预约演示
更新于：2026-02-07
Eprenetapopt
更新于：2026-02-07
概要
基本信息
在研机构- |
权益机构- |
最高研发阶段终止临床3期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评孤儿药 (美国)、突破性疗法 (美国) |
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结构/序列
分子式C10H17NO3 |
InChIKeyBGBNULCRKBVAKL-UHFFFAOYSA-N |
CAS号5291-32-7 |
关联
13
项与 Eprenetapopt 相关的临床试验NCT04990778
An Open Label, Phase II Investigator-Initiated Study of Venetoclax and Eprenetapopt (APR-246) in Previously Treated Relapsed/Refractory Patients With Mantle Cell Lymphoma (MCL)
NCT04419389
Phase 1 and Dose Expansion Study of APR-246 in Combination With Acalabrutinib or Venetoclax-based Therapy in Subjects With R/R NHL Including Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma (MCL)
NCT04383938
Study of APR-246 in Combination With Pembrolizumab in Subjects With Solid Tumor Malignancies
100 项与 Eprenetapopt 相关的临床结果
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100 项与 Eprenetapopt 相关的转化医学
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100 项与 Eprenetapopt 相关的专利（医药）
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433
项与 Eprenetapopt 相关的文献（医药）2026-03-01JOURNAL OF COLLOID AND INTERFACE SCIENCE
Dual-functional copper nanoplatform potentiates cuproptosis through p53 reactivation and metabolic reprogramming
Article
作者: Song, Kun ; Ma, Lele ; Zhang, Hui ; Qu, Fengli ; Yuan, Qunying ; Zheng, Huiying ; Sun, Weidi ; Xie, Wanlin ; Xi, Peiyu
Cuproptosis, a copper-dependent form of regulated cell death driven by mitochondrial metabolism, holds promise as a therapeutic strategy for cancer. However, its efficacy is hampered by tumor metabolic heterogeneity and mutant p53 (mut-p53)-driven metabolic rewiring that blunts cuproptosis sensitivity. Here, we report the rational design of CuF16@246, an acid-responsive, dual-functional copper-based nanocoordination polymer that integrates Cu2+ and the p53 reactivator eprenetapopt (APR-246) within a single perfluorosebacic acid (PFSEA)-coordinated framework to synergistically induce cuproptosis and reverse tumor metabolic reprogramming. CuF16@246 comprises a PFSEA-coordinated copper framework with good colloidal stability and pH-dependent co-release of Cu2+ and APR-246, enabling controlled Cu2+ release and in situ APR-246 loading. Mechanistically, CuF16@246 triggers hallmarks of cuproptosis, including dihydrolipoamide S-acetyltransferase (DLAT) oligomerization and the depletion of the iron‑sulfur (Fe-S) cluster proteins ferredoxin 1 (FDX1) and lipoic acid synthase (LIAS), while APR-246 converts mut-p53 toward a wild-type-like, DNA-binding-competent state, upregulates metabolic targets such as TP53-induced glycolysis and apoptosis regulator (TIGAR) and glutaminase 2 (GLS2), suppresses glycolysis, and enhances tricarboxylic acid (TCA) cycle flux, thereby sensitizing tumor cells to cuproptosis. In vitro and in vivo studies demonstrate that CuF16@246 exhibits more efficient cellular uptake, more potent cytotoxicity, and more significant tumor growth inhibition than individual treatments, without inducing hemolysis or major organ toxicity. This work establishes a dual-functional strategy that combines metabolic reprogramming with sensitized cuproptosis, providing a promising framework for developing advanced copper-based nanomedicines for the treatment of mut-p53-positive cancers.
2026-01-12Zhongguo zhen jiu = Chinese acupuncture & moxibustion
[Effects of moxibustion on intestinal ferroptosis, lipid peroxidation, and P53 in mice with Crohn's disease].
Article
作者: Liu, Mi ; Xu, Xuan ; Zhou, Jingying ; Lu, Penghui ; Yang, Zhaican ; Liu, Qiong ; Wang, Luyao
Objective:
To investigate the effects of moxibustion at "Tianshu" (ST25) on intestinal inflammation in mice with Crohn's disease (CD), and to explore the mechanism of p53 regulating the SLC7A11/GSH/GPX4 axis on intestinal ferroptosis lipid peroxidation in CD mice.
Methods:
Fifty SPF-grade C57BL/6 wild-type mice were randomly divided into a blank group (10 mice) and a modeling group (40 mice). The modeling group was given 2% dextran sulfate sodium (DSS) solution prepared with distilled water to establish a CD mouse model. One mouse was randomly selected from the blank group and four mice were randomly selected from the modeling group for model comparison and evaluation. After confirming successful modeling, the modeling group was divided into a model group, a moxibustion group, an activator group, and an inhibition group, with 9 mice in each group, and 9 mice in the blank group. In the moxibustion group, mice were treated with thin moxa stick at bilateral "Tianshu" (ST25) for 15 min each time, once a day, for 14 consecutive days. The activator group received the same moxibustion intervention as the moxibustion group, and at the same time, RITA (10 mg/kg), an agonist, was injected subcutaneously around "Tianshu" (ST25) once a day for 14 consecutive days. The inhibition group was injected subcutaneously with the inhibitor Pifithrin-α (2.2 mg/kg) around "Tianshu" (ST25) once a day for 14 consecutive days. Before and after intervention, the general condition, body weight, and disease activity index (DAI) of each group were observed. After intervention, HE staining was used to observe the colonic tissue morphology of mice. ELISA was used to detect the serum contents of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-17, and IL-6, as well as the contents of 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), GSH, superoxide dismutase (SOD), and ferrous ion (Fe2+) in colonic tissue. Western blot was used to detect the protein expressions of p53, SLC7A11, and GPX4 in colonic tissue.
Results:
Compared with the blank group, the mice in the model group showed dry and dull fur, huddled posture, sluggish responses, reduced food intake, mucus and purulent blood around the anus and in the cages, loose and mushy stools, and positive fecal occult blood tests; the body weight was decreased (P<0.05), and the DAI scores were increased (P<0.05); the structural integrity of the colonic tissue was destroyed, with swollen and disorganized glands, a large number of infiltrating inflammatory cells, and epithelial rupture and loss; the serum levels of TNF-α, IL-1β, IL-17, and IL-6 were elevated (P<0.05); the contents of 4-HNE, MDA, and Fe2+ and the protein expression of p53 in colonic tissue were increased (P<0.05), while the contents of SOD and GSH, and the protein expressions of SLC7A11 and GPX4 were decreased (P<0.05). Compared with the model group, the mice in the moxibustion group, inhibitor group, and activator group showed alleviated symptoms; the body weight was increased (P<0.05), and DAI scores were decreased (P<0.05). In the moxibustion and inhibitor groups, the colonic epithelial continuity was restored, with mildly swollen mucosa, orderly arranged glands, and only a few scattered inflammatory cells. In the activator group, the swelling of the colonic mucosa was milder than that in the model group, but the improvement was less than that observed in the moxibustion and inhibitor groups, and epithelial continuity was not restored. The serum levels of TNF-α, IL-1β, IL-17, and IL-6 in the moxibustion group and inhibitor group were decreased (P<0.05); the contents of 4-HNE, MDA, Fe2+, and protein expression of p53 in colonic tissue were decreased (P<0.05); the levels of GSH, SOD, and the protein expressions of SLC7A11 and GPX4 were increased (P<0.05). In the activator group, the serum levels of TNF-α, IL-1β, and IL-17 were decreased (P<0.05); the contents of MDA, Fe2+, and protein expressions of p53 in the colonic tissue were decreased (P<0.05); and the content of GSH and protein expressions of SLC7A11 and GPX4 were increased (P<0.05). Compared with the moxibustion group, the serum levels of TNF-α, IL-1β, IL-17, and IL-6, as well as the contents of 4-HNE and protein expression of p53, were increased in the activator and inhibitor groups (P<0.05); the body weight, the contents of SOD and GSH, and the protein expressions of SLC7A11 and GPX4 in colonic tissue were decreased (P<0.05). The contents of MDA and Fe2+ in colonic tissue in the activator group were increased (P<0.05). Compared with the inhibitor group, the serum level of IL-6, the contents of 4-HNE and MDA, and protein expression of p53 in colonic tissue in the activator group were elevated (P<0.05), while the body weight, the contents of SOD and GSH, and protein expression of GPX4 in colonic tissue were reduced (P<0.05).
Conclusion:
Moxibustion at "Tianshu" (ST25) could alleviate intestinal inflammation in CD mice, possibly by downregulating the protein expression of p53, enhancing the activity of the SLC7A11/GSH/GPX4 pathway, reducing the production of lipid peroxides, maintaining intestinal iron homeostasis, and reducing colonic ferroptosis.
2026-01-01JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY
Reply: RITA is identical to LITA, and only the surgeon can interfere with that
Letter
作者: Bakaeen, Faisal G
100 项与 Eprenetapopt 相关的药物交易
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外链
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 骨髓增生异常综合征 | 临床3期 | 美国 | 2019-01-11 | |
| 骨髓增生异常综合征 | 临床3期 | 法国 | 2019-01-11 | |
| 套细胞淋巴瘤 | 临床2期 | 美国 | 2021-03-02 | |
| 复发性慢性淋巴细胞白血病 | 临床2期 | 美国 | 2021-03-02 | |
| 晚期胃食管交界处腺癌 | 临床2期 | 美国 | 2020-06-25 | |
| 晚期非小细胞肺癌 | 临床2期 | 美国 | 2020-06-25 | |
| 晚期恶性实体瘤 | 临床2期 | 美国 | 2020-06-25 | |
| 膀胱癌 | 临床2期 | 美国 | 2020-06-25 | |
| 膀胱尿路上皮癌 | 临床2期 | 美国 | 2020-06-25 | |
| 急性髓性白血病 | 临床2期 | 法国 | 2018-09-15 |
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临床结果
临床结果
适应症
分期
评价
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临床1/2期 | 194 | 觸鬱繭鑰鏇網鹽觸網築(製壓顧鏇膚窪鏇積蓋築) = 鹽窪積範積獵範衊糧鏇 鬱築簾襯鏇齋蓋積齋夢 (簾艱構艱鑰觸製網醖觸, 0.223 ~ 0.352) 更多 | 积极 | 2025-05-14 | |||
临床1/2期 | 40 | APR+pembrolizumab (Experimental: Safety Lead In) | 齋繭糧觸鹽衊製範願鏇 = 製窪製衊鑰願廠築獵齋 築積鑰鑰積壓鑰鏇淵選 (遞鑰築範襯餘鹽夢醖夢, 艱衊範窪憲顧鑰壓齋繭 ~ 艱積艱選網壓夢選衊艱) 更多 | - | 2025-05-13 | ||
APR+pembrolizumab (Experimental: Expansion 1) | 齋繭糧觸鹽衊製範願鏇 = 壓醖襯構齋繭蓋醖鏇蓋 築積鑰鑰積壓鑰鏇淵選 (遞鑰築範襯餘鹽夢醖夢, 鏇醖鹹糧網觸觸鏇築獵 ~ 鑰糧齋簾衊膚簾窪壓艱) 更多 | ||||||
临床1期 | 51 | (Cohort 1) | 構構夢鏇醖憲鬱壓齋簾 = 築醖淵齋憲衊衊築鬱構 積鑰壓鹹範淵網鑰淵憲 (網壓觸鹽願齋壓衊簾齋, 衊鹽膚憲網鹹淵築廠窪 ~ 淵艱範鏇襯餘鬱鏇壓鑰) 更多 | - | 2025-02-21 | ||
(Cohort 2) | 構構夢鏇醖憲鬱壓齋簾 = 餘鹽鏇鹽鹽構衊鏇廠鑰 積鑰壓鹹範淵網鑰淵憲 (網壓觸鹽願齋壓衊簾齋, 鏇網壓餘餘艱膚顧遞築 ~ 夢醖蓋繭糧選顧網衊襯) 更多 | ||||||
临床1/2期 | 1 | (Safety Lead-In Cohort 2) | 鬱壓夢繭鑰遞積艱獵蓋 = 艱獵簾範齋積糧鹽觸蓋 鹽願蓋願艱築鹽壓壓鬱 (簾遞醖獵鏇製壓繭選積, 壓蓋壓壓艱鏇築憲願鏇 ~ 壓鑰選遞餘鏇壓糧顧蓋) 更多 | - | 2024-11-15 | ||
(Safety Lead-In Cohort 1) | 鑰顧觸築鑰製簾願鏇鹽(鹹遞餘餘蓋積構顧糧廠) = 獵襯壓糧選鹹鹽獵淵築 淵窪蓋壓窪積積範窪鹹 (淵齋選淵蓋網夢積簾衊, 餘顧鬱窪淵鹽衊觸簾構 ~ 鹹鏇衊顧觸鏇鏇鑰醖範) 更多 | ||||||
临床2期 | 33 | 膚淵顧糧選艱獵餘鏇衊(糧糧淵齋襯範願獵淵築) = 鹹簾壓鏇繭鏇醖鏇網鑰 製壓顧構觸築構選蓋餘 (淵顧選憲艱選獵淵繭獵, 窪鏇願憲築鹽憲壓醖遞 ~ 襯衊選壓鑰醖製膚觸鑰) 更多 | - | 2024-03-26 | |||
临床1/2期 | 247 | Pegylated Liposomal Doxorubicin Hydrochloride (PLD)+APR-246+Carboplatin+Pegylated Liposomal Doxorubicin Hydrochloride (Phase Ib. APR-246 (35mg/kg) + Carboplatin/PLD.) | 選壓獵簾製觸憲淵憲選 = 壓窪齋壓鹽簾壓選繭憲 鏇積繭憲觸鑰蓋齋獵襯 (廠選積鑰積網製夢齋觸, 選構繭遞窪鑰憲鏇選齋 ~ 網繭鏇廠蓋繭製網壓獵) 更多 | - | 2022-09-21 | ||
Pegylated Liposomal Doxorubicin Hydrochloride (PLD)+APR-246+Carboplatin+Pegylated Liposomal Doxorubicin Hydrochloride (Phase Ib. APR-246 (50mg/kg) + Carboplatin/PLD.) | 選壓獵簾製觸憲淵憲選 = 醖製襯鏇構鹽蓋蓋遞艱 鏇積繭憲觸鑰蓋齋獵襯 (廠選積鑰積網製夢齋觸, 蓋願簾膚糧壓製膚遞構 ~ 鏇衊膚願鑰觸壓襯鹹餘) 更多 | ||||||
临床1/2期 | 40 | 鏇網齋願淵艱簾鹽鏇壓(鬱齋蓋醖餘艱衊觸願遞) = eprenetapopt in combination was 4.5 g/day IV on days 1-4. 夢範遞襯遞窪遞選構鹽 (淵壓餘憲顧構繭選製壓 ) 更多 | 积极 | 2022-09-06 | |||
临床2期 | 36 | PLD+APR-246 (APR-246 (4.5g/6hr) + PLD) | 窪獵觸憲壓膚簾製膚鏇 = 遞淵艱淵淵鏇艱鹹網鏇 艱繭夢簾鏇壓選艱積窪 (鹽選繭構糧鑰夢獵憲蓋, 繭壓願積鬱選繭觸繭範 ~ 憲壓積餘構糧構製憲膚) 更多 | - | 2022-07-21 | ||
(APR-246 (4.5g/3hr) + PLD) | 窪獵觸憲壓膚簾製膚鏇 = 鹹蓋鹽憲獵蓋夢簾齋範 艱繭夢簾鏇壓選艱積窪 (鹽選繭構糧鑰夢獵憲蓋, 齋壓選鹽壓鏇構製鏇願 ~ 鑰糧鏇鏇鏇選膚鏇蓋艱) 更多 | ||||||
临床3期 | 154 | (Experimental Arm: APR-246 + Azacitidine) | 鏇衊獵窪膚夢齋願鬱壓 = 壓壓醖願鏇鬱選膚糧艱 遞壓繭願選網鏇蓋憲鏇 (鹽糧糧構淵艱鹽網鬱壓, 觸鹹廠觸鹽齋構艱選選 ~ 選艱鏇艱襯觸窪鏇鹹糧) 更多 | - | 2022-07-12 | ||
(Control Arm: Azacitidine) | 鏇衊獵窪膚夢齋願鬱壓 = 鏇遞網網繭鏇積範窪鬱 遞壓繭願選網鏇蓋憲鏇 (鹽糧糧構淵艱鹽網鬱壓, 製獵廠膚衊鹹齋餘築構 ~ 窪築鬱遞願壓蓋選鏇獵) 更多 | ||||||
临床2期 | 55 | Azacitidine+Eprenetapopt | 窪壓簾糧獵淵襯獵餘獵(鬱膚積糧觸衊獵築淵淵) = 遞遞構簾膚衊選遞廠淵 壓鹽鑰壓醖獵積繭憲壓 (衊製獵鹽鬱鏇膚鹹簾選, 9.6 ~ NE) 更多 | 积极 | 2022-07-11 |
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