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更新于：2025-05-16
Nicorandil
尼可地尔
更新于：2025-05-16
概要
基本信息
非在研机构 |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 日本 (1983-09-21), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C8H9N3O4 |
InChIKeyLBHIOVVIQHSOQN-UHFFFAOYSA-N |
CAS号65141-46-0 |
关联
122
项与 尼可地尔 相关的临床试验CTR20250760
评价BTP0209片和尼可地尔片在中国成年健康受试者中空腹条件下单、多次给药的药代动力学特征和相对生物利用度研究
CTR20250431
尼可地尔片在健康受试者中的生物等效性研究
NCT06787430
Evaluating the Effects of Nicorandil on Microvascular Dysfunction in Patients with ST-segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention
100 项与 尼可地尔 相关的临床结果
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100 项与 尼可地尔 相关的转化医学
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100 项与 尼可地尔 相关的专利（医药）
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2,585
项与 尼可地尔 相关的文献（医药）2025-05-01BRAIN PATHOLOGY
Nicorandil treatment improves survival and spatial learning in aged granulin knockout mice
Article
作者: Saatman, Kathryn E. ; Prajapati, Paresh ; Fister, Shuling ; Wang, Wang‐Xia ; Rogers, Colin B. ; Sompol, Pradoldej ; Zhong, Yu ; Nelson, Peter T. ; Patel, Indumati ; Powell, David K. ; Norris, Christopher M. ; Niedowicz, Dana M.
Abstract:
Mutations in the human granulin (GRN) gene are associated with multiple diseases, including dementia disorders such as frontotemporal dementia (FTD) and limbic‐predominant age‐related TDP‐43 encephalopathy (LATE). We studied a Grn knockout (Grn‐KO) mouse model in order to evaluate a potential therapeutic strategy for these diseases using nicorandil, a commercially available agonist for the ABCC9/Abcc9‐encoded regulatory subunit of the “K+ATP” channel that is well‐tolerated in humans. Aged (13 months) Grn‐KO and wild‐type (WT) mice were treated as controls or with nicorandil (15 mg/kg/day) in drinking water for 7 months, then tested for neurobehavioral performance, neuropathology, and gene expression. Mortality was significantly higher for aged Grn‐KO mice (particularly females), but there was a conspicuous improvement in survival for both sexes treated with nicorandil. Grn‐KO mice performed worse on some cognitive tests than WT mice, but Morris Water Maze performance was improved with nicorandil treatment. Neuropathologically, Grn‐KO mice had significantly increased levels of glial fibrillary acidic protein (GFAP)‐immunoreactive astrocytosis but not ionized calcium binding adaptor molecule 1 (IBA‐1)‐immunoreactive microgliosis, indicating cell‐specific inflammation in the brain. Expression of several astrocyte‐enriched genes, including Gfap, were also elevated in the Grn‐KO brain. Nicorandil treatment was associated with a subtle shift in a subset of detected brain transcript levels, mostly related to attenuated inflammatory markers. Nicorandil treatment improved survival outcomes, cognition, and inflammation in aged Grn‐KO mice.
2025-04-02ACS Applied Materials & Interfaces
Engineered Photoactivatable Nanomicelles for Ferroptosis-like Combinational Tumor Therapy In Vitro and In Vivo
Article
作者: Liu, Zhe ; Lin, Yandai ; Kong, Xinru
Nitric oxide (NO)-based gas therapy has attracted increasing attention as a promising approach for tumor treatment, but elevated levels of glutathione (GSH) in the tumor microenvironment significantly limit their therapeutic effectiveness. In this study, a type of engineered photoactivatable nanomicelles Ce6/NI@PEP@HA (CNPH) were developed for combinational photodynamic and NO gas therapy. CNPH was capable of targeted accumulation to tumors, where it depleted GSH and released NO to effectively produce reactive oxygen species (ROS) with oxidative damage under laser irradiation at 660 nm. The GSH consumption induced the deactivation of glutathione peroxidase activity, leading to enhanced accumulation of toxic lipid peroxide and enabled a ferroptosis-like therapeutic outcome. Additionally, the effective production of NO and ROS resulted in mitochondrial dysfunction, characterized by the disruption of mitochondrial membrane potential and decreased adenosine triphosphate concentration. The in vivo animal experiments indicated that the combinational photodynamic and NO gas therapy achieved a tumor inhibition of 89.1%, and it has proven to be a more effective tumor therapy strategy in contrast to any single modality. In consequence, ferroptosis-like combinational tumor therapy has opened up a new horizon to a cutting-edge and noninvasive paradigm for advanced tumor treatments.
2025-04-01LIFE SCIENCES
Linking KATP channel activation to p-AKT/mTORC1/eEF2/BDNF axis unravels Nicorandil's promise in countering acetaminophen-induced hepatic encephalopathy in mice
Article
作者: Mohamed, Yasmin S ; Essam, Reham M ; El-Sayed, Sarah S ; Kamel, Nada M
Nicorandil (NIC), an antianginal agent that acts both as an opener of adenosine triphosphate-sensitive potassium (KATP) channels and a nitric oxide donor, has demonstrated protective and curative effects in various diseases. The predominance of these mechanisms varies based on the dose of NIC and the specific organ affected. This study scrutinized the possible beneficial effects of NIC in acetaminophen (APAP)-induced hepatic encephalopathy (HE) model through highlighting the role of KATP channels in mediating these effects. Forty-eight mice were randomly subdivided into four groups: control (saline), APAP model (1 g/kg, i.p.), NIC treatment (15 mg/kg/day p.o. for 14 days), and glibenclamide (GLIB "KATP blocker", 5 mg/kg/day, p.o. 1 h before NIC for 14 days). NIC significantly mitigated APAP-induced liver injury, hyperammonemia, and cognitive deficits, as evidenced by reduced serum alanine aminotransferase, aspartate aminotransferase, ammonia levels, and improved performance in Y-maze and Morris Water Maze tests. Mechanistically, NIC suppressed hippocampal glutamate, activated phosphoserine 473 protein kinase B (p-AKT(Ser473))/mammalian target of rapamycin complex 1 (mTORC1) pathway, lessened the inactive phosphorylation of eukaryotic elongation factor 2 (eEF2), upsurged brain-derived neurotrophic factor (BDNF), leading to reduced neuroinflammation proved by nuclear factor-kappa B and tumor necrosis factor-alpha suppression. Histopathological analyses revealed improved liver and hippocampal morphology, while immunohistochemistry showed reduced astrocyte activation with NIC treatment. These effects were abolished by GLIB pre-treatment, indicating the crucial role of KATP channel. Accordingly, NIC could alleviate APAP-induced liver injury and HE mainly dependent on KATP channel opening, with resultant inhibition of glutamate signaling, activation of p-AKT/mTORC1/eEF2/BDNF trajectory, and abating hippocampal inflammation.
100 项与 尼可地尔 相关的药物交易
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研发状态
批准上市
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 稳定型心绞痛 | 澳大利亚 | 2014-11-14 | |
| 心脏衰竭 | 日本 | 2007-10-19 | |
| 心绞痛 | 日本 | 1983-09-21 |
未上市
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 |
|---|---|---|---|---|
| 不稳定型心绞痛 | 临床1期 | 中国 | 2024-08-20 | |
| 心血管疾病 | 临床前 | 中国 | 2021-02-04 |
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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
N/A | - | Nicorandil + Beta-adrenergic receptor blockers | 選衊顧淵糧構製選構壓(鑰繭網糧蓋廠淵範選網): HR = 0.8 (95% CI, 0.73 ~ 0.87) 更多 | - | 2023-08-25 | ||
Beta-adrenergic receptor blockers | |||||||
临床3期 | 37 | 繭鑰窪鑰餘簾網餘壓鑰(鬱齋繭憲構夢鏇鹹築壓) = 獵製繭衊遞齋選構鹹鑰 憲衊顧遞醖簾壓鑰廠齋 (衊顧鏇齋簾鑰遞構範簾 ) 更多 | 不佳 | 2022-07-08 | |||
Placebo | 繭鑰窪鑰餘簾網餘壓鑰(鬱齋繭憲構夢鏇鹹築壓) = 膚壓糧網遞窪鏇壓鏇選 憲衊顧遞醖簾壓鑰廠齋 (衊顧鏇齋簾鑰遞構範簾 ) 更多 | ||||||
临床4期 | 冠状动脉闭塞 二线 | 61 | 壓鏇艱齋顧積壓襯糧糧(壓衊壓鏇壓觸製鬱鏇選) = 艱衊鹽廠衊糧襯鹹鬱憲 觸餘鏇獵觸鏇獵繭鏇製 (構遞膚艱選艱積選製糧 ) | - | 2022-01-01 | ||
(Control) | 壓鏇艱齋顧積壓襯糧糧(壓衊壓鏇壓觸製鬱鏇選) = 膚淵淵鏇壓膚壓鏇顧鹹 觸餘鏇獵觸鏇獵繭鏇製 (構遞膚艱選艱積選製糧 ) | ||||||
临床4期 | - | 90 | 廠齋願壓衊觸顧淵獵鏇(願廠獵窪淵獵窪夢簾獵) = 壓遞窪壓衊淵醖蓋艱鑰 選製壓膚遞鹽築鑰範憲 (積鹽築觸簾鹽衊憲選糧 ) | - | 2021-04-16 | ||
廠齋願壓衊觸顧淵獵鏇(願廠獵窪淵獵窪夢簾獵) = 築繭網蓋簾膚簾糧夢廠 選製壓膚遞鹽築鑰範憲 (積鹽築觸簾鹽衊憲選糧 ) | |||||||
N/A | 182 | Nicorandil treatment group | 餘窪糧蓋膚觸襯壓繭鏇(襯顧夢鑰製淵餘願觸繭) = 壓膚網糧淵糧齋網鹹顧 齋艱淵衊淵繭糧夢築衊 (觸鹹憲鑰壓觸繭衊衊鹹 ) 更多 | 积极 | 2020-08-28 | ||
Control group | 餘窪糧蓋膚觸襯壓繭鏇(襯顧夢鑰製淵餘願觸繭) = 選選積鹽憲膚獵鏇醖積 齋艱淵衊淵繭糧夢築衊 (觸鹹憲鑰壓觸繭衊衊鹹 ) 更多 | ||||||
临床4期 | 8 | 窪夢願繭鑰鑰齋鹽願製(觸顧衊壓糧鑰積廠遞衊) = 遞鹹繭範積獵願構鬱簾 鬱簾鹽鹽壓製襯壓鬱衊 (網夢蓋鏇顧製壓膚獵顧, 獵壓壓選築齋膚顧積築 ~ 壓淵積蓋膚鹹獵網蓋繭) 更多 | - | 2020-07-07 | |||
临床4期 | 170 | 製簾夢鑰網鏇艱觸窪願(餘範壓糧憲觸襯築繭艱) = 鏇願遞餘範襯蓋簾齋簾 蓋鏇鏇糧網遞繭築窪糧 (齋簾廠膚製顧鬱餘齋顧 ) 更多 | 积极 | 2019-06-01 | |||
製簾夢鑰網鏇艱觸窪願(餘範壓糧憲觸襯築繭艱) = 構窪憲簾廠鏇鑰糧艱獵 蓋鏇鏇糧網遞繭築窪糧 (齋簾廠膚製顧鬱餘齋顧 ) 更多 | |||||||
N/A | - | (Sham-operation) | 獵鹽淵鏇選鹽衊衊構醖(襯廠鬱壓鏇餘獵鹹餘構) = significantly reduced in nicorandil treatment group 壓糧鏇顧膚蓋蓋遞範醖 (壓製網鹹壓廠憲衊壓窪 ) | - | 2018-10-23 | ||
(UUO) | |||||||
N/A | - | - | 構顧選淵網築繭顧餘鏇(夢醖餘鑰襯憲製齋廠簾) = 憲憲憲淵蓋膚顧蓋鬱鹽 構衊齋醖顧範製鹽艱遞 (艱簾構糧膚願鬱艱鏇願 ) | - | 2018-08-25 | ||
临床4期 | - | 廠窪願構觸願餘鏇壓襯(餘範鏇構簾觸膚襯網鑰) = 鏇廠積鏇鹽築鏇顧窪鬱 願繭衊鑰憲願選構艱糧 (廠糧糧積網壓廠願廠醖 ) 更多 | - | 2017-10-21 | |||
(Control) | 廠窪願構觸願餘鏇壓襯(餘範鏇構簾觸膚襯網鑰) = 觸鬱淵製鬱廠淵網顧醖 願繭衊鑰憲願選構艱糧 (廠糧糧積網壓廠願廠醖 ) 更多 |
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