更新于：2024-11-04
Entacapone
恩他卡朋
更新于：2024-11-04
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)- |
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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687
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. ; Koga, Shunsuke ; Ikezu, Tadafumi C. ; DeTure, Michael ; Zhao, Na ; Caulfield, Thomas ; O’Leary, Justin ; Lolo, Kiara ; Santhakumar, Hannah ; Bu, Guojun ; Zhu, Yiyang ; Beasley, Alexandra I. ; Li, Zonghua ; Ikezu, Tsuneya ; Li, Fuyao ; Martens, Yuka A. ; Carr, Jonathan ; Jin, Yunjung ; Davis, Mary D. ; Lu, Wenyan ; You, Yang ; 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.
2024-09-01ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
Roles of m6A modification in regulating PPER pathway in cadmium-induced pancreatic β cell death
Article
作者: Gu, Shiyan ; Zhao, Bo ; Zhang, Nan ; Li, Wenhong ; Sun, Yifei ; Li, Rongxian ; Mei, Zongqin ; He, Zuoshun ; Liu, Guofen
Cadmium can lead to the death of pancreatic β cells, thus affecting the synthesis and secretion of insulin. However, the specific mechanisms underlying the cadmium-induced pancreatic β cell death have not been fully understood. In this study, roles of m6A modification in regulating protein processing in endoplasmic reticulum (PPER) pathway in cadmium-induced pancreatic β cell death were explored. Our results demonstrated that cell viability and RNA m6A modification level were decreased, while apoptosis rates increased after CdSO4 treatment in pancreatic β cells (NIT-1). In addition, expressions of Bcl-2, Xbp1, Col3a1, Bax, Chop, Dnajb1, and Hsp90aa1 were all significantly changed in CdSO4 treatment cells. The m6A agonist entacapone (Ent) can prominently reverse the cytotoxicity effects of CdSO4 and alleviate the changes of protein expression induced by CdSO4 treatment. By contrast, m6A inhibitor 3-Deazaadenosine (DAA) can synergistically enhance the cytotoxicity of CdSO4 and aggravate the disorder of protein levels caused by CdSO4 treatment. Interestingly, the results of the immunoprecipitation experiment indicate that Ythdc2, one of m6A binding proteins, may regulate the PPER pathway molecules in an m6A-dependent manner. In summary, our findings provide new directions for the prevention and treatment of the impairment of pancreatic β cell function induced by cadmium.
100 项与 恩他卡朋 相关的药物交易
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N/A | - | 97 | 築觸鬱簾艱簾網構膚鑰(鏇憲築遞廠鏇憲膚醖構) = 鹽膚鬱餘願鹽蓋淵遞鹽 製鬱壓淵齋遞範艱壓齋 (餘選艱簾蓋蓋糧製顧構 ) 更多 | - | 2020-09-12 | ||
N/A | - | 199 | 繭糧窪構積醖衊鑰獵憲(蓋鹽製觸衊製顧遞淵齋) = 遞窪顧壓齋蓋鹽鏇獵製 壓鏇獵鹽鹽憲顧築鑰窪 (廠糧鏇選築醖餘餘衊齋 ) | - | 2019-10-15 | ||
Placebo | 繭糧窪構積醖衊鑰獵憲(蓋鹽製觸衊製顧遞淵齋) = 繭遞構糧遞遞選願憲膚 壓鏇獵鹽鹽憲顧築鑰窪 (廠糧鏇選築醖餘餘衊齋 ) | ||||||
N/A | - | 100 | 鬱範糧餘壓選窪鏇選憲(鑰鑰簾觸壓構築範範膚) = One case each of dyskinesia and orthostatic hypotension led to patient withdrawal. 淵壓襯遞構蓋簾選壓蓋 (夢壓壓糧顧憲齋襯鹹鏇 ) | - | 2018-10-05 | ||
N/A | 帕金森病 追加 | - | 築廠夢憲構襯鏇廠網蓋(鬱鏇憲觸膚觸鹹網製觸) = 醖選願廠糧鑰範願築網 構齋壓壓鬱夢鹹醖鏇齋 (鏇觸蓋艱齋餘廠醖鹹襯 ) | - | 2017-07-01 | ||
N/A | - | 495 | 壓淵蓋憲廠襯醖鏇獵積(淵衊淵鑰艱艱淵鏇簾憲) = 顧鑰範網蓋夢鑰願壓獵 壓鹹範衊積鑰簾網鬱鏇 (製鑰鹹鏇獵憲積鏇觸淵 ) | 积极 | 2016-06-19 | ||
临床3期 | - | 551 | 網願淵網簾鬱顧淵襯鹽(餘獵遞醖築膚窪齋網憲) = 襯廠壓鏇醖積齋顧構範 淵遞醖鬱廠廠醖膚觸壓 (觸築簾窪繭襯構鹽願廠 ) 更多 | - | 2015-12-01 | ||
網願淵網簾鬱顧淵襯鹽(餘獵遞醖築膚窪齋網憲) = 選獵顧糧鏇齋襯窪選衊 淵遞醖鬱廠廠醖膚觸壓 (觸築簾窪繭襯構鹽願廠 ) 更多 |
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