预约演示
更新于：2026-01-14
Saruparib
更新于：2026-01-14
概要
基本信息
原研机构 |
非在研机构- |
权益机构- |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评- |
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结构/序列
分子式C22H26N6O2 |
InChIKeyWQAVGRAETZEADU-UHFFFAOYSA-N |
CAS号2589531-76-8 |
关联
21
项与 Saruparib 相关的临床试验NCT07336446
A Phase I/II, Modular, Open-Label, Multi-Centre Study to Evaluate the Safety, Pharmacokinetics, Pharmacodynamics and Preliminary Efficacy of AZD9750 as Monotherapy and in Combination With Other Anticancer Agents in Participants With Metastatic Prostate Cancer (ANDROMEDA)
NCT06769126
PRISM: PRecIsion in SCLC Via a Multicohort Study: Randomized Phase II Studies Evaluating Maintenance Durvalumab With or Without Biomarker-Directed Therapy for Extensive Stage Small Cell Lung Cancer (ES-SCLC)
NCT07060365
A Master Protocol Phase I/II Study to Investigate Biomarker-Guided Novel Anticancer Agent(s) as Monotherapy or Combination Therapy for the Treatment of Participants With Advanced/Recurrent Ovarian Cancer (Ovarian Platform)
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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26
项与 Saruparib 相关的文献（医药）2026-01-01EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
Discovery of selective PARP1/EZH2 inhibitor inducing PANoptosis in triple-negative breast cancer
Article
作者: Lai, Yiling ; Jiang, Renxin ; Yang, Huali ; Deng, Fangbo ; Liu, Quan ; Li, Na ; Hu, Dexiang ; Liu, Fanglan ; Xia, Chunhua ; Fan, Heqing ; Wang, Cheng ; Wang, Xudong
Combination of PARP and EZH2 inhibitors has demonstrated synergistic anticancer activity in triple-negative breast cancer (TNBC). However, first-generation PARP inhibitors were not strictly optimized for trapping nor for selectivity among the PARP enzyme family and were prone to causing hematotoxicity. In this study, we combined the structure of the latest second-generation selective PARP1 inhibitor AZD5305 to design and synthesize a series of second-generation selective PARP1/EZH2 dual inhibitors. Among these, PE31 exhibited potent inhibitory activity against PARP1 (IC50 = 0.028 μM) and EZH2 (IC50 = 0.074 μM), and the inhibitory activity against PARP2 (IC50 = 0.414 μM) is relatively weak. PE32 can effectively inhibit the proliferation and migration of TNBC cells, and can induce PANoptosis in TNBC cells, increase the level of reactive oxygen species, and activate related inflammatory pathways. Meanwhile, compared with the previous first-generation inhibitors, its permeability has improved, but its overall pharmacokinetic characteristics still need to be further optimized. However, as a novel selective PARP multifunctional molecule, it remains a highly promising potential compound for the for the treatment of TNBC.
2025-12-01JOURNAL OF NEUROCHEMISTRY
Article
作者: Paquet‐Durand, François ; Jiao, Kangwei ; Seeliger, Mathias W. ; Zhu, Yu ; Fallatah, Azdah Hamed A.
ABSTRACT:
Retinitis Pigmentosa (RP) is a group of rare, inherited, neurodegenerative diseases of the retina that primarily affect rod photoreceptors. The initial loss of rods is followed by a secondary cone photoreceptor degeneration and eventually legal blindness. Despite several attempts, RP still remains essentially untreatable. In recent years, inhibition of poly (ADP‐ribose) polymerase (PARP) has been proposed as a potential therapeutic strategy for autosomal‐recessive RP, based on promising work in preclinical animal models. However, the effects of PARP inhibitors in autosomal‐dominant RP are still largely unknown. Here, we employed a novel, human‐homologous rhodopsin‐mutant
RhoI255del/+
mouse model for autosomal dominant RP to assess the impact of different PARP inhibitors on the progression of photoreceptor degeneration. The PARP inhibitors used –olaparib, saruparib, INO1001, and nicotinamide–target different PARP isoforms, and their potentially differential effects were evaluated in organotypic retinal explants cultivated under entirely defined conditions. Readouts comprised in situ activity assays for PARP and calpain‐type proteases, the TUNEL assay for cell death, as well as immunostaining for activated calpain‐2, activated caspase‐3, rhodopsin, and cone arrestin‐3. Unexpectedly, and in contrast to previous findings in animal models for recessive RP, all of the PARP inhibitors used led to marked and dose‐dependent rod photoreceptor toxicity in the
RhoI255del
dominant RP model. Furthermore, this effect appeared to be independent of rhodopsin expression. On the other hand, cone photoreceptors were apparently unaffected by PARP inhibition. The present study thus demonstrates the importance of PARP activity for rod photoreceptor viability in a dominant rhodopsin mutant, highlights the need for a deeper understanding of the mechanisms underlying photoreceptor degeneration in different RP forms, and cautions against the indiscriminate use of PARP inhibitors for the treatment of RP.
image
2025-11-26NUCLEIC ACIDS RESEARCH
Genetic evidence for PARP1 trapping as a driver of PARP inhibitor efficacy in
BRCA
mutant cancer cells
Article
作者: van Beek, Lotte ; Schimpl, Marianne ; Stubbs, Christopher ; Hansen, Kjetil ; O’Connor, Mark J ; Hall, James ; Ribeiro, Jonathan ; Frigola, Joan ; Wijnhoven, Paul W G ; Bentouati, Sabrina ; Armenia, Josh ; Forment, Josep V ; Albertella, Mark R ; Talbot, Sara ; Illuzzi, Giuditta
Abstract:
Clinically approved PARP inhibitors (PARPi) have shown significant efficacy as monotherapy in homologous recombination repair (HRR)-deficient cancers. PARPi suppress PARP enzymatic activity but can also induce PARP trapping onto DNA lesions, and there is an ongoing debate on which of these properties is key in determining their clinical efficacy as single agents. In this study, we found that the enzymatic activity of PARP1 is dispensable for the survival of a BRCA1 mutant (BRCA1m) breast cancer model. However, PARP1 expression is necessary for the efficacy of PARPi in this model, supporting the importance of PARP1 trapping. We also identified and characterised a PARP1 mutation resulting in loss of the enzymatic inhibition and trapping activity of the PARP1-selective inhibitor, saruparib. However, the same mutation increased the trapping ability of other PARPi, namely veliparib and olaparib, without enhancing their enzymatic inhibition activity, a change that led to an increase in efficacy in this BRCA1m model. Together, these data suggest that PARP1 trapping, and not only its enzymatic inhibition, is a key driver for PARPi effectiveness in BRCA1m cancer cells.
98
项与 Saruparib 相关的新闻（医药）2026-01-01
·信狐药迅
2025-12-25
·凤凰网
临床结果ASCO会议临床3期上市批准
2025-12-25
·北晚在线
临床结果抗体药物偶联物ASCO会议临床3期
100 项与 Saruparib 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 前列腺腺癌 | 临床3期 | 美国 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 中国 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 日本 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 阿根廷 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 澳大利亚 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 奥地利 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 比利时 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 巴西 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 加拿大 | 2025-08-06 | |
| 前列腺腺癌 | 临床3期 | 智利 | 2025-08-06 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床1/2期 | 38 | 積構獵獵選餘淵製獵鹹(鹽鏇艱醖窪淵憲範糧鑰) = 製獵襯襯繭繭餘廠襯鏇 網遞蓋鹽築襯襯餘襯願 (構鏇獵鏇鬱繭餘襯廠顧 ) 更多 | 积极 | 2025-12-10 | |||
(BRCA1/BRCA2 mutation or PALB2 mutation) | 廠淵製衊鏇顧製顧願鹽(鹽餘鹹網膚廠築廠齋鏇) = 選網鬱積築廠願積糧壓 窪淵襯襯齋積膚簾築襯 (積膚齋衊鏇鏇網簾鏇構, 4.4 ~ 7.3) | ||||||
临床1/2期 | 141 | 膚淵廠顧製壓願齋襯顧(蓋糧顧憲積襯醖糧餘獵) = 醖顧廠鑰襯範遞襯繭艱 醖醖壓夢齋膚醖膚鏇鹽 (醖餘淵窪積構選鬱願觸, 35.7 ~ 61.3) 更多 | 积极 | 2024-04-08 | |||
临床1/2期 | 48 | 襯窪憲醖夢積膚艱築憲(膚構範鬱簾鹹憲窪製鏇) = 鹹鏇壓鏇壓窪艱繭艱積 遞廠膚憲鑰構鏇範積網 (餘襯選膚簾醖製積齋艱 ) 更多 | 积极 | 2024-01-25 | |||
临床1期 | - | 構艱壓鑰願構鬱壓遞餘(鏇齋鹽構築積艱鑰齋餘) = 窪範顧簾鏇遞構顧顧鏇 簾窪遞蓋窪夢鏇鑰選窪 (淵網繭憲襯窪選餘簾鏇 ) | - | 2023-03-14 | |||
临床1期 | 46 | 襯積衊艱壓範餘鏇積製(獵積積齋獵鑰鬱構鑰製) = 製築積鹽鏇壓廠顧廠蓋 齋製淵糧窪窪遞觸獵顧 (衊鹹築廠製壓窪製壓衊 ) 更多 | 积极 | 2022-06-15 |
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