PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33941784-1	2021	ARIEL2 (NCT01891344) is a single-arm, open-label phase 2 study of the PARP inhibitor (PARPi) rucaparib in relapsed high-grade ovarian carcinoma.	rucaparib	93-102	poly(ADP-ribose) polymerase 1	Homo sapiens	70-74
33970687-0	2021	Phase II Study of Maintenance Rucaparib in Patients With Platinum-Sensitive Advanced Pancreatic Cancer and a Pathogenic Germline or Somatic Variant in BRCA1, BRCA2, or PALB2.	rucaparib	30-39	BRCA1 DNA repair associated	Homo sapiens	151-156
33970687-0	2021	Phase II Study of Maintenance Rucaparib in Patients With Platinum-Sensitive Advanced Pancreatic Cancer and a Pathogenic Germline or Somatic Variant in BRCA1, BRCA2, or PALB2.	rucaparib	30-39	BRCA2 DNA repair associated	Homo sapiens	158-163
33970687-0	2021	Phase II Study of Maintenance Rucaparib in Patients With Platinum-Sensitive Advanced Pancreatic Cancer and a Pathogenic Germline or Somatic Variant in BRCA1, BRCA2, or PALB2.	rucaparib	30-39	partner and localizer of BRCA2	Homo sapiens	168-173
33970687-14	2021	CONCLUSION: Maintenance rucaparib is a safe and effective therapy for platinum-sensitive, advanced PC with a PV in BRCA1, BRCA2, or PALB2.	rucaparib	24-33	BRCA1 DNA repair associated	Homo sapiens	115-120
33970687-14	2021	CONCLUSION: Maintenance rucaparib is a safe and effective therapy for platinum-sensitive, advanced PC with a PV in BRCA1, BRCA2, or PALB2.	rucaparib	24-33	BRCA2 DNA repair associated	Homo sapiens	122-127
33970687-14	2021	CONCLUSION: Maintenance rucaparib is a safe and effective therapy for platinum-sensitive, advanced PC with a PV in BRCA1, BRCA2, or PALB2.	rucaparib	24-33	partner and localizer of BRCA2	Homo sapiens	132-137
34327724-10	2022	Arrhythmia cases are potentially linked to the structural features of hERG ion-channel inhibition found in rucaparib and niraparib.	rucaparib	107-116	ETS transcription factor ERG	Homo sapiens	70-74
32795228-11	2020	CONCLUSION: Rucaparib has antitumor activity in patients with mCRPC and a deleterious BRCA alteration, but with a manageable safety profile consistent with that reported in other solid tumor types.	rucaparib	12-21	BRCA2 DNA repair associated	Homo sapiens	86-90
33941784-2	2021	In this post hoc exploratory biomarker analysis of pre- and post-platinum ARIEL2 samples, RAD51C and RAD51D mutations and high-level BRCA1 promoter methylation predict response to rucaparib, similar to BRCA1/BRCA2 mutations.	rucaparib	180-189	RAD51 paralog C	Homo sapiens	90-96
33941784-2	2021	In this post hoc exploratory biomarker analysis of pre- and post-platinum ARIEL2 samples, RAD51C and RAD51D mutations and high-level BRCA1 promoter methylation predict response to rucaparib, similar to BRCA1/BRCA2 mutations.	rucaparib	180-189	RAD51 paralog D	Homo sapiens	101-107
33941784-2	2021	In this post hoc exploratory biomarker analysis of pre- and post-platinum ARIEL2 samples, RAD51C and RAD51D mutations and high-level BRCA1 promoter methylation predict response to rucaparib, similar to BRCA1/BRCA2 mutations.	rucaparib	180-189	BRCA1 DNA repair associated	Homo sapiens	133-138
33941784-2	2021	In this post hoc exploratory biomarker analysis of pre- and post-platinum ARIEL2 samples, RAD51C and RAD51D mutations and high-level BRCA1 promoter methylation predict response to rucaparib, similar to BRCA1/BRCA2 mutations.	rucaparib	180-189	BRCA2 DNA repair associated	Homo sapiens	208-213
32795228-0	2020	Rucaparib in Men With Metastatic Castration-Resistant Prostate Cancer Harboring a BRCA1 or BRCA2 Gene Alteration.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	82-87
32795228-0	2020	Rucaparib in Men With Metastatic Castration-Resistant Prostate Cancer Harboring a BRCA1 or BRCA2 Gene Alteration.	rucaparib	0-9	BRCA2 DNA repair associated	Homo sapiens	91-96
32795228-2	2020	We present results from patients with mCRPC associated with a BRCA alteration treated with rucaparib 600 mg twice daily in the phase II TRITON2 study.	rucaparib	91-100	BRCA2 DNA repair associated	Homo sapiens	62-66
34958553-12	2022	The results from our mass spectrometry-based proteomic analysis highlights notable off-target effects produced by low-dose treatment of BRCA1-mutated HGSOC cells treated with rucaparib or niraparib.	rucaparib	175-184	BRCA1 DNA repair associated	Homo sapiens	136-141
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	poly(ADP-ribose) polymerase 1	Homo sapiens	13-40
34473525-4	2022	Poly-ADP ribose polymerase inhibitors (olaparib and rucaparib) have demonstrated significant clinical benefit for patients harboring deleterious mutations in genes belonging to the homologous recombination repair pathway and have received Food and Drug Administration approval.	rucaparib	52-61	poly(ADP-ribose) polymerase 1	Homo sapiens	0-26
34812476-1	2022	Poly (ADP-ribose) polymerase (PARP) inhibitors, including olaparib, niraparib, rucaparib, talazoparib and veliparib, have emerged as one of the most exciting new treatments for solid tumors, particularly in patients with breast-related cancer antigen 1/2 mutations.	rucaparib	79-88	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
34812476-1	2022	Poly (ADP-ribose) polymerase (PARP) inhibitors, including olaparib, niraparib, rucaparib, talazoparib and veliparib, have emerged as one of the most exciting new treatments for solid tumors, particularly in patients with breast-related cancer antigen 1/2 mutations.	rucaparib	79-88	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
34598946-0	2021	Response to rucaparib in BRCA-mutant metastatic castration-resistant prostate cancer identified by genomic testing in the TRITON2 study.	rucaparib	12-21	BRCA2 DNA repair associated	Homo sapiens	25-29
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	BRCA1 DNA repair associated	Homo sapiens	206-211
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	BRCA2 DNA repair associated	Homo sapiens	215-220
34598946-1	2021	PURPOSE: The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is approved in the US for patients with metastatic castration-resistant prostate cancer (mCRPC) and a deleterious germline and/or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	58-67	BRCA2 DNA repair associated	Homo sapiens	222-226
34598946-10	2021	CONCLUSION: Plasma, tissue, and local testing of mCRPC patients can be used to identify men with BRCA+ mCRPC who can benefit from treatment with the PARP inhibitor rucaparib.	rucaparib	164-173	BRCA2 DNA repair associated	Homo sapiens	97-101
34598946-10	2021	CONCLUSION: Plasma, tissue, and local testing of mCRPC patients can be used to identify men with BRCA+ mCRPC who can benefit from treatment with the PARP inhibitor rucaparib.	rucaparib	164-173	poly(ADP-ribose) polymerase 1	Homo sapiens	149-153
34602290-1	2021	OBJECTIVE: To describe molecular and clinical characteristics of patients with high-grade recurrent ovarian carcinoma (HGOC) who had long-term responses to the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib.	rucaparib	205-214	poly(ADP-ribose) polymerase 1	Homo sapiens	160-187
34602290-1	2021	OBJECTIVE: To describe molecular and clinical characteristics of patients with high-grade recurrent ovarian carcinoma (HGOC) who had long-term responses to the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib.	rucaparib	205-214	poly(ADP-ribose) polymerase 1	Homo sapiens	189-193
34107090-1	2021	Retraction: "Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway," by Dong Li, Jingyan Yang, Huanzhi Ma, Chengliang Sun, Rongjie Feng, J Cell Biochem.	rucaparib	62-71	protein tyrosine kinase 2 beta	Homo sapiens	162-178
34729995-3	2021	Olaparib and rucaparib, two PARP inhibitors, were successfully tested in clinical trials for HRR-deficient metastatic castration-resistant prostate cancer.	rucaparib	13-22	poly(ADP-ribose) polymerase 1	Homo sapiens	28-32
34819864-2	2021	Methods: The log normal hazard function model was established by using progression-free survival (PFS) data of 1,169 patients from published randomized trials on FDA-approved PARP inhibitors (olaparib, niraparib, and rucaparib).	rucaparib	217-226	poly(ADP-ribose) polymerase 1	Homo sapiens	175-179
34593565-4	2021	PRIMARY OBJECTIVES: In women with newly diagnosed ovarian, fallopian tube, or peritoneal cancer, we wish to assess the efficacy of frontline maintenance treatment with the PARP inhibitor rucaparib versus placebo following response to platinum-based chemotherapy (ATHENA-MONO), and to assess the combination of rucaparib plus nivolumab (a programmed death receptor 1 (PD-1)-blocking monoclonal antibody) versus rucaparib alone (ATHENA-COMBO).	rucaparib	187-196	poly(ADP-ribose) polymerase 1	Homo sapiens	172-176
34647981-0	2021	Preexisting TP53-Variant Clonal Hematopoiesis and Risk of Secondary Myeloid Neoplasms in Patients With High-grade Ovarian Cancer Treated With Rucaparib.	rucaparib	142-151	tumor protein p53	Homo sapiens	12-16
34647981-15	2021	Conclusions and Relevance: The findings of this genetic association study suggest that preexisting TP53 CHIP variants may be associated with t-MNs after rucaparib treatment.	rucaparib	153-162	tumor protein p53	Homo sapiens	99-103
34899683-6	2021	Targeting LDH, a secondary target of the PARP inhibitor rucaparib, resulted in decreased intracellular Mtb, suggesting a metabolic role in rucaparib-induced control of Mtb.	rucaparib	56-65	poly(ADP-ribose) polymerase 1	Homo sapiens	41-45
34904808-1	2021	ABSTRACT: In May 2020, the poly(ADP-ribose) polymerase (PARP) inhibitors rucaparib and olaparib were Food and Drug Administration approved for the management of metastatic castration-resistant prostate cancers.	rucaparib	73-82	poly(ADP-ribose) polymerase 1	Homo sapiens	27-54
34904808-1	2021	ABSTRACT: In May 2020, the poly(ADP-ribose) polymerase (PARP) inhibitors rucaparib and olaparib were Food and Drug Administration approved for the management of metastatic castration-resistant prostate cancers.	rucaparib	73-82	poly(ADP-ribose) polymerase 1	Homo sapiens	56-60
34904808-2	2021	Rucaparib was approved for tumors that harbor alterations in BRCA1 and BRCA2 following progression on chemotherapy and androgen receptor-directed therapy, whereas olaparib was approved for tumors that harbor alterations in a broader range of DNA damage repair genes following progression on androgen receptor-directed therapy.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	61-66
34904808-2	2021	Rucaparib was approved for tumors that harbor alterations in BRCA1 and BRCA2 following progression on chemotherapy and androgen receptor-directed therapy, whereas olaparib was approved for tumors that harbor alterations in a broader range of DNA damage repair genes following progression on androgen receptor-directed therapy.	rucaparib	0-9	BRCA2 DNA repair associated	Homo sapiens	71-76
34556698-5	2021	Cell death could be prevented by supplementation with 2-oxoglutarate (a TCA cycle intermediate), benfotiamine (the vitamin B1 derivative that suppresses the collateral pathways), or the poly (ADP-ribose) polymerase (PARP) inhibitor, rucaparib.	rucaparib	233-242	poly(ADP-ribose) polymerase 1	Homo sapiens	186-214
34549539-6	2021	Across subgroups, significantly longer median PFS was observed with rucaparib versus placebo in the BRCA-mutated and HRD cohorts.	rucaparib	68-77	BRCA1 DNA repair associated	Homo sapiens	100-104
34638791-9	2021	Rucaparib, a PARP inhibitor, potentiated the effects of ruthenium complexes.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	13-17
34556698-5	2021	Cell death could be prevented by supplementation with 2-oxoglutarate (a TCA cycle intermediate), benfotiamine (the vitamin B1 derivative that suppresses the collateral pathways), or the poly (ADP-ribose) polymerase (PARP) inhibitor, rucaparib.	rucaparib	233-242	poly(ADP-ribose) polymerase 1	Homo sapiens	216-220
34459606-1	2021	The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is used in the clinic to treat BRCA-mutated cancers.	rucaparib	49-58	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
34459606-1	2021	The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is used in the clinic to treat BRCA-mutated cancers.	rucaparib	49-58	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
34459606-1	2021	The poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib is used in the clinic to treat BRCA-mutated cancers.	rucaparib	49-58	BRCA1 DNA repair associated	Homo sapiens	90-94
34103386-8	2021	Across subgroups, median progression-free survival was also significantly longer with rucaparib versus placebo in the BRCA-mutant and homologous recombination deficient cohorts.	rucaparib	86-95	BRCA1 DNA repair associated	Homo sapiens	118-122
34572083-3	2021	The aim of this study is to assess the effects of the PARPi rucaparib in vitro using cell lines with BRCA2 mutations in comparison to those with BRCA2 wild type.	rucaparib	60-69	BRCA2 DNA repair associated	Homo sapiens	101-106
34572083-4	2021	METHODS: Cell proliferation assays, RT-qPCR, immunofluorescence, annexin V/PI assays were used to assess the effects of rucaparib in vitro.	rucaparib	120-129	annexin A5	Homo sapiens	65-74
34572083-6	2021	The migratory and proliferative capacity of PEO1 cells was compromised following treatment with rucaparib 10 microM compared to BRCA2 wild-type cell lines via a mechanism involving the mTOR pathway.	rucaparib	96-105	twinkle mtDNA helicase	Homo sapiens	44-48
34572083-6	2021	The migratory and proliferative capacity of PEO1 cells was compromised following treatment with rucaparib 10 microM compared to BRCA2 wild-type cell lines via a mechanism involving the mTOR pathway.	rucaparib	96-105	mechanistic target of rapamycin kinase	Homo sapiens	185-189
34572083-7	2021	Rucaparib treatment significantly increased DNA damage primarily in PEO1 cells and SKOV3 cells compared with wild type.	rucaparib	0-9	twinkle mtDNA helicase	Homo sapiens	68-72
34572083-10	2021	This study also demonstrates the mechanisms of action of rucaparib (PARPi) which may involve elements of the mTOR pathway.	rucaparib	57-66	mechanistic target of rapamycin kinase	Homo sapiens	109-113
34256353-4	2021	The recent regulatory approvals of PARP inhibitors olaparib and rucaparib represent the first molecular biomarker-guided drugs for men with prostate cancer.	rucaparib	64-73	poly(ADP-ribose) polymerase 1	Homo sapiens	35-39
34316715-6	2021	Analysis of ovarian cancer samples from the ARIEL2 Part 1 clinical trial of rucaparib monotherapy likewise indicated an association between loss of RAD51C methylation prior to on-study biopsy and limited response.	rucaparib	76-85	RAD51 paralog C	Homo sapiens	148-154
34321239-5	2021	PDX models lost meRAD51C following treatment with PARPi rucaparib or niraparib, where a single unmethylated copy of RAD51C was sufficient to drive PARPi resistance.	rucaparib	56-65	RAD51 paralog C	Homo sapiens	116-122
34778690-1	2021	Two poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and rucaparib) are US Food and Drug Administration-approved for patients with metastatic castration-resistant prostate cancer (mCRPC) harboring BRCA1/2 mutations, but the relative efficacy of PARP inhibition in BRCA1- versus BRCA2-altered mCRPC is understudied.	rucaparib	65-74	poly(ADP-ribose) polymerase 1	Homo sapiens	4-32
34778690-1	2021	Two poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and rucaparib) are US Food and Drug Administration-approved for patients with metastatic castration-resistant prostate cancer (mCRPC) harboring BRCA1/2 mutations, but the relative efficacy of PARP inhibition in BRCA1- versus BRCA2-altered mCRPC is understudied.	rucaparib	65-74	poly(ADP-ribose) polymerase 1	Homo sapiens	34-38
34778690-1	2021	Two poly (ADP-ribose) polymerase (PARP) inhibitors (olaparib and rucaparib) are US Food and Drug Administration-approved for patients with metastatic castration-resistant prostate cancer (mCRPC) harboring BRCA1/2 mutations, but the relative efficacy of PARP inhibition in BRCA1- versus BRCA2-altered mCRPC is understudied.	rucaparib	65-74	BRCA1 DNA repair associated	Homo sapiens	205-212
34377227-2	2021	Currently, two PARP inhibitors, olaparib and rucaparib, have received approval as monotherapy by the Food and Drug Administration for the treatment of men with castration resistant prostate cancer with selected mutations involving the homologous recombination (HR) pathway.	rucaparib	45-54	poly(ADP-ribose) polymerase 1	Homo sapiens	15-19
34069967-3	2021	In particular, derivatives of olaparib and rucaparib, which have reduced trapping potency by PARP-1 compared to talazoparib, have been radiolabeled for these purposes.	rucaparib	43-52	poly (ADP-ribose) polymerase family, member 1	Mus musculus	93-99
35614267-1	2022	PURPOSE: Rucaparib, an FDA-approved PARP inhibitor, is used as a single agent in maintenance therapy to provide promising treatment efficacy with an acceptable safety profile in various types of BRCA-mutated cancers.	rucaparib	9-18	poly(ADP-ribose) polymerase 1	Homo sapiens	36-40
34700141-1	2021	Cancers with mutations in BRCA2 have defective DNA repair capacity which is potentially targetable with poly-ADP(ribose) polymera se (PARP) inhibitors such as olaparib and rucaparib.	rucaparib	172-181	BRCA2 DNA repair associated	Homo sapiens	26-31
35614267-1	2022	PURPOSE: Rucaparib, an FDA-approved PARP inhibitor, is used as a single agent in maintenance therapy to provide promising treatment efficacy with an acceptable safety profile in various types of BRCA-mutated cancers.	rucaparib	9-18	BRCA1 DNA repair associated	Homo sapiens	195-199
35614267-4	2022	With this aim, we developed (18F)rucaparib, an 18F-labelled isotopologue of rucaparib, and employed it as a PARP-targeting agent for cancer imaging with PET.	rucaparib	33-42	poly(ADP-ribose) polymerase 1	Homo sapiens	108-112
35614267-7	2022	(18F)rucaparib binds to the DNA damage repair enzyme, PARP, allowing direct visualisation and measurement of PARP in cancerous models before and after PARP inhibition or other genotoxic cancer therapies, providing critical information for cancer diagnosis and therapy.	rucaparib	5-14	poly(ADP-ribose) polymerase 1	Homo sapiens	54-58
35614267-7	2022	(18F)rucaparib binds to the DNA damage repair enzyme, PARP, allowing direct visualisation and measurement of PARP in cancerous models before and after PARP inhibition or other genotoxic cancer therapies, providing critical information for cancer diagnosis and therapy.	rucaparib	5-14	poly(ADP-ribose) polymerase 1	Homo sapiens	109-113
35614267-9	2022	RESULTS: Uptake of (18F)rucaparib was found to be mainly dependent on PARP1 expression.	rucaparib	24-33	poly(ADP-ribose) polymerase 1	Homo sapiens	70-75
35614267-10	2022	Induction of DNA damage increased PARP expression, thereby increasing uptake of (18F)rucaparib.	rucaparib	85-94	poly(ADP-ribose) polymerase 1	Homo sapiens	34-38
35614267-11	2022	In vivo studies revealed relatively fast blood clearance of (18F)rucaparib in PSN1 tumour-bearing mice, with a tumour uptake of 5.5 +- 0.5%ID/g (1 h after i.v.	rucaparib	65-74	5'-nucleotidase, cytosolic III	Mus musculus	78-82
35614267-13	2022	In vitro and in vivo studies showed significant reduction of (18F)rucaparib uptake by addition of different PARP inhibitors, indicating PARP-selective binding.	rucaparib	66-75	poly(ADP-ribose) polymerase 1	Homo sapiens	108-112
35614267-13	2022	In vitro and in vivo studies showed significant reduction of (18F)rucaparib uptake by addition of different PARP inhibitors, indicating PARP-selective binding.	rucaparib	66-75	poly(ADP-ribose) polymerase 1	Homo sapiens	136-140
35614267-14	2022	CONCLUSION: Taken together, we demonstrate the potential of (18F)rucaparib as a non-invasive PARP-targeting imaging agent for pancreatic cancers.	rucaparib	65-74	poly(ADP-ribose) polymerase 1	Homo sapiens	93-97
35491267-13	2022	However, patients with ARID1A mutations had a higher response rate and PFS6 suggesting this subgroup may benefit from the combination of bevacizumab and rucaparib.	rucaparib	153-162	AT-rich interaction domain 1A	Homo sapiens	23-29
35594523-1	2022	INTRODUCTION: In May 2020, the approval of rucaparib (a poly-adenosine diphosphate-ribose polymerase (PARP) inhibitor) in the USA marked the arrival of a new class of targeted, life-prolonging therapeutics for the 15-25% of metastatic castration-resistant prostate cancer patients whose tumors harbor germline or somatic BRCA1/2 gene alterations.	rucaparib	43-52	poly(ADP-ribose) polymerase 1	Homo sapiens	56-100
35594523-1	2022	INTRODUCTION: In May 2020, the approval of rucaparib (a poly-adenosine diphosphate-ribose polymerase (PARP) inhibitor) in the USA marked the arrival of a new class of targeted, life-prolonging therapeutics for the 15-25% of metastatic castration-resistant prostate cancer patients whose tumors harbor germline or somatic BRCA1/2 gene alterations.	rucaparib	43-52	poly(ADP-ribose) polymerase 1	Homo sapiens	102-106
35594523-1	2022	INTRODUCTION: In May 2020, the approval of rucaparib (a poly-adenosine diphosphate-ribose polymerase (PARP) inhibitor) in the USA marked the arrival of a new class of targeted, life-prolonging therapeutics for the 15-25% of metastatic castration-resistant prostate cancer patients whose tumors harbor germline or somatic BRCA1/2 gene alterations.	rucaparib	43-52	BRCA1 DNA repair associated	Homo sapiens	321-328
35298905-0	2022	Rucaparib for BRCA1/2-mutated pretreated ovarian cancer: reflections from the ARIEL4 trial.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	14-21
35343196-6	2022	Four PARP inhibitors (olaparib, niraparib, rucaparib, and talazoparib) are currently approved by the Food and Drug Administration for OC, breast, and pancreatic cancer indications and are being evaluated for other BRCA-associated cancers.	rucaparib	43-52	poly(ADP-ribose) polymerase 1	Homo sapiens	5-9
35236893-1	2022	Rucaparib (RCP) is a potent selective inhibitor of both PARP-1 and PARP-2 enzymes that induces synthetic lethality in cancer cells.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	56-62
35236893-1	2022	Rucaparib (RCP) is a potent selective inhibitor of both PARP-1 and PARP-2 enzymes that induces synthetic lethality in cancer cells.	rucaparib	0-9	poly(ADP-ribose) polymerase 2	Homo sapiens	67-73
35236893-1	2022	Rucaparib (RCP) is a potent selective inhibitor of both PARP-1 and PARP-2 enzymes that induces synthetic lethality in cancer cells.	rucaparib	11-14	poly(ADP-ribose) polymerase 1	Homo sapiens	56-62
35236893-1	2022	Rucaparib (RCP) is a potent selective inhibitor of both PARP-1 and PARP-2 enzymes that induces synthetic lethality in cancer cells.	rucaparib	11-14	poly(ADP-ribose) polymerase 2	Homo sapiens	67-73
35281113-3	2022	Through analyzing the effect of HRD status on response efficacy of anticancer drugs and elucidating its related mechanisms of action, we found rucaparib (PARP inhibitor) and doxorubicin (anthracycline) sensitive in HR-deficient patients, while paclitaxel sensitive in the HR-proficient.	rucaparib	143-152	poly(ADP-ribose) polymerase 1	Homo sapiens	154-158
35267438-7	2022	We give a comprehensive overview over the preclinical development of PARP imaging agents, which are mostly based on the PARPi olaparib, rucaparib, and recently also talazoparib.	rucaparib	136-145	poly(ADP-ribose) polymerase 1	Homo sapiens	69-73
35205643-6	2022	Selective poly (ADP-ribose) polymerase (PARP) inhibitors such as Niraparib, Olaparib, Talazoparib, Rucaparib, and Veliparib are now approved for several cancers with loss of high-fidelity double-strand break homologous recombination (HR), namely those with deleterious mutations to BRCA1/2, PALB2, and other functionally related genes.	rucaparib	99-108	poly(ADP-ribose) polymerase 1	Homo sapiens	10-38
35210863-1	2022	Purpose: The US Food and Drug Administration has recently granted accelerated approval of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib as treatment for men with metastatic castration-resistant prostate cancer (mCRPC) associated with a deleterious germline or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	139-148	poly(ADP-ribose) polymerase 1	Homo sapiens	94-121
35210863-1	2022	Purpose: The US Food and Drug Administration has recently granted accelerated approval of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib as treatment for men with metastatic castration-resistant prostate cancer (mCRPC) associated with a deleterious germline or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	139-148	poly(ADP-ribose) polymerase 1	Homo sapiens	123-127
35210863-1	2022	Purpose: The US Food and Drug Administration has recently granted accelerated approval of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib as treatment for men with metastatic castration-resistant prostate cancer (mCRPC) associated with a deleterious germline or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	139-148	BRCA1 DNA repair associated	Homo sapiens	281-286
35210863-1	2022	Purpose: The US Food and Drug Administration has recently granted accelerated approval of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib as treatment for men with metastatic castration-resistant prostate cancer (mCRPC) associated with a deleterious germline or somatic BRCA1 or BRCA2 (BRCA) alteration.	rucaparib	139-148	BRCA2 DNA repair associated	Homo sapiens	290-295
35205643-6	2022	Selective poly (ADP-ribose) polymerase (PARP) inhibitors such as Niraparib, Olaparib, Talazoparib, Rucaparib, and Veliparib are now approved for several cancers with loss of high-fidelity double-strand break homologous recombination (HR), namely those with deleterious mutations to BRCA1/2, PALB2, and other functionally related genes.	rucaparib	99-108	poly(ADP-ribose) polymerase 1	Homo sapiens	40-44
35205643-6	2022	Selective poly (ADP-ribose) polymerase (PARP) inhibitors such as Niraparib, Olaparib, Talazoparib, Rucaparib, and Veliparib are now approved for several cancers with loss of high-fidelity double-strand break homologous recombination (HR), namely those with deleterious mutations to BRCA1/2, PALB2, and other functionally related genes.	rucaparib	99-108	BRCA1 DNA repair associated	Homo sapiens	282-289
35205643-6	2022	Selective poly (ADP-ribose) polymerase (PARP) inhibitors such as Niraparib, Olaparib, Talazoparib, Rucaparib, and Veliparib are now approved for several cancers with loss of high-fidelity double-strand break homologous recombination (HR), namely those with deleterious mutations to BRCA1/2, PALB2, and other functionally related genes.	rucaparib	99-108	partner and localizer of BRCA2	Homo sapiens	291-296
34039959-0	2021	BKM120 sensitizes glioblastoma to the PARP inhibitor rucaparib by suppressing homologous recombination repair.	rucaparib	53-62	collagen type XI alpha 2 chain	Homo sapiens	38-42
35159068-5	2022	The regulatory approval of two PARP inhibitors in 2020-rucaparib and olaparib-has provided the first targeted therapy option for patients harboring defects in selected DNA damage response and repair (DDR) pathway genes.	rucaparib	55-64	poly(ADP-ribose) polymerase 1	Homo sapiens	31-35
34039959-3	2021	Herein, we demonstrated that concurrent treatment with the PARP inhibitor rucaparib and the PI3K inhibitor BKM120 showed synergetic anticancer effects on GBM U251 and U87MG cells.	rucaparib	74-83	collagen type XI alpha 2 chain	Homo sapiens	59-63
33710534-10	2021	Differences in efficacy and safety across PARP inhibitors (olaparib, talazoparib, veliparib, niraparib, rucaparib) may relate to differences in potency of PARP trapping on DNA and cytotoxic specificity.	rucaparib	104-113	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
34039740-5	2021	Similarly, pharmacologic blockade of H6PD with rucaparib normalizes tumor glucocorticoid metabolism in human cell lines and reinstates responsiveness to enzalutamide in mouse xenograft models.	rucaparib	47-56	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	37-41
34030643-1	2021	BACKGROUND: ATLAS evaluated the efficacy and safety of the PARP inhibitor rucaparib in patients with previously treated locally advanced/unresectable or metastatic urothelial carcinoma (UC).	rucaparib	74-83	collagen type XI alpha 2 chain	Homo sapiens	59-63
33866131-3	2021	Targeting DNA damage response (DDR) pathways in prostate cancer became a promising treatment strategy and olaparib and rucaparib, Poly(ADP-ribose) polymerase (PARP) inhibitors, have been approved for patients carrying mutations in homologous recombination (HR) repair pathways.	rucaparib	119-128	poly(ADP-ribose) polymerase 1	Homo sapiens	130-157
33866131-3	2021	Targeting DNA damage response (DDR) pathways in prostate cancer became a promising treatment strategy and olaparib and rucaparib, Poly(ADP-ribose) polymerase (PARP) inhibitors, have been approved for patients carrying mutations in homologous recombination (HR) repair pathways.	rucaparib	119-128	poly(ADP-ribose) polymerase 1	Homo sapiens	159-163
33710534-10	2021	Differences in efficacy and safety across PARP inhibitors (olaparib, talazoparib, veliparib, niraparib, rucaparib) may relate to differences in potency of PARP trapping on DNA and cytotoxic specificity.	rucaparib	104-113	poly(ADP-ribose) polymerase 1	Homo sapiens	155-159
33906871-2	2021	He was being treated at the time with the poly ADP ribose polymerase inhibitor Rucaparib.	rucaparib	79-88	poly(ADP-ribose) polymerase 1	Homo sapiens	42-68
33827356-4	2021	AREAS COVERED: Here, the authors" review the clinical trials leading to the recent approvals of two PARP inhibitors (PARPi), olaparib and rucaparib, specifically TOPARP-A, TOPARP-B, PROfound and TRITON-2.	rucaparib	138-147	poly(ADP-ribose) polymerase 1	Homo sapiens	100-104
33827356-7	2021	We also recommend that olaparib or rucaparib be considered relatively early in the treatment sequence in metastatic castration-resistant prostate cancer patients with BRCA1 or BRCA2 mutations.	rucaparib	35-44	BRCA1 DNA repair associated	Homo sapiens	167-172
33753748-0	2021	Cisplatin +/- rucaparib after preoperative chemotherapy in patients with triple-negative or BRCA mutated breast cancer.	rucaparib	14-23	BRCA1 DNA repair associated	Homo sapiens	92-96
33495407-7	2021	Meanwhile, PARP1 inhibitor rucaparib and siRNA against PARP1 attenuated oxaliplatin-induced parthanatos in OSCC cells.	rucaparib	27-36	poly(ADP-ribose) polymerase 1	Homo sapiens	11-16
33630412-2	2021	The recent approvals of the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and rucaparib in the metastatic castration-resistant prostate cancer (mCRPC) setting signal the need to embed molecular diagnostics in the clinical pathway of patients with mCRPC to identify those who can benefit from targeted therapies.	rucaparib	87-96	poly(ADP-ribose) polymerase 1	Homo sapiens	28-55
33515503-4	2021	We aimed to test the hypothesis that BAP1-deficient or BRCA1-deficient mesotheliomas would be sensitive to PARP inhibition by rucaparib.	rucaparib	126-135	poly(ADP-ribose) polymerase 1	Homo sapiens	107-111
33515503-20	2021	INTERPRETATION: Rucaparib in patients with BAP1-negative or BRCA1-negative mesothelioma met the prespecified criteria for success, showing promising activity with manageable toxicity.	rucaparib	16-25	BRCA1 associated protein 1	Homo sapiens	43-47
33515503-20	2021	INTERPRETATION: Rucaparib in patients with BAP1-negative or BRCA1-negative mesothelioma met the prespecified criteria for success, showing promising activity with manageable toxicity.	rucaparib	16-25	BRCA1 DNA repair associated	Homo sapiens	60-65
32790034-1	2021	The U.S. Food and Drug Administration (FDA) recently approved two poly-ADP ribose polymerase (PARP) inhibitors, olaparib and rucaparib, for treatment of biomarker-positive metastatic castrate resistant prostate cancer.	rucaparib	125-134	poly(ADP-ribose) polymerase 1	Homo sapiens	66-92
32164505-3	2021	Currently, four PARP inhibitors including olaparib, rucaparib, niraparib, and talazoparib have been approved by FDA for cancer treatment and have achieved great success in the treatment of ovarian cancer, breast cancer, and pancreatic cancer etc.	rucaparib	52-61	poly(ADP-ribose) polymerase 1	Homo sapiens	16-20
33145877-1	2021	The U.S. Food and Drug Administration (FDA) granted accelerated approval to rucaparib in May 2020 for the treatment of adult patients with deleterious BRCA mutation (germline and/or somatic)-associated metastatic castrate resistant prostate cancer (mCRPC) who have been treated with androgen receptor-directed therapy and taxane.	rucaparib	76-85	BRCA1 DNA repair associated	Homo sapiens	151-155
33145877-12	2021	IMPLICATIONS FOR PRACTICE: The accelerated approval of rucaparib for the treatment of adult patients with deleterious BRCA mutation (germline and/or somatic)-associated mCRPC who have been treated with androgen receptor-directed therapy and a taxane represents the first approved therapy for this selected patient population.	rucaparib	55-64	BRCA1 DNA repair associated	Homo sapiens	118-122
33369704-8	2021	Two patients in the rucaparib 600-mg group had four grade 3 treatment-emergent adverse events: increased in alanine aminotransferase and aspartate aminotransferase levels, depression, and hallucinations.	rucaparib	20-29	glutamic--pyruvic transaminase	Homo sapiens	108-132
33332934-0	2021	Enhanced Efficacy of Combined Therapy with Checkpoint Kinase 1 Inhibitor and Rucaparib Via Regulation of Rad-51 Expression in BRCA Wild-Type Epithelial Ovarian Cancer Cells.	rucaparib	77-86	RAD51 recombinase	Homo sapiens	105-111
33406057-1	2020	The management of prostate cancer entered a new era of biomarker-driven therapy in May of 2020, when the US Food and Drug Administration (FDA) approved the poly (ADP-ribose) polymerase (PARP) inhibitors rucaparib and olaparib as the first targeted therapies in biomarker-preselected patients with metastatic castration-resistant prostate cancer.	rucaparib	203-212	poly(ADP-ribose) polymerase 1	Homo sapiens	156-184
33406057-1	2020	The management of prostate cancer entered a new era of biomarker-driven therapy in May of 2020, when the US Food and Drug Administration (FDA) approved the poly (ADP-ribose) polymerase (PARP) inhibitors rucaparib and olaparib as the first targeted therapies in biomarker-preselected patients with metastatic castration-resistant prostate cancer.	rucaparib	203-212	poly(ADP-ribose) polymerase 1	Homo sapiens	186-190
32367009-12	2020	Also rucaparib showed a benefit in terms of PSA response rate and ORR in patients with BRCA2 and BRCA1 mutation in a phase-II study.	rucaparib	5-14	BRCA2 DNA repair associated	Homo sapiens	87-92
32367009-12	2020	Also rucaparib showed a benefit in terms of PSA response rate and ORR in patients with BRCA2 and BRCA1 mutation in a phase-II study.	rucaparib	5-14	BRCA1 DNA repair associated	Homo sapiens	97-102
33293727-9	2020	Clinical studies have also shown the efficacy of angiogenesis inhibitors such as bevacizumab and the PARP inhibitors olaparib, niraparib and rucaparib.	rucaparib	141-150	poly(ADP-ribose) polymerase 1	Homo sapiens	101-105
33293727-12	2020	The PARP inhibitors niraparib, olaparib and rucaparib have already been approved for use by the FDA and the EMA.	rucaparib	44-53	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
32790034-1	2021	The U.S. Food and Drug Administration (FDA) recently approved two poly-ADP ribose polymerase (PARP) inhibitors, olaparib and rucaparib, for treatment of biomarker-positive metastatic castrate resistant prostate cancer.	rucaparib	125-134	poly(ADP-ribose) polymerase 1	Homo sapiens	94-98
32636098-1	2020	Recent data have revealed antitumor activity for four PARP inhibitors, two of which (olaparib and rucaparib) are approved by the US Food and Drug Administration for metastatic castrate-resistant prostate cancer with selected DNA repair defects.	rucaparib	98-107	poly(ADP-ribose) polymerase 1	Homo sapiens	54-58
33099187-4	2020	Recently, targeted therapy with the angiogenesis inhibitor bevacizumab and the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib, niraparib, and rucaparib have demonstrated significant clinical benefits as maintenance treatment for recurrent disease.	rucaparib	150-159	poly(ADP-ribose) polymerase 1	Homo sapiens	79-106
33099187-4	2020	Recently, targeted therapy with the angiogenesis inhibitor bevacizumab and the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib, niraparib, and rucaparib have demonstrated significant clinical benefits as maintenance treatment for recurrent disease.	rucaparib	150-159	poly(ADP-ribose) polymerase 1	Homo sapiens	108-112
32717310-0	2020	Rucaparib antagonize multidrug resistance in cervical cancer cells through blocking the function of ABC transporters.	rucaparib	0-9	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	100-103
32717310-2	2020	In the present study, we investigated the ability of rucaparib, a Poly (ADP-ribose) polymerase (PARP) inhibitor which is currently in clinical development, on overcoming ABC transporters-mediated MDR in cervical cancer cell lines.	rucaparib	53-62	poly(ADP-ribose) polymerase 1	Homo sapiens	66-94
32717310-2	2020	In the present study, we investigated the ability of rucaparib, a Poly (ADP-ribose) polymerase (PARP) inhibitor which is currently in clinical development, on overcoming ABC transporters-mediated MDR in cervical cancer cell lines.	rucaparib	53-62	poly(ADP-ribose) polymerase 1	Homo sapiens	96-100
32717310-2	2020	In the present study, we investigated the ability of rucaparib, a Poly (ADP-ribose) polymerase (PARP) inhibitor which is currently in clinical development, on overcoming ABC transporters-mediated MDR in cervical cancer cell lines.	rucaparib	53-62	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	170-173
32717310-6	2020	Molecular docking study indicated that rucaparib could bind to the active site of the ABC transporters.	rucaparib	39-48	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	86-89
32717310-7	2020	The present study indicated that rucaparib could antagonize MDR in cervical cancer cells by blocking the function of ABC transporters.	rucaparib	33-42	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	117-120
32840418-9	2020	Q-TWiST with TOX defined using select grade >= 2 TEAEs also consistently favored rucaparib.	rucaparib	81-90	twist family bHLH transcription factor 1	Homo sapiens	2-7
32840418-9	2020	Q-TWiST with TOX defined using select grade >= 2 TEAEs also consistently favored rucaparib.	rucaparib	81-90	thymocyte selection associated high mobility group box	Homo sapiens	13-16
32840418-10	2020	CONCLUSION: The significant differences in QA-PFS and Q-TWiST confirm the benefit of rucaparib versus placebo in all predefined cohorts.	rucaparib	85-94	twist family bHLH transcription factor 1	Homo sapiens	56-61
32927276-5	2020	FINDINGS: Firstly, we found that the PARPi rucaparib enhanced the effect of BET inhibitors (CPI-203 & CPI-0610) irrespective of clinical subtype or HRD status.	rucaparib	43-52	delta/notch like EGF repeat containing	Homo sapiens	76-79
32927276-7	2020	Secondly, rucaparib synergised with the BCL2 family inhibitor navitoclax, with preferential activity in ovarian carcinomas that harbour alterations in BRCA1/2, BARD1, or MSH2/6.	rucaparib	10-19	BCL2 apoptosis regulator	Homo sapiens	40-44
32927276-7	2020	Secondly, rucaparib synergised with the BCL2 family inhibitor navitoclax, with preferential activity in ovarian carcinomas that harbour alterations in BRCA1/2, BARD1, or MSH2/6.	rucaparib	10-19	BRCA1 DNA repair associated	Homo sapiens	151-158
32927276-7	2020	Secondly, rucaparib synergised with the BCL2 family inhibitor navitoclax, with preferential activity in ovarian carcinomas that harbour alterations in BRCA1/2, BARD1, or MSH2/6.	rucaparib	10-19	BRCA1 associated RING domain 1	Homo sapiens	160-165
32927276-7	2020	Secondly, rucaparib synergised with the BCL2 family inhibitor navitoclax, with preferential activity in ovarian carcinomas that harbour alterations in BRCA1/2, BARD1, or MSH2/6.	rucaparib	10-19	mutS homolog 2	Homo sapiens	170-176
32814685-2	2020	The recent Food and Drug Administration (FDA) approval of the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and rucaparib for the treatment of advanced prostate cancer heralds the onset of precision medicine for this disease.	rucaparib	121-130	poly(ADP-ribose) polymerase 1	Homo sapiens	62-89
32717529-4	2020	To date, four PARP1 inhibitors namely olaparib, rucaparib, niraparib and talazoparib, have been approved by Food and Drug Administration (FDA) for treating ovarian cancer and breast cancer with BRCA1/2 mutation.	rucaparib	48-57	poly(ADP-ribose) polymerase 1	Homo sapiens	14-19
32717529-4	2020	To date, four PARP1 inhibitors namely olaparib, rucaparib, niraparib and talazoparib, have been approved by Food and Drug Administration (FDA) for treating ovarian cancer and breast cancer with BRCA1/2 mutation.	rucaparib	48-57	BRCA1 DNA repair associated	Homo sapiens	194-201
32814685-2	2020	The recent Food and Drug Administration (FDA) approval of the poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and rucaparib for the treatment of advanced prostate cancer heralds the onset of precision medicine for this disease.	rucaparib	121-130	poly(ADP-ribose) polymerase 1	Homo sapiens	91-95
32814685-9	2020	The PARP inhibitors olaparib and rucaparib are now FDA approved for mCRPC patients with HRR mutations and BRCA1/2 mutations, respectively.	rucaparib	33-42	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
32814685-12	2020	PATIENT SUMMARY: The poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and rucaparib are now approved by the Food and Drug Administration for the treatment of advanced prostate cancer.	rucaparib	80-89	poly(ADP-ribose) polymerase 1	Homo sapiens	21-48
32814685-9	2020	The PARP inhibitors olaparib and rucaparib are now FDA approved for mCRPC patients with HRR mutations and BRCA1/2 mutations, respectively.	rucaparib	33-42	BRCA1 DNA repair associated	Homo sapiens	106-113
32814685-12	2020	PATIENT SUMMARY: The poly(ADP-ribose) polymerase (PARP) inhibitors olaparib and rucaparib are now approved by the Food and Drug Administration for the treatment of advanced prostate cancer.	rucaparib	80-89	poly(ADP-ribose) polymerase 1	Homo sapiens	50-54
32963528-5	2020	In addition, BRCA mutations predict good response to poly-ADP ribose polymerase (PARP) inhibitors, such as olaparib, rucaparib, and niraparib.	rucaparib	117-126	BRCA1 DNA repair associated	Homo sapiens	13-17
32861537-1	2020	BACKGROUND: In the phase 3 trial ARIEL3, maintenance treatment with the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib provided clinical benefit versus placebo for patients with recurrent, platinum-sensitive ovarian cancer.	rucaparib	117-126	poly(ADP-ribose) polymerase 1	Homo sapiens	72-99
32861537-1	2020	BACKGROUND: In the phase 3 trial ARIEL3, maintenance treatment with the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib provided clinical benefit versus placebo for patients with recurrent, platinum-sensitive ovarian cancer.	rucaparib	117-126	poly(ADP-ribose) polymerase 1	Homo sapiens	101-105
32963528-5	2020	In addition, BRCA mutations predict good response to poly-ADP ribose polymerase (PARP) inhibitors, such as olaparib, rucaparib, and niraparib.	rucaparib	117-126	poly(ADP-ribose) polymerase 1	Homo sapiens	53-79
32963528-5	2020	In addition, BRCA mutations predict good response to poly-ADP ribose polymerase (PARP) inhibitors, such as olaparib, rucaparib, and niraparib.	rucaparib	117-126	poly(ADP-ribose) polymerase 1	Homo sapiens	81-85
32129697-0	2020	Evaluation of in vitro absorption, distribution, metabolism, and excretion and assessment of drug-drug interaction of rucaparib, an orally potent poly(ADP-ribose) polymerase inhibitor.	rucaparib	118-127	poly(ADP-ribose) polymerase 1	Homo sapiens	146-173
33053351-0	2020	Rucaparib Treatment Alters p53 Oscillations in Single Cells to Enhance DNA-Double-Strand-Break-Induced Cell Cycle Arrest.	rucaparib	0-9	tumor protein p53	Homo sapiens	27-30
33053351-4	2020	The small-molecule rucaparib, an inhibitor of the alternative end-joining-associated protein poly (ADP-ribose) polymerase (PARP), increased p53 pulse duration, altering the temporal expression of multiple p53 target genes.	rucaparib	19-28	poly(ADP-ribose) polymerase 1	Homo sapiens	123-127
33053351-4	2020	The small-molecule rucaparib, an inhibitor of the alternative end-joining-associated protein poly (ADP-ribose) polymerase (PARP), increased p53 pulse duration, altering the temporal expression of multiple p53 target genes.	rucaparib	19-28	tumor protein p53	Homo sapiens	140-143
33053351-4	2020	The small-molecule rucaparib, an inhibitor of the alternative end-joining-associated protein poly (ADP-ribose) polymerase (PARP), increased p53 pulse duration, altering the temporal expression of multiple p53 target genes.	rucaparib	19-28	tumor protein p53	Homo sapiens	205-208
32129697-9	2020	Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 microM, respectively) and slightly inhibited OATP1B1, OATP1B3, OAT1, and OAT3 (66%, 58%, 58%, and 42% inhibition, respectively) at 300 microM.	rucaparib	0-9	solute carrier family 22 member 8	Homo sapiens	125-129
32129697-2	2020	The absorption, distribution, metabolism, elimination, and drug-drug interaction (DDI) potential of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib was characterised in vitro.2.	rucaparib	149-158	poly(ADP-ribose) polymerase 1	Homo sapiens	104-131
32129697-10	2020	Rucaparib inhibited OCT1, OCT2, MATE1, and MATE2-K (IC50, 4.3, 31, 0.63, and 0.19 muM, respectively).3.	rucaparib	0-9	POU class 2 homeobox 1	Homo sapiens	20-24
32129697-2	2020	The absorption, distribution, metabolism, elimination, and drug-drug interaction (DDI) potential of the poly(ADP-ribose) polymerase (PARP) inhibitor rucaparib was characterised in vitro.2.	rucaparib	149-158	poly(ADP-ribose) polymerase 1	Homo sapiens	133-137
32129697-4	2020	In HLMs, cytochrome P450 (CYP) 1A2 and CYP3A contributed to the metabolism of rucaparib to its major metabolite M324 with estimated fractions of metabolism catalysed by CYP (fm,CYP) of 0.27 and 0.64, respectively.	rucaparib	78-87	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	9-34
32129697-10	2020	Rucaparib inhibited OCT1, OCT2, MATE1, and MATE2-K (IC50, 4.3, 31, 0.63, and 0.19 muM, respectively).3.	rucaparib	0-9	POU class 2 homeobox 2	Homo sapiens	26-30
32129697-4	2020	In HLMs, cytochrome P450 (CYP) 1A2 and CYP3A contributed to the metabolism of rucaparib to its major metabolite M324 with estimated fractions of metabolism catalysed by CYP (fm,CYP) of 0.27 and 0.64, respectively.	rucaparib	78-87	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	39-44
32129697-10	2020	Rucaparib inhibited OCT1, OCT2, MATE1, and MATE2-K (IC50, 4.3, 31, 0.63, and 0.19 muM, respectively).3.	rucaparib	0-9	solute carrier family 47 member 1	Homo sapiens	32-37
32129697-10	2020	Rucaparib inhibited OCT1, OCT2, MATE1, and MATE2-K (IC50, 4.3, 31, 0.63, and 0.19 muM, respectively).3.	rucaparib	0-9	solute carrier family 47 member 2	Homo sapiens	43-50
32129697-10	2020	Rucaparib inhibited OCT1, OCT2, MATE1, and MATE2-K (IC50, 4.3, 31, 0.63, and 0.19 muM, respectively).3.	rucaparib	0-9	latexin	Homo sapiens	82-85
32129697-12	2020	Caution is advised when co-administering rucaparib with sensitive substrates of MATEs, OCT1, and OCT2.	rucaparib	41-50	POU class 2 homeobox 1	Homo sapiens	87-91
32129697-12	2020	Caution is advised when co-administering rucaparib with sensitive substrates of MATEs, OCT1, and OCT2.	rucaparib	41-50	POU class 2 homeobox 2	Homo sapiens	97-101
32129697-4	2020	In HLMs, cytochrome P450 (CYP) 1A2 and CYP3A contributed to the metabolism of rucaparib to its major metabolite M324 with estimated fractions of metabolism catalysed by CYP (fm,CYP) of 0.27 and 0.64, respectively.	rucaparib	78-87	peptidylprolyl isomerase G	Homo sapiens	26-29
32129697-4	2020	In HLMs, cytochrome P450 (CYP) 1A2 and CYP3A contributed to the metabolism of rucaparib to its major metabolite M324 with estimated fractions of metabolism catalysed by CYP (fm,CYP) of 0.27 and 0.64, respectively.	rucaparib	78-87	peptidylprolyl isomerase G	Homo sapiens	39-42
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	31-37
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	39-45
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	47-54
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	56-62
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	166-172
32129697-5	2020	Rucaparib reversibly inhibited CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3As (IC50, 3.55, 12.9, 5.42, 41.6, and 17.2-22.9 microM [2 substrates], respectively), but not CYP2B6 or CYP2C8 (>190 microM).	rucaparib	0-9	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	176-182
32129697-7	2020	In cultured human hepatocytes, rucaparib showed concentration-dependent induction of CYP1A2 mRNA and downregulation of CYP3A4 and CYP2B6 mRNA.	rucaparib	31-40	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	85-91
32129697-7	2020	In cultured human hepatocytes, rucaparib showed concentration-dependent induction of CYP1A2 mRNA and downregulation of CYP3A4 and CYP2B6 mRNA.	rucaparib	31-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	119-125
32129697-7	2020	In cultured human hepatocytes, rucaparib showed concentration-dependent induction of CYP1A2 mRNA and downregulation of CYP3A4 and CYP2B6 mRNA.	rucaparib	31-40	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	130-136
32129697-8	2020	In transfected cells expressing drug transporters, rucaparib was a substrate for P-gp and BCRP, but not for OATP1B1, OATP1B3, OAT1, OAT3, or OCT2.	rucaparib	51-60	phosphoglycolate phosphatase	Homo sapiens	81-85
32129697-8	2020	In transfected cells expressing drug transporters, rucaparib was a substrate for P-gp and BCRP, but not for OATP1B1, OATP1B3, OAT1, OAT3, or OCT2.	rucaparib	51-60	BCR pseudogene 1	Homo sapiens	90-94
32129697-9	2020	Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 microM, respectively) and slightly inhibited OATP1B1, OATP1B3, OAT1, and OAT3 (66%, 58%, 58%, and 42% inhibition, respectively) at 300 microM.	rucaparib	0-9	phosphoglycolate phosphatase	Homo sapiens	20-24
32129697-9	2020	Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 microM, respectively) and slightly inhibited OATP1B1, OATP1B3, OAT1, and OAT3 (66%, 58%, 58%, and 42% inhibition, respectively) at 300 microM.	rucaparib	0-9	BCR pseudogene 1	Homo sapiens	29-33
32129697-9	2020	Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 microM, respectively) and slightly inhibited OATP1B1, OATP1B3, OAT1, and OAT3 (66%, 58%, 58%, and 42% inhibition, respectively) at 300 microM.	rucaparib	0-9	solute carrier organic anion transporter family member 1B1	Homo sapiens	97-104
32129697-9	2020	Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 microM, respectively) and slightly inhibited OATP1B1, OATP1B3, OAT1, and OAT3 (66%, 58%, 58%, and 42% inhibition, respectively) at 300 microM.	rucaparib	0-9	solute carrier organic anion transporter family member 1B3	Homo sapiens	106-113
32129697-9	2020	Rucaparib inhibited P-gp and BCRP (IC50, 169 and 55 microM, respectively) and slightly inhibited OATP1B1, OATP1B3, OAT1, and OAT3 (66%, 58%, 58%, and 42% inhibition, respectively) at 300 microM.	rucaparib	0-9	potassium two pore domain channel subfamily K member 3	Homo sapiens	115-119
32709004-5	2020	Interestingly, NIH-OVCAR3 cells showed sensitivity to carboplatin and rucaparib which was explained by functional loss of homologous recombination repair (HRR) identified by plasmid re-joining assay, despite the ability to form RAD51 foci and absence of mutations in HRR genes.	rucaparib	70-79	RAD51 recombinase	Homo sapiens	228-233
32427631-4	2020	Several PARPis have been successfully tested in clinical trials for HRR-deficient metastatic castration-resistant prostate cancer (mCRPC), and olaparib and rucaparib have recently received breakthrough approval in BRCA1/2 mutated mCRPC.	rucaparib	156-165	BRCA1 DNA repair associated	Homo sapiens	214-221
32527552-1	2020	We describe the synthesis and in vitro activity of drug-dye conjugate 1, which is a combination of the PARP inhibitor rucaparib and heptamethine cyanine dye IR-786.	rucaparib	118-127	poly(ADP-ribose) polymerase 1	Homo sapiens	103-107
32086346-0	2020	Non-BRCA DNA Damage Repair Gene Alterations and Response to the PARP Inhibitor Rucaparib in Metastatic Castration-Resistant Prostate Cancer: analysis from the phase 2 TRITON2 study.	rucaparib	79-88	collagen type XI alpha 2 chain	Homo sapiens	64-68
32371137-5	2020	The US Food and Drug Administration (FDA) and European Medicines Agency (EMA) recently approved several PARP inhibitors, such as olaparib, niraparib, talazoparib, and rucaparib, for the treatment of ovarian and germline BRCA-mutant breast cancers.	rucaparib	167-176	poly(ADP-ribose) polymerase 1	Homo sapiens	104-108
32371137-5	2020	The US Food and Drug Administration (FDA) and European Medicines Agency (EMA) recently approved several PARP inhibitors, such as olaparib, niraparib, talazoparib, and rucaparib, for the treatment of ovarian and germline BRCA-mutant breast cancers.	rucaparib	167-176	BRCA1 DNA repair associated	Homo sapiens	220-224
32215876-4	2020	US Food and Drug Administration (FDA)-approved PARP inhibitors include olaparib, rucaparib, and niraparib, while veliparib is in the late stage of clinical development.	rucaparib	81-90	poly(ADP-ribose) polymerase 1	Homo sapiens	47-51
32086346-8	2020	Conclusions: In this prospective, genomics-driven study of rucaparib in mCRPC, we found limited radiographic/PSA responses to PARP inhibition in men with alterations in ATM, CDK12, or CHEK2 However, patients with alterations in other DDR-associated genes (eg, PALB2) may benefit from PARP inhibition.	rucaparib	59-68	collagen type XI alpha 2 chain	Homo sapiens	126-130
32523631-2	2020	The PARP inhibitor rucaparib is indicated in the UK, European Union and the United States for use in the treatment and maintenance settings for patients with relapsed ovarian cancer.	rucaparib	19-28	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
32539918-8	2020	After Rubraca  treatment, the apoptotic rate of SKOV3 and A2780 cells (Annexin V+/PI-cells) did not change significantly, but the proportion of necrotic cells (PI+cells or Annexin V+/PI+cells) increased significantly, which was different from the control group.	rucaparib	6-13	annexin A5	Homo sapiens	71-80
32495160-1	2020	The poly(ADP-ribose) polymerase inhibitor rucaparib is approved as monotherapy in the treatment and maintenance settings for women with relapsed ovarian cancer in the European Union and the United States.	rucaparib	42-51	poly(ADP-ribose) polymerase 1	Homo sapiens	4-31
32268868-4	2021	RESULTS: Fifteen out of 329 flavonoids achieved better docking score as compared to rucaparib which is an FDA approved PARP inhibitor.	rucaparib	84-93	poly(ADP-ribose) polymerase 1	Homo sapiens	119-123
32359490-13	2020	CFI, TFST, PFS2, and TSST were also significantly longer with rucaparib than placebo in the BRCA-mutant and homologous recombination-deficient cohorts.	rucaparib	62-71	GINS complex subunit 2	Homo sapiens	11-15
32260355-5	2020	The BRCA2 mutated V-C8 cells were 1000x more sensitive to rucaparib cytotoxicity than their matched BRCA2 corrected V-C8.B2 cells, but no more sensitive to PF-477736 despite having seven-fold higher levels of RS.	rucaparib	58-67	LOW QUALITY PROTEIN: breast cancer type 2 susceptibility protein	Cricetulus griseus	4-9
32235451-7	2020	Niraparib, Olaparib, and Rucaparib also demonstrated effective inhibitory potency in both advanced TNBC and ER-/HER2+ cells with and without BRCA-mutations.	rucaparib	25-34	estrogen receptor 1	Homo sapiens	108-110
32235451-7	2020	Niraparib, Olaparib, and Rucaparib also demonstrated effective inhibitory potency in both advanced TNBC and ER-/HER2+ cells with and without BRCA-mutations.	rucaparib	25-34	erb-b2 receptor tyrosine kinase 2	Homo sapiens	112-116
32171277-0	2020	Polyclonal BRCA2 mutations following carboplatin treatment confer resistance to the PARP inhibitor rucaparib in a patient with mCRPC: a case report.	rucaparib	99-108	BRCA2 DNA repair associated	Homo sapiens	11-16
32171277-0	2020	Polyclonal BRCA2 mutations following carboplatin treatment confer resistance to the PARP inhibitor rucaparib in a patient with mCRPC: a case report.	rucaparib	99-108	poly(ADP-ribose) polymerase 1	Homo sapiens	84-88
32171277-3	2020	CASE PRESENTATION: A patient with mCRPC associated with a germline BRCA2 mutation was sequentially treated with carboplatin and the PARP inhibitor rucaparib.	rucaparib	147-156	BRCA2 DNA repair associated	Homo sapiens	67-72
32171277-3	2020	CASE PRESENTATION: A patient with mCRPC associated with a germline BRCA2 mutation was sequentially treated with carboplatin and the PARP inhibitor rucaparib.	rucaparib	147-156	poly(ADP-ribose) polymerase 1	Homo sapiens	132-136
31813938-2	2020	6-mercaptopurine (6MP) was found to selectively kill BRCA-defective cells in a xenograft model as effectively as the PARP inhibitor AG014699, even after these cells acquired resistance to a PARP inhibitor or cisplatin.	rucaparib	132-140	poly(ADP-ribose) polymerase 1	Homo sapiens	117-121
31931287-7	2020	To date, three PARP inhibitor drugs have been approved for treating ovarian cancer by FDA in United States, namely Olaparib, Rucaparib, and Niraparib.	rucaparib	125-134	poly(ADP-ribose) polymerase 1	Homo sapiens	15-19
31669203-1	2020	PARP1 inhibitor (Niraparib, Olaparib, Rucaparib) maintenance therapy improves progression-free survival in platinum sensitive sporadic epithelial ovarian cancers.	rucaparib	38-47	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
31939072-10	2020	Finally, an additional targeted approach being pursued involves PARP inhibitors (rucaparib and olaparib are both in Phase II) based on earlier study results.	rucaparib	81-90	poly(ADP-ribose) polymerase 1	Homo sapiens	64-68
30612311-0	2019	Sensitization of colorectal cancer to irinotecan therapy by PARP inhibitor rucaparib.	rucaparib	75-84	poly(ADP-ribose) polymerase 1	Homo sapiens	60-64
32128485-3	2020	Case summary: We describe a case of PARP inhibitor-induced torsades de pointes (TdP) in an 86-year-old gentleman prescribed rucaparib due to chemotherapy-resistant, metastatic prostate cancer with pre-existing long QT, with an apparent dose-dependent increase in QT interval.	rucaparib	124-133	poly(ADP-ribose) polymerase 1	Homo sapiens	36-40
31625002-3	2019	Since 2014, four PARP inhibitors have been approved in various indications: olaparib, niraparib, and rucaparib in high-grade serous ovarian cancer, and olaparib and talazoparib in metastatic breast cancer.	rucaparib	101-110	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
31685558-0	2019	Antitumor activity of the poly(ADP-ribose) polymerase inhibitor rucaparib as monotherapy in patients with platinum-sensitive, relapsed, BRCA-mutated, high-grade ovarian cancer, and an update on safety.	rucaparib	64-73	poly(ADP-ribose) polymerase 1	Homo sapiens	26-53
31685558-0	2019	Antitumor activity of the poly(ADP-ribose) polymerase inhibitor rucaparib as monotherapy in patients with platinum-sensitive, relapsed, BRCA-mutated, high-grade ovarian cancer, and an update on safety.	rucaparib	64-73	BRCA1 DNA repair associated	Homo sapiens	136-140
31685558-1	2019	OBJECTIVE: To report results from an integrated efficacy and safety analysis supporting the European Commission"s approval of the poly(ADP-ribose) polymerase inhibitor rucaparib as monotherapy treatment for relapsed, platinum-sensitive, BRCA-mutated ovarian cancer.	rucaparib	168-177	poly(ADP-ribose) polymerase 1	Homo sapiens	130-157
31685558-1	2019	OBJECTIVE: To report results from an integrated efficacy and safety analysis supporting the European Commission"s approval of the poly(ADP-ribose) polymerase inhibitor rucaparib as monotherapy treatment for relapsed, platinum-sensitive, BRCA-mutated ovarian cancer.	rucaparib	168-177	BRCA1 DNA repair associated	Homo sapiens	237-241
31685558-9	2019	CONCLUSIONS: In patients with platinum-sensitive, BRCA-mutated ovarian cancer, rucaparib demonstrated antitumor activity and is the first and currently the only poly(ADP-ribose) polymerase inhibitor approved by the European Commission as treatment for this population.	rucaparib	79-88	BRCA1 DNA repair associated	Homo sapiens	50-54
31685558-9	2019	CONCLUSIONS: In patients with platinum-sensitive, BRCA-mutated ovarian cancer, rucaparib demonstrated antitumor activity and is the first and currently the only poly(ADP-ribose) polymerase inhibitor approved by the European Commission as treatment for this population.	rucaparib	79-88	poly(ADP-ribose) polymerase 1	Homo sapiens	161-188
30988430-10	2019	We found that rucaparib can target PARP11 to stabilize IFNAR1 and therefore exhibits efficient enhancement of IFN-I signalling and the host antiviral response.	rucaparib	14-23	poly(ADP-ribose) polymerase family member 11	Homo sapiens	35-41
30988430-10	2019	We found that rucaparib can target PARP11 to stabilize IFNAR1 and therefore exhibits efficient enhancement of IFN-I signalling and the host antiviral response.	rucaparib	14-23	interferon alpha and beta receptor subunit 1	Homo sapiens	55-61
30988430-10	2019	We found that rucaparib can target PARP11 to stabilize IFNAR1 and therefore exhibits efficient enhancement of IFN-I signalling and the host antiviral response.	rucaparib	14-23	interferon alpha 1	Homo sapiens	55-58
32758032-4	2020	Several PARP inhibitors (PARPi) are under development, such as olaparib, talazoparib, niraparib, rucaparib, and veliparib.	rucaparib	97-106	poly(ADP-ribose) polymerase 1	Homo sapiens	8-12
31219654-9	2019	Forced activation of canonical Wnt signaling in several PARPi-sensitive cells via WNT3A reduced olaparib and rucaparib sensitivity.	rucaparib	109-118	Wnt family member 3A	Homo sapiens	31-34
31219654-9	2019	Forced activation of canonical Wnt signaling in several PARPi-sensitive cells via WNT3A reduced olaparib and rucaparib sensitivity.	rucaparib	109-118	Wnt family member 3A	Homo sapiens	82-87
31218365-4	2019	In this review, we summarize a decade of PARP inhibitor clinical development, a work which has resulted in the registration of several PARP inhibitors in breast (olaparib and talazoparib) and ovarian cancer (olaparib, niraparib and rucaparib, either alone or following platinum chemotherapy as maintenance therapy).	rucaparib	232-241	poly(ADP-ribose) polymerase 1	Homo sapiens	41-45
31218365-4	2019	In this review, we summarize a decade of PARP inhibitor clinical development, a work which has resulted in the registration of several PARP inhibitors in breast (olaparib and talazoparib) and ovarian cancer (olaparib, niraparib and rucaparib, either alone or following platinum chemotherapy as maintenance therapy).	rucaparib	232-241	poly(ADP-ribose) polymerase 1	Homo sapiens	135-139
30880062-2	2019	Because histone-dependent activation is unique to PARP-1, non-NAD-like PARP-1 inhibitors have the potential to bypass the off-target effects of classical NAD-dependent PARP-1 inhibitors, such as olaparib, veliparib, and rucaparib.	rucaparib	220-229	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
30880062-2	2019	Because histone-dependent activation is unique to PARP-1, non-NAD-like PARP-1 inhibitors have the potential to bypass the off-target effects of classical NAD-dependent PARP-1 inhibitors, such as olaparib, veliparib, and rucaparib.	rucaparib	220-229	poly(ADP-ribose) polymerase 1	Homo sapiens	71-77
31404966-5	2019	Among them, olaparib and rucaparib have breakthrough designations for BRCA1/2-mutated mCRPC.	rucaparib	25-34	BRCA1 DNA repair associated	Homo sapiens	70-77
33343988-1	2019	Rucaparib and niraparib are two of the newest U.S. Food and Drug Administration-approved PARP inhibitors, joining olaparib with indications in ovarian cancer.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	89-93
30977683-0	2019	Rucaparib in the landscape of PARP inhibition in ovarian cancer.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
31119062-3	2019	Herein, we evaluated the therapeutic effect of PARP1 inhibitor, rucaparib, for keloids.	rucaparib	64-73	poly(ADP-ribose) polymerase 1	Homo sapiens	47-52
31119062-8	2019	Rucaparib (20 muM) significantly suppressed the proliferation of keloid fibroblasts.	rucaparib	0-9	latexin	Homo sapiens	14-17
31119062-9	2019	Moreover, the combination of rucaparib (20 muM) and triamcinolone (50 muM) showed additive suppressive effect on keloid fibroblasts.	rucaparib	29-38	latexin	Homo sapiens	43-46
31119062-9	2019	Moreover, the combination of rucaparib (20 muM) and triamcinolone (50 muM) showed additive suppressive effect on keloid fibroblasts.	rucaparib	29-38	latexin	Homo sapiens	70-73
31119062-10	2019	Migration assay showed that rucaparib (10 muM) significantly suppressed the migration of keloid fibroblasts.	rucaparib	28-37	latexin	Homo sapiens	42-45
31119062-11	2019	Fibrosis markers in keloid fibroblasts significantly decreased after rucaparib treatment (20 muM).	rucaparib	69-78	latexin	Homo sapiens	93-96
31119062-14	2019	PARP1 inhibitor, rucaparib, might be a promising therapeutic drug for the treatment of keloid disease.	rucaparib	17-26	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
30912451-3	2019	PARP inhibitors olaparib, veliparib, talazoparib, niraparib and rucaparib have predominantly been studied in women with breast or ovarian cancers associated with deleterious germline mutations in BRCA1 and BRCA2 (gBRCA1/2+).	rucaparib	64-73	BRCA1 DNA repair associated	Homo sapiens	196-201
30939057-0	2019	Germline BRCA1 Deletion as Driver Mutation for Metastatic Urachal Adenocarcinoma in Patient Who Achieved Complete Response to Rucaparib.	rucaparib	126-135	BRCA1 DNA repair associated	Homo sapiens	9-14
30895466-4	2019	Three PARP inhibitors (olaparib, niraparib, and rucaparib) are now approved for use in women with recurrent EOC.	rucaparib	48-57	poly(ADP-ribose) polymerase 1	Homo sapiens	6-10
30940721-1	2019	In an interim analysis, the targeted PARP inhibitor rucaparib showed encouraging signs of disease control when used as a maintenance therapy for patients with platinum-sensitive advanced pancreatic cancer and a pathogenic mutation in BRCA1, BRCA2, or PALB2.	rucaparib	52-61	collagen type XI alpha 2 chain	Homo sapiens	37-41
30940721-1	2019	In an interim analysis, the targeted PARP inhibitor rucaparib showed encouraging signs of disease control when used as a maintenance therapy for patients with platinum-sensitive advanced pancreatic cancer and a pathogenic mutation in BRCA1, BRCA2, or PALB2.	rucaparib	52-61	BRCA1 DNA repair associated	Homo sapiens	234-239
30940721-1	2019	In an interim analysis, the targeted PARP inhibitor rucaparib showed encouraging signs of disease control when used as a maintenance therapy for patients with platinum-sensitive advanced pancreatic cancer and a pathogenic mutation in BRCA1, BRCA2, or PALB2.	rucaparib	52-61	BRCA2 DNA repair associated	Homo sapiens	241-246
30940721-1	2019	In an interim analysis, the targeted PARP inhibitor rucaparib showed encouraging signs of disease control when used as a maintenance therapy for patients with platinum-sensitive advanced pancreatic cancer and a pathogenic mutation in BRCA1, BRCA2, or PALB2.	rucaparib	52-61	partner and localizer of BRCA2	Homo sapiens	251-256
31074636-2	2019	Three different poly ADP ribose polymerase inhibitors (olaparib, niraparib and rucaparib) have been already approved as maintenance after response to platinum-based chemotherapy; two of them (olaparib and rucaparib) also as single agents.	rucaparib	79-88	poly(ADP-ribose) polymerase 1	Homo sapiens	16-42
31069647-5	2019	Olaparib and rucaparib are utilized in recurrent germline or somatic BRCA mutated ovarian cancer.	rucaparib	13-22	BRCA1 DNA repair associated	Homo sapiens	69-73
31191001-3	2019	Currently, PARP inhibitors such as olaparib, rucaparib and niraparib, which improve progression-free survival, particularly in patients harboring BRCA mutations, are approved by the Food and Drug Administration (FDA) and European Medicine Agency (EMA) for the treatment of ovarian cancers.	rucaparib	45-54	poly(ADP-ribose) polymerase 1	Homo sapiens	11-15
31191001-3	2019	Currently, PARP inhibitors such as olaparib, rucaparib and niraparib, which improve progression-free survival, particularly in patients harboring BRCA mutations, are approved by the Food and Drug Administration (FDA) and European Medicine Agency (EMA) for the treatment of ovarian cancers.	rucaparib	45-54	BRCA1 DNA repair associated	Homo sapiens	146-150
31117037-2	2019	Additionally, 3 new PARP inhibitors (olaparib, rucaparib, niraparib) have been approved for use in ovarian cancer, with different indications as maintenance therapy or treatment of recurrence.	rucaparib	47-56	poly(ADP-ribose) polymerase 1	Homo sapiens	20-24
31040352-6	2019	By combining this dual metabolic labelling strategy with highly sensitive tandem mass tag (TMT) isobaric mass spectrometry and hierarchical Bayesian analysis, we have quantified the responses of thousands of endogenous proteins to clinical PARP inhibitors Olaparib and Rucaparib.	rucaparib	269-278	poly(ADP-ribose) polymerase 1	Homo sapiens	240-244
30672100-2	2019	To date, three PARP inhibitors, namely, olaparib, rucaparib and niraparib have been approved for the treatment of ovarian cancer in the United States.	rucaparib	50-59	poly(ADP-ribose) polymerase 1	Homo sapiens	15-19
29166829-3	2019	In patients with deleterious BRCA1/2 mutation, an overall response rate of 80% was achieved in the phase II trial Assessment of Rucaparib in Ovarian CancEr Trial 2 (ARIEL2).	rucaparib	128-137	BRCA1 DNA repair associated	Homo sapiens	29-34
29166829-6	2019	CONCLUSION: Rucaparib appears to be a safe and effective new option in the treatment of relapsed, advanced BRCA1/2 mutant ovarian cancer.	rucaparib	12-21	BRCA1 DNA repair associated	Homo sapiens	107-114
30871186-2	2019	In cultures of ovarian cancer cells, we have previously shown that HRR function, based upon RAD51 foci quantification, correlated with growth inhibition ex vivo induced by rucaparib (a PARPi) and 12-month survival following platinum chemotherapy.	rucaparib	172-181	RAD51 recombinase	Homo sapiens	92-97
30737031-2	2019	PARP inhibitors including olaparib and rucaparib, have been specially developed against breast and ovarian cancers deficient in DNA repair systems.	rucaparib	39-48	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
30737031-3	2019	In this study, we found that PARP1-defective olaparib-resistant A2780 cells (ola-R cells) cells were still sensitive to two PARP inhibitors, rucaparib and veliparib.	rucaparib	141-150	poly(ADP-ribose) polymerase 1	Homo sapiens	29-34
30737031-3	2019	In this study, we found that PARP1-defective olaparib-resistant A2780 cells (ola-R cells) cells were still sensitive to two PARP inhibitors, rucaparib and veliparib.	rucaparib	141-150	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
30830551-1	2019	Rucaparib (Rubraca ) is a small molecule poly(ADP-ribose) polymerase (PARP) inhibitor with potent activity against PARP-1, -2 and -3.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	41-68
30830551-1	2019	Rucaparib (Rubraca ) is a small molecule poly(ADP-ribose) polymerase (PARP) inhibitor with potent activity against PARP-1, -2 and -3.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	70-74
30830551-1	2019	Rucaparib (Rubraca ) is a small molecule poly(ADP-ribose) polymerase (PARP) inhibitor with potent activity against PARP-1, -2 and -3.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	115-132
30830551-4	2019	Based on an analysis of patients across two phase II clinical trials, rucaparib displayed clinical activity as third- (or later-) line treatment of BRCA-mutated ovarian cancer, with rucaparib-treated patients having a confirmed objective response rate of 54%.	rucaparib	70-79	BRCA1 DNA repair associated	Homo sapiens	148-152
30333088-6	2019	Three different PARP inhibitors (olaparib, niraparib, and rucaparib) have been approved for the treatment of ovarian cancer and one (olaparib) for breast cancer harboring BRCA mutations.	rucaparib	58-67	poly(ADP-ribose) polymerase 1	Homo sapiens	16-20
30684797-7	2019	There are currently three FDA approved PARP1 inhibitors namely Olaparib, Rucaparib and Niraparib in the market while Veliparib and Talazoparib are in the late stage of clinical development.	rucaparib	73-82	poly(ADP-ribose) polymerase 1	Homo sapiens	39-44
30589644-4	2019	We demonstrated that clinical PARPi, including olaparib and rucaparib, have cell-autonomous immunomodulatory properties in ERCC1-defective NSCLC and BRCA1-defective triple-negative breast cancer (TNBC) cells.	rucaparib	60-69	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	123-128
30589644-4	2019	We demonstrated that clinical PARPi, including olaparib and rucaparib, have cell-autonomous immunomodulatory properties in ERCC1-defective NSCLC and BRCA1-defective triple-negative breast cancer (TNBC) cells.	rucaparib	60-69	BRCA1 DNA repair associated	Homo sapiens	149-154
29872938-9	2019	Results Rucaparib suppressed proliferation, induced G2/M phase arrest, and reduced the expression of cyclin D1 and CDK4 in cervical cancer cells.	rucaparib	8-17	cyclin dependent kinase 4	Homo sapiens	115-119
30425037-0	2019	BRCA Reversion Mutations in Circulating Tumor DNA Predict Primary and Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma.	rucaparib	112-121	BRCA1 DNA repair associated	Homo sapiens	0-4
30425037-0	2019	BRCA Reversion Mutations in Circulating Tumor DNA Predict Primary and Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma.	rucaparib	112-121	poly(ADP-ribose) polymerase 1	Homo sapiens	97-101
30425037-4	2019	Patients without BRCA reversion mutations detected in pretreatment cfDNA had significantly longer rucaparib progression-free survival than those with reversion mutations (median, 9.0 vs. 1.8 months; HR, 0.12; P < 0.0001).	rucaparib	98-107	BRCA1 DNA repair associated	Homo sapiens	17-21
30425037-6	2019	SIGNIFICANCE: BRCA reversion mutations are detected in cfDNA from platinum-resistant or platinum-refractory HGOC and are associated with decreased clinical benefit from rucaparib treatment.	rucaparib	169-178	BRCA1 DNA repair associated	Homo sapiens	14-18
30409489-8	2019	Lastly, it reviews key trials for the three poly-adenosine diphosphate [ADP]-ribose polymerases (PARP) inhibitors that have been FDA-approved for maintenance therapy in platinum-sensitive recurrent EOC: olaparib, rucaparib, and niraparib.	rucaparib	213-222	poly(ADP-ribose) polymerase 1	Homo sapiens	97-101
29872938-0	2019	The poly (ADP-ribose) polymerase inhibitor rucaparib suppresses proliferation and serves as an effective radiosensitizer in cervical cancer.	rucaparib	43-52	poly(ADP-ribose) polymerase 1	Homo sapiens	4-32
29872938-6	2019	Immunofluorescence staining assay was performed to detect the expression of the DNA injury marker tsadi-H2AX after treatment with rucaparib and radiotherapy.	rucaparib	130-139	H2A.X variant histone	Homo sapiens	104-108
30427584-0	2019	Evaluation of Drug-Drug Interactions of Rucaparib and CYP1A2, CYP2C9, CYP2C19, CYP3A, and P-gp Substrates in Patients With an Advanced Solid Tumor.	rucaparib	40-49	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	70-77
29872938-9	2019	Results Rucaparib suppressed proliferation, induced G2/M phase arrest, and reduced the expression of cyclin D1 and CDK4 in cervical cancer cells.	rucaparib	8-17	cyclin D1	Homo sapiens	101-110
30427584-0	2019	Evaluation of Drug-Drug Interactions of Rucaparib and CYP1A2, CYP2C9, CYP2C19, CYP3A, and P-gp Substrates in Patients With an Advanced Solid Tumor.	rucaparib	40-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	79-84
30427584-0	2019	Evaluation of Drug-Drug Interactions of Rucaparib and CYP1A2, CYP2C9, CYP2C19, CYP3A, and P-gp Substrates in Patients With an Advanced Solid Tumor.	rucaparib	40-49	ATP binding cassette subfamily B member 1	Homo sapiens	90-94
30105925-0	2018	Rucaparib in ovarian cancer: extending the use of PARP inhibitors in the recurrent disease.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	50-54
30449210-2	2018	Poly-ADP ribose polymerase (PARP) inhibitors like rucaparib are daily oral medication that exploit the DNA repair pathway.	rucaparib	50-59	poly(ADP-ribose) polymerase 1	Homo sapiens	0-26
30449210-2	2018	Poly-ADP ribose polymerase (PARP) inhibitors like rucaparib are daily oral medication that exploit the DNA repair pathway.	rucaparib	50-59	poly(ADP-ribose) polymerase 1	Homo sapiens	28-32
30449210-6	2018	The side effect profile of rucaparib is similar or more favorable when evaluating it against other PARP inhibitors.	rucaparib	27-36	poly(ADP-ribose) polymerase 1	Homo sapiens	99-103
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	65-69
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	71-76
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase 2	Homo sapiens	78-83
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 3	Homo sapiens	88-93
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 4	Homo sapiens	119-124
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 10	Homo sapiens	126-132
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 12	Homo sapiens	134-140
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 15	Homo sapiens	142-148
30105925-1	2018	Rucaparib is a potent inhibitor of poly (ADP-ribose) polymerase (PARP) PARP1, PARP2 and PARP3, and to a lesser extent, PARP4, PARP10, PARP12, PARP15 and PARP16.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 16	Homo sapiens	153-159
30105925-2	2018	Study 10 and ARIEL2 evaluated the use of rucaparib as treatment in patients with recurrent high-grade ovarian carcinoma and resulting in approval of rucaparib for patients with both germline and somatic BRCA mutation.	rucaparib	41-50	BRCA1 DNA repair associated	Homo sapiens	203-207
30105925-2	2018	Study 10 and ARIEL2 evaluated the use of rucaparib as treatment in patients with recurrent high-grade ovarian carcinoma and resulting in approval of rucaparib for patients with both germline and somatic BRCA mutation.	rucaparib	149-158	BRCA1 DNA repair associated	Homo sapiens	203-207
30116283-3	2018	The small-molecule NAD+ mimetics, olaparib, niraparib, rucaparib, veliparib, and talazoparib, inhibit the catalytic activity of PARP-1 and PARP-2 and are currently being studied in later-stage clinical trials.	rucaparib	55-64	poly(ADP-ribose) polymerase 1	Homo sapiens	128-134
30132953-0	2018	Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway.	rucaparib	49-58	protein tyrosine kinase 2 beta	Homo sapiens	149-165
30132953-6	2018	Western blot assay uncovered the combined effects of INPP4B and rucaparib on cell cycle, apoptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signal pathway.	rucaparib	64-73	protein tyrosine kinase 2 beta	Homo sapiens	129-145
30132953-6	2018	Western blot assay uncovered the combined effects of INPP4B and rucaparib on cell cycle, apoptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signal pathway.	rucaparib	64-73	AKT serine/threonine kinase 1	Homo sapiens	152-155
30132953-12	2018	Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells.	rucaparib	50-59	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	69-72
30132953-12	2018	Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells.	rucaparib	50-59	cyclin E1	Homo sapiens	74-83
30132953-12	2018	Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells.	rucaparib	50-59	cyclin D1	Homo sapiens	88-97
30132953-12	2018	Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells.	rucaparib	50-59	AKT serine/threonine kinase 1	Homo sapiens	182-185
30132953-14	2018	The study demonstrated that INPP4B and rucaparib exhibited synergistic antitumor effect by regulating PI3K/AKT pathway in OS cells.	rucaparib	39-48	AKT serine/threonine kinase 1	Homo sapiens	107-110
30426062-0	2018	Pharmacokinetics and clinical response to single agent rucaparib in a dialysis dependent patient with BRCA associated breast and recurrent ovarian cancer.	rucaparib	55-64	BRCA1 DNA repair associated	Homo sapiens	102-106
30426062-1	2018	A 56-year old woman with BRCA-associated breast cancer and recurrent ovarian cancer was treated with a poly (ADP-ribose) polymerase enzyme (PARP) inhibitor, rucaparib, in the setting of dialysis-dependence which required dose modification.	rucaparib	157-166	BRCA1 DNA repair associated	Homo sapiens	25-29
30426062-1	2018	A 56-year old woman with BRCA-associated breast cancer and recurrent ovarian cancer was treated with a poly (ADP-ribose) polymerase enzyme (PARP) inhibitor, rucaparib, in the setting of dialysis-dependence which required dose modification.	rucaparib	157-166	poly(ADP-ribose) polymerase 1	Homo sapiens	140-144
30535808-3	2018	Olaparib and rucaparib currently have indications for treatment of recurrent BRCA mutant ovarian cancer.	rucaparib	13-22	BRCA1 DNA repair associated	Homo sapiens	77-81
30266954-0	2018	Methylation of all BRCA1 copies predicts response to the PARP inhibitor rucaparib in ovarian carcinoma.	rucaparib	72-81	BRCA1 DNA repair associated	Homo sapiens	19-24
30266954-0	2018	Methylation of all BRCA1 copies predicts response to the PARP inhibitor rucaparib in ovarian carcinoma.	rucaparib	72-81	poly(ADP-ribose) polymerase 1	Homo sapiens	57-61
30266954-4	2018	Among BRCA1-methylated PDX, silencing of all BRCA1 copies predicts rucaparib response, whilst heterozygous methylation is associated with resistance.	rucaparib	67-76	BRCA1 DNA repair associated	Homo sapiens	6-11
30266954-4	2018	Among BRCA1-methylated PDX, silencing of all BRCA1 copies predicts rucaparib response, whilst heterozygous methylation is associated with resistance.	rucaparib	67-76	BRCA1 DNA repair associated	Homo sapiens	45-50
30266954-5	2018	Analysis of 21 BRCA1-methylated platinum-sensitive recurrent HGSOC (ARIEL2 Part 1 trial) confirmed that homozygous or hemizygous BRCA1 methylation predicts rucaparib clinical response, and that methylation loss can occur after exposure to chemotherapy.	rucaparib	156-165	ADP-ribosyltransferase 1	Homo sapiens	68-81
30266954-5	2018	Analysis of 21 BRCA1-methylated platinum-sensitive recurrent HGSOC (ARIEL2 Part 1 trial) confirmed that homozygous or hemizygous BRCA1 methylation predicts rucaparib clinical response, and that methylation loss can occur after exposure to chemotherapy.	rucaparib	156-165	BRCA1 DNA repair associated	Homo sapiens	129-134
30116283-3	2018	The small-molecule NAD+ mimetics, olaparib, niraparib, rucaparib, veliparib, and talazoparib, inhibit the catalytic activity of PARP-1 and PARP-2 and are currently being studied in later-stage clinical trials.	rucaparib	55-64	poly(ADP-ribose) polymerase 2	Homo sapiens	139-145
29572258-0	2018	Direct Imaging of Drug Distribution and Target Engagement of the PARP Inhibitor Rucaparib.	rucaparib	80-89	poly(ADP-ribose) polymerase 1	Homo sapiens	65-69
29572258-2	2018	Here, we describe the intrinsic fluorescence properties of the clinically approved PARP inhibitor rucaparib and its potential to directly measure drug distribution and target engagement-a critical factor for understanding drug action and improving efficacy.	rucaparib	98-107	poly(ADP-ribose) polymerase 1	Homo sapiens	83-87
29572258-7	2018	Nuclear rucaparib uptake increased with higher PARP1 expression, and we determined an intracellular half-life of 6.4 h. Conclusion: The label-free, intrinsic fluorescence of rucaparib can be exploited to interrogate drug distribution and target binding, critical factors toward improving treatment efficacy and outcome.	rucaparib	8-17	poly(ADP-ribose) polymerase 1	Homo sapiens	47-52
30080919-3	2018	Two PARP inhibitors, olaparib and rucaparib, have been approved by the US Food and Drug Administration (FDA) for the treatment of recurrent, BRCA-associated ovarian cancer.	rucaparib	34-43	poly(ADP-ribose) polymerase 1	Homo sapiens	4-8
29393407-1	2018	Poly (ADP-ribose) polymerase (PARP) inhibitors, such as olaparib or rucaparib, have shown treatment efficacy in BRCA1/2-deficient tumors.	rucaparib	68-77	poly(ADP-ribose) polymerase 1	Homo sapiens	0-28
30046392-0	2018	Epigenetic activation of HORMAD1 in basal-like breast cancer: role in Rucaparib sensitivity.	rucaparib	70-79	HORMA domain containing 1	Homo sapiens	25-32
30046392-7	2018	On the other hand, investigation of the Genomics of Drug Sensitivity in Cancer dataset revealed significantly reduced sensitivity of HORMAD1-overexpressing BLBC cell lines to Rucaparib, a commonly used PARPi.	rucaparib	175-184	HORMA domain containing 1	Homo sapiens	133-140
30046392-9	2018	Ectopic expression of HORMAD1 enhances tumor formations in two of these models, and significantly reduces sensitivity to Rucaparib in the HCC1954 model.	rucaparib	121-130	HORMA domain containing 1	Homo sapiens	22-29
30046392-10	2018	Taken together, our data suggest that epigenetic activation of HORMAD1 by hypomethylation in BLBC may endow reduced sensitivity to Rucaparib treatment in some tumor models.	rucaparib	131-140	HORMA domain containing 1	Homo sapiens	63-70
30067621-3	2018	PARP inhibitors that have undergone clinical investigation in the treatment of breast cancer include olaparib, talazoparib, veliparib, niraparib, and rucaparib.	rucaparib	150-159	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
29750420-3	2018	We review key trials that have led to the approval of three PARP inhibitors-olaparib, niraparib and rucaparib-as maintenance therapy for platinum-sensitive recurrent ovarian cancer.	rucaparib	100-109	poly(ADP-ribose) polymerase 1	Homo sapiens	60-64
29977351-1	2018	Rucaparib is a poly (ADP-ribose) polymerase (PARP) inhibitor and potent inhibitor of PARP1, PARP2 and PARP3 enzymes.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	15-43
29977351-1	2018	Rucaparib is a poly (ADP-ribose) polymerase (PARP) inhibitor and potent inhibitor of PARP1, PARP2 and PARP3 enzymes.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	45-49
29977351-1	2018	Rucaparib is a poly (ADP-ribose) polymerase (PARP) inhibitor and potent inhibitor of PARP1, PARP2 and PARP3 enzymes.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	85-90
29977351-1	2018	Rucaparib is a poly (ADP-ribose) polymerase (PARP) inhibitor and potent inhibitor of PARP1, PARP2 and PARP3 enzymes.	rucaparib	0-9	poly(ADP-ribose) polymerase 2	Homo sapiens	92-97
29977351-1	2018	Rucaparib is a poly (ADP-ribose) polymerase (PARP) inhibitor and potent inhibitor of PARP1, PARP2 and PARP3 enzymes.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 3	Homo sapiens	102-107
29977351-2	2018	Phase II and III trials have documented that rucaparib has single-agent antitumor activity in patients with high-grade ovarian carcinoma, with both BRCA-mutated (germline and somatic) and with homologous recombination deficiency (HRD).	rucaparib	45-54	BRCA1 DNA repair associated	Homo sapiens	148-153
29605737-0	2018	Rucaparib: An emerging parp inhibitor for treatment of recurrent ovarian cancer.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	23-27
29605737-5	2018	Rucaparib inhibits PARP-1, 2 and 3, PARP-4, -12, -15 and -16, as well as tankyrase 1 and 2.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	19-34
29605737-5	2018	Rucaparib inhibits PARP-1, 2 and 3, PARP-4, -12, -15 and -16, as well as tankyrase 1 and 2.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 4	Homo sapiens	36-42
29605737-5	2018	Rucaparib inhibits PARP-1, 2 and 3, PARP-4, -12, -15 and -16, as well as tankyrase 1 and 2.	rucaparib	0-9	tankyrase	Homo sapiens	73-90
29605737-6	2018	On December 2016, it was granted accelerated approval by the FDA, based on data from two multicenter, single arm, phase II trials that evaluated the efficacy of Rucaparib in patients with deleterious, germline and/or somatic BRCA mutation-associated, advanced OC, who have been treated with two or more lines of chemotherapy.	rucaparib	161-170	BRCA1 DNA repair associated	Homo sapiens	225-229
29393407-1	2018	Poly (ADP-ribose) polymerase (PARP) inhibitors, such as olaparib or rucaparib, have shown treatment efficacy in BRCA1/2-deficient tumors.	rucaparib	68-77	poly(ADP-ribose) polymerase 1	Homo sapiens	30-34
30051098-0	2018	Rucaparib Monotherapy in Patients With Pancreatic Cancer and a Known Deleterious BRCA Mutation.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	81-85
29606854-0	2018	Rucaparib: a novel PARP inhibitor for BRCA advanced ovarian cancer.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	19-23
29606854-1	2018	Rucaparib is a potent small-molecule inhibitor of poly (ADP-ribose) polymerase (PARP) proteins (PARP-1, PARP-2 and PARP-3) that play an important role in repairing DNA damage and maintaining genomic stability.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	80-84
29606854-1	2018	Rucaparib is a potent small-molecule inhibitor of poly (ADP-ribose) polymerase (PARP) proteins (PARP-1, PARP-2 and PARP-3) that play an important role in repairing DNA damage and maintaining genomic stability.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	96-102
29606854-1	2018	Rucaparib is a potent small-molecule inhibitor of poly (ADP-ribose) polymerase (PARP) proteins (PARP-1, PARP-2 and PARP-3) that play an important role in repairing DNA damage and maintaining genomic stability.	rucaparib	0-9	poly(ADP-ribose) polymerase 2	Homo sapiens	104-110
29606854-1	2018	Rucaparib is a potent small-molecule inhibitor of poly (ADP-ribose) polymerase (PARP) proteins (PARP-1, PARP-2 and PARP-3) that play an important role in repairing DNA damage and maintaining genomic stability.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 3	Homo sapiens	115-121
29606854-3	2018	Rucaparib has been investigated in several preclinical and clinical studies showing promising activity in BRCA-mutant and BRCA-wild-type epithelial ovarian cancers (EOCs).	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	106-110
29895102-5	2018	PARP inhibitors, currently mainly including Olaparib, Niraparib, Velaparib, Rucaparib, and Talazoparib, have demonstrated promising activity in EOC treatment.	rucaparib	76-85	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
29189915-10	2018	First, the PARP1 inhibitors, rucaparib and talazoparib, were selectively synergistic with CNDAC in BRCA1/2 deficient OC cells (combination index < 1) at a relatively low concentration range.	rucaparib	29-38	poly(ADP-ribose) polymerase 1	Homo sapiens	11-16
29189915-10	2018	First, the PARP1 inhibitors, rucaparib and talazoparib, were selectively synergistic with CNDAC in BRCA1/2 deficient OC cells (combination index < 1) at a relatively low concentration range.	rucaparib	29-38	BRCA1 DNA repair associated	Homo sapiens	99-104
29327913-6	2018	Indeed, three PARP1 inhibitors (Olaparib, Rucaparib, and Niraparib) have recently been approved by the Food and Drug Administration for the treatment of ovarian cancer.	rucaparib	42-51	poly(ADP-ribose) polymerase 1	Homo sapiens	14-19
28806493-1	2018	BACKGROUND AND PURPOSE: Olaparib, rucaparib and niraparib, potent inhibitors of poly(ADP-ribose) polymerase (PARP) are approved as anti-cancer drugs in humans.	rucaparib	34-43	poly(ADP-ribose) polymerase 1	Homo sapiens	109-113
30051098-17	2018	Conclusion: Rucaparib provided clinical benefit to patients with advanced pancreatic cancer and a BRCA1/2 mutation, and demonstrated an acceptable safety profile.	rucaparib	12-21	BRCA2 DNA repair associated	Homo sapiens	98-105
28751443-0	2017	FDA Approval Summary: Rucaparib for the Treatment of Patients with Deleterious BRCA Mutation-Associated Advanced Ovarian Cancer.	rucaparib	22-31	BRCA1 DNA repair associated	Homo sapiens	79-83
28751443-1	2017	On December 19, 2016, the FDA granted accelerated approval to rucaparib (RUBRACA; Clovis Oncology, Inc.) for the treatment of patients with deleterious BRCA mutation (germline and/or somatic)-associated advanced ovarian cancer who have been treated with two or more chemotherapies.	rucaparib	62-71	BRCA1 DNA repair associated	Homo sapiens	152-156
28751443-2	2017	The FDA also approved the FoundationFocus CDx BRCA test (Foundation Medicine, Inc.), the first next-generation sequencing-based companion diagnostic, for identifying patients with advanced ovarian cancer eligible for treatment with rucaparib based on detection of deleterious BRCA1 and/or BRCA2 mutations in tumor tissue.	rucaparib	232-241	BRCA1 DNA repair associated	Homo sapiens	46-50
28751443-2	2017	The FDA also approved the FoundationFocus CDx BRCA test (Foundation Medicine, Inc.), the first next-generation sequencing-based companion diagnostic, for identifying patients with advanced ovarian cancer eligible for treatment with rucaparib based on detection of deleterious BRCA1 and/or BRCA2 mutations in tumor tissue.	rucaparib	232-241	BRCA1 DNA repair associated	Homo sapiens	276-281
28751443-2	2017	The FDA also approved the FoundationFocus CDx BRCA test (Foundation Medicine, Inc.), the first next-generation sequencing-based companion diagnostic, for identifying patients with advanced ovarian cancer eligible for treatment with rucaparib based on detection of deleterious BRCA1 and/or BRCA2 mutations in tumor tissue.	rucaparib	232-241	BRCA2 DNA repair associated	Homo sapiens	289-294
28751443-3	2017	Rucaparib"s approval was based primarily on efficacy data from 106 patients with BRCA mutation-associated ovarian cancer who had prior treatment with two or more chemotherapies and safety data from 377 patients with ovarian cancer treated with rucaparib 600 mg orally twice daily on two open-label, single-arm trials.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	81-85
28543772-6	2017	Liver extracts from PARP1 WT mice showed a significant increase in NAD+ levels after rucaparib treatment compared with untreated mouse liver, and a significant decrease in NAD+ levels in the temozolomide-treated group.	rucaparib	85-94	poly (ADP-ribose) polymerase family, member 1	Mus musculus	20-25
28882436-0	2017	Antitumor activity and safety of the PARP inhibitor rucaparib in patients with high-grade ovarian carcinoma and a germline or somatic BRCA1 or BRCA2 mutation: Integrated analysis of data from Study 10 and ARIEL2.	rucaparib	52-61	poly(ADP-ribose) polymerase 1	Homo sapiens	37-41
28882436-0	2017	Antitumor activity and safety of the PARP inhibitor rucaparib in patients with high-grade ovarian carcinoma and a germline or somatic BRCA1 or BRCA2 mutation: Integrated analysis of data from Study 10 and ARIEL2.	rucaparib	52-61	BRCA1 DNA repair associated	Homo sapiens	134-139
28882436-0	2017	Antitumor activity and safety of the PARP inhibitor rucaparib in patients with high-grade ovarian carcinoma and a germline or somatic BRCA1 or BRCA2 mutation: Integrated analysis of data from Study 10 and ARIEL2.	rucaparib	52-61	BRCA2 DNA repair associated	Homo sapiens	143-148
28882436-13	2017	CONCLUSIONS: Rucaparib has antitumor activity in advanced BRCA1/2-mutated HGOC and a manageable safety profile.	rucaparib	13-22	BRCA2 DNA repair associated	Homo sapiens	58-65
28916367-1	2017	BACKGROUND: Rucaparib, a poly(ADP-ribose) polymerase inhibitor, has anticancer activity in recurrent ovarian carcinoma harbouring a BRCA mutation or high percentage of genome-wide loss of heterozygosity.	rucaparib	12-21	BRCA1 DNA repair associated	Homo sapiens	132-136
28916367-11	2017	Median progression-free survival in patients with a BRCA-mutant carcinoma was 16 6 months (95% CI 13 4-22 9; 130 [35%] patients) in the rucaparib group versus 5 4 months (3 4-6 7; 66 [35%] patients) in the placebo group (hazard ratio 0 23 [95% CI 0 16-0 34]; p<0 0001).	rucaparib	136-145	BRCA1 DNA repair associated	Homo sapiens	52-56
29138572-3	2017	Indeed, three PARP inhibitors, olaparib, rucaparib and niraparib have already been approved in the US or Europe, mainly for the treatment of BRCA-mutant ovarian cancer.	rucaparib	41-50	BRCA1 DNA repair associated	Homo sapiens	141-145
28588062-0	2017	Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma.	rucaparib	114-123	RAD51 paralog C	Homo sapiens	38-44
28588062-0	2017	Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma.	rucaparib	114-123	RAD51 paralog D	Homo sapiens	49-55
28588062-0	2017	Secondary Somatic Mutations Restoring RAD51C and RAD51D Associated with Acquired Resistance to the PARP Inhibitor Rucaparib in High-Grade Ovarian Carcinoma.	rucaparib	114-123	collagen type XI alpha 2 chain	Homo sapiens	99-103
28588062-5	2017	Four distinct secondary mutations and spatial heterogeneity were observed for RAD51CIn vitro complementation assays and a patient-derived xenograft, as well as predictive molecular modeling, confirmed that resistance to rucaparib was associated with secondary mutations.Significance: Analyses of primary and secondary mutations in RAD51C and RAD51D provide evidence for these primary mutations in conferring PARPi sensitivity and secondary mutations as a mechanism of acquired PARPi resistance.	rucaparib	220-229	RAD51 paralog C	Homo sapiens	78-84
28588062-5	2017	Four distinct secondary mutations and spatial heterogeneity were observed for RAD51CIn vitro complementation assays and a patient-derived xenograft, as well as predictive molecular modeling, confirmed that resistance to rucaparib was associated with secondary mutations.Significance: Analyses of primary and secondary mutations in RAD51C and RAD51D provide evidence for these primary mutations in conferring PARPi sensitivity and secondary mutations as a mechanism of acquired PARPi resistance.	rucaparib	220-229	RAD51 paralog D	Homo sapiens	342-348
28543772-0	2017	PARP inhibitor rucaparib induces changes in NAD levels in cells and liver tissues as assessed by MRS. Poly(adenosine diphosphate ribose) polymerases (PARPs) are multifunctional proteins which play a role in many cellular processes.	rucaparib	15-24	poly (ADP-ribose) polymerase family, member 1	Mus musculus	0-4
28543772-0	2017	PARP inhibitor rucaparib induces changes in NAD levels in cells and liver tissues as assessed by MRS. Poly(adenosine diphosphate ribose) polymerases (PARPs) are multifunctional proteins which play a role in many cellular processes.	rucaparib	15-24	poly (ADP-ribose) polymerase family, member 1	Mus musculus	150-155
28543772-1	2017	Namely, PARP1 and PARP2 have been shown to be involved in DNA repair, and therefore are valid targets in cancer treatment with PARP inhibitors, such as rucaparib, currently in clinical trials.	rucaparib	152-161	poly (ADP-ribose) polymerase family, member 1	Mus musculus	8-13
28543772-1	2017	Namely, PARP1 and PARP2 have been shown to be involved in DNA repair, and therefore are valid targets in cancer treatment with PARP inhibitors, such as rucaparib, currently in clinical trials.	rucaparib	152-161	poly (ADP-ribose) polymerase family, member 2	Mus musculus	18-23
28543772-1	2017	Namely, PARP1 and PARP2 have been shown to be involved in DNA repair, and therefore are valid targets in cancer treatment with PARP inhibitors, such as rucaparib, currently in clinical trials.	rucaparib	152-161	poly (ADP-ribose) polymerase family, member 1	Mus musculus	8-12
28264872-10	2017	Among 98 patients, 5 (5.1%) discontinued because of an adverse event (excluding disease progression).Conclusions: Rucaparib was tolerable and had activity in patients with platinum-sensitive germline BRCA1/2-mutated HGOC.	rucaparib	114-123	BRCA1 DNA repair associated	Homo sapiens	200-205
28399901-0	2017	Activity of trabectedin and the PARP inhibitor rucaparib in soft-tissue sarcomas.	rucaparib	47-56	poly(ADP-ribose) polymerase 1	Homo sapiens	32-36
27702817-5	2017	Cytotoxicities of cisplatin and the PARP inhibitor rucaparib were assessed using sulforhodamine B (SRB) assays.	rucaparib	51-60	collagen type XI alpha 2 chain	Homo sapiens	36-40
28264872-0	2017	A Phase I-II Study of the Oral PARP Inhibitor Rucaparib in Patients with Germline BRCA1/2-Mutated Ovarian Carcinoma or Other Solid Tumors.	rucaparib	46-55	collagen type XI alpha 2 chain	Homo sapiens	31-35
28264872-0	2017	A Phase I-II Study of the Oral PARP Inhibitor Rucaparib in Patients with Germline BRCA1/2-Mutated Ovarian Carcinoma or Other Solid Tumors.	rucaparib	46-55	BRCA1 DNA repair associated	Homo sapiens	82-87
28264872-1	2017	Purpose: Rucaparib is a potent, oral, small-molecule PARP inhibitor.	rucaparib	9-18	collagen type XI alpha 2 chain	Homo sapiens	53-57
28790837-0	2017	Rucaparib: the past, present, and future of a newly approved PARP inhibitor for ovarian cancer.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	61-65
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	65-71
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	0-9	poly(ADP-ribose) polymerase 2	Homo sapiens	73-79
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 3	Homo sapiens	85-91
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	29-38	poly(ADP-ribose) polymerase 1	Homo sapiens	65-71
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	29-38	poly(ADP-ribose) polymerase 2	Homo sapiens	73-79
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	29-38	poly(ADP-ribose) polymerase family member 3	Homo sapiens	85-91
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	40-51	poly(ADP-ribose) polymerase 1	Homo sapiens	65-71
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	40-51	poly(ADP-ribose) polymerase 2	Homo sapiens	73-79
28790837-1	2017	Rucaparib camsylate (CO-338, AG-014699, PF-01367338) is a potent PARP-1, PARP-2, and PARP-3 inhibitor.	rucaparib	40-51	poly(ADP-ribose) polymerase family member 3	Homo sapiens	85-91
28790837-3	2017	Rucaparib has received the US Food and Drug Administration (FDA) approval for patients with deleterious BRCA mutation (germline and/or somatic)-associated advanced ovarian cancer who have been treated with two or more chemotherapies.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	104-108
28790837-5	2017	Rucaparib"s companion diagnostic FoundationFocus  CDx BRCA test is the first FDA-approved next-generation sequencing-based companion diagnostic test designed to identify patients likely to respond to rucaparib.	rucaparib	200-209	BRCA1 DNA repair associated	Homo sapiens	54-58
28790837-6	2017	This article reviews the mechanisms of action, safety, approval, and indications for use of the PARP inhibitor rucaparib as well as future trials and use of rucaparib"s companion diagnostic test.	rucaparib	111-120	poly(ADP-ribose) polymerase 1	Homo sapiens	96-100
28388401-1	2017	Rucaparib is an inhibitor of nuclear poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Olaparib.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	82-88
28388401-1	2017	Rucaparib is an inhibitor of nuclear poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Olaparib.	rucaparib	0-9	poly(ADP-ribose) polymerase 2	Homo sapiens	94-100
28388401-1	2017	Rucaparib is an inhibitor of nuclear poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Olaparib.	rucaparib	0-9	poly(ADP-ribose) polymerase family member 3	Homo sapiens	106-112
28388401-3	2017	Rucaparib is approved for recurrent ovarian cancers with germline or somatic mutations in BRCA1/2.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	90-97
27440269-3	2017	EXPERIMENTAL DESIGN: Efficacy of PARP inhibitors olaparib, rucaparib, and veliparib, as well as etoposide and cisplatin in SCLC cell lines, and gene expression correlates, was analyzed using public datasets.	rucaparib	59-68	poly(ADP-ribose) polymerase 1	Homo sapiens	33-37
28250698-1	2017	Insulin degludec/liraglutide (Xultophy 100/3.6) for type-2 diabetes; rucaparib (Rubraca) for the treatment of deleterious BRCA mutation-associated ovarian cancer; and nusinersen (Spinraza) for the treatment of spinal muscular atrophy.	rucaparib	69-78	BRCA1 DNA repair associated	Homo sapiens	122-126
28001384-4	2017	Veliparib and niraparib are selective inhibitors of PARP1 and PARP2; olaparib, rucaparib, and talazoparib are more potent inhibitors of PARP1 but are less selective.	rucaparib	79-88	poly(ADP-ribose) polymerase 1	Homo sapiens	136-141
28222073-10	2017	The rucaparib/carboplatin combination had radiologic antitumour activity, primarily in BRCA1- or BRCA2-mutated breast and ovarian/peritoneal cancers.	rucaparib	4-13	BRCA1 DNA repair associated	Homo sapiens	87-92
28222073-10	2017	The rucaparib/carboplatin combination had radiologic antitumour activity, primarily in BRCA1- or BRCA2-mutated breast and ovarian/peritoneal cancers.	rucaparib	4-13	BRCA2 DNA repair associated	Homo sapiens	97-102
28057616-1	2017	The FDA approved the PARP inhibitor rucaparib to treat women with advanced ovarian cancer who have already been treated with at least two chemotherapies and have a BRCA1 or BRCA2 gene mutation identified by an approved companion diagnostic test.	rucaparib	36-45	collagen type XI alpha 2 chain	Homo sapiens	21-25
28057616-1	2017	The FDA approved the PARP inhibitor rucaparib to treat women with advanced ovarian cancer who have already been treated with at least two chemotherapies and have a BRCA1 or BRCA2 gene mutation identified by an approved companion diagnostic test.	rucaparib	36-45	BRCA1 DNA repair associated	Homo sapiens	164-169
28057616-1	2017	The FDA approved the PARP inhibitor rucaparib to treat women with advanced ovarian cancer who have already been treated with at least two chemotherapies and have a BRCA1 or BRCA2 gene mutation identified by an approved companion diagnostic test.	rucaparib	36-45	BRCA2 DNA repair associated	Homo sapiens	173-178
27908594-0	2017	Rucaparib in relapsed, platinum-sensitive high-grade ovarian carcinoma (ARIEL2 Part 1): an international, multicentre, open-label, phase 2 trial.	rucaparib	0-9	ADP-ribosyltransferase 1	Homo sapiens	72-85
28695516-1	2017	This chapter describes the approaches taken in the development of the first PARP inhibitor to enter clinical trial, rucaparib (now called Rubraca), in 2003.	rucaparib	116-125	poly(ADP-ribose) polymerase 1	Homo sapiens	76-80
27908594-24	2017	INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type LOH low carcinomas.	rucaparib	127-136	BRCA2 DNA repair associated	Homo sapiens	48-52
27908594-24	2017	INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type LOH low carcinomas.	rucaparib	127-136	BRCA2 DNA repair associated	Homo sapiens	48-52
27908594-25	2017	Our results suggest that assessment of tumour LOH can be used to identify patients with BRCA wild-type platinum-sensitive ovarian cancers who might benefit from rucaparib.	rucaparib	161-170	BRCA2 DNA repair associated	Homo sapiens	88-92
27908594-3	2017	In ARIEL2, we assessed the ability of tumour genomic LOH, quantified with a next-generation sequencing assay, to predict response to rucaparib, an oral PARP inhibitor.	rucaparib	133-142	poly(ADP-ribose) polymerase 1	Homo sapiens	152-156
27908594-18	2017	Median progression-free survival after rucaparib treatment was 12 8 months (95% CI 9 0-14 7) in the BRCA mutant subgroup, 5 7 months (5 3-7 6) in the LOH high subgroup, and 5 2 months (3 6-5 5) in the LOH low subgroup.	rucaparib	39-48	BRCA2 DNA repair associated	Homo sapiens	100-104
27908594-24	2017	INTERPRETATION: In patients with BRCA mutant or BRCA wild-type and LOH high platinum-sensitive ovarian carcinomas treated with rucaparib, progression-free survival was longer than in patients with BRCA wild-type LOH low carcinomas.	rucaparib	127-136	BRCA2 DNA repair associated	Homo sapiens	33-37
27530326-9	2016	In Trp53-/-;Brca2-/- mutant cells, we documented a relative increase in sensitivity to the PARP inhibitor rucaparib and slower orthotopic tumor growth compared with Trp53-/- cells, with an appearance of intratumoral tertiary lymphoid structures rich in CD3+ T cells.	rucaparib	106-115	transformation related protein 53	Mus musculus	3-8
27866910-4	2016	However, in addition to the canonical targets PARP1, PARP2, and several of their binding partners, we also identified hexose-6-phosphate dehydrogenase (H6PD) and deoxycytidine kinase (DCK) as previously unrecognized targets of rucaparib and niraparib, respectively.	rucaparib	227-236	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	118-150
27866910-4	2016	However, in addition to the canonical targets PARP1, PARP2, and several of their binding partners, we also identified hexose-6-phosphate dehydrogenase (H6PD) and deoxycytidine kinase (DCK) as previously unrecognized targets of rucaparib and niraparib, respectively.	rucaparib	227-236	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	152-156
27866910-4	2016	However, in addition to the canonical targets PARP1, PARP2, and several of their binding partners, we also identified hexose-6-phosphate dehydrogenase (H6PD) and deoxycytidine kinase (DCK) as previously unrecognized targets of rucaparib and niraparib, respectively.	rucaparib	227-236	deoxycytidine kinase	Homo sapiens	162-182
27866910-4	2016	However, in addition to the canonical targets PARP1, PARP2, and several of their binding partners, we also identified hexose-6-phosphate dehydrogenase (H6PD) and deoxycytidine kinase (DCK) as previously unrecognized targets of rucaparib and niraparib, respectively.	rucaparib	227-236	deoxycytidine kinase	Homo sapiens	184-187
27530326-9	2016	In Trp53-/-;Brca2-/- mutant cells, we documented a relative increase in sensitivity to the PARP inhibitor rucaparib and slower orthotopic tumor growth compared with Trp53-/- cells, with an appearance of intratumoral tertiary lymphoid structures rich in CD3+ T cells.	rucaparib	106-115	breast cancer 2, early onset	Mus musculus	12-17
27530326-9	2016	In Trp53-/-;Brca2-/- mutant cells, we documented a relative increase in sensitivity to the PARP inhibitor rucaparib and slower orthotopic tumor growth compared with Trp53-/- cells, with an appearance of intratumoral tertiary lymphoid structures rich in CD3+ T cells.	rucaparib	106-115	poly (ADP-ribose) polymerase family, member 1	Mus musculus	91-95
27716873-8	2016	There are a number of other PARP inhibitors in late phase clinical development in ovarian cancer including rucaparib, niraparib, veliparib, and talazoparib.	rucaparib	107-116	poly(ADP-ribose) polymerase 1	Homo sapiens	28-32
27087632-0	2016	Evaluation of rucaparib and companion diagnostics in the PARP inhibitor landscape for recurrent ovarian cancer therapy.	rucaparib	14-23	poly(ADP-ribose) polymerase 1	Homo sapiens	57-61
27515310-5	2016	Therefore, our purpose was to determine whether the more specific PARP-1 inhibitors rucaparib and olaparib enhanced the efficacy of X-radiation or (131)I-MIBG.	rucaparib	84-93	poly(ADP-ribose) polymerase 1	Homo sapiens	66-72
27515310-10	2016	Rucaparib and olaparib were equally effective inhibitors of PARP-1 activity.	rucaparib	0-9	poly(ADP-ribose) polymerase 1	Homo sapiens	60-66
27415012-8	2016	Active efflux of paclitaxel, olaparib, doxorubicin and rucaparib was confirmed in drug-resistant cells and in ABCB1-expressing bacterial membranes.	rucaparib	55-64	ATP binding cassette subfamily B member 1	Homo sapiens	110-115
27228289-0	2016	Phase 2 multicentre trial investigating intermittent and continuous dosing schedules of the poly(ADP-ribose) polymerase inhibitor rucaparib in germline BRCA mutation carriers with advanced ovarian and breast cancer.	rucaparib	130-139	BRCA1 DNA repair associated	Homo sapiens	152-156
27087632-4	2016	Rucaparib received US FDA Breakthrough Therapy designation for treatment of platinum-sensitive BRCA-mutated advanced ovarian cancer patients who received greater than two lines of platinum-based therapy.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	95-99
27016230-11	2016	Among 19 OvCa cell lines, the RAD50 copy number deletion is significantly associated with better responses to two structurally distinct PARPis (i.e. olaparib and rucaparib).	rucaparib	162-171	RAD50 double strand break repair protein	Homo sapiens	30-35
26905328-7	2016	RESULTS: In the carcinoma cell line, the PTEN knockdown enhanced sensitivity to cisplatin, rucaparib, doxorubicin, camptothecin, paclitaxel, and irradiation.	rucaparib	91-100	phosphatase and tensin homolog	Homo sapiens	41-45
27022037-8	2016	IMPLICATIONS FOR PRACTICE: The poly(ADP-ribose) polymerase (PARP) inhibitor olaparib has recently received approval from the Food and Drug Administration (FDA) and European Medicines Agency (EMA), with a second agent (rucaparib) likely to be approved in the near future.	rucaparib	218-227	poly(ADP-ribose) polymerase 1	Homo sapiens	60-64
27055253-5	2016	Using reverse-phase protein array, we found the proteins most significantly upregulated following treatment with the PARP inhibitors olaparib and rucaparib were in the PI3K/mTOR pathway (p-mTOR, p-AKT, and pS6) (p<=0.02).	rucaparib	146-155	poly(ADP-ribose) polymerase 1	Homo sapiens	117-121
27055253-5	2016	Using reverse-phase protein array, we found the proteins most significantly upregulated following treatment with the PARP inhibitors olaparib and rucaparib were in the PI3K/mTOR pathway (p-mTOR, p-AKT, and pS6) (p<=0.02).	rucaparib	146-155	mechanistic target of rapamycin kinase	Homo sapiens	173-177
27055253-5	2016	Using reverse-phase protein array, we found the proteins most significantly upregulated following treatment with the PARP inhibitors olaparib and rucaparib were in the PI3K/mTOR pathway (p-mTOR, p-AKT, and pS6) (p<=0.02).	rucaparib	146-155	mechanistic target of rapamycin kinase	Homo sapiens	189-193
27055253-5	2016	Using reverse-phase protein array, we found the proteins most significantly upregulated following treatment with the PARP inhibitors olaparib and rucaparib were in the PI3K/mTOR pathway (p-mTOR, p-AKT, and pS6) (p<=0.02).	rucaparib	146-155	AKT serine/threonine kinase 1	Homo sapiens	197-200
27055253-5	2016	Using reverse-phase protein array, we found the proteins most significantly upregulated following treatment with the PARP inhibitors olaparib and rucaparib were in the PI3K/mTOR pathway (p-mTOR, p-AKT, and pS6) (p<=0.02).	rucaparib	146-155	taste 2 receptor member 63 pseudogene	Homo sapiens	206-209
27141070-8	2016	Similar trials with other PARP inhibitors (rucaparib, niraparib and veliparib) are in progress and include non-BRCA-mutated ovarian cancer.	rucaparib	43-52	poly(ADP-ribose) polymerase 1	Homo sapiens	26-30
26518726-4	2016	We report here that while the activities of the four human sirtuin isoforms SIRT1, SIRT2, SIRT3 and SIRT6 are blocked by sirtuin inhibitor Ex527 in vitro, they are unaffected by the seven clinical and commonly used PARP inhibitors niraparib, olaparib, rucaparib, talazoparib, veliparib, PJ34, and XAV939.	rucaparib	252-261	sirtuin 1	Homo sapiens	76-81
27002934-0	2016	Phase 2 multicentre trial investigating intermittent and continuous dosing schedules of the poly(ADP-ribose) polymerase inhibitor rucaparib in germline BRCA mutation carriers with advanced ovarian and breast cancer.	rucaparib	130-139	poly(ADP-ribose) polymerase 1	Homo sapiens	92-119
27002934-0	2016	Phase 2 multicentre trial investigating intermittent and continuous dosing schedules of the poly(ADP-ribose) polymerase inhibitor rucaparib in germline BRCA mutation carriers with advanced ovarian and breast cancer.	rucaparib	130-139	BRCA1 DNA repair associated	Homo sapiens	152-156
27002934-1	2016	BACKGROUND: Rucaparib is an orally available potent selective small-molecule inhibitor of poly(ADP-ribose) polymerase (PARP) 1 and 2.	rucaparib	12-21	poly(ADP-ribose) polymerase 1	Homo sapiens	90-132
27002934-2	2016	Rucaparib induces synthetic lethality in cancer cells defective in the homologous recombination repair pathway including BRCA-1/2.	rucaparib	0-9	BRCA1 DNA repair associated	Homo sapiens	121-129
27002934-3	2016	We investigated the efficacy and safety of single-agent rucaparib in germline (g) BRCA mutation carriers with advanced breast and ovarian cancers.	rucaparib	56-65	BRCA1 DNA repair associated	Homo sapiens	82-86
27002934-4	2016	METHODS: Phase II, open-label, multicentre trial of rucaparib in proven BRCA-1/2 mutation carriers with advanced breast and or ovarian cancer, WHO PS 0-1 and normal organ function.	rucaparib	52-61	BRCA1 DNA repair associated	Homo sapiens	72-78
27002934-7	2016	RESULTS: Rucaparib was well tolerated in patients up to doses of 480 mg per day and is a potent inhibitor of PARP, with sustained inhibition >=24 h after single doses.	rucaparib	9-18	poly(ADP-ribose) polymerase 1	Homo sapiens	109-113
27002934-12	2016	CONCLUSIONS: Rucaparib is well tolerated and results in high levels of PARP inhibition in surrogate tissues even at the lowest dose levels.	rucaparib	13-22	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
26518726-4	2016	We report here that while the activities of the four human sirtuin isoforms SIRT1, SIRT2, SIRT3 and SIRT6 are blocked by sirtuin inhibitor Ex527 in vitro, they are unaffected by the seven clinical and commonly used PARP inhibitors niraparib, olaparib, rucaparib, talazoparib, veliparib, PJ34, and XAV939.	rucaparib	252-261	sirtuin 2	Homo sapiens	83-88
26518726-4	2016	We report here that while the activities of the four human sirtuin isoforms SIRT1, SIRT2, SIRT3 and SIRT6 are blocked by sirtuin inhibitor Ex527 in vitro, they are unaffected by the seven clinical and commonly used PARP inhibitors niraparib, olaparib, rucaparib, talazoparib, veliparib, PJ34, and XAV939.	rucaparib	252-261	sirtuin 3	Homo sapiens	90-95
26518726-4	2016	We report here that while the activities of the four human sirtuin isoforms SIRT1, SIRT2, SIRT3 and SIRT6 are blocked by sirtuin inhibitor Ex527 in vitro, they are unaffected by the seven clinical and commonly used PARP inhibitors niraparib, olaparib, rucaparib, talazoparib, veliparib, PJ34, and XAV939.	rucaparib	252-261	sirtuin 6	Homo sapiens	100-105
26438157-2	2015	The aim of this study was to evaluate the combination of the PARP inhibitor rucaparib with temozolomide and to correlate pharmacokinetic and pharmacodynamic studies with efficacy in patient-derived GBM xenograft models.	rucaparib	76-85	collagen type XI alpha 2 chain	Homo sapiens	61-65
26438157-5	2015	Using Madin-Darby canine kidney (MDCK) II cells stably expressing murine BCRP1 or human MDR1, cell accumulation studies demonstrated that rucaparib is transported by both transporters.	rucaparib	138-147	BAF nuclear assembly factor 1	Mus musculus	73-78
26438157-0	2015	Efficacy of PARP Inhibitor Rucaparib in Orthotopic Glioblastoma Xenografts Is Limited by Ineffective Drug Penetration into the Central Nervous System.	rucaparib	27-36	poly (ADP-ribose) polymerase family, member 1	Mus musculus	12-16
26438157-5	2015	Using Madin-Darby canine kidney (MDCK) II cells stably expressing murine BCRP1 or human MDR1, cell accumulation studies demonstrated that rucaparib is transported by both transporters.	rucaparib	138-147	ATP binding cassette subfamily B member 1	Homo sapiens	88-92
26438157-6	2015	Consistent with the influence of these efflux pumps on central nervous system drug distribution, Mdr1a/b(-/-)Bcrp1(-/-) knockout mice had a significantly higher brain to plasma ratio for rucaparib (1.61 +- 0.25) than wild-type mice (0.11 +- 0.08).	rucaparib	187-196	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	97-102
26438157-6	2015	Consistent with the influence of these efflux pumps on central nervous system drug distribution, Mdr1a/b(-/-)Bcrp1(-/-) knockout mice had a significantly higher brain to plasma ratio for rucaparib (1.61 +- 0.25) than wild-type mice (0.11 +- 0.08).	rucaparib	187-196	BAF nuclear assembly factor 1	Mus musculus	109-114
26438157-7	2015	A pharmacokinetic and pharmacodynamic evaluation after a single dose confirmed limited accumulation of rucaparib in the brain is associated with substantial residual PARP enzymatic activity.	rucaparib	103-112	poly (ADP-ribose) polymerase family, member 1	Mus musculus	166-170
26342868-1	2015	A series of AG014699 derivatives containing a novel scaffold of 2,3-dihydro-1H-[1,2]diazepino[4,5,6-cd]indole-1,4(6H)-dione were synthesized and evaluated for their inhibitory activities toward PARP-1 enzyme and two cell lines, MCF-7 cells and the BRCA1-deficient MDA-MB-436 cells.	rucaparib	12-20	poly(ADP-ribose) polymerase 1	Homo sapiens	194-200
26095183-8	2015	To inhibit the functions of CHD4 that are mediated through histone deacetylase and poly (ADP-ribose) polymerase, we evaluated the effect of the histone deacetylase inhibitor suberohydroxamic acid and the poly (ADP-ribose) polymerase inhibitor AG-014699.	rucaparib	243-252	chromodomain helicase DNA binding protein 4	Homo sapiens	28-32
26095183-9	2015	Treatment with either suberohydroxamic acid or AG-014699 reduced the number of EpCAM(+) liver cancer stem cells in vitro, and suberohydroxamic acid and AG-014699 in combination successfully inhibited tumor growth in a mouse xenograft model.	rucaparib	47-56	epithelial cell adhesion molecule	Mus musculus	79-84
26342868-2	2015	Our results demonstrated that of all AG014699 derivatives synthesized in this work, compounds 6 and 7 showed strong PARP-1 inhibitory activity (IC50=3.5 nM and 2.4 nM, respectively), only four and three times less potent than AG014699.	rucaparib	37-45	poly(ADP-ribose) polymerase 1	Homo sapiens	116-122
26281686-5	2015	Other PARP inhibitors under clinical trials include rucaparib, niraparib, veliparib, and the "PARP-trapping" BMN-673.	rucaparib	52-61	poly(ADP-ribose) polymerase 1	Homo sapiens	6-10
27128213-0	2015	PARP activity in peripheral blood lymphocytes as a predictive biomarker for PARP inhibition in tumor tissues - A population pharmacokinetic/pharmacodynamic analysis of rucaparib.	rucaparib	168-177	poly(ADP-ribose) polymerase 1	Homo sapiens	0-4
25667168-0	2015	The Combination of the PARP Inhibitor Rucaparib and 5FU Is an Effective Strategy for Treating Acute Leukemias.	rucaparib	38-47	poly(ADP-ribose) polymerase 1	Homo sapiens	23-27
27128213-0	2015	PARP activity in peripheral blood lymphocytes as a predictive biomarker for PARP inhibition in tumor tissues - A population pharmacokinetic/pharmacodynamic analysis of rucaparib.	rucaparib	168-177	poly(ADP-ribose) polymerase 1	Homo sapiens	76-80
27128213-1	2015	PURPOSE: Rucaparib is a potent Poly (ADP-ribose) Polymerase (PARP) inhibitor currently under clinical development.	rucaparib	9-18	poly(ADP-ribose) polymerase 1	Homo sapiens	61-65
27128213-9	2015	CONCLUSION: Population PK and PK/PD models have been established to describe population PK of rucaparib and the relationship between rucaparib plasma concentration and PARP inhibition in both PBLs and tumor issues.	rucaparib	133-142	poly(ADP-ribose) polymerase 1	Homo sapiens	168-172
25128455-7	2014	RESULTS: In a panel of four HER2 overexpressing breast cancer cell lines, both olaparib and rucaparib significantly decreased cell growth and enhanced anti-tumour effects of trastuzumab.	rucaparib	92-101	erb-b2 receptor tyrosine kinase 2	Homo sapiens	28-32
25689628-0	2015	Vasoactivity of rucaparib, a PARP-1 inhibitor, is a complex process that involves myosin light chain kinase, P2 receptors, and PARP itself.	rucaparib	16-25	poly(ADP-ribose) polymerase 1	Homo sapiens	29-35
25689628-0	2015	Vasoactivity of rucaparib, a PARP-1 inhibitor, is a complex process that involves myosin light chain kinase, P2 receptors, and PARP itself.	rucaparib	16-25	myosin light chain kinase	Homo sapiens	82-107
25689628-0	2015	Vasoactivity of rucaparib, a PARP-1 inhibitor, is a complex process that involves myosin light chain kinase, P2 receptors, and PARP itself.	rucaparib	16-25	poly(ADP-ribose) polymerase 1	Homo sapiens	29-33
25689628-2	2015	We previously reported that the first PARP inhibitor to enter clinical trial, rucaparib (AG014699), induced vasodilation in vivo in xenografts, potentiating response to temozolomide.	rucaparib	78-87	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
25689628-2	2015	We previously reported that the first PARP inhibitor to enter clinical trial, rucaparib (AG014699), induced vasodilation in vivo in xenografts, potentiating response to temozolomide.	rucaparib	89-97	poly(ADP-ribose) polymerase 1	Homo sapiens	38-42
25689628-3	2015	We now report that rucaparib inhibits the activity of the muscle contraction mediator myosin light chain kinase (MLCK) 10-fold more potently than its commercially available inhibitor ML-9.	rucaparib	19-28	myosin light chain kinase	Homo sapiens	86-111
25689628-3	2015	We now report that rucaparib inhibits the activity of the muscle contraction mediator myosin light chain kinase (MLCK) 10-fold more potently than its commercially available inhibitor ML-9.	rucaparib	19-28	myosin light chain kinase	Homo sapiens	113-117
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-32
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	34-38
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	39-44
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	ATP binding cassette subfamily B member 1	Homo sapiens	50-64
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	phosphoglycolate phosphatase	Homo sapiens	66-70
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	ATP binding cassette subfamily B member 1	Homo sapiens	71-76
24962512-0	2015	Breast cancer resistance protein (BCRP/ABCG2) and P-glycoprotein (P-GP/ABCB1) restrict oral availability and brain accumulation of the PARP inhibitor rucaparib (AG-014699).	rucaparib	150-159	poly(ADP-ribose) polymerase 1	Homo sapiens	135-139
24962512-1	2015	BACKGROUND: Rucaparib is a potent, orally available, small-molecule inhibitor of poly ADP-ribose polymerase (PARP) 1 and 2.	rucaparib	12-21	poly(ADP-ribose) polymerase 1	Homo sapiens	81-122
24962512-3	2015	PURPOSE: We aimed to establish whether the multidrug efflux transporters ABCG2 (BCRP) and ABCB1 (P-gp, MDR1) affect the oral availability and brain penetration of rucaparib in mice.	rucaparib	163-172	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	73-78
24962512-3	2015	PURPOSE: We aimed to establish whether the multidrug efflux transporters ABCG2 (BCRP) and ABCB1 (P-gp, MDR1) affect the oral availability and brain penetration of rucaparib in mice.	rucaparib	163-172	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	80-84
24962512-3	2015	PURPOSE: We aimed to establish whether the multidrug efflux transporters ABCG2 (BCRP) and ABCB1 (P-gp, MDR1) affect the oral availability and brain penetration of rucaparib in mice.	rucaparib	163-172	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	90-95
24962512-3	2015	PURPOSE: We aimed to establish whether the multidrug efflux transporters ABCG2 (BCRP) and ABCB1 (P-gp, MDR1) affect the oral availability and brain penetration of rucaparib in mice.	rucaparib	163-172	phosphoglycolate phosphatase	Mus musculus	97-101
24962512-3	2015	PURPOSE: We aimed to establish whether the multidrug efflux transporters ABCG2 (BCRP) and ABCB1 (P-gp, MDR1) affect the oral availability and brain penetration of rucaparib in mice.	rucaparib	163-172	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	103-107
24962512-4	2015	RESULTS: In vitro, rucaparib was efficiently transported by both human ABCB1 and ABCG2, and very efficiently by mouse Abcg2.	rucaparib	19-28	ATP binding cassette subfamily B member 1	Homo sapiens	71-76
24962512-4	2015	RESULTS: In vitro, rucaparib was efficiently transported by both human ABCB1 and ABCG2, and very efficiently by mouse Abcg2.	rucaparib	19-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	81-86
24962512-4	2015	RESULTS: In vitro, rucaparib was efficiently transported by both human ABCB1 and ABCG2, and very efficiently by mouse Abcg2.	rucaparib	19-28	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	118-123
24962512-6	2015	In vivo, oral availability (plasma AUC0-1 and AUC0-24) and brain levels of rucaparib at 1 and 24 h were increased by the absence of both Abcg2 and Abcb1a/1b after oral administration of rucaparib at 10 mg/kg.	rucaparib	75-84	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	137-142
24962512-8	2015	This may have clinical relevance for improvement of rucaparib therapy in PARP inhibitor-resistant tumors with ABCB1 and/or ABCG2 expression and in patients with brain (micro)metastases positioned behind a functional blood-brain barrier.	rucaparib	52-61	poly(ADP-ribose) polymerase 1	Homo sapiens	73-77
24962512-8	2015	This may have clinical relevance for improvement of rucaparib therapy in PARP inhibitor-resistant tumors with ABCB1 and/or ABCG2 expression and in patients with brain (micro)metastases positioned behind a functional blood-brain barrier.	rucaparib	52-61	ATP binding cassette subfamily B member 1	Homo sapiens	110-115
24962512-8	2015	This may have clinical relevance for improvement of rucaparib therapy in PARP inhibitor-resistant tumors with ABCB1 and/or ABCG2 expression and in patients with brain (micro)metastases positioned behind a functional blood-brain barrier.	rucaparib	52-61	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	123-128
25689628-4	2015	Moreover, rucaparib produces additive relaxation above the maximal degree achievable with ML-9, suggesting that MLCK inhibition is not solely responsible for dilation.	rucaparib	10-19	myosin light chain kinase	Homo sapiens	112-116
24632590-3	2014	Here, we demonstrate that three PARP drug candidates, namely, rucaparib, veliparib, and olaparib, have a clearly different in vitro affinity profile across a panel of diverse kinases selected using a computational approach that relates proteins by ligand similarity.	rucaparib	62-71	collagen type XI alpha 2 chain	Homo sapiens	32-36
25017803-9	2014	Rucaparib-sensitive and rucaparib-resistant groups showed significant differences in gammaH2AX and RAD51 foci formation after rucaparib exposure.	rucaparib	0-9	RAD51 recombinase	Homo sapiens	99-104
25017803-9	2014	Rucaparib-sensitive and rucaparib-resistant groups showed significant differences in gammaH2AX and RAD51 foci formation after rucaparib exposure.	rucaparib	24-33	RAD51 recombinase	Homo sapiens	99-104
25017803-9	2014	Rucaparib-sensitive and rucaparib-resistant groups showed significant differences in gammaH2AX and RAD51 foci formation after rucaparib exposure.	rucaparib	126-135	RAD51 recombinase	Homo sapiens	99-104
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	85-89
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	Pim-2 proto-oncogene, serine/threonine kinase	Homo sapiens	91-95
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	protein kinase D2	Homo sapiens	97-102
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	dual specificity tyrosine phosphorylation regulated kinase 1A	Homo sapiens	104-110
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	cyclin dependent kinase 1	Homo sapiens	112-116
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	cyclin dependent kinase 9	Homo sapiens	118-122
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	homeodomain interacting protein kinase 2	Homo sapiens	124-129
24632590-4	2014	In this respect, rucaparib inhibits nine kinases with micromolar affinity, including PIM1, PIM2, PRKD2, DYRK1A, CDK1, CDK9, HIPK2, CK2, and ALK.	rucaparib	17-26	ALK receptor tyrosine kinase	Homo sapiens	140-143
24420152-0	2014	INPP4B overexpression enhances the antitumor efficacy of PARP inhibitor AG014699 in MDA-MB-231 triple-negative breast cancer cells.	rucaparib	72-80	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	0-6
24556618-2	2014	Early clinical trial data with rucaparib suggested that it caused sustained PARP inhibition.	rucaparib	31-40	poly (ADP-ribose) polymerase family, member 1	Mus musculus	76-80
24556618-7	2014	Rucaparib is retained in cells and inhibits PARP >=50% for >=72 h days after a 30-min pulse of 400 nM.	rucaparib	0-9	poly (ADP-ribose) polymerase family, member 1	Mus musculus	44-48
24556618-11	2014	CONCLUSIONS: Rucaparib accumulates and is retained in tumour cells and inhibits PARP for long periods such that weekly schedules have equivalent anticancer activity to daily dosing in a pre-clinical model, suggesting that clinical evaluation of alternative schedules of rucaparib should be considered.	rucaparib	13-22	poly (ADP-ribose) polymerase family, member 1	Mus musculus	80-84
24420152-2	2014	The main aim of this study was to evaluate whether overexpressing inositol polyphosphate 4-phosphatase type II (INPP4B) gene, a novel tumor suppressor gene negatively regulating the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway, could enhance the antitumor efficacy of PARP inhibitor AG014699 used in the treatment of triple-negative breast cancer (TNBC).	rucaparib	297-305	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	112-118
24420152-2	2014	The main aim of this study was to evaluate whether overexpressing inositol polyphosphate 4-phosphatase type II (INPP4B) gene, a novel tumor suppressor gene negatively regulating the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway, could enhance the antitumor efficacy of PARP inhibitor AG014699 used in the treatment of triple-negative breast cancer (TNBC).	rucaparib	297-305	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	182-211
24420152-2	2014	The main aim of this study was to evaluate whether overexpressing inositol polyphosphate 4-phosphatase type II (INPP4B) gene, a novel tumor suppressor gene negatively regulating the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway, could enhance the antitumor efficacy of PARP inhibitor AG014699 used in the treatment of triple-negative breast cancer (TNBC).	rucaparib	297-305	AKT serine/threonine kinase 1	Homo sapiens	219-222
24420152-6	2014	However, PARP inhibitor AG014699 could activate the PI3K/AKT signaling pathway activity and partially offset its therapeutic efficacy.	rucaparib	24-32	AKT serine/threonine kinase 1	Homo sapiens	57-60
24420152-7	2014	In our study, a significant enhancement of proliferation inhibition was observed when INPP4B overexpression was combined with PARP inhibitor AG014699 in comparison with either single treatment.	rucaparib	141-149	inositol polyphosphate-4-phosphatase type II B	Homo sapiens	86-92
24791791-0	2014	[Effects of poly(ADP-ribose)polymerase inhibitor AG014699 combined with chemotherapy on the proliferation of triple-negative breast cancer cell line MDA-MB-231].	rucaparib	49-57	poly(ADP-ribose) polymerase 1	Homo sapiens	12-38
24791791-2	2014	METHODS: MDA-MB-231 cells were treated by PARP inhibitor AG014699 alone or combination with DTX or CBP.	rucaparib	57-65	poly(ADP-ribose) polymerase 1	Homo sapiens	42-46
24791791-5	2014	RESULTS: Treatment with PARP inhibitor AG014699, DTX, or CBP alone inhibited the proliferation, induced apoptosis and blocked the cell cycle.	rucaparib	39-47	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
24791791-8	2014	A combination of PARP inhibitor AG014699 and DTX or CBP promoted apoptosis and increased the proportion of G2/M stage cells.	rucaparib	32-40	poly(ADP-ribose) polymerase 1	Homo sapiens	17-21
24791791-9	2014	CONCLUSION: PARP inhibitor AG014699 combined with DTX or CBP can remarkably inhibit MDA-MB-231 cell proliferation, showing additive or synergistic antitumor effects.	rucaparib	27-35	poly(ADP-ribose) polymerase 1	Homo sapiens	12-16
25558828-11	2014	Disruption of Rad51 foci formation, which compromises homologous recombination, was consistent with increased sensitivity of PCa cells to the PARP inhibitor Rucaparib.	rucaparib	157-166	RAD51 recombinase	Homo sapiens	14-19
24411611-6	2014	In irradiated H460 xenografts, concurrent therapy with BEZ235 and AG014699 resulted in sustained Gamma-H2AX (gammaH2AX) staining and prominent beta-galactosidase activity.	rucaparib	66-74	galactosidase beta 1	Homo sapiens	143-161
25558828-11	2014	Disruption of Rad51 foci formation, which compromises homologous recombination, was consistent with increased sensitivity of PCa cells to the PARP inhibitor Rucaparib.	rucaparib	157-166	collagen type XI alpha 2 chain	Homo sapiens	142-146
24216281-0	2014	Liquid chromatography-tandem mass spectrometric assay for the PARP inhibitor rucaparib in plasma.	rucaparib	77-86	poly (ADP-ribose) polymerase family, member 1	Mus musculus	62-66
24216281-1	2014	A quantitative bioanalytical liquid chromatography-tandem mass spectrometric (LC-MS/MS) assay for the poly(ADP-ribose) polymerase-1 inhibitor rucaparib was developed and validated.	rucaparib	142-151	poly (ADP-ribose) polymerase family, member 1	Mus musculus	102-131
24900770-7	2014	The clinical ARTD1 inhibitor candidate rucaparib was the most potent tankyrase inhibitor identified (24 and 14 nM for tankyrases), which indicates that inhibition of tankyrases would affect the cellular responses of this compound.	rucaparib	39-48	poly(ADP-ribose) polymerase 1	Homo sapiens	13-18
24336406-4	2013	Decreasing the intracellular calcium levels using BAPTA, or direct reconstitution of BRCA2 protein levels either by recombinant expression or by small molecule inhibition of both Skp2 and miR-1245 restored sensitivity to rucaparib to wild-type levels.	rucaparib	221-230	BRCA2 DNA repair associated	Homo sapiens	85-90
24336406-4	2013	Decreasing the intracellular calcium levels using BAPTA, or direct reconstitution of BRCA2 protein levels either by recombinant expression or by small molecule inhibition of both Skp2 and miR-1245 restored sensitivity to rucaparib to wild-type levels.	rucaparib	221-230	S-phase kinase associated protein 2	Homo sapiens	179-183
24336406-4	2013	Decreasing the intracellular calcium levels using BAPTA, or direct reconstitution of BRCA2 protein levels either by recombinant expression or by small molecule inhibition of both Skp2 and miR-1245 restored sensitivity to rucaparib to wild-type levels.	rucaparib	221-230	microRNA 1245a	Homo sapiens	188-196
24336406-2	2013	Herein, we demonstrate that depletion of the mitochondrial genome (mtDNA) in breast, prostate and thyroid transformed cells resulted in elevated steady-state cytosolic calcium concentration and activation of calcineurin/PI3-kinase/AKT signaling leading to upregulation of miR-1245 and the ubiquitin ligase Skp2, two potent negative regulators of the tumor suppressor protein BRCA2, thus resulting in BRCA2 protein depletion, severe reduction in homologous recombination (HR) and increased sensitivity to the PARP inhibitor rucaparib.	rucaparib	523-532	AKT serine/threonine kinase 1	Homo sapiens	231-234
23729402-4	2013	Concentration-dependent antiproliferative effects of rucaparib were seen in 26 of 39 (67%) cell lines and were not restricted to cell lines with BRCA1/2 mutations.	rucaparib	53-62	BRCA1 DNA repair associated	Homo sapiens	145-152
24077350-2	2013	We have previously identified elevated PARP1 levels in SCLC and demonstrated in vitro sensitivity to the PARP inhibitors AZD 2281 and AG014699.	rucaparib	134-142	poly [ADP-ribose] polymerase	Bombyx mori	39-43
23729402-1	2013	Here, we investigate the potential role of the PARP inhibitor rucaparib (CO-338, formerly known as AG014699 and PF-01367338) for the treatment of sporadic ovarian cancer.	rucaparib	62-71	poly(ADP-ribose) polymerase 1	Homo sapiens	47-51
22343925-3	2012	Many of the best-known inhibitors, including TIQ-A, 6(5H)-phenanthridinone, olaparib, ABT-888 and rucaparib, bound to several PARP family members, suggesting that these molecules lack specificity and have promiscuous inhibitory activity.	rucaparib	98-107	poly(ADP-ribose) polymerase 1	Homo sapiens	126-130
23423489-0	2013	A phase II study of the potent PARP inhibitor, Rucaparib (PF-01367338, AG014699), with temozolomide in patients with metastatic melanoma demonstrating evidence of chemopotentiation.	rucaparib	47-56	poly(ADP-ribose) polymerase 1	Homo sapiens	31-35
23423489-2	2013	A phase I study of rucaparib and temozolomide showed that full-dose temozolomide could be given during PARP inhibition.	rucaparib	19-28	poly(ADP-ribose) polymerase 1	Homo sapiens	103-107
23423489-11	2013	CONCLUSIONS: This study showed that temozolomide (150-200 mg/m(2)/day) can safely be given with a PARP inhibitory dose of rucaparib, increasing progression-free survival over historical controls in metastatic melanoma patients.	rucaparib	122-131	poly(ADP-ribose) polymerase 1	Homo sapiens	98-102
23565244-4	2013	We evaluated the effectiveness of radiation in combination with the PARP inhibitor, rucaparib in PCa cells.	rucaparib	84-93	poly(ADP-ribose) polymerase 1	Homo sapiens	68-72
23565244-8	2013	Increased radiosensitivity in the presence of rucaparib was associated with persistent DNA breaks, as determined by chi-H2AX, p53BP1, and Rad51 foci.	rucaparib	46-55	tumor protein p53 binding protein 1	Homo sapiens	126-132
23565244-8	2013	Increased radiosensitivity in the presence of rucaparib was associated with persistent DNA breaks, as determined by chi-H2AX, p53BP1, and Rad51 foci.	rucaparib	46-55	RAD51 recombinase	Homo sapiens	138-143
23565244-9	2013	VCaP cells, which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar construct (fusion III) showed enhanced sensitivity towards rucaparib, which, in turn, increased the radiation response to a similar extent as the DNA-PKcs inhibitor NU7441.	rucaparib	156-165	transmembrane serine protease 2	Homo sapiens	29-36
23565244-9	2013	VCaP cells, which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar construct (fusion III) showed enhanced sensitivity towards rucaparib, which, in turn, increased the radiation response to a similar extent as the DNA-PKcs inhibitor NU7441.	rucaparib	156-165	ETS transcription factor ERG	Homo sapiens	37-40
23565244-9	2013	VCaP cells, which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar construct (fusion III) showed enhanced sensitivity towards rucaparib, which, in turn, increased the radiation response to a similar extent as the DNA-PKcs inhibitor NU7441.	rucaparib	156-165	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	243-251
23148997-2	2013	In this study, the PARP-1 inhibitor Rucaparib was utilized to increase the sensitivity to chemoradiotherapy treatment in BRCA-2-deficient and -proficient pancreatic cancer cells.	rucaparib	36-45	poly(ADP-ribose) polymerase 1	Homo sapiens	19-25
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	rucaparib	46-54	poly(ADP-ribose) polymerase 1	Homo sapiens	0-5
23917378-2	2013	PARP1 inhibitors [AZD2281 ; ABT888 ; NU1025 ; AG014699] interacted with CHK1 inhibitors [UCN-01 ; AZD7762 ; LY2603618] to kill mammary carcinoma cells.	rucaparib	46-54	checkpoint kinase 1	Homo sapiens	72-76
22678161-6	2012	These PARP inhibitors exhibited differential anti-tumor activities, with the relative potencies of AG-014699 > AZD-2281 > ABT-888 > BSI-201.	rucaparib	99-108	poly(ADP-ribose) polymerase 1	Homo sapiens	6-10
21926192-0	2011	The clinically active PARP inhibitor AG014699 ameliorates cardiotoxicity but does not enhance the efficacy of doxorubicin, despite improving tumor perfusion and radiation response in mice.	rucaparib	37-45	poly (ADP-ribose) polymerase family, member 1	Mus musculus	22-26
21706052-0	2012	NF-kappaB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699.	rucaparib	64-73	nuclear factor kappa B subunit 1	Homo sapiens	0-9
21706052-0	2012	NF-kappaB mediates radio-sensitization by the PARP-1 inhibitor, AG-014699.	rucaparib	64-73	poly(ADP-ribose) polymerase 1	Homo sapiens	46-52
21706052-8	2012	As preventing SSB repair did not radio-sensitize p65(-/-) cells, we conclude that radio-sensitization by AG-014699 is due to downstream inhibition of NF-kappaB activation, and independent of SSB repair inhibition.	rucaparib	105-114	nuclear factor kappa B subunit 1	Homo sapiens	150-159
21926192-1	2011	AG014699 was the first inhibitor of the DNA repair enzyme PARP-1 to enter clinical trial in cancer patients.	rucaparib	0-8	poly(ADP-ribose) polymerase 1	Homo sapiens	58-64
21870278-1	2011	This chapter describes the approaches taken in the development of the first PARP inhibitor to enter into clinical trial, AG-014699.	rucaparib	121-130	poly(ADP-ribose) polymerase 1	Homo sapiens	76-80
22015278-8	2011	Early phase trials with efficacy endpoints have been presented for the PARP inhibitors AG014699, olaparib, veliparib, iniparib and MK4827.	rucaparib	87-95	poly(ADP-ribose) polymerase 1	Homo sapiens	71-75
21183737-0	2011	Therapeutic potential of poly(ADP-ribose) polymerase inhibitor AG014699 in human cancers with mutated or methylated BRCA1 or BRCA2.	rucaparib	63-71	poly(ADP-ribose) polymerase 1	Homo sapiens	25-52
21183737-0	2011	Therapeutic potential of poly(ADP-ribose) polymerase inhibitor AG014699 in human cancers with mutated or methylated BRCA1 or BRCA2.	rucaparib	63-71	BRCA1 DNA repair associated	Homo sapiens	116-121
21183737-0	2011	Therapeutic potential of poly(ADP-ribose) polymerase inhibitor AG014699 in human cancers with mutated or methylated BRCA1 or BRCA2.	rucaparib	63-71	BRCA2 DNA repair associated	Homo sapiens	125-130
21183737-11	2011	Growth of xenograft tumors with BRCA1/2 mutations or with epigenetically silenced BRCA1 was reduced by AG014699 treatment, and combination treatment with AG014699 plus carboplatin was more effective than either drug alone.	rucaparib	103-111	BRCA2 DNA repair associated	Homo sapiens	32-39
21183737-11	2011	Growth of xenograft tumors with BRCA1/2 mutations or with epigenetically silenced BRCA1 was reduced by AG014699 treatment, and combination treatment with AG014699 plus carboplatin was more effective than either drug alone.	rucaparib	103-111	BRCA1 DNA repair associated	Homo sapiens	32-37
21183737-13	2011	CONCLUSION: Human cancer cells or xenograft tumors with mutated or epigenetically silenced BRCA1/2 were sensitive to AG014699 monotherapy, indicating a potential role for PARP inhibitors in sporadic human cancers.	rucaparib	117-125	BRCA2 DNA repair associated	Homo sapiens	91-98
21183737-13	2011	CONCLUSION: Human cancer cells or xenograft tumors with mutated or epigenetically silenced BRCA1/2 were sensitive to AG014699 monotherapy, indicating a potential role for PARP inhibitors in sporadic human cancers.	rucaparib	117-125	poly(ADP-ribose) polymerase 1	Homo sapiens	171-175
20978505-0	2010	Central nervous system penetration and enhancement of temozolomide activity in childhood medulloblastoma models by poly(ADP-ribose) polymerase inhibitor AG-014699.	rucaparib	153-162	poly(ADP-ribose) polymerase 1	Homo sapiens	115-142
20978505-3	2010	METHODS: We assessed the effect of AG-014699, a clinically active PARP inhibitor, on temozolomide-induced growth inhibition in human medulloblastoma models.	rucaparib	35-44	poly(ADP-ribose) polymerase 1	Homo sapiens	66-70
19174487-4	2009	EXPERIMENTAL DESIGN: We evaluated the chemosensitizing properties of the PARP inhibitor AG014699 (Pfizer, Inc.) in combination with temozolomide and topotecan, against human neuroblastoma cells and xenografts, alongside associated pharmacologic and toxicologic indices.	rucaparib	88-96	poly(ADP-ribose) polymerase 1	Homo sapiens	73-77
20371688-4	2010	We developed a functional assay of HR status in primary cultures of EOCs based on Rad51 focus formation that correlates well with sensitivity to the potent PARP inhibitor AG014699.	rucaparib	171-179	RAD51 recombinase	Homo sapiens	82-87
20371688-4	2010	We developed a functional assay of HR status in primary cultures of EOCs based on Rad51 focus formation that correlates well with sensitivity to the potent PARP inhibitor AG014699.	rucaparib	171-179	poly(ADP-ribose) polymerase 1	Homo sapiens	156-160
20371688-9	2010	Following exposure to AG014699, there was an increase in Rad51 foci (HR competent) in 9 of 24 (36%) but no increase (HR deficient) in 16 of 24 (64%) cultures.	rucaparib	22-30	RAD51 recombinase	Homo sapiens	57-62
19789326-0	2009	Vasoactivity of AG014699, a clinically active small molecule inhibitor of poly(ADP-ribose) polymerase: a contributory factor to chemopotentiation in vivo?	rucaparib	16-24	poly(ADP-ribose) polymerase 1	Homo sapiens	74-101
19789326-2	2009	AG014699 is a potent PARP inhibitor in phase II clinical development.	rucaparib	0-8	poly(ADP-ribose) polymerase 1	Homo sapiens	21-25
19789326-11	2009	AG014699 inhibited MLCK at concentrations that relaxed isolated arteries, whereas AG14361 had no effect.	rucaparib	0-8	myosin light chain kinase	Homo sapiens	19-23
19174487-5	2009	RESULTS: Addition of PARP-inhibitory concentrations of AG014699 significantly potentiated growth inhibition by both topotecan (1.5- to 2.3-fold) and temozolomide (3- to 10-fold) in vitro, with equivalent effects confirmed in clonogenic assays.	rucaparib	55-63	poly(ADP-ribose) polymerase 1	Homo sapiens	21-25
19174487-11	2009	Coupled with the acceptable pharmacokinetic, pharmacodynamic, and toxicity profiles of AG014699, our findings provide strong rationale for investigation of PARP inhibitors in pediatric early clinical studies.	rucaparib	87-95	poly(ADP-ribose) polymerase 1	Homo sapiens	156-160
19047122-4	2008	The article reports safety, efficacy, pharmacokinetic, and pharmacodynamic results of the first-in-class trial of a PARP inhibitor, AG014699, combined with temozolomide in adults with advanced malignancy.	rucaparib	132-140	poly(ADP-ribose) polymerase 1	Homo sapiens	116-120