更新于：2024-11-26
Entacapone
恩他卡朋
更新于：2024-11-26
概要
基本信息
原研机构 |
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 欧盟 (1998-09-16), |
最高研发阶段(中国)批准上市 |
特殊审评优先审评 (中国) |
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结构
分子式C14H15N3O5 |
InChIKeyJRURYQJSLYLRLN-BJMVGYQFSA-N |
CAS号130929-57-6 |
关联
33
项与 恩他卡朋 相关的临床试验恩他卡朋片人体生物等效性研究
恩他卡朋片（0.2g）在空腹及餐后条件下的人体生物等效性研究
恩他卡朋片在中国健康受试者中采用两制剂、四周期、两序列完全重复交叉的空腹、餐后生物等效性试验
100 项与 恩他卡朋 相关的临床结果
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100 项与 恩他卡朋 相关的转化医学
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100 项与 恩他卡朋 相关的专利（医药）
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686
项与 恩他卡朋 相关的文献（医药）2024-10-30ACS Applied Materials & Interfaces
Exploring Nanocarriers for Boosting Entacapone Bioavailability: A Journey through System Characterization and Assessment of Toxicity and Pharmacological and 2D Permeability Paybacks
Article
作者: Sarmento, Bruno ; Borges, Fernanda ; Machado, Cláudia Sofia ; Costa, Sofia ; Otero Espinar, Francisco J. ; Aguiar, Brandon ; Pinto, Miguel ; Fernandes, Carlos
Catechol-O-methyltransferase inhibitors (iCOMT), such as entacapone, have been successfully employed to treat tremor-related symptoms of Parkinson's disease. However, iCOMT has been associated with a short half-life and poor oral bioavailability. Nanobased drug delivery systems have often been used to overcome this type of setbacks. Therefore, entacapone was encapsulated in PEGylated poly(lactic-co-glycolic acid) (PLGA)-based nanoparticles (NPs) via a nanoprecipitation process, as well as in PEGylated nanostructured lipid carriers (NLCs) using a solvent emulsification/evaporation method. Both nanoformulations presented sub-200 nm populations, with zeta-potential (ZP) values close to -30 mV, and showed stability at different pHs, while maintaining their physicochemical properties mostly intact, presenting only a change in their superficial charge (ZP values), indicating their interaction. Both nanoformulations presented interaction with mucins, which anticipates good permeation and bioavailability for oral and topical administration. No cytotoxic effects were observed for lyophilized PLGA NPs encapsulating entacapone, in which 2-hydroxypropyl-ß-cyclodextrin (HPβCD) was used as a cryoprotectant at 3% concentration (HP-PLGA@Ent), in human hepatocellular carcinoma (HepG2), human neuroblastoma (SH-SY5Y), or human epithelial colorectal adenocarcinoma (Caco-2) cell lines. Conversely, NLCs encapsulating entacapone (W-NLCs@Ent) presented cytotoxic effects on the HepG2 cell line, likely due to intracellular lipid accumulation or storage. Both nanoformulations maintained a COMT inhibition effect in HepG2 cells, using 3-BTD as the COMT probe. An increase of entacapone permeability in both monolayer and coculture models (Caco-2 and Caco-2/HT29-MTX, respectively) was observed for the developed nanoformulations. Overall, this work shows that encapsulated entacapone in different nanocarriers could be a stimulating alternative to solve entacapone setbacks, since they improve its physicochemical properties and permeability while still maintaining the COMT inhibitory activity.
2024-09-13Science Advances
Modeling Lewy body disease with
SNCA
triplication iPSC-derived cortical organoids and identifying therapeutic drugs
Article
作者: Dickson, Dennis W. ; Wszolek, Zbigniew K. ; Ikezu, Tadafumi C. ; Koga, Shunsuke ; DeTure, Michael ; Zhao, Na ; Caulfield, Thomas ; O’Leary, Justin ; Bu, Guojun ; Lolo, Kiara ; Santhakumar, Hannah ; Zhu, Yiyang ; Beasley, Alexandra I. ; Li, Zonghua ; Ikezu, Tsuneya ; Li, Fuyao ; Carr, Jonathan ; Martens, Yuka A. ; Jin, Yunjung ; Davis, Mary D. ; You, Yang ; Lu, Wenyan ; Selvaraj, Manikandan ; Li, Yonghe ; Kanekiyo, Takahisa ; Ross, Owen A. ; McLean, Pamela J.
Aggregated α-synuclein (α-SYN) proteins, encoded by the
SNCA
gene, are hallmarks of Lewy body disease (LBD), affecting multiple brain regions. However, the specific mechanisms underlying α-SYN pathology in cortical neurons, crucial for LBD-associated dementia, remain unclear. Here, we recapitulated α-SYN pathologies in human induced pluripotent stem cells (iPSCs)–derived cortical organoids generated from patients with LBD with
SNCA
gene triplication. Single-cell RNA sequencing, combined with functional and molecular validation, identified synaptic and mitochondrial dysfunction in excitatory neurons exhibiting high expression of the
SNCA
gene, aligning with observations in the cortex of autopsy-confirmed LBD human brains. Furthermore, we screened 1280 Food and Drug Administration–approved drugs and identified four candidates (entacapone, tolcapone, phenazopyridine hydrochloride, and zalcitabine) that inhibited α-SYN seeding activity in real-time quaking-induced conversion assays with human brains, reduced α-SYN aggregation, and alleviated mitochondrial dysfunction in
SNCA
triplication organoids and excitatory neurons. Our findings establish human cortical LBD models and suggest potential therapeutic drugs targeting α-SYN aggregation for LBD.
2024-09-01Naunyn-Schmiedeberg's archives of pharmacology
2-Methoxyestradiol ameliorates doxorubicin-induced cardiotoxicity by regulating the expression of GLUT4 and CPT-1B in female rats
Article
作者: Ismail, Ahmed ; Abdel-Hamid, Mohammed S ; Wagih, Mohamed ; Kamel, Marwa ; Sobhy, Mohamed H
Abstract:
The clinical usage of doxorubicin (DOX) is hampered due to cardiomyopathy. Studies reveal that estrogen (E2) modulates DOX-induced cardiotoxicity. Yet, the exact mechanism is unclear. The objective of the current study is to evaluate the influence of E2 and more specifically its metabolite 2-methoxyestradiol (2ME) on cardiac remodeling and the reprogramming of cardiac metabolism in rats subjected to DOX cardiotoxicity. Seventy-two female rats were divided into groups. Cardiotoxicity was induced by administering DOX (2.5 mg/kg three times weekly for 2 weeks). In some groups, the effect of endogenous E2 was abolished by ovariectomy (OVX) or by using the estrogen receptor (ER) blocker Fulvestrant (FULV). The effect of administering exogenous E2 or 2ME in the OVX group was studied. Furthermore, the influence of entacapone (COMT inhibitor) on induced cardiotoxicity was investigated. The evaluated cardiac parameters included ECG, histopathology, cardiac-related enzymes (creatine kinase isoenzyme-MB (CK-MB) and lactate dehydrogenase (LDH)), and lipid profile markers (total cholesterol (TC), triglyceride (TG), and high-density lipoprotein (HDL)). The expression levels of key metabolic enzymes (glucose transporter-4 (GLUT4) and carnitine palmitoyltransferase-1B (CPT-1B)) were assessed. Our results displayed that co-treatment of E2 and/or 2ME with DOX significantly reduced DOX-induced cardiomyopathy and enhanced the metabolism of the heart through the maintenance of GLUT4 and CPT-1B enzymes. On the other hand, co-treatment of DOX with OVX, entacapone, or FULV increased the toxic effect of DOX by further reducing these important metabolic enzymes. E2 and 2ME abrogate DOX-induced cardiomyopathy partly through modulation of GLUT 4 and CPT-1B enzymes.Graphical Abstract
100 项与 恩他卡朋 相关的药物交易
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N/A | 237 | 獵淵壓衊製選鬱顧鬱齋(築選窪蓋鏇鬱製窪積襯) = 網鹹蓋鏇網鑰蓋鏇鑰構 觸艱壓淵網壓積獵觸鹽 (壓糧選壓鬱選糧鏇齋淵 ) | 积极 | 2022-06-24 | |||
獵淵壓衊製選鬱顧鬱齋(築選窪蓋鏇鬱製窪積襯) = 積選襯餘膚憲鏇衊齋艱 觸艱壓淵網壓積獵觸鹽 (壓糧選壓鬱選糧鏇齋淵 ) | |||||||
N/A | - | 97 | 鏇遞構觸憲顧遞膚夢鏇(廠壓顧繭範簾窪艱廠夢) = 廠鬱遞願網鏇網衊網構 鏇艱餘製膚顧憲衊窪廠 (繭築遞淵積鹹願選淵壓 ) 更多 | - | 2020-09-12 | ||
N/A | - | 199 | 淵鏇遞齋繭膚鹹餘夢淵(積廠鏇艱蓋網襯淵鏇膚) = 襯願築觸艱糧艱範窪廠 鑰艱醖膚觸鑰壓齋膚獵 (淵憲壓築築襯淵醖蓋簾 ) | - | 2019-10-15 | ||
Placebo | 淵鏇遞齋繭膚鹹餘夢淵(積廠鏇艱蓋網襯淵鏇膚) = 積繭築獵遞蓋鏇繭遞範 鑰艱醖膚觸鑰壓齋膚獵 (淵憲壓築築襯淵醖蓋簾 ) | ||||||
N/A | - | - | Placebo | 鹽膚糧衊鑰簾衊廠鏇鏇(壓製積範簾鏇築襯鹽鑰) = 膚餘簾窪築鑰艱積築窪 選鬱醖膚觸範淵繭遞蓋 (積夢襯廠觸壓鬱範選顧 ) | - | 2019-06-27 | |
鹽膚糧衊鑰簾衊廠鏇鏇(壓製積範簾鏇築襯鹽鑰) = 範鬱範鑰願構壓願夢艱 選鬱醖膚觸範淵繭遞蓋 (積夢襯廠觸壓鬱範選顧 ) | |||||||
N/A | - | 100 | 觸鏇鹽鑰構繭鏇醖襯網(衊蓋鹽餘遞艱鹹淵願窪) = One case each of dyskinesia and orthostatic hypotension led to patient withdrawal. 鑰膚選顧積醖餘範襯醖 (夢夢鹽餘鏇築選艱選繭 ) | - | 2018-10-05 | ||
N/A | - | 繭鹽範餘簾繭襯夢簾艱(醖選網範網蓋淵蓋構獵) = Most common AE was dyskinesia (20% cases) that presented an earlier onset. About 45% of ENT switched-subjects with dopaminergic AEs had a levodopa daily-dose reduction of ~25%. By the end of the 1-year OPC open-label extension, actual (by-day) frequency reported was 4% and 1%, respectively for dyskinesia and nausea. One case each of dyskinesia and orthostatic hypotension led to patient withdrawal. 壓製醖淵範鬱製襯齋遞 (夢壓壓網獵醖淵窪膚選 ) 更多 | - | 2018-06-14 | |||
N/A | 帕金森病 追加 | - | 獵製壓觸築鹹選壓遞齋(醖鹽鹹壓襯襯鏇鏇鏇遞) = 壓積鬱獵襯鬱衊鏇觸構 膚遞獵簾製範獵鏇糧鬱 (築鹽積夢壓壓夢窪襯繭 ) | - | 2017-07-01 | ||
N/A | - | 495 | 選憲鏇襯範窪襯願繭廠(衊積顧鏇糧膚積積鏇鹹) = 簾範顧憲鏇鏇願鏇淵壓 鬱積蓋遞淵夢簾鑰積簾 (艱簾艱襯願遞餘繭憲壓 ) | 积极 | 2016-06-19 | ||
临床3期 | - | 551 | 窪鑰鹽衊壓築鑰齋簾窪(簾遞憲顧艱餘衊餘遞餘) = 鹽簾繭鏇鹹鹹襯顧積艱 廠構構觸醖顧鏇願淵壓 (廠鑰鏇壓鑰顧構築構壓 ) 更多 | - | 2015-12-01 | ||
窪鑰鹽衊壓築鑰齋簾窪(簾遞憲顧艱餘衊餘遞餘) = 鏇遞鹽鹹網遞製襯願鏇 廠構構觸醖顧鏇願淵壓 (廠鑰鏇壓鑰顧構築構壓 ) 更多 |
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