline
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.		2.610aromatic ether;
benzimidazoles;
pyridines;
sulfoxide
osalmide
osalmide: structure		2.610organic molecular entity
oxethazaine
[no description available]		2.610amino 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.		2.610endocannabinoid;
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.		2.610benzylisoquinoline alkaloid;
dimethoxybenzene;
isoquinolines		antispasmodic drug;
vasodilator agent
pentoxifylline
[no description available]		2.610oxopurine
perhexiline
Perhexiline: 2-(2,2-Dicyclohexylethyl)piperidine. Coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis.		2.610piperidinescardiovascular 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.		2.610diaminopyridine;
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.		2.610monocarboxylic acidantineoplastic 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.		2.610acyl fluorideserine proteinase inhibitor
pimobendan
pimobendan: produces arterial & venous dilatation in dogs; structure given in first source		2.610benzimidazoles;
pyridazinone		cardiotonic drug;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
vasodilator agent
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.		2.6620phenanthridines;
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		2.610isoquinolines
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.		2.610benzoic 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.		2.610dithioketal;
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.		2.610phenothiazines;
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.		2.610phenothiazines;
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.		2.610naphthalenes;
propanolamine;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
pyrimethamine
Maloprim: contains above 2 cpds		4.811aminopyrimidine;
monochlorobenzenes		antimalarial;
antiprotozoal drug;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
rimantadine
Rimantadine: An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza.		2.610alkylamine
rolipram
[no description available]		2.610pyrrolidin-2-onesantidepressant;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor
scriptaid
scriptide: provokes translocation of GLUT4 to increase glucose uptake; structure in first source		2.610isoquinolines
sebacic acid
sebacic acid : An alpha,omega-dicarboxylic acid that is the 1,8-dicarboxy derivative of octane.		2.610alpha,omega-dicarboxylic acid;
dicarboxylic fatty acid		human metabolite;
plant metabolite
sodium fluoride
[no description available]		4.811fluoride saltmutagen
fenofibrate
[no description available]		2.610benzochromenone;
delta-lactone;
naphtho-alpha-pyrone		platelet aggregation inhibitor;
Sir2 inhibitor
imatinib
[no description available]		2.610aromatic amine;
benzamides;
N-methylpiperazine;
pyridines;
pyrimidines		antineoplastic agent;
apoptosis inducer;
tyrosine kinase inhibitor
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.		2.610aromatic 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
temozolomide
[no description available]		5.0521imidazotetrazine;
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.		2.610phthalimides;
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.		2.610monochlorobenzenes;
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.		2.610pteridinesdiuretic;
sodium channel blocker
trifluoperazine
[no description available]		2.610N-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.		2.610organofluorine 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.		2.610alkaloid;
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.		2.610benzamides;
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.		2.610aminopyrimidine;
methoxybenzenes		antibacterial drug;
diuretic;
drug allergen;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
environmental contaminant;
xenobiotic
tyrphostin a9
[no description available]		2.610alkylbenzenegeroprotector
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.		2.610aminopyridine;
indolecarboxamide;
N-acylpiperazine;
sulfonamide		antiviral drug;
HIV-1 reverse transcriptase inhibitor
vesnarinone
[no description available]		2.610organic molecular entity
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.		8.027511-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
idoxuridine
[no description available]		2.610organoiodine compound;
pyrimidine 2'-deoxyribonucleoside		antiviral drug;
DNA synthesis inhibitor
chloramphenicol
Amphenicol: Chloramphenicol and its derivatives.		2.610C-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.		4.811amino 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.		2.610aspartate 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
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.		2.610benzenes;
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.		4.811amino 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.		2.610benzoxazole
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.		2.610antibiotic 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.		2.610psoralensplant 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.		2.610antibiotic antifungal agent;
N-glycosylpyrrolopyrimidine;
ribonucleoside		antimetabolite;
antineoplastic agent;
bacterial metabolite
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.		2.610nucleoside analogue;
organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
EC 2.1.1.45 (thymidylate synthase) inhibitor
phencyclidine
Phencyclidine: A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to KETAMINE in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE). As a drug of abuse, it is known as PCP and Angel Dust.. phencyclidine : A member of the class of piperidines that is piperidine in which the nitrogen is substituted with a 1-phenylcyclohexyl group. Formerly used as an anaesthetic agent, it exhibits both hallucinogenic and neurotoxic effects.		4.811benzenes;
piperidines		anaesthetic;
neurotoxin;
NMDA receptor antagonist;
psychotropic drug
acrylic acid
acrylic acid: RN given refers to parent cpd. acrylic acid : A alpha,beta-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group.		4.811alpha,beta-unsaturated monocarboxylic acidmetabolite
rhodamine b
rhodamine B: RN & N1 from 9th CI Form Index; RN given refers to parent cpd; structure in Merck Index, 9th ed, #7973; TETRAETHYLRHODAMINE was see RHODAMINES 1975-93; use RHODAMINES to search TETRAETHYLRHODAMINE 1975-93. rhodamine B : An organic chloride salt having N-[9-(2-carboxyphenyl)-6-(diethylamino)-3H-xanthen-3-ylidene]-N-ethylethanaminium as the counterion. An amphoteric dye commonly used as a fluorochrome.		4.811organic chloride salt;
xanthene dye		fluorescent probe;
fluorochrome;
histological dye
9,10-anthraquinone
9,10-anthraquinone : An anthraquinone that is anthracene in which positions 9 and 10 have been oxidised to carbonyls.		2.610anthraquinone
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.		2.610benzanilide fungicide;
salicylamides;
salicylanilides
gramine
gramine : An aminoalkylindole that is indole carrying a dimethylaminomethyl substituent at postion 3.		2.610aminoalkylindole;
indole alkaloid;
tertiary amino compound		antibacterial agent;
antiviral agent;
plant metabolite;
serotonergic antagonist
n-vinyl-2-pyrrolidinone
N-vinyl-2-pyrrolidinone: monomer of POVIDONE; structure given in first source		4.811pyrrolidin-2-ones
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.		2.610aminoacridines;
primary amino compound		acid-base indicator;
antiinfective agent;
antiseptic drug;
fluorescent dye;
MALDI matrix material;
mutagen
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.		2.610gallate esteranti-inflammatory agent;
antioxidant;
plant metabolite
ethylbenzene
[no description available]		4.811alkylbenzene
monobenzone
monobenzone: structure. monobenzone : The monobenzyl ether of hydroquinone. It is used as a topical drug for medical depigmentation.		2.610benzyl etherallergen;
dermatologic drug;
melanin synthesis inhibitor
allyl chloride
[no description available]		2.2110organochlorine compound
thiophenes
Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.		2.2510mancude organic heteromonocyclic parent;
monocyclic heteroarene;
thiophenes;
volatile organic compound		non-polar solvent
framycetin
Framycetin: A component of NEOMYCIN that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed). framycetin : A tetracyclic antibacterial agent derived from neomycin, being a glycoside ester of neamine and neobiosamine B.		4.811aminoglycosideallergen;
antibacterial drug;
Escherichia coli metabolite
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.		2.610dithiocarbamic acidschelator;
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.		2.610catechinantioxidant;
plant metabolite
indazoles
Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.		20.2218853indazole
thiazoles
[no description available]		5.17211,3-thiazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
hydrazine
diamine : Any polyamine that contains two amino groups.		4.811azane;
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.		2.610N-glycosyl-1,3,5-triazine;
nucleoside analogue		antineoplastic agent
hydantoins
Hydantoins: Compounds based on imidazolidine dione. Some derivatives are ANTICONVULSANTS.. imidazolidine-2,4-dione : An imidazolidinone with oxo groups at position 2 and 4.		4.811imidazolidine-2,4-dione
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.		2.610thioxanthenesadjuvant;
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.		2.610bisbenzylisoquinoline 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.		2.610aromatic 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.		2.610dihydroxyanthraquinoneanti-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.		2.610isoquinoline 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		2.610botanical 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.		2.610flavanones
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.		2.610hydroxy monocarboxylic acidplant metabolite
oleanolic acid
[no description available]		2.610hydroxy monocarboxylic acid;
pentacyclic triterpenoid		plant metabolite
angelicin
angelicin: used as tranquillizer; sedative; or anticonvulsant; structure		2.610furanocoumarin
diperodon
diperodon: RN given refers to parent cpd; structure given in first source		2.610carbamate ester
megestrol acetate
[no description available]		2.61020-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.		2.610acetylcysteine;
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]		2.610
levonorgestrel
Levonorgestrel: A synthetic progestational hormone with actions similar to those of PROGESTERONE and about twice as potent as its racemic or (+-)-isomer (NORGESTREL). It is used for contraception, control of menstrual disorders, and treatment of endometriosis.		4.81117beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound		contraceptive drug;
female contraceptive drug;
progestin;
synthetic oral contraceptive
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.		2.610ethanolamines;
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.		2.610hydrochlorideenvironmental contaminant;
hypoglycemic agent;
xenobiotic
calcium peroxide
[no description available]		4.811calcium oxides
manganese dioxide
[no description available]		4.811manganese molecular entity;
metal oxide
zinc oxide
Zinc Oxide: A mild astringent and topical protectant with some antiseptic action. It is also used in bandages, pastes, ointments, dental cements, and as a sunblock.		4.811zinc molecular entity
antimycin a
[no description available]		2.610benzamides;
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		2.610bipyridines
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.		2.610benzyl alcohols;
dichlorobenzene		antiseptic drug
tetrachloroisophthalonitrile
tetrachloroisophthalonitrile: structure. chlorothalonil : A dinitrile that is benzene-1,3-dicarbonitrile substituted by four chloro groups. A non-systemic fungicide first introduced in the 1960s, it is used to control a range of diseases in a wide variety of crops.		2.3110aromatic fungicide;
dinitrile;
tetrachlorobenzene		antifungal agrochemical
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		2.610dihydrofuran;
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.		2.610adenosines;
purine 2',3'-dideoxyribonucleoside		EC 3.5.4.4 (adenosine deaminase) inhibitor;
EC 4.6.1.1 (adenylate cyclase) inhibitor
vidarabine
adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.		2.610beta-D-arabinoside;
purine nucleoside		antineoplastic agent;
bacterial metabolite;
nucleoside antibiotic
3-deazaadenosine
3-deazaadenosine: RN given refers to parent cpd.		2.610
manganese
Manganese: A trace element with atomic symbol Mn, atomic number 25, and atomic weight 54.94. It is concentrated in cell mitochondria, mostly in the pituitary gland, liver, pancreas, kidney, and bone, influences the synthesis of mucopolysaccharides, stimulates hepatic synthesis of cholesterol and fatty acids, and is a cofactor in many enzymes, including arginase and alkaline phosphatase in the liver. (From AMA Drug Evaluations Annual 1992, p2035). manganese(4+) : A manganese cation that is monoatomic and has a formal charge of +4.		4.811elemental manganese;
manganese group element atom		Escherichia coli metabolite;
micronutrient
mercury
Mercury: A silver metallic element that exists as a liquid at room temperature. It has the atomic symbol Hg (from hydrargyrum, liquid silver), atomic number 80, and atomic weight 200.59. Mercury is used in many industrial applications and its salts have been employed therapeutically as purgatives, antisyphilitics, disinfectants, and astringents. It can be absorbed through the skin and mucous membranes which leads to MERCURY POISONING. Because of its toxicity, the clinical use of mercury and mercurials is diminishing.. mercury(0) : Elemental mercury of oxidation state zero.		4.811elemental mercury;
zinc group element atom		neurotoxin
molybdenum
Molybdenum: A metallic element with the atomic symbol Mo, atomic number 42, and atomic weight 95.95. It is an essential trace element, being a component of the enzymes xanthine oxidase, aldehyde oxidase, and nitrate reductase.		4.811chromium group element atommicronutrient
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.		8.88125elemental platinum;
nickel group element atom;
platinum group metal atom
rhodium
Rhodium: A hard and rare metal of the platinum group, atomic number 45, atomic weight 102.905, symbol Rh.. rhodium atom : A cobalt group element atom of atomic number 45.		2.2110cobalt group element atom
silver
Silver: An element with the atomic symbol Ag, atomic number 47, and atomic weight 107.87. It is a soft metal that is used medically in surgical instruments, dental prostheses, and alloys. Long-continued use of silver salts can lead to a form of poisoning known as ARGYRIA.		4.811copper group element atom;
elemental silver		Escherichia coli metabolite
titanium
Titanium: A dark-gray, metallic element of widespread distribution but occurring in small amounts with atomic number, 22, atomic weight, 47.867 and symbol, Ti; specific gravity, 4.5; used for fixation of fractures.		4.811titanium group element atom
gold
Gold: A yellow metallic element with the atomic symbol Au, atomic number 79, and atomic weight 197. It is used in jewelry, goldplating of other metals, as currency, and in dental restoration. Many of its clinical applications, such as ANTIRHEUMATIC AGENTS, are in the form of its salts.		4.811copper group element atom;
elemental gold
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.		2.610pyrimidine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
galactosamine
2-amino-2-deoxy-D-galactopyranose : The pyranose form of D-galactosamine.. D-galactosamine : The D-stereoisomer of galactosamine.		4.811D-galactosamine;
primary amino compound		toxin
zinc sulfate
Zinc Sulfate: A compound given in the treatment of conditions associated with zinc deficiency such as acrodermatitis enteropathica. Externally, zinc sulfate is used as an astringent in lotions and eye drops. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995). zinc sulfate : A metal sulfate compound having zinc(2+) as the counterion.		4.811metal sulfate;
zinc molecular entity		fertilizer
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.		4.811calcium phosphate
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.		2.610diol;
organic heterotricyclic compound		antimetabolite;
antineoplastic agent;
prodrug
chloropyramine
chloropyramine: RN given refers to parent cpd; structure		2.610aminopyridine
titanium dioxide
titanium dioxide: used medically as protectant against externally caused irritation & sunlight; high concentrations of dust may cause irritation to respiratory tract; RN given refers to titanium oxide (TiO2); structure. titanium dioxide : A titanium oxide with the formula TiO2. A naturally occurring oxide sourced from ilmenite, rutile and anatase, it has a wide range of applications.		4.811titanium oxidesfood colouring
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.		2.6106-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazoleantinematodal 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		2.610pyridines;
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.		2.610aminoglycoside antibiotic;
anthracycline;
p-quinones;
tetracenequinones		antineoplastic agent;
bacterial metabolite
transferrin
Transferrin: An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.		2.610
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.		2.2510ADP-sugarEscherichia 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.		2.610azide;
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).		12.1942taxane diterpenoid;
tetracyclic diterpenoid		antineoplastic agent;
human metabolite;
metabolite;
microtubule-stabilising agent
etoposide
[no description available]		2.2510beta-D-glucoside;
furonaphthodioxole;
organic heterotetracyclic compound		antineoplastic agent;
DNA synthesis inhibitor
ribavirin
Rebetron: Rebetron is tradename		2.6101-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
pyridoxal phosphate
[no description available]		2.610pyridinecarbaldehyde
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		2.610benzamides;
carboxylic ester
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.		2.610alkanethiol;
L-proline derivative;
N-acylpyrrolidine;
pyrrolidinemonocarboxylic acid		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
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.		2.6101,2-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.		2.610
salmeterol xinafoate
Salmeterol Xinafoate: A selective ADRENERGIC BETA-2 RECEPTOR agonist that functions as a BRONCHODILATOR when administered by inhalation. It is used to manage the symptoms of ASTHMA and CHRONIC OBSTRUCTIVE PULMONARY DISEASE.		4.811naphthoic acid
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.		2.610aromatic 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.		2.610biphenyls;
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.		2.610imidazoquinolineantineoplastic 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.		2.6106-aminopurines;
ether;
phosphonic acids		antiviral drug;
DNA synthesis inhibitor;
drug metabolite;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent
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.		2.610phosphonic acids;
pyrimidone		anti-HIV agent;
antineoplastic agent;
antiviral drug;
photosensitizing agent
celgosivir
celgosivir: inhibits glycoprotein processing & the growth of HIVs		2.610
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.		2.610organofluorine 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]		2.610monothioacetal;
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]		7.3110carbamate 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.		2.610biphenylyltetrazole;
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.		2.610guanidinesantiviral 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.		2.6106-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.		2.610monothioacetal;
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.		2.1710carbamate ester;
cytidines;
organofluorine compound		antimetabolite;
antineoplastic agent;
prodrug
adenosine
quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit		4.811adenosines;
purines D-ribonucleoside		analgesic;
anti-arrhythmia drug;
fundamental metabolite;
human metabolite;
vasodilator agent
octyl gallate
[no description available]		2.610gallate esterfood antioxidant;
hypoglycemic agent;
plant metabolite
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.		2.610acetylenic 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.		2.610aryl sulfide;
benzamides;
organic heterobicyclic compound;
phenols;
secondary alcohol;
tertiary amino compound		antineoplastic agent;
HIV protease inhibitor
glucose, (beta-d)-isomer
beta-D-glucose : D-Glucopyranose with beta configuration at the anomeric centre.. (1->4)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->4) linkages.. (1->3)-beta-D-glucan : A beta-D-glucan in which the glucose units are connected by (1->3) linkages.		4.811D-glucopyranoseepitope;
mouse metabolite
betulinic acid
[no description available]		2.610hydroxy 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		2.610lignan
baicalin
[no description available]		2.610dihydroxyflavone;
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.		2.610azacycloalkane;
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]		2.610carbamate 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.		2.610acetamides;
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.		2.610flavans;
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.		2.610gallate ester;
galloyl beta-D-glucose		anti-inflammatory agent;
antineoplastic agent;
geroprotector;
hepatoprotective agent;
plant metabolite;
radiation protective agent;
radical scavenger
cephalotaxine
[no description available]		2.610benzazepine 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.		2.610hydrochloridedrug allergen
mefloquine hydrochloride
[no description available]		2.610hydrochloride
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.		2.610epoxide;
ethyl ester;
L-leucine derivative;
monocarboxylic acid amide		anticoronaviral agent;
cathepsin B inhibitor
propazole
propazole: RN given refers to parent cpd; structure		2.610benzimidazoles
prulifloxacin
prulifloxacin: structure given in first source		2.610fluoroquinolone 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.		2.610benzimidazoles;
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		2.610trihydroxybenzoic acidmetabolite
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)		4.8112-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.		2.6101,1-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.		2.610organic peroxide;
sesquiterpene lactone		antimalarial;
plant metabolite
brinzolamide
brinzolamide: an antiglaucoma agent		2.610sulfonamide;
thienothiazine		antiglaucoma drug;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
dipropylacetamide
dipropylacetamide: structure. valpromide : A fatty amide derived from valproic acid.		2.610fatty amidegeroprotector;
metabolite;
teratogenic agent
oxprenolol hydrochloride
[no description available]		2.610
opipramol hydrochloride
[no description available]		2.610
moroxydine
[no description available]		2.610biguanides
thioxolone
tioxolone : A 1,3-benzoxathiole having a hydroxy substituent at the 6-position.		2.610benzoxathioleantiseborrheic
honokiol
[no description available]		2.610biphenyls
nobiletin
nobiletin : A methoxyflavone that is flavone substituted by methoxy groups at positions 5, 6, 7, 8, 3' and 4' respectively.		2.610methoxyflavoneantineoplastic 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.		2.610indolizidine alkaloidanticoronaviral agent;
antimalarial;
plant metabolite;
protein synthesis inhibitor
leupeptin
[no description available]		2.610aldehyde;
tripeptide		bacterial metabolite;
calpain inhibitor;
cathepsin B inhibitor;
EC 3.4.21.4 (trypsin) inhibitor;
serine protease inhibitor
tetrandrine
tetrandrine: a bisbenzylisoquinoline that exhibits antifibrogenic activity		2.610bisbenzylisoquinoline alkaloid;
isoquinolines
calpeptin
[no description available]		2.610amino acid amide
fangchinoline
[no description available]		2.610aromatic 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		2.610dihydroxy 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.		2.610hydroxy-1,2-naphthoquinone
loganin
[no description available]		2.610beta-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
fibrinogen
Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.. D-iditol : The D-enantiomer of iditol.		4.811iditolfungal metabolite
moexipril
[no description available]		2.610peptide
aucubin
[no description available]		2.610organic molecular entitymetabolite
catalpol
[no description available]		2.610organic molecular entitymetabolite
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.		2.6102-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile
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.		2.610methyladenosine
sivelestat
sivelestat: inhibitor of neutrophil elastase; structure given in first source		2.610N-acylglycine;
pivalate ester
pyronaridine
[no description available]		2.610aminoquinoline
geniposide
[no description available]		2.610terpene glycoside
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).		2.6107-hydroxyisoflavones 7-O-beta-D-glucoside;
hydroxyisoflavone;
monosaccharide derivative		plant metabolite
homoorientin
homoorientin: isolated from Swertia japonica; structure given in first source		4.811flavone C-glycoside;
tetrahydroxyflavone		antineoplastic agent;
radical scavenger
sophocarpine
[no description available]		2.610
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.		2.610hydroxamic acid;
secondary carboxamide		antineoplastic agent;
matrix metalloproteinase inhibitor
elacridar
Elacridar: inhibitor of MDR1 PROTEIN; structure given in first source		2.610
celastrol
[no description available]		2.610monocarboxylic acid;
pentacyclic triterpenoid		anti-inflammatory drug;
antineoplastic agent;
antioxidant;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
Hsp90 inhibitor;
metabolite
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)		2.610leucine derivative
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.		2.610monocarboxylic 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.-)		2.610dicarboxylic acid monoamide;
epoxy monocarboxylic acid;
guanidines;
L-leucine derivative;
zwitterion		antimalarial;
antiparasitic agent;
protease inhibitor
umifenovir
umifenovir: an antiviral agent		2.610indolyl carboxylic acid
safinamide
safinamide: short-acting inhibitor of MOA-B; FCE 26743 is (S)-isomer, FCE 28073 is (R)-isomer; structure in first source		2.610amino 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		2.610hydroxamic 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]		6.05223beta-hydroxy-Delta(5)-steroid;
3beta-sterol;
pyridines		antineoplastic agent;
EC 1.14.99.9 (steroid 17alpha-monooxygenase) inhibitor
3,4-dihydro-5-methyl-1(2h)-isoquinolinone
3,4-dihydro-5-methyl-1(2H)-isoquinolinone: structure given in first source		3.3110isoquinolines
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).		2.610carbohydrazideantiviral drug;
HIV protease inhibitor
vx 497
N-3-(3-(3-methoxy-4-oxazol-5-ylphenyl)ureido)benzylcarbamic acid tetrahydrofuran-3-yl ester: structure in first source		2.610
bcx 1812
[no description available]		2.6103-hydroxy monocarboxylic acid;
acetamides;
cyclopentanols;
guanidines		antiviral drug;
EC 3.2.1.18 (exo-alpha-sialidase) inhibitor
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.		2.610methoxynaphthalene;
monocarboxylic acid		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
gout suppressant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
olmesartan
olmesartan: an active metabolite of CS 866		2.610biphenylyltetrazoleangiotensin receptor antagonist;
antihypertensive agent
telbivudine
[no description available]		2.610pyrimidine 2'-deoxyribonucleosideantiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) 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		2.610carboxylic ester
resiquimod
S 28463: structure given in first source		2.610imidazoquinoline
tanshinone ii a
tashinone IIA: a cardiovascular agent with antineoplastic activity; isolated from Salvia miltiorrhiza; structure in first source		2.610abietane diterpenoid
cyclo(alanylalanyl)
[no description available]		3.3110
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.		2.610hydroxy 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
angiotensin ii
Giapreza: injectable form of angiotensin II used to increase blood pressure in adult patients with septic or other distributive shock. Ile(5)-angiotensin II : An angiotensin II that acts on the central nervous system (PDB entry: 1N9V).		4.811amino acid zwitterion;
angiotensin II		human metabolite
migalastat
migalastat: a potent inhibitor of glycolipid biosynthesis		2.610piperidines
erlotinib
[no description available]		2.610aromatic ether;
quinazolines;
secondary amino compound;
terminal acetylenic compound		antineoplastic agent;
epidermal growth factor receptor antagonist;
protein kinase inhibitor
organophosphonates
hydrogenphosphite : A divalent inorganic anion resulting from the removal of a proton from two of the hydroxy groups of phosphorous acid.		4.811divalent inorganic anion;
phosphite ion
limonin
[no description available]		2.610epoxide;
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.		2.610glucosiduronic acid;
glycosyloxyflavone;
monosaccharide derivative;
trihydroxyflavone		antineoplastic agent;
proteasome inhibitor
etravirine
[no description available]		2.610aminopyrimidine;
aromatic ether;
dinitrile;
organobromine compound		antiviral agent;
HIV-1 reverse transcriptase inhibitor
chelidonine
chelidonine: benzophenanthridine derived from scoulerine from Chelidonium majus; RN given refers to parent cpd (chelidonine, (5bR-(5balpha,6beta,12alpha))-isomer)		2.610alkaloid antibiotic;
alkaloid fundamental parent;
benzophenanthridine alkaloid
4-n-butylresorcinol
4-n-butylresorcinol: structure in first source		2.610resorcinols
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.		2.610carbamate 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		2.610
lenalidomide
[no description available]		4.811aromatic amine;
dicarboximide;
isoindoles;
piperidones		angiogenesis inhibitor;
antineoplastic agent;
immunomodulator
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.		2.610amidobenzoic acid;
monohydroxybenzoic acid;
tosylate ester		STAT3 inhibitor
berbamine
[no description available]		2.610bisbenzylisoquinoline alkaloid;
isoquinolines
u-104
SLC-0111: a carbonic anhydrase inhibitor; structure in first source		2.610
7-hydroxy-5-methyl-2-(2-oxopropyl)-8-[3,4,5-trihydroxy-6-(hydroxymethyl)-2-oxanyl]-1-benzopyran-4-one
[no description available]		2.610glycoside
bortezomib
[no description available]		5.321amino 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.		2.6101,3-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		2.610salicylamides
carboplatin
[no description available]		7.0732
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.		2.610beta-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.		2.610cinchona alkaloidalpha-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.		2.610steroid 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.		2.610L-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.		2.6102,6-diaminopurinesantiviral drug;
drug allergen;
HIV-1 reverse transcriptase inhibitor
linezolid
[no description available]		2.610acetamides;
morpholines;
organofluorine compound;
oxazolidinone		antibacterial drug;
protein synthesis inhibitor
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.		2.610pyridoisoquinoline
(-)-usnic acid
(-)-usnic acid : The (-)-enantiomer of usnic acid.		2.610usnic acidEC 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.		2.610aldehyde;
tripeptide		cysteine protease inhibitor
resveratrol
trans-resveratrol : A resveratrol in which the double bond has E configuration.		2.610resveratrolantioxidant;
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.		2.610macrolide lactambacterial metabolite;
immunosuppressive agent
lycopene
[no description available]		2.610acyclic caroteneantioxidant;
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.		2.610macrolide antibioticantibacterial drug;
environmental contaminant;
xenobiotic
roflumilast
[no description available]		2.610aromatic 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.		2.6104-amino-1,2-oxazolidin-3-oneanti-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.		2.610N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide
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.		2.610dicarboxylic acid monoester;
monocarboxylic acid;
pentacyclic triterpenoid		HIV-1 maturation inhibitor;
metabolite
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.		2.610amino 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.		2.610nucleoside analogue;
phosphonic acids		antiviral drug;
drug metabolite;
HIV-1 reverse transcriptase inhibitor
posaconazole
[no description available]		2.610aromatic ether;
conazole antifungal drug;
N-arylpiperazine;
organofluorine compound;
oxolanes;
triazole antifungal drug;
triazoles		trypanocidal drug
gw 257406x
maribavir: has antiviral activity against human cytomegalovirus		2.610
shikonin
shikonin: a naphthazarin; has antineoplastic and angiogenesis inhibiting activities		2.610hydroxy-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]		2.610tropane alkaloid
cmx 001
[no description available]		2.610
amd 8664
[no description available]		2.610
bay 41-4109
BAY 41-4109: structure in first source		2.610
bay 57-1293
pritelivir: herpes simplex virus 1 helicase-primase inhibitor		2.610
2'-c-methylcytidine
2'-C-methylcytidine: structure in first source		2.610
isoxanthohumol
isoxanthohumol: structure in first source		2.610flavanones
4-(4-chloro-2-methylphenoxy)-n-hydroxybutanamide
4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide: a c-FLIP inhibitor; structure in first source		2.610aromatic ether
mecarbinate
[no description available]		2.610
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.		2.610tetrapeptideprotease 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.		2.610
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.		2.610aryl 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		2.610
3,4'-dihydroxyflavone
3,4'-dihydroxyflavone: an antioxidant; structure in first source		2.610
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.		2.610methoxycinnamic acid
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.		2.610ferulic acidsantioxidant;
biomarker;
metabolite
cyclouridine
cyclouridine: structure given in third source		2.610
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.		2.610aromatic 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
thiohydantoins
Thiohydantoins: Sulfur analogs of hydantoins with one or both carbonyl groups replaced by thiocarbonyl groups.		7.833
zucapsaicin
[no description available]		2.610methoxybenzenes;
phenols
nbd 556
[no description available]		2.610
chlorogenic acid
caffeoylquinic acid: Antiviral Agent; structure in first source. chlorogenate : A monocarboxylic acid anion that is the conjugate base of chlorogenic acid; major species at pH 7.3.		4.811cinnamate ester;
tannin		food component;
plant metabolite
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.		2.6102-aminopurinesanticoronaviral agent;
antimetabolite;
antineoplastic agent
thiourea
Thiourea: A photographic fixative used also in the manufacture of resins. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance may reasonably be anticipated to be a carcinogen (Merck Index, 9th ed). Many of its derivatives are ANTITHYROID AGENTS and/or FREE RADICAL SCAVENGERS.. thiourea : The simplest member of the thiourea class, consisting of urea with the oxygen atom substituted by sulfur.		4.811one-carbon compound;
thioureas;
ureas		antioxidant;
chromophore
4,5,6,7-tetrachloroindan-1,3-dione
4,5,6,7-tetrachloroindan-1,3-dione: inhibits ubiquitin C-terminal hydrolase L1		2.610
srpin340
SRPIN340: Serine-Arginine-Rich Protein Kinase Inhibitor		2.610
pr-619
[no description available]		2.610
p5091
P5091: inhibits ubiquitin-specific protease 7; structure in first source		2.610
fusidic acid
Fusidic Acid: An antibiotic isolated from the fermentation broth of Fusidium coccineum. (From Merck Index, 11th ed). It acts by inhibiting translocation during protein synthesis.. fusidic acid : A steroid antibiotic that is isolated from the fermentation broth of Fusidium coccineum.		7.61011alpha-hydroxy steroid;
3alpha-hydroxy steroid;
alpha,beta-unsaturated monocarboxylic acid;
steroid acid;
steroid antibiotic;
sterol ester		EC 2.7.1.33 (pantothenate kinase) inhibitor;
Escherichia coli metabolite;
protein synthesis inhibitor
trovirdine
trovirdine: HIV-1 reverse transcriptase inhibitor		2.610
fti 277
[no description available]		2.610
u 0126
U 0126: protein kinase kinase inhibitor; structure in first source		2.610aryl sulfide;
dinitrile;
enamine;
substituted aniline		antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
osteogenesis regulator;
vasoconstrictor agent
vicriviroc
vicriviroc: structure in first source		2.610(trifluoromethyl)benzenes
telaprevir
[no description available]		2.610cyclopentapyrrole;
cyclopropanes;
oligopeptide;
pyrazines		antiviral drug;
hepatitis C protease inhibitor;
peptidomimetic
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.		2.610beta-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
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).		2.6101,3-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
yya-021
YYA-021: an HIV entry inhibitor; structure in first source		2.610
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		2.610C-nitro compound;
maleimides;
monochlorobenzenes;
phenols;
secondary amino compound;
substituted aniline		antioxidant;
apoptosis inducer;
EC 2.7.11.26 (tau-protein kinase) inhibitor;
neuroprotective agent
sitagliptin
sitagliptin : A triazolopyrazine that exhibits hypoglycemic activity.		2.610triazolopyrazine;
trifluorobenzene		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
environmental contaminant;
hypoglycemic agent;
serine proteinase inhibitor;
xenobiotic
tak-220
TAK-220: structure in first source		2.610
jtk-303
[no description available]		2.610aromatic ether;
monochlorobenzenes;
organofluorine compound;
quinolinemonocarboxylic acid;
quinolone		HIV-1 integrase inhibitor
nbd 557
[no description available]		2.610
luteolin
[no description available]		4.8113'-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.		2.610cinnamate 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.		2.610beta-D-glucoside;
glycosyloxyflavone;
monosaccharide derivative;
trihydroxyflavone		antioxidant;
plant metabolite
cyclosporine
[no description available]		2.610
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.		2.610harmala alkaloidanti-HIV agent;
EC 1.4.3.4 (monoamine oxidase) inhibitor;
metabolite
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.		2.610dicarboxylic 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.		2.610carboxylic 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.		2.6102-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]		2.610biflavonoid;
hydroxyflavone;
ring assembly		angiogenesis inhibitor;
antiviral agent;
cathepsin B inhibitor;
P450 inhibitor;
plant metabolite
baicalein
[no description available]		2.610trihydroxyflavoneangiogenesis 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.		2.610dihydroxyflavone;
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.		2.610beta-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.		2.610aromatic 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.		2.6107-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.		2.6107-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.		2.6103'-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.		2.610tetrahydroxyflavonemetabolite
trans-2,3',4,5'-tetrahydroxystilbene
trans-2,3',4,5'-tetrahydroxystilbene: hydroxystilbene oxyresveratrol		2.610stilbenoid
polydatin
trans-piceid : A stilbenoid that is trans-resveratrol substituted at position 3 by a beta-D-glucosyl residue.		2.610beta-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		2.610organooxygen compoundgeroprotector;
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.		2.610catechols;
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.		2.610sulfonamide;
thiophenes		antiglaucoma drug;
antihypertensive agent;
EC 4.2.1.1 (carbonic anhydrase) 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.		2.610cyclic ketal;
ketohexose derivative;
sulfamate ester		anticonvulsant;
sodium channel blocker
fluticasone
Fluticasone: A STEROID with GLUCOCORTICOID RECEPTOR activity that is used to manage the symptoms of ASTHMA; ALLERGIC RHINITIS, and ATOPIC DERMATITIS.. fluticasone : A trifluorinated corticosteroid used in the form of its propionate ester for treatment of allergic rhinitis.		4.81111beta-hydroxy steroid;
17alpha-hydroxy steroid;
3-oxo-Delta(4) steroid;
corticosteroid;
fluorinated steroid;
thioester		anti-allergic agent;
anti-asthmatic drug
benzyloxycarbonyl-phe-ala-fluormethylketone
cathepsin B inhibitor : A cysteine protease inhibitor which inhibits cathepsin B (EC 3.4.22.1).		2.610
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.		2.610carboxylic ester;
difluorobenzene;
dipeptide;
tert-butyl ester		EC 3.4.23.46 (memapsin 2) inhibitor
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.		2.610dihydroxyflavone;
tetramethoxyflavone		apoptosis inducer;
plant 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.		2.610dihydroxyflavone;
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.		2.610beta-D-glucoside;
resorcinols;
stilbenoid		anti-inflammatory agent;
antioxidant;
apoptosis inhibitor;
cardioprotective agent;
cyclooxygenase 2 inhibitor;
platelet aggregation inhibitor
tyrphostin ag 555
[no description available]		2.610
pd 151746
[no description available]		2.610
strontium
Strontium: An element of the alkaline earth family of metals. It has the atomic symbol Sr, atomic number 38, and atomic weight 87.62.		4.811alkaline earth metal atom
bismuth
Bismuth: A metallic element that has the atomic symbol Bi, and atomic number 83. Its principal isotope is Bismuth 209.		4.811metal atom;
pnictogen
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.		2.610dipeptideEC 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.		2.610
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.		2.610hydroxamic 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.		2.610dicarboxylic acid diamide;
N-(2-hydroxyethyl)piperazine;
piperazinecarboxamide		HIV protease inhibitor
sulfur
Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight [32.059; 32.076]. It is found in the amino acids cysteine and methionine.		4.811chalcogen;
nonmetal atom		macronutrient
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).		2.610nonaprenol;
primary alcohol		plant metabolite
pepstatin
pepstatin: inhibits the aspartic protease endothiapepsin		2.610pentapeptide;
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.		2.610carbamate ester;
monocarboxylic acid amide;
peptide;
secondary alcohol		EC 3.4.23.46 (memapsin 2) inhibitor;
peptidomimetic
bms 806
BMS 806: prevents entry of HIV into cells by binding HIV envelope protein gp120; no further info available 4/2002		2.610
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
[no description available]		2.610
tulobuterol hydrochloride
[no description available]		2.610organic molecular entity
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).		2.610aminal;
organochlorine compound;
quinolines;
secondary carboxamide;
thioureas
radium
Radium: A radioactive element of the alkaline earth series of metals. It has the atomic symbol Ra and atomic number 88. Radium is the product of the disintegration of URANIUM and is present in pitchblende and all ores containing uranium. It is used clinically as a source of beta and gamma-rays in radiotherapy, particularly BRACHYTHERAPY.		8.9911alkaline earth metal atom
germacrone
germacrone: isolated from Curcuma wenyujin		2.610germacrane 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		2.610
lithospermic acid
[no description available]		2.610
laq824
LAQ824: Histone deacetylase inhibitor		2.610
ekb 569
EKB 569: an EGF receptor kinase inhibitor		2.610aminoquinoline;
monocarboxylic acid amide;
monochlorobenzenes;
nitrile		protein kinase inhibitor
rilpivirine
[no description available]		2.610aminopyrimidine;
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]		2.610germacranolide
4,5-di-O-caffeoylquinic acid
[no description available]		2.610quinic 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.		2.610
artesunate
artesunic acid: RN given for (3R-(3alpha,5abeta,6beta,8abeta,9alpha,10alpha,12beta,(2aR*))-isomer; succinic ester of artemether		2.610artemisinin derivative;
cyclic acetal;
dicarboxylic acid monoester;
hemisuccinate;
semisynthetic derivative;
sesquiterpenoid		antimalarial;
antineoplastic agent;
ferroptosis inducer
(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]		2.610oligopeptide
pd 184352
2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide: inhibits MAP kinase kinase; structure in first source		2.3110aminobenzoic acid
vildagliptin
[no description available]		2.610amino acid amide
belinostat
[no description available]		2.610hydroxamic acid;
olefinic compound;
sulfonamide		antineoplastic agent;
EC 3.5.1.98 (histone deacetylase) inhibitor
hdac-42
HDAC-42: structure in first source		2.610amidobenzoic acid
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.		2.610biguanides;
monochlorobenzenes		antibacterial agent;
antiinfective agent
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.		2.6106-aminopurines;
ether;
isopropyl ester;
L-alanine derivative;
phosphoramidate ester		antiviral drug;
HIV-1 reverse transcriptase inhibitor;
prodrug
iniparib
[no description available]		4.0830carbonyl compound;
organohalogen compound
n-(2-amino-5-fluorobenzyl)-4-(n-(pyridine-3-acrylyl)aminomethyl)benzamide
[no description available]		2.610
pri-2205
[no description available]		2.610
mk 0752
[no description available]		2.610
givinostat
[no description available]		2.610carbamate ester
pd 144418
[no description available]		2.610
bicyclol
bicyclol: an antihepatitis drug, on the metabolism and hepatotoxicity of aflatoxin B1 (AFB1) in rats.		2.610
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.		6.1663pyridines;
sterol ester		antineoplastic agent;
EC 1.14.99.9 (steroid 17alpha-monooxygenase) inhibitor;
prodrug
midostaurin
midostaurin : An organic heterooctacyclic compound that is the N-benzoyl derivative of staurosporine.		2.610benzamides;
gamma-lactam;
indolocarbazole;
organic heterooctacyclic compound		antineoplastic agent;
EC 2.7.11.13 (protein kinase C) inhibitor
ly 450139
[no description available]		2.610peptide
akr 501
avatrombopag: enhances megakaryocytopoiesis; structure in first source		2.2510
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).		2.610aminopyrimidine;
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
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.		2.610aromatic 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		2.610aromatic ether
ginsenoside rb1
[no description available]		2.610ginsenoside;
glycoside;
tetracyclic triterpenoid		anti-inflammatory drug;
anti-obesity agent;
apoptosis inhibitor;
neuroprotective agent;
plant metabolite;
radical scavenger
hki 272
[no description available]		2.1710nitrile;
quinolines		antineoplastic agent;
tyrosine kinase inhibitor
rucaparib
AG14447: Poly(ADP-ribose) polymerase inhibitor; structure in first source		8.73380azepinoindole;
caprolactams;
organofluorine compound;
secondary amino compound		antineoplastic agent;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
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]		2.610organonitrogen heterocyclic compound;
organosulfur heterocyclic compound
cetilistat
cetilistat: lipase inhibitor in randomized, placebo-controlled study of weight reduction in obese patients (3/2007)		2.610benzoxazine
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		2.610aromatic amide
aluminum oxide
Aluminum Oxide: An oxide of aluminum, occurring in nature as various minerals such as bauxite, corundum, etc. It is used as an adsorbent, desiccating agent, and catalyst, and in the manufacture of dental cements and refractories.		4.811
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.		2.610aminopiperidine;
quinazolines		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
azd 6244
AZD 6244: a MEK inhibitor		2.610benzimidazoles;
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		2.610
apilimod
[no description available]		2.610
apixaban
[no description available]		2.610aromatic ether;
lactam;
piperidones;
pyrazolopyridine		anticoagulant;
EC 3.4.21.6 (coagulation factor Xa) inhibitor
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.		2.610benzamides;
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.		2.610chloropyridine;
monocarboxylic acid amide;
tertiary amino compound;
thiazolopyridine		anticoagulant;
EC 3.4.21.6 (coagulation factor Xa) inhibitor;
platelet aggregation inhibitor
saracatinib
[no description available]		2.610aromatic 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
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.		2.610tripeptide;
ureas		antiviral drug;
hepatitis C protease inhibitor;
peptidomimetic
ly 411575
[no description available]		2.610dibenzoazepine;
difluorobenzene;
lactam;
secondary alcohol		EC 3.4.23.46 (memapsin 2) inhibitor
galidesivir
[no description available]		2.610
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.		2.610aromatic ether;
piperazines;
tetralins		anticoronaviral agent;
antineoplastic agent;
apoptosis inducer;
sigma-2 receptor agonist
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		2.610
epoxomicin
[no description available]		2.610morpholines;
tripeptide		proteasome inhibitor
bms 477118
[no description available]		2.610adamantanes;
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		2.610
tmc 353121
[no description available]		2.610
amd 070
mavorixafor: a derivative of AMD3100; a CXCR4 blocker		2.610aminoquinoline
danoprevir
[no description available]		2.610
bms-626529
[no description available]		2.610
bms-663068
fostemsavir: an HIV-1 attachment inhibitor; structure in first source		2.610
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		2.1710cyclic ketal;
cyclic ketone;
macrocycle;
polycyclic ether;
polyether;
primary amino compound		antineoplastic agent;
microtubule-destabilising agent
amenamevir
ASP2151: a herpesvirus helicase-primase inhibitor, in a guinea pig model of genital herpes; structure in first source		2.610
vx 765
belnacasan: a NSAID		2.610dipeptide
Dihydrotanshinone I
dihydrotanshinone I: extracted from Radix Salviae		2.610abietane diterpenoidanticoronaviral agent
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.		2.610nitrile;
piperidines;
primary amino compound;
pyrimidines		EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
hypoglycemic agent
fr 180204
FR 180204: structure in first source		2.610pyrazoles;
ring assembly
quisinostat
[no description available]		2.610indoles
carfilzomib
[no description available]		5.321epoxide;
morpholines;
tetrapeptide		antineoplastic agent;
proteasome inhibitor
hcv 796
HCV 796: inhibits HCV RdRp; structure in first source		2.610
resminostat
resminostat: a histone deacetylase inhibitor; structure in first source		2.610
zk 756326
2-(2-(4-(3-phenoxybenzyl)piperazin-1-yl)ethoxy)ethanol: a CC chemokine receptor CCR8 agonist; structure in first source		2.610aromatic ether
balapiravir
balapiravir: a prodrug of R1479; structure in first source		2.610
trametinib
[no description available]		2.610acetamides;
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
deoxyarbutin
4-((tetrahydro-2H-pyran-2-yl)oxy)phenol: has antineoplastic activity; structure in first source		2.610
abexinostat
abexinostat: structure in first source		2.610benzofurans
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.		2.610dioxanes;
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.		2.610azabicyclohexane;
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
empagliflozin
[no description available]		4.811aromatic ether;
C-glycosyl compound;
monochlorobenzenes;
tetrahydrofuryl ether		hypoglycemic agent;
sodium-glucose transport protein subtype 2 inhibitor
teneligliptin
[no description available]		2.610amino acid amide
ly2603618
[no description available]		3.1910ureas
dextrothyroxine
[no description available]		2.610
veliparib
[no description available]		7.07200benzimidazolesEC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
pf 03491390
[no description available]		2.610
alloin
[no description available]		2.610anthracenes;
C-glycosyl compound;
cyclic ketone;
phenols		laxative;
metabolite
nad
NAD(1-) : An anionic form of nicotinamide adenine dinucleotide arising from deprotonation of the two OH groups of the diphosphate moiety.		2.2510organophosphate oxoanioncofactor;
human metabolite;
hydrogen acceptor;
Saccharomyces cerevisiae metabolite
mdv 3100
[no description available]		2.610(trifluoromethyl)benzenes;
benzamides;
imidazolidinone;
monofluorobenzenes;
nitrile;
thiocarbonyl compound		androgen antagonist;
antineoplastic agent
bms-650032
asunaprevir: an NS3 protease inhibitor against hepatitis C virus		2.610oligopeptide
rg 7128
2'-fluoro-2'-methyl-3',5'-diisobutyryldeoxycytidine: inhibits HCV polymerase; structure in first source		2.610
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.		2.610disaccharide derivative;
glycopeptide;
semisynthetic derivative		antibacterial drug;
antimicrobial agent
cellulose
DEAE-Cellulose: Cellulose derivative used in chromatography, as ion-exchange material, and for various industrial applications.		4.811glycoside
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.		2.610cyclopentanols;
indanes;
pyrrolopyrimidine;
secondary amino compound;
sulfamidate		antineoplastic agent;
apoptosis inducer
uk 453,061
UK 453,061: a reverse transcriptase inhibitor/anti-HIV agent; structure in first source		2.610aromatic ether
N-(2-aminophenyl)-2-pyrazinecarboxamide
[no description available]		2.610aromatic amide
tegobuvir
tegobuvir: a non-structural protein 5B polymerase inhibitor		2.610
pf-429242
PF-429242: a subtilisin kexin isozyme-1/site-1 protease inhibitor		2.610
olaparib
[no description available]		9.21560cyclopropanes;
monofluorobenzenes;
N-acylpiperazine;
phthalazines		antineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
cx 4945
[no description available]		2.610
pci 34051
PCI 34051: an HDAC8 inhibitor		2.610indolecarboxamide
cep-9722
CEP-9722: a prodrug of the poly(ADP-ribose) polymerase inhibitor CEP-8983		3.2710
lomibuvir
lomibuvir: an antiviral agent with polymerase NS5 inhibitory activity		2.610thiophenecarboxylic acid
delanzomib
[no description available]		2.610C-terminal boronic acid peptide;
phenylpyridine;
secondary alcohol;
threonine derivative		antineoplastic agent;
apoptosis inducer;
proteasome inhibitor
pitavastatin(1-)
pitavastatin(1-) : A hydroxy monocarboxylic acid anion that is the conjugate base of pitavastatin, obtained by deprotonation of the carboxy group.		2.610hydroxy monocarboxylic acid anion
mk-1775
adavosertib: a Wee1 kinase inhibitor; structure in first source		3.8620piperazines
apalutamide
[no description available]		6.0522
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).		2.610benzamides;
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		2.610carbamate ester
jzl 184
JZL 184: inhibits monoacylglycerol lipase; structure in first source		2.610benzodioxoles
gsk 650394
[no description available]		2.610phenylpyridine
oprozomib
ONX 0912: antineoplastic; an orally active proteasome inhibitor; structure in first source		2.610
az 960
[no description available]		2.610
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).		2.610diastereoisomeric mixturecis-Golgi ArfGEF GBF inhibitor
cobicistat
[no description available]		2.6101,3-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.		2.610biphenyls;
carbamate ester;
carboxamide;
imidazoles;
valine derivative		antiviral drug;
nonstructural protein 5A inhibitor
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.		2.610benzamides;
boronic acids;
dichlorobenzene;
glycine derivative		antineoplastic agent;
apoptosis inducer;
drug metabolite;
orphan drug;
proteasome inhibitor
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		2.610
plx4032
[no description available]		4.811aromatic ketone;
difluorobenzene;
monochlorobenzenes;
pyrrolopyridine;
sulfonamide		antineoplastic agent;
B-Raf inhibitor
5-(3-methylsulfonylphenyl)-4-[(1-methyl-5-tetrazolyl)thio]thieno[2,3-d]pyrimidine
[no description available]		2.610aryl sulfide;
thienopyrimidine
baricitinib
[no description available]		2.610azetidines;
nitrile;
pyrazoles;
pyrrolopyrimidine;
sulfonamide		anti-inflammatory agent;
antirheumatic drug;
antiviral agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
immunosuppressive agent
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).		2.610acetamides;
benzamides;
naphthalenes;
secondary carboxamide		anticoronaviral agent;
protease inhibitor
piperidines
Piperidines: A family of hexahydropyridines.		20.0517849
e-52862
[no description available]		2.610
ly2811376
[no description available]		2.610
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.		2.1510benzamides;
bridged compound;
dicarboximide;
quinolines		axin stabilizer;
Wnt signalling inhibitor
anagliptin
anagliptin: anagliptin hydrochloride salt is the active compound		2.610amino acid amide
gardiquimod
[no description available]		2.610
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.		2.610aromatic ether;
azamacrocycle;
carbamate ester;
cyclopropanes;
lactam;
N-sulfonylcarboxamide;
quinoxaline derivative		antiviral drug;
hepatitis C protease inhibitor;
hepatoprotective agent
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.		2.610
letermovir
letermovir: has antiviral activity; structure in first source		2.610
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.		2.610isopropyl 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		2.610benzoxazole
blz 945
[no description available]		2.610
azd3839
AZD3839: a BACE1 inhibitor; structure in first source		2.610
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.		2.610
unc 0638
UNC 0638: inhibits lysine methyltransferases G9a and GLP; structure in first source		2.610quinazolines
gs-9620
[no description available]		2.610
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		2.610
bms 708163
BMS 708163: structure in first source		2.610oxadiazole;
ring assembly
jq1 compound
[no description available]		2.610carboxylic 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
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		2.610
gsk525762a
molibresib: mimicks acetylated histones; structure in first source		2.610benzodiazepine
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).		2.610aromatic amine;
aromatic ether;
benzimidazoles;
primary amino compound;
quinazolines;
secondary amino compound		antineoplastic agent
birinapant
birinapant: a Smac mimetic with antineoplastic activity		2.610dipeptide
ly2886721
[no description available]		2.610
nms-p118
NMS-P118: a PARP-1 inhibitor; structure in first source		2.8220
tubastatin a
[no description available]		2.610hydroxamic acid;
pyridoindole;
tertiary amino compound		EC 3.5.1.98 (histone deacetylase) inhibitor
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.		2.610benzimidazole;
hydroxamic acid;
olefinic compound;
tertiary amino compound		antimalarial;
antineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor
spautin-1
[no description available]		2.610
ldn 57444
LDN 57444: inhibitor of ubiquitin C-terminal hydrolase-L1; structure in first source		2.610
gsk1210151a
GSK1210151A: inhibitor of the BET family of proteins; structure in first source		2.610imidazoquinoline
i-bet726
[no description available]		2.610
acy-1215
ricolinostat: an HDAC6 inhibitor; structure in first source		2.610pyrimidinecarboxylic acid
cudc-907
[no description available]		2.610
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.		2.6101,3-thiazoles;
benzothiazine;
monocarboxylic acid amide		analgesic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
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.		2.610sulfonamideantiviral 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		2.610
gsk1265744
[no description available]		2.610difluorobenzene;
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.		2.610aromatic 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.		2.610aromatic ether;
naphthalenes;
pyrimidone;
sulfonamide		antiviral drug;
nonnucleoside hepatitis C virus polymerase inhibitor
byl719
[no description available]		4.811proline derivative
rgfp966
[no description available]		2.610
rg2833
RG2833: a histone deacetylase inhibitor; structure in first source		2.610
pi-1840
PI-1840: has both antineoplastic and proteasome inhibitory activities; structure in first source		2.610
acy-738
[no description available]		2.610
pelabresib
CPI-0610: a bromodomain and extra-terminal protein inhibitor with antineoplastic activity; structure in first source		2.610monochlorobenzenes;
organic heterotricyclic compound;
primary carboxamide		antineoplastic agent;
bromodomain-containing protein 4 inhibitor
gs-5806
presatovir: a respiratory syncytial virus entry inhibitor		2.610
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		3.5110
doravirine
[no description available]		2.610
gn6958
GN6958: inhibits SUMO-sentrin specific protease 1 (SENP1); structure in first source		2.610
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		2.610
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.		2.610azaspiro 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.		2.610carbamate 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		2.610
4-((1-butyl-3-phenylureido)methyl)-n-hydroxybenzamide
4-((1-butyl-3-phenylureido)methyl)-N-hydroxybenzamide: inhibits HDAC6; structure in first source		2.610
selinexor
selinexor: inhibits karyopherin XPO1		2.610
verdinexor
verdinexor: a selective inhibitor of nuclear export		2.610
cb-839
[no description available]		2.610
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.		2.610carbamate 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).		2.610
etp-46464
ETP-46464: inhibits ATM and Rad3-related kinase; structure in first source		3.1910
xen445
[no description available]		2.610
santacruzamate a
santacruzamate A: HDAC2 inhibitor from the Panamanian marine cyanobacterium cf. Symploca sp.; structure in first source		2.610organonitrogen compound;
organooxygen compound
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.		2.610aromatic 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]		2.6101,3,5-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		2.2510
s 8932
[no description available]		2.610aromatic amine;
C-nucleoside;
carboxylic ester;
nitrile;
phosphoramidate ester;
pyrrolotriazine		anticoronaviral agent;
antiviral drug;
prodrug
triciribine
triciribine: structure. triciribine : A nucleoside analogue in which the nucleobase portion is a 1,4,5,6,8-pentaazaacenaphthylene ring system substituted with an amino group at position 3, and a methyl group at position 5 and is bound to the beta-D-ribofuranosyl moiety by an N(1)-glycosidic linkage.		2.3110
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.		2.6102-aminopurines;
oxopurine;
primary alcohol;
secondary alcohol		antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
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.		2.6102-aminopurines;
oxopurine		antimetabolite;
antiviral drug
nu 1025
NU 1064: structure in first source		3.8220phenols;
quinazolines		EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
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.		2.610folic acids;
N-acyl-amino acid		human metabolite;
mouse metabolite;
nutrient
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.		2.610purine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor;
geroprotector;
HIV-1 reverse transcriptase inhibitor
ganciclovir
[no description available]		2.6102-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.		2.610L-valyl esterantiviral 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.		2.6102-aminopurines;
propane-1,3-diols		antiviral drug
4-hydroxyquinazoline
4-oxo-3,4-dihydroquinazoline: structure in first source		2.610quinazolines
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		2.610carboxamidine;
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.		2.610dibenzodiazepine;
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).		2.610N-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
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.		2.610(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.		2.6101,2,4-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.		2.1510(trifluoromethyl)benzenes;
thiopyranopyrimidine		tankyrase inhibitor
hesperadin
[no description available]		2.610
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		2.610
n'-(3,4-dihydroxybenzylidene)-3-hydroxy-2-naphthahydrazide
[no description available]		2.610catechols;
hydrazide;
hydrazone;
naphthols		EC 3.6.5.5 (dynamin GTPase) inhibitor
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.		2.610benzofuropyrimidine;
organochlorine compound;
pyrrolidines		antineoplastic agent;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
bmn 673
talazoparib: inhibits both PARP1 and PARP2; structure in first source		7.71230
me0328
ME0328: inhibits ARTD3; structure in first source		2.610
nvp-tnks656
[no description available]		2.610
leptin
Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.		4.811
pyrimidinones
Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.		2.3110
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.		2.1510
ConditionIndicatedRelationship StrengthStudiesTrials
Cell Transformation, Neoplastic
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.		02.4520
Benign Neoplasms
[description not available]		013.082212
Neoplasms
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.		117.694224
Congenital Zika Syndrome
[description not available]		02.6620
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		010.27139
Zika Virus Infection
A viral disease transmitted by the bite of AEDES mosquitoes infected with ZIKA VIRUS. Its mild DENGUE-like symptoms include fever, rash, headaches and ARTHRALGIA. The viral infection during pregnancy, in rare cases, is associated with congenital brain and ocular abnormalities, called Congenital Zika Syndrome, including MICROCEPHALY and may also lead to GUILLAIN-BARRE SYNDROME.		02.6620
Breast Cancer
[description not available]		011.23195
Breast Neoplasms
Tumors or cancer of the human BREAST.		117.315715
ER-Negative PR-Negative HER2-Negative Breast Cancer
[description not available]		03.8330
Triple Negative Breast Neoplasms
Breast neoplasms that do not express ESTROGEN RECEPTORS; PROGESTERONE RECEPTORS; and do not overexpress the NEU RECEPTOR/HER-2 PROTO-ONCOGENE PROTEIN.		03.8330
Epithelial Ovarian Cancer
[description not available]		015.354916
Cancer of Ovary
[description not available]		021.03191100
Carcinoma, Ovarian Epithelial
A malignant neoplasm that originates in cells on the surface EPITHELIUM of the ovary and is the most common form of ovarian cancer. There are five histologic subtypes: papillary serous, endometrioid, mucinous, clear cell, and transitional cell. Mutations in BRCA1, OPCML, PRKN, PIK3CA, AKT1, CTNNB1, RRAS2, and CDH1 genes are associated with this cancer.		015.354916
Ovarian Neoplasms
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.		127.4573300
Carcinoma, Non-Small Cell Lung
[description not available]		09.76106
Cancer of Lung
[description not available]		010.12137
Carcinoma, Non-Small-Cell Lung
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.		111.76106
Lung Neoplasms
Tumors or cancer of the LUNG.		112.12137
Peritoneal Carcinomatosis
[description not available]		010.87127
Local Neoplasm Recurrence
[description not available]		017.026836
Peritoneal Neoplasms
Tumors or cancer of the PERITONEUM.		112.87127
Cancer of Pancreas
[description not available]		08.9454
Cancer of Prostate
[description not available]		013.312013
Chromosome Instability Syndromes
[description not available]		04.2120
Pancreatic Neoplasms
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).		110.9454
Prostatic Neoplasms
Tumors or cancer of the PROSTATE.		119.556039
HPV Infection
[description not available]		03.3310
Cancer of Cervix
[description not available]		03.8120
Cancer of Endometrium
[description not available]		05.4131
Uterine Cervical Neoplasms
Tumors or cancer of the UTERINE CERVIX.		16.7940
Endometrial Neoplasms
Tumors or cancer of ENDOMETRIUM, the mucous lining of the UTERUS. These neoplasms can be benign or malignant. Their classification and grading are based on the various cell types and the percent of undifferentiated cells.		110.0393
Papillomavirus Infections
Neoplasms of the skin and mucous membranes caused by papillomaviruses. They are usually benign but some have a high risk for malignant progression.		03.3310
Erythema Multiforme
A skin and mucous membrane disease characterized by an eruption of macules, papules, nodules, vesicles, and/or bullae with characteristic bull's-eye lesions usually occurring on the dorsal aspect of the hands and forearms.		07.4110
Thrombopenia
[description not available]		011.251714
Androgen-Independent Prostatic Cancer
[description not available]		09.77129
Thrombocytopenia
A subnormal level of BLOOD PLATELETS.		016.251714
Prostatic Neoplasms, Castration-Resistant
Tumors or cancer of the PROSTATE which can grow in the presence of low or residual amount of androgen hormones such as TESTOSTERONE.		111.77129
Pancytopenia
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.		07.610
Esophageal Squamous Cell Carcinoma
A carcinoma that originates usually from cells on the surface of the middle and lower third of the ESOPHAGUS. Tumor cells exhibit typical squamous morphology and form large polypoid lesions. Mutations in RNF6, LZTS1, TGFBR2, DEC1, and WWOX1 genes are associated with this cancer.		010.0721
Cancer of Esophagus
[description not available]		05.0721
Esophageal Neoplasms
Tumors or cancer of the ESOPHAGUS.		05.0721
Bone Cancer
[description not available]		02.4110
Bone Neoplasms
Tumors or cancer located in bone tissue or specific BONES.		02.4110
Minimal Disease, Residual
[description not available]		04.7211
Female Genital Neoplasms
[description not available]		03.3310
Genital Neoplasms, Female
Tumor or cancer of the female reproductive tract (GENITALIA, FEMALE).		03.3310
Blood Pressure, High
[description not available]		08.3965
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.		08.3965
Neutropenia
A decrease in the number of NEUTROPHILS found in the blood.		04.421
Carcinoma, Neuroendocrine
A group of carcinomas which share a characteristic morphology, often being composed of clusters and trabecular sheets of round blue cells, granular chromatin, and an attenuated rim of poorly demarcated cytoplasm. Neuroendocrine tumors include carcinoids, small (oat) cell carcinomas, medullary carcinoma of the thyroid, Merkel cell tumor, cutaneous neuroendocrine carcinoma, pancreatic islet cell tumors, and pheochromocytoma. Neurosecretory granules are found within the tumor cells. (Segen, Dictionary of Modern Medicine, 1992)		02.610
Body Weight
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.		0151010
Adenocarcinoma, Endometrioid
[description not available]		08.7754
Carcinoma, Endometrioid
An adenocarcinoma characterized by the presence of cells resembling the glandular cells of the ENDOMETRIUM. It is a common histological type of ovarian CARCINOMA and ENDOMETRIAL CARCINOMA. There is a high frequency of co-occurrence of this form of adenocarcinoma in both tissues.		08.7754
Male Genital Neoplasms
[description not available]		03.5210
Genital Neoplasms, Male
Tumor or cancer of the MALE GENITALIA.		03.5210
Pregnancy
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.		08.1554
Bladder Cancer
[description not available]		05.6822
Cancer of the Urinary Tract
[description not available]		03.9911
Urinary Bladder Neoplasms
Tumors or cancer of the URINARY BLADDER.		19.2844
Carcinoma, Transitional Cell
A malignant neoplasm derived from TRANSITIONAL EPITHELIAL CELLS, occurring chiefly in the URINARY BLADDER; URETERS; or RENAL PELVIS.		03.9911
Anemia
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.		02.6920
Malignant Mesothelioma
[description not available]		04.9132
Mesothelioma
A tumor derived from mesothelial tissue (peritoneum, pleura, pericardium). It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos. (Dorland, 27th ed)		111.0421
Adenoma, Prostatic
[description not available]		02.610
Prostatic Hyperplasia
Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.		02.610
Benign Neoplasms, Brain
[description not available]		08.1874
Brain Neoplasms
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.		08.1874
Cystadenocarcinoma, Serous
A malignant cystic or semicystic neoplasm. It often occurs in the ovary and usually bilaterally. The external surface is usually covered with papillary excrescences. Microscopically, the papillary patterns are predominantly epithelial overgrowths with differentiated and undifferentiated papillary serous cystadenocarcinoma cells. Psammoma bodies may be present. The tumor generally adheres to surrounding structures and produces ascites. (From Hughes, Obstetric-Gynecologic Terminology, 1972, p185)		02.6120
Disease Exacerbation
[description not available]		011.24108
Anemia, Hypoplastic
[description not available]		07.6344
Anemia, Aplastic
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.		07.6344
Proteinuria
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.		07.6344
Nausea
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.		07.8154
Cancer of Larynx
[description not available]		02.2110
Laryngeal Neoplasms
Cancers or tumors of the LARYNX or any of its parts: the GLOTTIS; EPIGLOTTIS; LARYNGEAL CARTILAGES; LARYNGEAL MUSCLES; and VOCAL CORDS.		02.2110
Cancer of Head
[description not available]		02.6920
Head and Neck Neoplasms
Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)		14.6920
Cancer of the Fallopian Tube
[description not available]		010.62117
Fallopian Tube Neoplasms
Benign or malignant neoplasms of the FALLOPIAN TUBES. They are uncommon. If they develop, they may be located in the wall or within the lumen as a growth attached to the wall by a stalk.		112.62117
Anxiety
Feelings or emotions of dread, apprehension, and impending disaster but not disabling as with ANXIETY DISORDERS.		07.2510
Depression
Depressive states usually of moderate intensity in contrast with MAJOR DEPRESSIVE DISORDER present in neurotic and psychotic disorders.		07.2510
Glial Cell Tumors
[description not available]		05.1931
Glioma
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)		05.1931
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		04.9921
Malignant Melanoma
[description not available]		05.2931
Cancer of Skin
[description not available]		02.2510
Melanoma
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)		112.2931
Skin Neoplasms
Tumors or cancer of the SKIN.		02.2510
Genetic Predisposition
[description not available]		05.4921
Chronic Illness
[description not available]		04.6211
Attachment Loss, Periodontal
[description not available]		04.6211
Infections, Coronavirus
[description not available]		04.6211
Chemical Dependence
[description not available]		04.6211
Cerebral Infarction, Middle Cerebral Artery
[description not available]		04.6211
Osteoarthritis of Knee
[description not available]		04.6211
Deafness, Transitory
[description not available]		04.6211
Liver Abscess, Pyogenic
Single or multiple areas of PUS due to bacterial infection within the hepatic parenchyma. It can be caused by a variety of BACTERIA, local or disseminated from infections elsewhere such as in APPENDICITIS; CHOLECYSTITIS; PERITONITIS; and after LIVER TRANSPLANTATION.		04.6211
Complications of Diabetes Mellitus
[description not available]		07.7444
Acute Liver Injury, Drug-Induced
[description not available]		04.6211
Acute Kidney Failure
[description not available]		07.7444
Carcinogenesis
The origin, production or development of cancer through genotypic and phenotypic changes which upset the normal balance between cell proliferation and cell death. Carcinogenesis generally requires a constellation of steps, which may occur quickly or over a period of many years.		07.7444
Adverse Drug Event
[description not available]		04.9421
Fatty Liver, Nonalcoholic
[description not available]		04.6211
2019 Novel Coronavirus Disease
[description not available]		07.7444
Ancylostomiasis
Infection of humans or animals with hookworms of the genus ANCYLOSTOMA. Characteristics include anemia, dyspepsia, eosinophilia, and abdominal swelling.		04.6211
Auricular Fibrillation
[description not available]		04.6211
Bladder Disorder, Neurogenic
[description not available]		04.6211
Acute Brain Injuries
[description not available]		04.6211
Carcinoma, Epidermoid
[description not available]		04.6211
Cerebral Ischemia
[description not available]		04.6211
Caries, Dental
[description not available]		04.6211
Alloxan Diabetes
[description not available]		04.6211
Diabetes Mellitus, Adult-Onset
[description not available]		04.6211
Canine Diseases
[description not available]		04.6211
Fistula
Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body.		04.6211
Cancer of Gastrointestinal Tract
[description not available]		04.6211
Astrocytoma, Grade IV
[description not available]		04.6211
Focal Segmental Glomerulosclerosis
[description not available]		04.6211
Cardiac Failure
[description not available]		07.7444
Bleeding
[description not available]		04.6211
Hepatocellular Carcinoma
[description not available]		04.9921
Innate Inflammatory Response
[description not available]		07.7444
Infections, Klebsiella
[description not available]		04.6211
Cirrhosis, Liver
[description not available]		04.6211
Liver Dysfunction
[description not available]		04.6211
Cancer of Liver
[description not available]		04.9921
Mitral Incompetence
[description not available]		04.6211
Kahler Disease
[description not available]		04.6211
Cardiomyopathies, Primary
[description not available]		04.6211
Angiogenesis, Pathologic
[description not available]		07.7444
Morbid Obesity
[description not available]		04.6211
Arthritis, Degenerative
[description not available]		04.6211
Pocket, Periodontal
[description not available]		04.6211
Pericementitis
[description not available]		04.6211
Complication, Postoperative
[description not available]		04.6211
Condition, Preneoplastic
[description not available]		04.6211
Embolism, Pulmonary
[description not available]		04.6211
Acute Respiratory Distress Syndrome
[description not available]		04.6211
Sarcoma, Epithelioid
[description not available]		04.6211
Linear Skull Fracture
[description not available]		04.6211
Cancer of Stomach
[description not available]		09.9399
Nicotine Addiction
[description not available]		04.6211
Zoonoses
Diseases of non-human animals that may be transmitted to HUMANS or may be transmitted from humans to non-human animals.		04.6211
Coxarthrosis
[description not available]		04.6211
Injury, Ischemia-Reperfusion
[description not available]		07.7444
MPTP Neurotoxicity Syndrome
[description not available]		04.6211
Shoulder Injuries
Injuries involving the SHOULDERS and SHOULDER JOINT.		04.6211
Hemorrhage, Gingival
[description not available]		04.6211
Acute Disease
Disease having a short and relatively severe course.		04.6211
Atrial Fibrillation
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.		04.6211
Biliary Tract Diseases
Diseases in any part of the BILIARY TRACT including the BILE DUCTS and the GALLBLADDER.		04.6211
Urinary Bladder, Neurogenic
Dysfunction of the URINARY BLADDER due to disease of the central or peripheral nervous system pathways involved in the control of URINATION. This is often associated with SPINAL CORD DISEASES, but may also be caused by BRAIN DISEASES or PERIPHERAL NERVE DISEASES.		04.6211
Brain Injuries
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.		04.6211
Carcinoma, Squamous Cell
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)		18.0522
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		07.7444
Brain Ischemia
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.		04.6211
Chronic Disease
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).		04.6211
Dental Caries
Localized destruction of the tooth surface initiated by decalcification of the enamel followed by enzymatic lysis of organic structures and leading to cavity formation. If left unchecked, the cavity may penetrate the enamel and dentin and reach the pulp.		04.6211
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		04.6211
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.		04.6211
Gingival Hemorrhage
The flowing of blood from the marginal gingival area, particularly the sulcus, seen in such conditions as GINGIVITIS, marginal PERIODONTITIS, injury, and ASCORBIC ACID DEFICIENCY.		04.6211
Glioblastoma
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.		16.6211
Glomerulosclerosis, Focal Segmental
A clinicopathological syndrome or diagnostic term for a type of glomerular injury that has multiple causes, primary or secondary. Clinical features include PROTEINURIA, reduced GLOMERULAR FILTRATION RATE, and EDEMA. Kidney biopsy initially indicates focal segmental glomerular consolidation (hyalinosis) or scarring which can progress to globally sclerotic glomeruli leading to eventual KIDNEY FAILURE.		04.6211
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.		07.7444
Hemorrhage
Bleeding or escape of blood from a vessel.		04.6211
Carcinoma, Hepatocellular
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.		04.9921
Inflammation
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.		07.7444
Ischemia
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.		04.6211
Klebsiella Infections
Infections with bacteria of the genus KLEBSIELLA.		04.6211
Liver Cirrhosis
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.		04.6211
Liver Diseases
Pathological processes of the LIVER.		04.6211
Liver Neoplasms
Tumors or cancer of the LIVER.		04.9921
Mitral Valve Insufficiency
Backflow of blood from the LEFT VENTRICLE into the LEFT ATRIUM due to imperfect closure of the MITRAL VALVE. This can lead to mitral valve regurgitation.		04.6211
Multiple Myeloma
A malignancy of mature PLASMA CELLS engaging in monoclonal immunoglobulin production. It is characterized by hyperglobulinemia, excess Bence-Jones proteins (free monoclonal IMMUNOGLOBULIN LIGHT CHAINS) in the urine, skeletal destruction, bone pain, and fractures. Other features include ANEMIA; HYPERCALCEMIA; and RENAL INSUFFICIENCY.		04.6211
Cardiomyopathies
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).		04.6211
Obesity, Morbid
The condition of weighing two, three, or more times the ideal weight, so called because it is associated with many serious and life-threatening disorders. In the BODY MASS INDEX, morbid obesity is defined as having a BMI greater than 40.0 kg/m2.		04.6211
Osteoarthritis
A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.		04.6211
Periodontal Pocket
An abnormal extension of a gingival sulcus accompanied by the apical migration of the epithelial attachment and bone resorption.		04.6211
Periodontitis
Inflammation and loss of connective tissues supporting or surrounding the teeth. This may involve any part of the PERIODONTIUM. Periodontitis is currently classified by disease progression (CHRONIC PERIODONTITIS; AGGRESSIVE PERIODONTITIS) instead of age of onset. (From 1999 International Workshop for a Classification of Periodontal Diseases and Conditions, American Academy of Periodontology)		04.6211
Pneumonia, Viral
Inflammation of the lung parenchyma that is caused by a viral infection.		04.6211
Postoperative Complications
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.		04.6211
Precancerous Conditions
Pathological conditions that tend eventually to become malignant.		04.6211
Pulmonary Embolism
Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS.		04.6211
Respiratory Distress Syndrome
A syndrome characterized by progressive life-threatening RESPIRATORY INSUFFICIENCY in the absence of known LUNG DISEASES, usually following a systemic insult such as surgery or major TRAUMA.		04.6211
Sarcoma
A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.		04.6211
Stomach Neoplasms
Tumors or cancer of the STOMACH.		111.9399
Tobacco Use Disorder
Tobacco used to the detriment of a person's health or social functioning. Tobacco dependence is included.		04.6211
Vitiligo
A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.		04.6211
Osteoarthritis, Hip
Noninflammatory degenerative disease of the hip joint which usually appears in late middle or old age. It is characterized by growth or maturational disturbances in the femoral neck and head, as well as acetabular dysplasia. A dominant symptom is pain on weight-bearing or motion.		04.6211
Reperfusion Injury
Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA.		07.7444
Coronavirus Infections
Virus diseases caused by the CORONAVIRUS genus. Some specifics include transmissible enteritis of turkeys (ENTERITIS, TRANSMISSIBLE, OF TURKEYS); FELINE INFECTIOUS PERITONITIS; and transmissible gastroenteritis of swine (GASTROENTERITIS, TRANSMISSIBLE, OF SWINE).		04.6211
Substance-Related Disorders
Disorders related to substance use or abuse.		04.6211
Infarction, Middle Cerebral Artery
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.		04.6211
Osteoarthritis, Knee
Noninflammatory degenerative disease of the knee joint consisting of three large categories: conditions that block normal synchronous movement, conditions that produce abnormal pathways of motion, and conditions that cause stress concentration resulting in changes to articular cartilage. (Crenshaw, Campbell's Operative Orthopaedics, 8th ed, p2019)		04.6211
Hearing Loss
A general term for the complete or partial loss of the ability to hear from one or both ears.		04.6211
Lipid Metabolism Disorders
Pathological conditions resulting from abnormal anabolism or catabolism of lipids in the body.		04.6211
Chemical and Drug Induced Liver Injury
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, herbal and dietary supplements and chemicals from the environment.		04.6211
Acute Kidney Injury
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.		07.7444
Drug-Related Side Effects and Adverse Reactions
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.		04.9421
Non-alcoholic Fatty Liver Disease
Fatty liver finding without excessive ALCOHOL CONSUMPTION.		04.6211
Neoplasms, Pleural
[description not available]		0421
Colorectal Cancer
[description not available]		07.3110
Colorectal Neoplasms
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.		14.3110
Metastase
[description not available]		03.4720
Neoplasm Metastasis
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.		03.4720
Carcinoma, Lewis Lung
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.		02.3110
Adenocarcinoma, Basal Cell
[description not available]		02.3110
Adenocarcinoma
A malignant epithelial tumor with a glandular organization.		02.3110
Experimental Lung Inflammation
Inflammation of any part, segment or lobe, of the lung parenchyma.		03.5520
Pneumonia
Infection of the lung often accompanied by inflammation.		03.5520
Epithelial Neoplasms
[description not available]		04.2430
Exanthem
[description not available]		02.1710
Lassitude
[description not available]		02.1710
Leukocytopenia
[description not available]		02.1710
Dysmyelopoietic Syndromes
[description not available]		02.1710
Nasopharyngitis
Inflammation of the NASOPHARYNX, usually including its mucosa, related lymphoid structure, and glands.		02.1710
Emesis
[description not available]		02.1710
Exanthema
Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke's disease), fifth (ERYTHEMA INFECTIOSUM), and sixth (EXANTHEMA SUBITUM) numeric designations survive as occasional synonyms in current terminology.		02.1710
Fatigue
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.		02.1710
Leukopenia
A decrease in the number of LEUKOCYTES in a blood sample below the normal range (LEUKOCYTE COUNT less than 4000).		02.1710
Myelodysplastic Syndromes
Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.		02.1710
Vomiting
The forcible expulsion of the contents of the STOMACH through the MOUTH.		02.1710
Blood Diseases
[description not available]		02.2110
Hematologic Diseases
Disorders of the blood and blood forming tissues.		02.2110
Atypical Ductal Hyperplasia
[description not available]		02.1710
Invasiveness, Neoplasm
[description not available]		02.1710
Carcinoma, Intraductal, Noninfiltrating
A noninvasive (noninfiltrating) carcinoma of the breast characterized by a proliferation of malignant epithelial cells confined to the mammary ducts or lobules, without light-microscopy evidence of invasion through the basement membrane into the surrounding stroma.		02.1710
Cardiac Toxicity
[description not available]		03.5911
Electrocardiogram QT Prolonged
[description not available]		03.5911
Long QT Syndrome
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.		03.5911
Cardiotoxicity
Damage to the HEART or its function secondary to exposure to toxic substances such as drugs used in CHEMOTHERAPY; IMMUNOTHERAPY; or RADIATION.		03.5911
Genome Instability
[description not available]		03.1210
Neuroblastoma
A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)		02.0810
Experimental Neoplasms
[description not available]		02.1110
Brain Stem Neoplasms, Primary
[description not available]		02.1110
Anaplastic Astrocytoma
[description not available]		02.1110
Astrocytoma
Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)		02.1110
Brain Stem Neoplasms
Benign and malignant intra-axial tumors of the MESENCEPHALON; PONS; or MEDULLA OBLONGATA of the BRAIN STEM. Primary and metastatic neoplasms may occur in this location. Clinical features include ATAXIA, cranial neuropathies (see CRANIAL NERVE DISEASES), NAUSEA, hemiparesis (see HEMIPLEGIA), and quadriparesis. Primary brain stem neoplasms are more frequent in children. Histologic subtypes include GLIOMA; HEMANGIOBLASTOMA; GANGLIOGLIOMA; and EPENDYMOMA.		02.1110