RegulationBreakthrough Therapy (United States), Orphan Drug (United States), Priority Review (China), Conditional marketing approval (China), Orphan Drug (South Korea), Fast Track (United States)

Structure/Sequence

Molecular FormulaC26H30N4O5S

InChIKeyACNPUCQQZDAPJH-FMOMHUKBSA-N

CAS Registry1613220-15-7

238

Clinical Trials associated with Niraparib Tosylate

NCT06412120

/ RecruitingPhase 4IIT

Single-Arm, Prospective, Multicenter Study Evaluating Safety, Tolerability, and Metabolism of Niraparib as Maintenance Following Front-Line Treatment for Ovarian Cancer in Women of African Ancestry

The purpose of this study is to identify the genetic characteristic(s), specifically degree of African ancestry, and environmental characteristic(s) that appear to be related to the effects, both good and bad, that the maintenance treatment has women with ovarian cancer. In this study, an investigational medication called niraparib is being tested for the treatment of ovarian cancer. Niraparib works by blocking the ability of cancer cells to fix their genes. Cancer cells with damaged genes have a harder time growing and spreading in the body and can even die.

Start Date01 Jun 2026

Sponsor / Collaborator

University of Miami

[+1]

CTRI/2025/01/079290

/ Not yet recruitingNot Applicable

A multi-centre, open label, balanced, randomized, two-treatment, two-period,two-sequence, two-way crossover, multiple-dose, steady state, pharmacokineticendpoint bioequivalence study of Niraparib tablets 200 mg of Natco Pharma(test product) against ZEJULA (niraparib) tablet 200 mg of GlaxoSmithKline(reference product) under fasting conditions in female patients with advancedepithelial ovarian, fallopian tube, or primary peritoneal cancer who are in acomplete or partial response to first-line platinum-based chemotherapy. - NIL

Start Date01 Dec 2025

Sponsor / Collaborator

NATCO Pharma Ltd.

[+1]

CTRI/2025/08/092636

/ Not yet recruitingNot Applicable

A multi-centre, open label, balanced, randomised, two-treatment, two-period, two-sequence, two-way crossover, multiple-dose, steady state, pharmacokinetic endpoint bioequivalence study of niraparib tablets 2x100 mg of Natco Pharma Ltd. (test product) against Zejula (niraparib) tablet 2x100 mg of GlaxoSmithKline (Ireland) (reference product) under fasting conditions in female participants with advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in a complete or partial response to first-line platinum-based chemotherapy. - NIL

Start Date25 Nov 2025

Sponsor / Collaborator

NATCO Pharma Ltd.

[+1]

100 Clinical Results associated with Niraparib Tosylate

100 Translational Medicine associated with Niraparib Tosylate

100 Patents (Medical) associated with Niraparib Tosylate

1,020

Literatures (Medical) associated with Niraparib Tosylate

31 Dec 2026·JOURNAL OF ENZYME INHIBITION AND MEDICINAL CHEMISTRY

Design, synthesis and anti-breast cancer activity evaluation of 6,7-dihydro-5 H -pyrrolo[3,4- d ]pyrimidine-based PARP1/ATR dual inhibitors

Article

Author: Wang, Xiao-Xian ; He, Meng-Lan ; Gao, Yuan ; Du, Bo-Qun ; Wang, Zong-Hao ; Chen, Yong-Hao ; Yao, Xia ; Wang, Chen-Chen ; Ye, Xiang-Yang ; Ye, Lu-Lu ; Luo, Hui

PARP1 inhibitors are FDA-approved for BRCA1/2-mutated breast cancer but show limited efficacy in wild-type cancers and face resistance issues. To overcome these, we designed novel 6,7-dihydro-5H-pyrrolo[3,4-d]pyrimidine-based compounds integrating PARP1 inhibitor pharmacophores with the ATR inhibitor AZD6738 scaffold. Substituent modifications influenced PARP1 and ATR selectivity, yielding dual inhibitors or selective PARP1 inhibitors. Compound 38a, the lead candidate, exhibited potent dual inhibition (IC₅₀ < 20 nM) and strong antitumor effects in MDA-MB-231 (IC₅₀ < 0.048 μM) and MDA-MB-468 (IC₅₀: 0.01 μM) cell lines in vitro. Mechanistically, 38a arrested cell cycle progression, induced apoptosis, inhibited colony formation and migration, and suppressed DNA damage repair pathways, outperforming combined Niraparib and AZD6738. These findings underscore the therapeutic potential of PARP1/ATR dual inhibitors for breast cancer and support further investigation.

31 Dec 2026·CANCER BIOLOGY & THERAPY

Evaluating carboplatin and PARP inhibitor combination efficacy using high-grade serous carcinoma spheroids and organoids

Article

Author: Tomas, Emily J. ; Davis, Jennifer ; Ramos Valdes, Yudith ; Shepherd, Trevor G.

BACKGROUND:

PARP inhibitors (PARPis) are new targeted agents that exploit homologous recombination DNA repair deficiencies (HRDs), which are present in 50% of high-grade serous carcinoma (HGSC) cases. Currently, olaparib is approved as maintenance therapy for BRCA1/2-mutated HGSC, and niraparib is approved for platinum-sensitive recurrent disease. However, research is currently expanding their potential as front-line agents or in combination with carboplatin, a standard HGSC chemotherapeutic.

METHODS:

Immortalized ovarian cancer (iOvCa) cell lines, developed from HGSC patient ascites, were treated with carboplatin, olaparib and niraparib to determine their sensitivity. Immunofluorescence analysis of RAD51 was conducted for HRD testing of all the cell lines. The cell lines were cultured as three-dimensional organoids and spheroids to mimic tumor growth and metastasis, respectively, and then treated to assess the effects of different drug combinations.

RESULTS:

The half-maximal inhibitory concentrations of olaparib and niraparib varied across our iOvCa cell lines, with iOvCa195 BRCA1-mutant line exhibiting the expected high sensitivity to both PARPis. Direct combination of carboplatin with olaparib or niraparib enhanced cell killing, yet achieved cell viability levels to those of carboplatin alone. In sequential experiments, carboplatin followed by either PARPi or vice versa showed no significant difference in cell viability to carboplatin alone, except in iOvCa195 organoids when treated with a PARPi first.

CONCLUSIONS:

Overall, first-line carboplatin treatment remains ideal, yet there may be select utility for PARPi prior to chemotherapy. Using patient-derived tumor models such as spheroids and organoids may provide insights for on-going and future clinical trials to enhance therapeutic outcomes for HGSC patients.

01 Dec 2026·JOURNAL OF MOLECULAR MEDICINE-JMM

Combined targeting poly (ADP-ribose) polymerase and receptor tyrosine kinase inhibits ovarian clear cell carcinoma progression through disrupted ribosome biogenesis

Article

Author: Lai, Chyong-Huey ; Chao, Angel ; Fu, Chiung-Hui ; Chao, An-Shine ; Yu, Alice L ; Teng, Yu-Chuan ; Wu, Ren-Chin ; Huang, Ruby Yun-Ju ; Lin, Chiao-Yun

OCCC has extremely poor prognosis. ARID1A mutation-related chromatin remodeling errors are key molecular features of OCCC. Dysregulation of receptor tyrosine kinases-related signaling pathways is common in OCCC. Here we show that combination of niraparib and lenvatinib exhibits significant synergistic inhibitory effects against platinum-resistant OCCC cell lines, xenografts, patient-derived tumoroid (PDT) models, and prolonged survival in the platinum-refractory patient-derived xenograft (PDX) model. RNA-sequencing revealed the most differently expressed genes in PDX treated with a combination of niraparib and lenvatinib versus control were in structural ribosomal components. Selected differently expressed ribosomal proteins (RPs: RPS2, RPS5, RPS9, and RPL3) was validated using quantitative polymerase chain reaction. Nucleophosmin (NPM1) expression, which is involved in ribosome biogenesis, was inhibited by niraparib and lenvatinib. Our findings imply that combined niraparib and lenvatinib reduces platinum-resistant OCCC progression by attenuating Src phosphorylation, NPM1 expression and ribosome biogenesis. These results highlight the necessity for continued exploration of this promising treatment strategy, particularly in future clinical trials for platinum-resistant or platinum-refractory OCCC. KEY MESSAGES: The combination of niraparib and lenvatinib synergistically inhibits platinum-resistant OCCC. This combination prolongs survival in a platinum-refractory PDX model. RNA sequencing revealed that the most differentially expressed genes in PDX models treated with this combination were associated with structural ribosomal components. This combination suppresses Src phosphorylation, NPM1 expression, and ribosomal protein levels in OCCC.

363

News (Medical) associated with Niraparib Tosylate

27 Mar 2026

·www.sciencedaily.com

Scientists discover why cancer drugs don’t work for everyone

Scientists have uncovered a hidden reason why cancer treatments don’t work equally well for everyone. Certain drugs can become trapped inside lysosomes within tumor cells, forming slow-release reservoirs that create uneven drug distribution. This means some cancer cells are heavily exposed while others are barely affected. Understanding this process could help doctors better tailor treatments and improve outcomes.One of the biggest challenges in cancer care is that the same therapy can be highly effective for some patients yet fail entirely for others. A new study published in Nature Communications, led by Dr. Louise Fets at the MRC Laboratory of Medical Sciences (LMS), takes a closer look at why this happens. The researchers focused on PARP inhibitors, a class of targeted cancer drugs, and tracked how they move through ovarian tumor samples using advanced imaging tools. Their findings show that these drugs can accumulate inside lysosomes, small structures within cells that act as "recycling centers." Once inside, the drugs can become trapped and later released, influencing how well the treatment performs. Mapping How Cancer Drugs Spread Inside Tumors Cancer treatment options have expanded rapidly in recent years, improving outcomes for many patients. PARP inhibitors, in particular, have transformed care for ovarian cancer. However, not all patients benefit, and some develop resistance over time. For these drugs to work, they must build up inside cancer cells at levels high enough to trigger cell death. Despite this, scientists still have limited understanding of how drugs distribute within tumors and what controls that process. This research shows that effectiveness depends not only on whether a drug reaches a tumor, but also on how it spreads within it and inside individual cells. To study this, researchers used thin slices of ovarian tumors taken from patients and kept alive in the lab. These samples, known as "explants," were treated with PARP inhibitors so scientists could directly observe how the drugs moved through real human tumor tissue. Using mass spectrometry imaging, the team produced detailed maps showing exactly where the drugs accumulated. They paired this with spatial transcriptomics, which allowed them to examine gene activity in areas with high and low drug levels within the same sample. The results revealed striking differences in drug distribution, both within individual tumors and between patients, even when the same dose was used. "A novel aspect of this study was the use of mass spectrometry imaging to directly measure and visualize drug uptake in patient tumour tissue. Through the spatial mapping of drug molecules, we could pinpoint regions of high and low drug and compare gene expression, from the same tissue slice, using spatial transcriptomics," says Dr. Zoe Hall, senior author and Associate Professor at Imperial's Department of Metabolism, Digestion and Reproduction. Lysosomes Act as Hidden Drug Reservoirs The researchers discovered that lysosomes play a central role in this uneven distribution. Some PARP inhibitors are drawn into these compartments and stored there instead of spreading evenly throughout the cell. This creates internal pockets where drugs accumulate. These lysosomes act as slow release reservoirs -- holding onto the drug and releasing it gradually -- which increases exposure in certain cells while leaving others with much lower levels. Not all PARP inhibitors behave in the same way. The study found that drugs like rucaparib and niraparib are affected by this process, while others such as olaparib are not. "We were surprised to see large variability in drug accumulation at the single-cell level. This variability was driven by the build-up of a drug in lysosomes, which are acting as reservoirs, increasing the exposure of cancer cells to drugs, by storing and releasing the drug when needed," says Dr. Carmen Ramirez Moncayo, first author and Postdoctoral Researcher at the LMS. What This Means for the Future of Cancer Treatment PARP inhibitors are already widely used to treat ovarian, breast, and prostate cancers, and they are being tested in many other cancer types. Gaining a better understanding of how these drugs are stored and distributed inside cells could lead to more personalized treatment strategies, improving effectiveness while reducing resistance and relapse. "By understanding how drugs are taken up into cells, we can understand whether this influences why cancer drugs work for some people and not for others. Eventually, we hope to be able study the molecular signature of a patient's tumor to help to tailor therapeutic approaches in a more personalized way," says Dr. Louise Fets, senior author and Head of the LMS' Drug Transport and Tumour metabolism Group. This study was conducted using tumor tissue maintained outside the body. In real patients, drugs are delivered through the bloodstream, and tumor blood vessels are often disorganized, which may further contribute to uneven drug distribution. Future studies will use animal models and larger patient groups to better understand how drug delivery, tumor structure, and lysosomal storage interact in clinical settings, including in relapsed cancers. This research was supported by funding from the Medical Research Council, Cancer Research UK, a PhD studentship from the Integrative Toxicology Training Partnership administered by the MRC Toxicology Unit, and a Victoria's Secret Global Fund for Women's Cancers Career Development Award, in partnership with Pelotonia and AACR.

19 Mar 2026

·allsci.com

Pfizer’s PARP Talzenna plus enzalutamide posts late stage success in mCSPC

Pfizer (NYSE: PFE) reported positive Phase III results for Talzenan (talazoparib) plus enzalutamide in HRR-mutated metastatic castration-sensitive prostate cancer, marking the first late-stage evidence for a PARP inhibitor combination in this earlier disease setting. The TALAPRO-3 trial met its primary endpoint of radiographic progression-free survival, with an interim analysis suggesting a trend toward improved overall survival. Trial specifics The TALAPRO-3 trial (NCT04821622) is a multicenter, randomized, double-blind, placebo-controlled study that enrolled 599 patients with metastatic castration-sensitive prostate cancer (mCSPC) harboring alterations in one or more of 12 HRR genes. Patients had received no more than three months of androgen deprivation therapy, with or without an approved androgen receptor pathway inhibitor in the mCSPC setting, and were randomized to receive either talazoparib 0.5 mg daily plus enzalutamide 160 mg daily or placebo plus enzalutamide 160 mg daily. Sites spanned the United States, Canada, Europe, South America, and the Asia-Pacific region. The primary endpoint, investigator-assessed radiographic progression-free survival defined by RECIST 1.1 for soft tissue and PCWG3 criteria for bone, was met with a statistically significant reduction in the risk of disease progression or death for the talazoparib enzalutamide combination versus placebo plus enzalutamide. The company reported that the observed hazard ratio exceeded the pre-specified target of 0.63, and that the majority of patients in the trial remained progression-free at the time of analysis. Consistent rPFS benefit was observed across patients whose tumors harbored BRCA alterations and those with non-BRCA HRR gene mutations, according to the data. At the interim analysis, overall survival — a key secondary endpoint — showed what Pfizer described as a strong trend toward improvement, though the data were not yet mature. Benefits were also reported across other secondary endpoints, including objective response rate, duration of response, and time to PSA progression. Pfizer did not disclose the specific hazard ratio, median rPFS values, or the number of events in either arm. The absence of these quantitative details limits independent assessment of the magnitude of benefit, and the full dataset is expected at an upcoming medical congress. The safety profile of the combination was consistent with the known adverse event profiles of each agent and no new safety signals were identified. Combining PARP inhibition with androgen receptor blockade Talazoparib is an oral PARP inhibitor that blocks PARP enzyme activity and traps PARP proteins at sites of DNA damage, leading to the accumulation of double-strand breaks and cell death in tumors deficient in homologous recombination repair. Enzalutamide is an androgen receptor pathway inhibitor that blocks androgen binding, nuclear translocation, and transcriptional activity. The biological rationale for the combination rests on evidence that androgen receptor signaling supports DNA repair in prostate cancer cells; inhibiting this pathway may deepen the vulnerability of HRR-deficient tumors to PARP inhibition. This synthetic lethality concept has been validated in the mCRPC setting through the TALAPRO-2 trial, which led to the FDA approval of the combination in June 2023 for HRR gene-mutated mCRPC. Positioning and context No therapy is currently approved specifically for HRR gene-mutated mCSPC. Standard treatment for mCSPC generally consists of androgen deprivation therapy combined with an androgen receptor pathway inhibitor such as enzalutamide, apalutamide, or abiraterone, or with docetaxel — none of which are tailored to HRR mutation status. PARP inhibitor approvals in prostate cancer, including talazoparib plus enzalutamide and olaparib (Lynparza, AstraZeneca/Merck), are limited to the castration-resistant setting. The TALAPRO-3 results represent the first Phase III readout of a PARP inhibitor combination in mCSPC selected by HRR gene status. Data from the PROpel and MAGNITUDE trials established the activity of olaparib plus abiraterone and niraparib plus abiraterone, respectively, in mCRPC, but neither program has reported Phase III data in the castration-sensitive population with HRR selection. Cross-trial comparisons are limited by differences in study design, patient populations, comparator arms, and disease stage. Approximately 25% of metastatic prostate cancers harbor HRR gene alterations, according to Pfizer, and these patients face a worse prognosis and reduced responsiveness to current standards of care. Data suggest that 50% to 65% of mCSPC patients progress to castration-resistant disease within two years, with HRR-mutated patients at increased risk of early progression. Next steps, regulatory plans Pfizer stated that the TALAPRO-3 results will be submitted for presentation at an upcoming medical congress and discussed with global health authorities to support potential regulatory submissions for expanding the Talzenna indication to this earlier disease stage. The combination of Talzenna plus Xtandi is currently approved in 60 countries for mCRPC, with the US approval granted in June 2023 and the European Commission approval following in January 2024. If the overall survival data mature favorably, the combination could become the first precision therapy approved for HRR gene-mutated metastatic castration-sensitive prostate cancer, a population where no biomarker-directed treatment currently exists. Leave a Reply Cancel reply Your email address will not be published. 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Phase 3Clinical ResultDrug ApprovalGene Therapy

18 Mar 2026

·www.biospace.com

Myriad Genetics Receives FDA Approval of the MyChoice CDx Test as the Companion Diagnostic for Zejula (niraparib) for Patients with Ovarian Cancer

Approval reinforces Myriad’s leadership in comprehensive HRD testing and establishes MyChoice CDx as the only FDA-approved companion diagnostic for Zejula in the United States SALT LAKE CITY, March 17, 2026 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc., (NASDAQ: MYGN), a leader in molecular diagnostic testing and precision medicine, today announced that the U.S. Food and Drug Administration (FDA) has approved the MyChoice ® CDx Test as the Companion Diagnostic (CDx) for Zejula ® (niraparib), a PARP inhibitor from GSK , for patients with advanced ovarian cancer. This approval is based on final data from the PRIMA trial, where the MyChoice CDx Test determined homologous recombination deficiency (HRD) status and was used to stratify advanced ovarian cancer patients. The MyChoice CDx is the only FDA-approved companion diagnostic test in the United States to identify patients with HRD-positive status eligible for treatment with Zejula. The test determines HRD status by leveraging next generation sequencing technology to conduct a comprehensive assessment of BRCA1/2 genes -- including large rearrangements -- and tumor genomic instability score (GIS) that includes loss of heterozygosity (LOH), telomeric allelic imbalance (TAI) and large-scale state transitions (LST). “The FDA approval reinforces Myriad’s long-standing leadership in ovarian cancer diagnostics and underscores the clinical importance of comprehensive HRD testing,” said Brian Donnelly, Chief Commercial Officer, Myriad Genetics. “By enabling precise identification of patients who may benefit from PARP inhibitors, MyChoice CDx helps ensure that treatment decisions are guided by robust genomic insights.” Nearly 50% of patients with advanced ovarian cancer have HRD positive (HRD+) tumors. 1 Identifying these patients is critical to ensuring appropriate use of PARP inhibitor therapy and improving personalized treatment decisions. 1-4 Z ejula is a prescription medicine used for the maintenance treatment of adult patients with advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer whose cancer is associated with HRD+ status defined by a deleterious or suspected deleterious BRCA mutation and/or genomic instability. Z ejula is used after the cancer has responded (complete or partial response) to treatment with first-line platinum-based chemotherapy (Zejula indications referenced here apply to the US only). (For other indications, see “About Zejula” section below). To learn more about the MyChoice CDx Test and how it can support treatment decisions for patients eligible for Zejula, please visit . About the MyChoice CDx Test The MyChoice ® CDx Test is the only FDA-approved homologous recombination deficiency (HRD) test specifically mentioned in American Society of Clinical Oncology (ASCO) guidelines for selecting patients with ovarian cancer who may benefit from poly [ADP-ribose] polymerase (PARP) inhibitors. 5 The MyChoice CDx Test determines HRD status by conducting a comprehensive assessment of BRCA1 /2 genes and tumor genomic instability score (GIS) that includes loss of heterozygosity (LOH), telomeric allelic imbalance (TAI) and large-scale state transitions (LST). The MyChoice CDx Test can identify 34% more patients with HRD than other tumor tests that use %LOH alone. 1 About Zejula (niraparib) Zejula is an oral, once-daily poly (ADP ribose) polymerase (PARP) inhibitor that works by preventing DNA repair in tumor cells, ultimately leading to their death. Zejula is indicated in the US for the maintenance treatment of adult patients with advanced epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in complete or partial response to first-line platinum-based chemotherapy and whose cancer is associated with homologous recombination deficiency (HRD)-positive status. Zejula is also indicated for the maintenance treatment of adult patients with deleterious or suspected deleterious germline BRCA-mutated recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in a complete or partial response to platinum-based chemotherapy and who have been selected based on a US FDA-approved companion diagnostic for Zejula (Zejula indications referenced here apply to the US only). Please see the US Prescribing Information for Zejula . About Myriad Genetics Myriad Genetics is a leading molecular diagnostic and precision medicine company committed to advancing health and well-being for all. Myriad Genetics develops and commercializes molecular tests that help patients and providers uncover genetic insights. Myriad Genetics tests assess the risk of developing disease or disease progression and guide treatment decisions across medical specialties where molecular insights can significantly improve patient care, support earlier detection, enable more precise treatment and contribute to lowering healthcare costs. For more information, visit . Safe Harbor Statement This press release contains “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995, including statements that this FDA approval reinforces the company’s long-standing leadership in ovarian cancer diagnostics and underscores the clinical importance of comprehensive HRD testing, and that, by enabling precise identification of patients who may benefit from PARP inhibitors, MyChoice CDx helps ensure that treatment decisions are guided by robust genomic insights. These “forward-looking statements” are management’s expectations of future events as of the date hereof and are subject to known and unknown risks and uncertainties that could cause actual results, conditions, and events to differ materially and adversely from those anticipated. Such factors include those risks described in the company’s filings with the U.S. Securities and Exchange Commission, including the company’s Annual Report on Form 10-K filed on February 24, 2026, as well as any updates to those risk factors filed from time to time in the company’s Quarterly Reports on Form 10-Q or Current Reports on Form 8-K. Myriad is not under any obligation, and it expressly disclaims any obligation, to update or alter any forward-looking statements, whether as a result of new information, future events or otherwise except as required by law. Konstantinopoulos PA, Ceccaldi R, Shapiro GI, D’Andrea AD. Homologous Recombination Deficiency: Exploiting the Fundamental Vulnerability of Ovarian Cancer. Cancer Discov. 2015;5(11):1137-1154. Timms KM, Abkevich V, Hughes E, et al. Comparison of genomic instability test scores used for predicting PARP activity in ovarian cancer. J Clin Oncol. 2020;38(15_suppl):1586. da Cunha Colombo Bonadio RR, Fogace RN, Miranda VC, Diz MDPE. Homologous recombination deficiency in ovarian cancer: a review of its epidemiology and management. Clinics (Sao Paulo). 2018;73(suppl 1):e450s. Watkins JA, Irshad S, Grigoriadis A, Tutt AN. Genomic scars as biomarkers of homologous recombination deficiency and drug response in breast and ovarian cancers. Breast Cancer Res. 2014;16(3):211. Tew WP, Lacchetti C, Birrer MJ, et al. PARP inhibitors in the management of ovarian cancer: ASCO guideline. J Clin Oncol. 2020;38(30):3468-3493 Investor Contact Matt Scalo (801) 584-3532 IR@myriad.com Media Contact Kate Schraml (224) 875-4493 PR@myriad.com

ASCOClinical Result

100 Deals associated with Niraparib Tosylate

External Link

KEGG	Wiki	ATC	Drug Bank
-	Niraparib Tosylate	L01XX54	DB11793

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Recurrent Primary Peritoneal Carcinoma	United States	GlaxoSmithKline LLC	27 Mar 2026
BRCA-mutated Ovarian Cancer	United States	GlaxoSmithKline LLC	23 Oct 2019
Ovarian Cancer	Switzerland	Tesaro, Inc.	03 Oct 2018
Peritoneal Neoplasms	Switzerland	Tesaro, Inc.	03 Oct 2018
Platinum-sensitive epithelial ovarian cancer	European Union	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-sensitive epithelial ovarian cancer	Iceland	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-sensitive epithelial ovarian cancer	Liechtenstein	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-sensitive epithelial ovarian cancer	Norway	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Fallopian Tube Carcinoma	European Union	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Fallopian Tube Carcinoma	Iceland	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Fallopian Tube Carcinoma	Liechtenstein	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Fallopian Tube Carcinoma	Norway	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Primary Peritoneal Carcinoma	European Union	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Primary Peritoneal Carcinoma	Iceland	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Primary Peritoneal Carcinoma	Liechtenstein	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Platinum-Sensitive Primary Peritoneal Carcinoma	Norway	GlaxoSmithKline Trading Services Ltd.	16 Nov 2017
Fallopian Tube Carcinoma	United States	GlaxoSmithKline LLC	27 Mar 2017
Ovarian Epithelial Carcinoma	United States	GlaxoSmithKline LLC	27 Mar 2017
Primary peritoneal carcinoma	United States	GlaxoSmithKline LLC	27 Mar 2017

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
BRCA Mutation Castration-Resistant Prostate Cancer	NDA/BLA	European Union	GlaxoSmithKline (Ireland) Ltd.	27 Feb 2023
Glioblastoma Multiforme	Phase 3	United States	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Australia	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Canada	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	France	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Germany	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Italy	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Netherlands	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Norway	GSK Plc	19 Jun 2024
Glioblastoma Multiforme	Phase 3	Spain	GSK Plc	19 Jun 2024

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04288687 (CTgov)	Phase 2	DNA Repair-Deficiency Disorders \| Castration-Resistant Prostatic Cancer \| Metastatic castration-resistant prostate cancer ... View more	11	Niraparib Pill	qxjrmvsgzm = ginucyglyh kdqcsgiodc (aownysooxz, pzfrpspbvm - evsxjhhnyc) View more	-	04 Mar 2026
NCT02655016 (PRIMA, ESGO2026)	Phase 3	Ovarian Cancer First line \| Maintenance	487	Niraparib	vmqaxmtcjf(pdrizkteno) = zvtwxmgeki dkxiunvhrr (ztfyplvksb )	Positive	28 Feb 2026
NCT05460000 (ENGOT-ov62, ESGO2026)	Phase 3	Ovarian Cancer HRD-positive	379	3 cycles of platinum-based chemotherapy (carboplatin + paclitaxel) + Niraparib maintenance therapy	fykijaznok(fsuxiawkbb) = mzinxvwgng zwzatswoev (pqljxaxovo )	Positive	28 Feb 2026
				6 cycles of platinum-based chemotherapy (carboplatin + paclitaxel) + Niraparib maintenance therapy	fykijaznok(fsuxiawkbb) = uhsvafprmk zwzatswoev (pqljxaxovo ) View more
ESGO2026	Not Applicable	Female Genital Neoplasms	28	Olaparib	haocdyqykt(nlsjaqoyvy) = pbnpgauyto jplatmplio (ejvztcvfee ) View more	Positive	28 Feb 2026
				Niraparib	vufxnaaijf(tfgqgsqukr) = prquejitaw oapylqhbcz (fxvoklivkh )
NCT04544995 (SCOOP, CTgov)	Phase 1	Adrenocortical Carcinoma \| Relapsed Solid Neoplasm \| Solid tumor ... View more	47	Niraparib+Dostarlimab (Part 1A Cohort 0: Niraparib 100 Milligram (mg) + Dostarlimab 3 mg/Kilogram (kg))	ongrcikqes = zubfwunnlm qmjqblkdxi (bxldclomls, duvogtjlvj - ftaysarykk) View more	-	21 Jan 2026
				Niraparib+Dostarlimab (Part 1A Cohort 1A: Niraparib 100 mg + Dostarlimab 7.5 mg/kg)	ongrcikqes = mdytyfmphd qmjqblkdxi (bxldclomls, njfqmdiknu - suobsexzsg) View more
SABCS2025	Phase 2	BRCA mutation positive Breast Cancer Neoadjuvant BRCA-Mutation Positive \| Hormone-Receptor Positive	34	Niraparib + Dostarlimab (HR+ BRCA-mutated breast cancer)	mxcjehqfgy(ijrwtrooxe) = Commonly reported adverse events included rash (25.0%), elevated liver function tests (18.8%), diarrhea (12.5%), and hypertension (12.5%). grofdtacib (wgmidwygue ) View more	Positive	10 Dec 2025
				Pembrolizumab + Carboplatin (HR+ BRCA-mutated breast cancer)
NCT05311579 (ESMO_ASIA2025)	Phase 2	Ovarian Cancer First line \| Maintenance	22	AnlotinibNiraparib + AnlotinibNiraparib	klxkkftymx(ohptlyjglr) = fmdhtxrmju rzefnjljzv (xntlrkwonq ) View more	Positive	05 Dec 2025
NCT05169437 (PAVO, CTgov)	Phase 2	Locally Advanced Malignant Solid Neoplasm \| Lung Cancer \| Esophageal Carcinoma ... View more	22	niraparib	ikzcbmulmw = wwridbdknr lrwnzfyile (prfkmwvify, ykgghdhsbg - zbemoxhnjd) View more	-	29 Oct 2025
NCT03748641 (MAGNITUDE, ESMO2025)	Phase 3	Metastatic castration-resistant prostate cancer First line BRCA1 \| BRCA2 \| FANCA ... View more	423	Niraparib and Abiraterone Acetate Plus Prednisone (NIRA+AAP)	ixitsfylqb(nxpdgtfbti) = wlocktliqf kymrydfbky (ahrnwhcnnx ) View more	Positive	17 Oct 2025
				Placebo + Abiraterone Acetate Plus Prednisone (PBO+AAP)	tyblwleoli(nqrcyylpkw) = oaihoefdnz njlpinnvdi (izjczafywh )
1NSPIRE (ESMO2025)	Not Applicable	Ovarian Epithelial Carcinoma First line \| Maintenance homologous recombination deficient (HRd) \| homologous recombination proficient (HRp) \| BRCA wild-type/HRD status unknown (BRCAwt/HRDunk)	218	Niraparib (HRd)	slftqvlgpe(jxhceaaeqy) = udmzngjnfo brugxlttay (eutstlnvya, 20.1 - NE) View more	Positive	17 Oct 2025
				Niraparib (HRp)	slftqvlgpe(jxhceaaeqy) = rxlvqudghk brugxlttay (eutstlnvya, 6.9 - 19.9) View more

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