评估AZD5305联合NHA对照安慰剂联合NHA的有效性和安全性。包括对以下终点的评价：即无影像学进展生存期、第二次无进展生存期、无症状性骨骼事件生存期、至首次发生去势抵抗性事件的时间、疼痛进展时间、泌尿系统症状恶化时间、疲劳恶化时间、身体机能恶化时间、至首次后续治疗或死亡时间、总生存期、以及有效性和安全性的评估。

开始日期2024-04-26

申办/合作机构

AstraZeneca AB

[+1]

NCT06380751 / Not yet recruiting临床3期

A Randomised, Open-Label, Phase III Study of Saruparib (AZD5305) Plus Camizestrant Compared With Physician's Choice CDK4/6 Inhibitor Plus Endocrine Therapy or Plus Camizestrant for the First-Line Treatment of Patients With BRCA1, BRCA2, or PALB2 Mutations and Hormone Receptor Positive, HER2-Negative (IHC 0, 1+, 2+/ ISH Non-amplified) Advanced Breast Cancer (EvoPAR-Breast01)

The primary objective of the study is to measure efficacy of saruparib (AZD5305) plus camizestrant compared with physician's choice CDK4/6i plus ET in patients with BRCA1, BRCA2, or PALB2m, HR-positive, HER2-negative (defined as IHC 0, 1+, 2+/ ISH non-amplified) advanced breast cancer.

开始日期2024-04-18

申办/合作机构

AstraZeneca PLC

NL-OMON56674 / Suspended临床3期

IVD1: Clinical Performance Study Plan For The Use of Myriad MyChoice® For Patient Enrolment Into the AZD5305 (Saruparib) vs Placebo in Participants with Metastatic Castration-Sensitive Prostate Cancer Receiving Physician*s Choice New Hormonal Agents;IVD2: Clinical Performance Study Plan for F1LCDx Used in Clinical Trial EvoPAR-Prostate01 ;Main: A Randomized, 2-cohort, Double-blind, Placebo-controlled, Phase III Study of AZD5305 in Combination with Physician*s Choice New Hormonal Agents in Patien - EvoPAR-Prostate01

开始日期2024-04-12

申办/合作机构-

100 项与 Saruparib 相关的临床结果

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100 项与 Saruparib 相关的转化医学

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100 项与 Saruparib 相关的专利（医药）

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项与 Saruparib 相关的文献（医药）

2023-05-04·Journal of experimental & clinical cancer research : CR

Targeting homologous recombination deficiency in uterine leiomyosarcoma.

Article

作者: Genevieve Dall ; Cassandra J Vandenberg ; Ksenija Nesic ; Gayanie Ratnayake ; Wenying Zhu ; Joseph H A Vissers ; Justin Bedő ; Jocelyn Penington ; Matthew J Wakefield ; Damien Kee ; Amandine Carmagnac ; Ratana Lim ; Kristy Shield-Artin ; Briony Milesi ; Amanda Lobley ; Elizabeth L Kyran ; Emily O'Grady ; Joshua Tram ; Warren Zhou ; Devindee Nugawela ; Kym Pham Stewart ; Reece Caldwell ; Lia Papadopoulos ; Ashley P Ng ; Alexander Dobrovic ; Stephen B Fox ; Orla McNally ; Jeremy D Power ; Tarek Meniawy ; Teng Han Tan ; Ian M Collins ; Oliver Klein ; Stephen Barnett ; Inger Olesen ; Anne Hamilton ; Oliver Hofmann ; Sean Grimmond ; Anthony T Papenfuss ; Clare L Scott ; Holly E Barker

BACKGROUND:

Uterine leiomyosarcoma (uLMS) is a rare and aggressive gynaecological malignancy, with individuals with advanced uLMS having a five-year survival of < 10%. Mutations in the homologous recombination (HR) DNA repair pathway have been observed in ~ 10% of uLMS cases, with reports of some individuals benefiting from poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) therapy, which targets this DNA repair defect. In this report, we screened individuals with uLMS, accrued nationally, for mutations in the HR repair pathway and explored new approaches to therapeutic targeting.

METHODS:

A cohort of 58 individuals with uLMS were screened for HR Deficiency (HRD) using whole genome sequencing (WGS), whole exome sequencing (WES) or NGS panel testing. Individuals identified to have HRD uLMS were offered PARPi therapy and clinical outcome details collected. Patient-derived xenografts (PDX) were generated for therapeutic targeting.

RESULTS:

All 13 uLMS samples analysed by WGS had a dominant COSMIC mutational signature 3; 11 of these had high genome-wide loss of heterozygosity (LOH) (> 0.2) but only two samples had a CHORD score > 50%, one of which had a homozygous pathogenic alteration in an HR gene (deletion in BRCA2). A further three samples harboured homozygous HRD alterations (all deletions in BRCA2), detected by WES or panel sequencing, with 5/58 (9%) individuals having HRD uLMS. All five individuals gained access to PARPi therapy. Two of three individuals with mature clinical follow up achieved a complete response or durable partial response (PR) with the subsequent addition of platinum to PARPi upon minor progression during initial PR on PARPi. Corresponding PDX responses were most rapid, complete and sustained with the PARP1-specific PARPi, AZD5305, compared with either olaparib alone or olaparib plus cisplatin, even in a paired sample of a BRCA2-deleted PDX, derived following PARPi therapy in the patient, which had developed PARPi-resistance mutations in PRKDC, encoding DNA-PKcs.

CONCLUSIONS:

Our work demonstrates the value of identifying HRD for therapeutic targeting by PARPi and platinum in individuals with the aggressive rare malignancy, uLMS and suggests that individuals with HRD uLMS should be included in trials of PARP1-specific PARPi.

2023-03-24·Science advances

Clinical PARP inhibitors allosterically induce PARP2 retention on DNA.

Article

作者: Marie-France Langelier ; Xiaohui Lin ; Shan Zha ; John M Pascal

PARP1 and PARP2 detect DNA breaks, which activates their catalytic production of poly(ADP-ribose) that recruits repair factors and contributes to PARP1/2 release from DNA. PARP inhibitors (PARPi) are used in cancer treatment and target PARP1/2 catalytic activity, interfering with repair and increasing PARP1/2 persistence on DNA damage. In addition, certain PARPi exert allosteric effects that increase PARP1 retention on DNA. However, no clinical PARPi exhibit this allosteric behavior toward PARP1. In contrast, we show that certain clinical PARPi exhibit an allosteric effect that retains PARP2 on DNA breaks in a manner that depends on communication between the catalytic and DNA binding regions. Using a PARP2 mutant that mimics an allosteric inhibitor effect, we observed increased PARP2 retention at cellular damage sites. The PARPi AZD5305 also exhibited a clear reverse allosteric effect on PARP2. Our results can help explain the toxicity of clinical PARPi and suggest ways to improve PARPi moving forward.

2023-03-01·Cancer research communications

The PARP1 Inhibitor AZD5305 Impairs Ovarian Adenocarcinoma Progression and Visceral Metastases in Patient-derived Xenografts Alone and in Combination with Carboplatin.

Article

作者: Giulia Dellavedova ; Alessandra Decio ; Laura Formenti ; Mark R Albertella ; Joanne Wilson ; Anna D Staniszewska ; Elisabetta Leo ; Raffaella Giavazzi ; Carmen Ghilardi ; Maria Rosa Bani

PARP inhibitors (PARPi) have changed the management of patients with ovarian cancer and their effectiveness has been demonstrated especially in homologous recombination repair-deficient tumors. These first-generation drugs target PARP1, but also PARP2 and other family members potentially responsible for adverse effects that limit their therapeutic potential and restrict their use in combination with chemotherapeutic agents. We investigated ovarian cancer patient-derived xenografts (OC-PDXs) to assess whether malignant progression could be impaired by a novel inhibitor selective for PARP1 (AZD5305) and to assess the potential of its combination with carboplatin (CPT), the standard-of-care for patients with ovarian cancer. In BRCA-mutated OC-PDXs, AZD5305 achieved greater tumor regressions and longer duration of response as well as a superior impairment of visceral metastasis and improved survival benefit compared with the first-generation dual PARP1/2 inhibitors. The combination of AZD5305 plus CPT was more efficacious than single agents. Subcutaneously growing tumors experienced regression that persisted after therapy stopped. Combination efficacy was greater against tumors that did not respond well to platinum, even at a dose at which AZD5305 monotherapy was ineffective. The combination therapy impaired metastatic dissemination and significantly prolonged the lifespan of mice bearing OC-PDXs in their abdomen. This combination benefit was evident even when CPT was used at suboptimal doses, and was superior to full-dose platinum treatment. These preclinical studies demonstrate that the PARP1-selective inhibitor AZD5305 retains and improves the therapeutic benefit of the first-generation PARPi, providing an opportunity to maximize benefits for this class of anticancer agents.

Significance:

Selective PARP1i AZD5305 can exceed the efficacy of first-generation PARPi, which target both PARP1 and PARP2, and potentiates the efficacy of CPT when given in combination. AZD5305 alone or in combination with platinum delayed visceral metastasis, ultimately extending the lifespan of OC-PDX-bearing mice. These preclinical models mimic the progression of the disease occurring in patients after debulking surgery, and are translationally relevant.

项与 Saruparib 相关的新闻（医药）

2024-04-08

·PRNewswire

Laekna Announces Two Poster Presentations on Internally Discovered Drug Candidates at AACR 2024

SHANGHAI and WARREN, N.J., April 7, 2024 /PRNewswire/ -- Laekna (2105.HK) announced that the company has presented two internally-discovered preclinical candidates, in addition to a poster presentation on a clinical trial, at the 2024 Annual Meeting of the American Association for Cancer Research (AACR) in San Diego, California. The presentations featured preclinical data of two novel selective inhibitors, LAE119, a novel PARP1 selective inhibitor and trapper, and LAE120, a novel selective USP1 inhibitor. "After advancing LAE102, our internally discovered antibody against ActRIIA, into IND stage, Laekna continues to strengthen our internal discovery efforts, with new drug candidates emerging", said Dr. Justin Gu, Chief Scientific Officer of Laekna. "The MOA of LAE119 and LAE120 is synthetic lethality, both exhibit strong anti-tumor efficacy and good safety in preclinical models. LAE 119 is a PARP1-selective inhibitor with the strongest DNA-trapping activity among all the PARP inhibitors tested. It shows good activity even in tumor cells with low PARP1 protein level. LAE120 is a novel USP1 inhibitor currently at IND-enabling studies stage. It has a unique chemical scaffold differentiated from all the other disclosed USP1 inhibitors and is expected to induce a different conformational change in USP1. The quick advance of these two projects into PCC stage demonstrates the effectiveness of the close collaboration among Med Chem, Biology and AIDD (AI-driven Drug Discovery) teams. Laekna will continue our internal effort of discovery novel drug candidates to provide more options for patients." Laekna's internal discovery focuses on innovation, scarcity, and differentiation, covering three areas: cancer, metabolic diseases，and liver fibrosis. The company has internally discovered 14 drug candidates, among which seven have been optimized and advanced to PCC (pre-clinical candidate) stage. The company plans to have one drug candidate entering the clinical stage each year. The Annual Meeting of AACR is set for April 05 to 10, 2024 at the San Diego Convention Center, California, USA. It is the focal point of the cancer research community, where scientists, clinicians, other health care professionals, survivors, patients, and advocates gather to share the latest advances in cancer science and medicine. [1] Presentation details are as follows: Title: Preclinical characterization of LAE119, a novel PARP1 selective inhibitor and trapper Authors: Ming Li, Yan Chen, Junyan Chen, Ling Jiang, Xiaofen Lin, Justin Gu Session Category: Experimental and Molecular Therapeutics Session Title: DNA Damage and Repair Session Date and Time: Wednesday, Apr 10, 2024 9:00 AM- 12:30 PM (PT) Location: Poster Section 22 Poster Board Number: 27 Abstract Highlights: LAE119 is a potent and selective PARP1 inhibitor and PARP1-DNA trapper. It demonstrates more than 1000-fold selectivity for PARP1 DNA trapping activity over PARP2. In comparison to most PARP inhibitors including AZD5305, LAE119 exhibits extremely long residence time on PARP1 in both biochemical and cellular assays and shows good activity even in tumor cells with low PARP1 protein level. It demonstrates robust anti-tumor effect in BRCA2-/- DLD-1 and MDA-MB-436 Xenograft models and has minimal effects on hematologic parameters. Full texts of the abstracts are available here. Title: Preclinical candidate LAE120, a novel selective USP1 inhibitor shows effective anticancer and combination activity with PARP inhibitors Authors: Jintao Wang, Yan Chen, Junyan Chen, Ling Jiang, Xiaofen Lin, Chaojun Cai, Minhua Zhang, Ming Li, Justin Gu Session Category: Experimental and Molecular Therapeutics Session Title: Novel Antitumor Agents 2 Session Date and Time: Sunday, Apr 7, 2024 1:30 PM- 5:00 PM (PT) Location: Poster Section 27 Poster Board Number: 16 Abstract Highlights: LAE120 is a novel, allosteric and highly potent USP1 inhibitor, displaying monotherapy potency and combination activity with PARP inhibitor in HRD (homologous recombination deficiency) cancers. It has a unique chemical structure differentiated from all the other disclosed USP1 inhibitors and is expected to induce a different conformational change in USP1. LAE120 shows robust tumor inhibitory activity in MDA-MB-436 and K562 xenograft models as a single agent and exhibits synergistic effect in combination with PARP inhibitors. LAE120 demonstrates good therapeutic window in DRF study and is currently at IND-enabling stage. Full texts of the abstracts are available here. About Laekna Founded in 2016, Laekna is a science-driven, clinical-stage biotechnology company committed to bringing novel therapies to cancer, metabolic diseases and liver fibrosis patients worldwide. As of December 31, 2023, we have initiated six clinical trials for Afuresertib (LAE002), LAE001 and LAE005 for the treatment of breast cancer, prostate cancer, ovarian cancer and PD-1/ PD-L1 drug-resistant solid tumors to address the unmet medical needs. Among the six clinical trials, three are multi-regional clinical trials (MRCTs). Afuresertib is a potent AKT inhibitor that inhibits all three AKT isoforms (AKT1, AKT2 and AKT3) as well as one of the only two AKT inhibitors in or completed the pivotal-stage clinical development for anti-cancer treatment globally. Laekna's internal drug discovery platform has discovered 14 drug candidates. LAE102 is our internally discovered antibody against ActRIIA. We've submitted IND applications to CDE and FDA respectively for LAE102 in relation to obesity in the first quarter of 2024. Blocking Activin-ActRII pathway could promote skeletal muscle regeneration and decrease fat mass. Laekna team has accumulated tremendous experiences and deep knowhow in this specific field and is developing more drug candidates (LAE103 and LAE123) to maximize the value of targeting ActRII receptors. Laekna, Inc. was listed on the Main Board of The Stock Exchange of Hong Kong Limited (the "Hong Kong Stock Exchange") on June 29, 2023, with the stock code 2105.HK. For more information, please visit: or Forward Looking Statements This press release may contain certain "forward-looking statements" which are not historical facts, but instead are predictions about future events based on Laekna's current beliefs, assumptions, and expectations, commonly identified by words such as "would", "may", "expects", "believes", "plans", "intends", "projects" and other terms with similar meaning. Although we believe that our predictions are reasonable, future events are inherently uncertain and our actual future results or performance may be materially different from what we expect. Accordingly, you are strongly cautioned that reliance on any forward-looking statements is subject to significant known and unknown risks and uncertainties. All forward-looking statements contained herein are qualified by reference to the cautionary statements set forth in this section. All information provided in this press release is as of the date of this press release and are based on assumptions that we believe to be reasonable as of this date, and we do not undertake any obligation to update any forward-looking statement, except as required under applicable law. SOURCE Laekna

AACR会议临床申请

2024-01-24

·FierceBiotech

Incyte vets, with phase 1 within reach, raise $102M for new biotech to create better PARP, PI3K drugs

Armed with medical chemistry expertise, the biotech has worked to create better molecules against validated targets. A group of familiar faces to Incyte watchers has broken off to start their own biotech, pulling in $102 million to develop competitors to approved cancer drugs from AstraZeneca, GSK, Novartis and Pfizer. The biotech, Synnovation Therapeutics, was founded by Wenqing Yao, Ph.D., and Liangxing Wu, Ph.D. Yao spent 19 years at Incyte, rising to the post of head of discovery chemistry, before leaving and setting up Synnovation in 2021. Wu worked alongside Yao at Incyte, where he spent almost a decade to end up with the title executive director, medicinal chemistry. Armed with medical chemistry expertise that contributed to Incyte products such as Olumiant, Pemazyre and Tabrecta, the pair have worked to create better molecules against validated targets, namely PARP and PI3K. It is now almost 10 years since the first drugs against the targets were approved, with AstraZeneca and Merck & Co.’s PARP inhibitor Lynparza and Gilead’s PI3K inhibitor Zydelig both winning authorizations in 2014. Other companies have since secured approval for competitors to those first-in-class products but work to address the limitations of Lynparza and Zydelig is yet to yield a flawless therapy. Synnovation, which officially launched today, has identified hematologic toxicity as a weakness of first-generation PARP inhibitors. Like other companies, the biotech has fingered inhibition of PARP2 as the cause of the toxicity and bet that it can expand the therapeutic index by selectively targeting PARP1. That isn’t a new idea. AstraZeneca has taken one selective PARP1 inhibitor, AZD5305, into phase 3 and moved its brain-penetrating sibling AZD9574 into the clinic. Gilead joined the race last year by acquiring XinThera and Merck KGaA has placed two PARP1 bets, one on Nerviano Medical Sciences and another on Jiangsu Hengrui Pharmaceuticals. Synnovation plans to start dosing patients in a phase 1 clinical trial of its brain-penetrating challenger, SNV1521, in the coming weeks. In preclinical tests, the biotech showed the molecule has greater than 500-fold selectivity against PARP2 and is more effective at inhibiting tumor growth than Lynparza. The biotech’s second candidate, SNV4818, is aimed at a target that has proven particularly troublesome. Zydelig and three other Gilead drugs that are too small to warrant their own line in the earnings collectively brought in $171 million over the first nine months of the year. Potential rivals have fled the space amid concerns PI3K inhibitors may shorten life expectancy and a resulting regulatory pushback. Synnovation’s attempt to crack the PI3K puzzle has resulted in a molecule that targets the alpha form of the kinase and, according to the biotech, “is differentiated from competitor molecules by virtue of its excellent selectivity for H1047X and moderate selectivity over relevant E545/542X mutants.” The design reflects the belief that a lack of selectivity against wild type PI3K-alpha has held the class back to date. Wu and Yao respectively work as CEO and senior vice president, drug discovery at Synnovation. The pair have been joined at the new biotech by two other leaders with lengthy stays at Incyte on their résumés. Phillip Liu, Ph.D., came on board as SVP, head of biology, while Kevin O’Hayer, M.D., Ph.D., took up the SVP, head of clinical development position last year.

临床1期高管变更上市批准临床3期

2024-01-24

·CPHI制药在线

市场 | 前有追兵，后有来者，阿斯利康重磅明星药如何突围？

关注并星标CPHI制药在线近日，药监局官网显示，科伦药业奥拉帕利片获批上市。这是继齐鲁制药的奥拉帕利首仿获批上市后，国内第2款获批上市的奥拉帕利仿制药。奥拉帕利原研产品为阿斯利康的Lynparza（Olaparib，利普卓），是全球首款获批上市的PARP（腺苷二磷酸核糖聚合酶）抑制剂。2014年12月，Lynparza获FDA批准上市，用于治疗卵巢癌。目前，Lynparza已相继获批卵巢癌、乳腺癌、去势抵抗性前列腺癌等多项适应症，是阿斯利康的重磅明星产品。基于"合成致死"概念，Lynparza掘金能力显著 Lynparza是利用"合成致死"概念在临床上取得成功的药物。所谓合成致死，即诱导细胞死亡的一种生物过程，其基于同时抑制在细胞存活所需的过程中的两种途径并行作用，而仅抑制其中一种途径则会导致细胞存活。 PARP在人体细胞内具有关键的DNA单链损伤修复功能。其通过快速识别并结合DNA受损单链，参与DNA损伤信号传导，募集修饰后受体蛋白到DNA损伤部位，完成修复。研究还发现，PARP抑制剂与BRCA1/2突变存在"合成致死"相互作用。作为双链修复的主力军，BRCA1/2存在于人体正常细胞里，在肿瘤细胞中，由于存在BRCA1/2突变，使肿瘤细胞的DNA损伤修复功能受限，导致双链损伤无法修复，从而增加了癌细胞对于PARP抑制剂的敏感性，破坏肿瘤细胞的合成以达到抗肿瘤目的。 Lynparza获FDA批准上市后，放量迅速，2022年销售额为26.38亿美元。Lynparza于2018年获NMPA批准在国内上市，第二年进入国家医保目录。仅在国内市场，2023上半年其销售额就超过6亿元。仿制药、创新药围攻，阿斯利康下一战如何打？ Lynparza作为里程碑式药物，引来诸多药企关注。在仿制药方面，齐鲁制药的奥拉帕利片于2023年5月获批上市，夺得首仿。在齐鲁、科伦之后，还有宣泰医药、石药集团、华东医药、江西香山药业等厂家的仿制药递交了上市申请。 Lynparza的化合物专利将在2024年3月到期，制剂专利将在2029年10月到期。虽然在专利到期前，这些仿制药无法上市销售，但随着专利悬崖的临近，阿斯利康不得不通过拓展适应症等手段应对未来激烈的市场竞争。除了仿制药外，Lynparza还面临着其他PARP抑制剂的竞争。目前，全球范围内共有6款PARP抑制剂获批上市，分别是Lynparza、Clovis Oncology的Rubraca（芦卡帕利，rucaparib，2016年12月获FDA批准）、GSK的Zejula（尼拉帕利，Niraparib，2017年3月获FDA批准）、辉瑞的Talzenna（他拉唑帕尼，talazoparib，2018年10月获FDA批准）、恒瑞医药的氟唑帕利（商品名：艾瑞颐，2020年12月获NMPA批准）以及百济神州的帕米帕利（品名：百汇择，2021年5月获NMPA批准）。其中Lynparza、Zejula、氟唑帕利、帕米帕利获NMPA批准在国内上市。一直以来，药企对PARP抑制剂的研发热情不减。全球在研的PARP抑制剂还有超80个。面对前后夹击的局面，阿斯利康正在开发新一代PARP抑制剂AZD5305。临床前研究显示，与第一代PARP抑制剂相比，AZD5305具有更好的耐受性，以及和靶点更强的结合力与疗效。在首个人类临床试验中，研究人员用AZD5305治疗了61位晚期乳腺癌、卵巢癌、前列腺癌或胰腺癌患者。在40位可评估疗效的患者中，10位获得部分缓解，11位疾病稳定。在接受循环肿瘤DNA（ctDNA）检测的13名患者中，8位患者的ctDNA水平下降。除了单靶点抑制剂，PARP抑制剂还在双靶点研发方面取得了进展。例如研究人员开发了可同时靶向PARP和PI3K的双重抑制剂，在异种移植小鼠模型中，与单独给药Lynparza或PI3K抑制剂和联合使用Lynparza和PI3K抑制剂相比，双重抑制剂抗肿瘤疗效更为显著。研究人员还在进行PARP与HDAC，PARP与TOPO，PARP与HSP90等双靶点抑制剂的研发。据公开数据，仅2022年，全球PARP抑制剂市场就超过55.1亿美元，预测2022-2026年将以11.2%的复合年增长率增长，2026年，PARP抑制剂全球市场将超过84.3亿美元。那么阿斯利康能否在未来的激烈竞争中取得突破，值得期待。主要参考资料： 1、CDE官网；2、AZD5305 Yields Promising Clinical and Safety Findings Across Several Solid Malignancies. Retrieved April 12, 2022, from https://www.cancernetwork.com/view/azd5305-yields-promising-clinical-and-safety-findings-across-several-solid-malignancies； 3、AstraZeneca unveils next-gen PARP inhibitor, looking to follow up on success of first-gen success story Lynparza. 【企业推荐】来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com▼更多制药资讯，请关注CPHI制药在线▼点击阅读原文，进入智药研习社~

上市批准专利到期

100 项与 Saruparib 相关的药物交易

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研发状态

适应症	最高研发状态	国家/地区	公司
去势抵抗性前列腺癌	临床3期	荷兰更多	AstraZeneca PLC 更多
子宫内膜癌	临床2期	法国更多	AstraZeneca PLC 更多
转移性去势抵抗性前列腺癌	临床2期	日本更多	AstraZeneca PLC 更多
卵巢癌	临床2期	德国更多	AstraZeneca PLC 更多
结直肠癌	临床2期	美国更多	AstraZeneca PLC 更多

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT04644068 (PETRA, AACR2022) 人工标引	临床1期	卵巢癌 \| 乳腺癌 \| 前列腺癌 \| 胰腺癌 BRCA1 Mutation \| BRCA2 Mutation \| PALB2 Mutation ... 更多	46	AZD5305	(鑰醖襯蓋醖製艱鬱觸糧) = 醖網觸製醖壓積構蓋網淵簾獵艱夢簾顧遞鏇獵 (遞廠膚糧壓醖蓋艱範繭 ) 更多	积极	2022-06-15
NCT05367440 (PETRANHA, ASCO_GU2024) 人工标引	临床1/2期	前列腺癌转移	48	enzalutamide or abiraterone acetate or darolutamide+AZD5305	(廠簾願壓艱艱選鬱夢鬱) = 遞壓觸繭廠艱鑰繭簾鑰鹹壓鹽衊繭顧襯構糧範 (夢膚糧艱製夢積願繭顧 ) 更多	积极	2024-01-25