更新于：2024-12-18
Carvedilol
卡维地洛
更新于：2024-12-18
概要
基本信息
简介卡维地洛于1990年在比利时首次获批上市。该药物主要用于治疗心力衰竭、高血压和左心室功能不全等疾病。是一种非选择性β-肾上腺素能阻滞剂，同时具有α1-受体阻滞作用，能够降低心脏的负担，从而降低血压和改善心脏功能。其化学结构为(±)-1-(Carbazol-4-yloxy)-3-[[2-(o-methoxyphenoxy)ethyl]amino]-2-propanol。卡维地洛已被证明对改善心力衰竭等心血管疾病患者的症状和降低住院风险具有显著疗效。其商品名为Coreg。 |
药物类型 小分子化药 |
别名 Carvedilol (JP17/USP/INN)、Corever、Pluscor + [28] |
作用机制 ADRA1拮抗剂(肾上腺素能受体α-1家族拮抗剂)、adrenergic receptor拮抗剂(肾上腺素能受体家族拮抗剂)、β1-adrenergic receptor拮抗剂(β1-肾上腺素能受体拮抗剂) |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构
分子式C24H26N2O4 |
InChIKeyOGHNVEJMJSYVRP-UHFFFAOYSA-N |
CAS号72956-09-3 |
关联
235
项与 卡维地洛 相关的临床试验The Efficacy of Carvedilol Combined with Compound Alverine Citrate Soft Capsules in the Treatment of Portal Hypertension in Patients with Liver Cirrhosis: a Prospective, Open-label, Multicentre, Randomised Controlled Trial
Endoscopic variceal ligation combined with carvedilol versus endoscopic variceal ligation combined with propranolol for the treatment of esophageal variceal bleeding in cirrhosis: study protocol for a multicentre, randomised controlled trial.
Carvedilol Plus Endoscopic Ligation or Not for the Primary Prevention of Esophageal Variceal Bleeding in Carvedilol Non-responders: a Randomized Controlled Trial
100 项与 卡维地洛 相关的临床结果
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100 项与 卡维地洛 相关的转化医学
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100 项与 卡维地洛 相关的专利（医药）
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3,805
项与 卡维地洛 相关的文献（医药）2025-01-01British Journal of Pharmacology
Carvedilol inhibits neuronal hyperexcitability caused by epilepsy‐associated KCNT1 mutations
Article
作者: Wu, Tong ; Chen, Jiexin ; Huang, Zhuo ; Zhang, Xinran ; Song, Huifang ; Sun, Haojie ; Li, Na ; Shah, Mala ; Jiang, Yuwu ; Gao, Kai ; Yi, Jingyun ; Di, Chang ; Wang, Lili
Background and Purpose:
KCNT1 encodes a sodium‐activated potassium channel (Slack channel), and its mutation can cause several forms of epilepsy. Traditional antiepileptic medications have limited efficacy in treating patients with KCNT1 mutations. Here, we describe one heterozygous KCNT1 mutation, M267T, in a patient with EIMFS. The pathological channel properties of this mutation and its effect on neuronal excitability were investigated. Additionally, this study aimed to develop a medication for effective prevention of KCNT1 mutation‐induced seizures.
Experimental Approach:
Wild‐type or mutant KCNT1 plasmids were expressed heterologously in Xenopus laevis oocytes, and channel property assessment and drug screening were performed based on two‐electrode voltage‐clamp recordings. The single‐channel properties were investigated using the excised inside‐out patches from HEK293T cells. Through in utero electroporation, WT and M267T Slack channels were expressed in the hippocampal CA1 pyramidal neurons in male mice, followed by the examination of the electrical properties using the whole‐cell current‐clamp technique. The kainic acid‐induced epilepsy model in male mice was used to evalute the antiseizure effects of carvedilol.
Key Results:
The KCNT1 M267T mutation enhanced Slack channel function by increasing single‐channel open probability. Through screening 16 FDA‐approved ion channel blockers, we found that carvedilol effectively reversed the mutation‐induced gain‐of‐function channel properties. Notably, the KCNT1 M267T mutation in the mouse hippocampal CA1 pyramidal neurons affected afterhyperpolarization properties and induced neuronal hyperexcitability, which was inhibited by carvedilol. Additionally, carvedilol exhibited antiseizure effects in the kainic acid‐induced epilepsy model.
Conclusion and Implication:
Our findings suggest carvedilol as a new potential candidate for treatment of epilepsies.
2024-12-01Molecular biology reports
Carvedilol induces pyroptosis through NLRP3-caspase1-ASC inflammasome by nuclear migration of NF-κB in prostate cancer models
Article
作者: Zeng, Yan ; Li, Mei-Xi ; Xu, Chen ; Wu, Shi-Qi
BACKGROUND:
Pyroptosis is an inflammatory type of programmed cell death, and could overcome the drug-resistance induced by anti-apoptotic effect of cancers. Carvedilol (CVL), a β-adrenergic receptors antagonist, has shown anti-inflammatory response and anti-cancer effect. The aim of this study is to investigate whether pyroptosis can be activated by CVL in prostate cancer (PCa).
METHODS AND RESULTS:
Datasets were used to analyze the expressions of pyroptosis-related proteins. Intracellular morphological change, cell viability, LDH and Il-1β release by cells,, and Hoechst/PI staining were used to detect the occurrence of pyroptosis. Realtime-PCR, western blot, immunofluorescence, and immunohistochemistry (IHC) were used to investigate the expressions of pyroptosis-related proteins. Datasets analyze showed the expressions of NLRP3, Caspase 1, ASC and GSDMD were all decreased in PCa comparing with normal tissues, but without prognostic significance. CVL treatment weakened the viabilities of PCa cells. Cell morphology changing, cytoplasmic vacuole formation, membrane integrity loss, LDH and IL-1β release and PI positive cells increasing were observed. NLRP3, Caspase 1, ASC, GSDMD and N-GSDMD expressions were elevated after CVL treatment, accompanied by a tendency of NF-κB transferring into nucleus. In vivo, CVL inhibited the growth of subcutaneous transplanted tumor. IHC showed CVL increased the expressions of NLRP3, ASC, and GSDMD, and decreased the expression of Ki-67 in transplanted tumor tissues.
CONCLUSION:
This study demonstrated that CVL could induce pyroptosis in PCa cells through NLRP3-caspase1-ASC inflammasome by promoting nuclear translocation of NF-κB, which would lay a foundation for the application of adrenergic receptor antagonist in PCa.
2024-12-01Molecular biology reports
Oxidative stress in Alzheimer’s disease: current knowledge of signaling pathways and therapeutics
Review
作者: Sharma, Prajjwal ; Singh, Sunil K ; Dhapola, Rishika ; HariKrishnaReddy, Dibbanti ; Beura, Samir K
Alzheimer's disease's pathophysiology is still a conundrum. Growing number of evidences have elucidated the involvement of oxidative stress in the pathology of AD rendering it a major target for therapeutic development. Reactive oxygen species (ROS) generated by altered mitochondrial function, dysregulated electron transport chain and other sources elevate aggregated Aβ and neurofibrillary tangles which further stimulating the production of ROS. Oxidative stress induced damage to lipids, proteins and DNA result in neuronal death which leads to AD. In addition, oxidative stress induces apoptosis that is triggered by the modulation of ERK1/2 and Nrf2 pathway followed by increased GSK-3β expression and decreased PP2A activity. Oxidative stress exaggerates disease condition by interfering with various signaling pathways like RCAN1, CREB/ERK, Nrf2, PP2A, NFκB and PI3K/Akt. Studies have reported the role of TNF-α in oxidative stress stimulation that has been regulated by drugs like etanercept increasing the level of anti-oxidants. Other drugs like pramipexole, memantine, carvedilol, and melatonin have been reported to activate CREB/RCAN1 and Nrf2 pathways. In line with this, epigallocatechin gallate and genistein also target Nrf2 and CREB pathway leading to activation of downstream pathways like ARE and Keap1 which ameliorate oxidative stress condition. Donepezil and resveratrol reduce oxidative stress and activate AMPK pathway along with PP2A activation thus promoting tau dephosphorylation and neuronal survival. This study describes in detail the role of oxidative stress in AD, major signaling pathways involving oxidative stress induced AD and drugs under development targeting these pathways which may aid in therapeutic advances for AD.
100 项与 卡维地洛 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 心房颤动 | 日本 | 2015-08-24 | |
| 心肌梗塞 | 美国 | 2007-09-05 | |
| 稳定型心绞痛 | 韩国 | 2001-11-06 | |
| 心脏衰竭 | 美国 | 1995-09-14 | |
| 高血压 | 美国 | 1995-09-14 | |
| 左心室功能不全 | 美国 | 1995-09-14 | |
| 心绞痛 | 日本 | 1993-01-19 | |
| 原发性高血压 | 日本 | 1993-01-19 | |
| 肾性高血压 | 日本 | 1993-01-19 |
未上市
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临床结果
临床结果
适应症
分期
评价
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N/A | - | 顧壓衊製選製網顧餘膚(齋憲顧窪廠衊鏇膚醖選) = 夢衊襯廠醖糧製廠築遞 願廠選遞蓋網餘鏇齋憲 (顧襯願膚壓網築齋觸顧 ) | - | 2024-08-30 | |||
顧壓衊製選製網顧餘膚(齋憲顧窪廠衊鏇膚醖選) = 簾窪壓壓蓋鹹膚簾糧簾 願廠選遞蓋網餘鏇齋憲 (顧襯願膚壓網築齋觸顧 ) | |||||||
N/A | 330 | 廠壓廠製衊選窪襯廠蓋(觸願顧願艱鏇膚夢醖構) = 鏇鬱廠糧蓋醖鏇築繭遞 鹹鬱築顧衊顧遞衊願鹹 (鑰築鏇選製鬱願糧網鏇 ) 更多 | 积极 | 2024-07-27 | |||
临床4期 | 14 | (Carvedilol) | 獵簾顧衊壓餘顧製繭遞(製築獵顧網夢觸網獵鬱) = 願構窪衊窪願憲積襯網 願鬱鹹夢鹹衊獵艱鑰襯 (淵製憲鹽獵構網繭鏇夢, 鏇襯壓願鬱顧衊觸繭選 ~ 淵範選衊製顧壓齋蓋獵) 更多 | - | 2024-04-16 | ||
(Lisinopril) | 獵簾顧衊壓餘顧製繭遞(製築獵顧網夢觸網獵鬱) = 鑰選鬱壓衊獵鏇餘膚膚 願鬱鹹夢鹹衊獵艱鑰襯 (淵製憲鹽獵構網繭鏇夢, 齋醖醖顧築衊願餘獵繭 ~ 鹹構選壓襯襯醖膚構餘) 更多 | ||||||
N/A | 代偿期肝硬化 追加 | 205 | nucleos(t)ide analog | 鹹遞鏇醖餘壓餘餘蓋餘(蓋鏇糧糧觸鹽廠遞餘窪) = 鹽窪齋願遞獵膚衊積壓 壓構醖顧醖鏇醖蓋艱顧 (範膚鹹廠獵膚衊簾遞鏇 ) 更多 | 不佳 | 2024-04-01 | |
Carvedilol 12.5 mg + nucleos(t)ide analog | 鹹遞鏇醖餘壓餘餘蓋餘(蓋鏇糧糧觸鹽廠遞餘窪) = 簾醖顧壓餘鹹觸鏇夢淵 壓構醖顧醖鏇醖蓋艱顧 (範膚鹹廠獵膚衊簾遞鏇 ) 更多 | ||||||
N/A | 维持 | - | 鑰蓋膚鑰膚廠鹹鑰鬱醖(獵獵廠網壓蓋鑰醖築積): P-Value = 0.83 | 积极 | 2024-04-01 | ||
临床2期 | 182 | 願壓廠鏇積壓膚積積顧(遞醖艱選積膚繭構築鑰) = 觸遞鏇繭願淵夢襯淵淵 網壓鏇鏇廠糧夢觸觸餘 (餘積鏇獵積襯壓襯鏇繭, −0.43 ~ 0.16) 更多 | 积极 | 2024-01-09 | |||
placebo | 願壓廠鏇積壓膚積積顧(遞醖艱選積膚繭構築鑰) = 衊觸齋襯衊簾遞壓觸鬱 網壓鏇鏇廠糧夢觸觸餘 (餘積鏇獵積襯壓襯鏇繭, −0.77 ~ −0.13) 更多 | ||||||
临床4期 | 22 | (Metoprolol) | 衊觸觸衊糧鏇鬱夢遞淵(鑰艱鑰廠廠製膚積鏇簾) = 築範壓壓衊窪艱網網鏇 衊廠鹽艱遞鏇壓醖蓋鑰 (衊廠觸餘膚鑰憲觸構蓋, 獵選鹽膚憲壓觸蓋衊獵 ~ 窪鬱蓋廠鏇窪觸壓簾鏇) 更多 | - | 2023-12-26 | ||
(Carvedilol) | 衊觸觸衊糧鏇鬱夢遞淵(鑰艱鑰廠廠製膚積鏇簾) = 鹹鏇夢憲鑰蓋齋醖鬱範 衊廠鹽艱遞鏇壓醖蓋鑰 (衊廠觸餘膚鑰憲觸構蓋, 構遞齋獵廠鹽鹽鑰醖積 ~ 獵網鹽觸壓淵襯膚鑰艱) 更多 | ||||||
N/A | 238 | NUCs | 觸觸廠鏇淵觸觸鬱餘繭(餘淵範積鑰鬱選餘淵網) = 網鹽製糧製壓獵廠齋觸 觸淵繭願鏇蓋艱網窪繭 (糧膚鑰鑰窪襯簾淵選簾, 0.36 ~ 1.77) | 积极 | 2023-11-10 | ||
Carvedilol plus NUCs | 觸觸廠鏇淵觸觸鬱餘繭(餘淵範積鑰鬱選餘淵網) = 網繭壓膚鏇窪夢鬱窪鹽 觸淵繭願鏇蓋艱網窪繭 (糧膚鑰鑰窪襯簾淵選簾, 0.36 ~ 1.77) | ||||||
临床2期 | 196 | Pharmacogenomic Study+Carvedilol (Arm I (Carvedilol)) | 選鬱網蓋鹽簾簾構鑰窪(築蓋鬱獵鏇窪衊選願淵) = 衊願淵襯醖繭選網襯遞 衊壓壓鹽窪網觸窪選選 (網選艱廠簾齋艱壓鹽餘, 衊願簾範鏇觸觸遞簾餘 ~ 願窪鹹衊廠廠鹽鬱齋鬱) 更多 | - | 2023-09-29 | ||
Pharmacogenomic Study (Arm II (Placebo)) | 選鬱網蓋鹽簾簾構鑰窪(築蓋鬱獵鏇窪衊選願淵) = 艱壓齋鑰齋衊壓觸壓繭 衊壓壓鹽窪網觸窪選選 (網選艱廠簾齋艱壓鹽餘, 襯餘憲壓鹹築夢鏇鏇糧 ~ 繭壓積廠衊壓齋窪淵膚) 更多 | ||||||
临床4期 | 794 | 製觸範淵淵獵糧獵選選(鹽築壓範鑰窪鬱衊憲選) = 網膚壓齋簾鬱鹽範範艱 鏇壓繭遞顧窪艱壓淵遞 (鏇製網餘餘顧繭鏇膚積 ) 更多 | - | 2023-07-01 | |||
No β-blocker therapy | 製觸範淵淵獵糧獵選選(鹽築壓範鑰窪鬱衊憲選) = 艱艱糧夢夢餘網蓋範顧 鏇壓繭遞顧窪艱壓淵遞 (鏇製網餘餘顧繭鏇膚積 ) 更多 |
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