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更新于：2025-10-26
Eprosartan Mesylate
依普沙坦
更新于：2025-10-26
概要
基本信息
药物类型 小分子化药 |
别名 (E)-2-butyl-1-(p-carboxybenzyl)-α-2-thenylimidazole-5-acrylic acid、(E)-3-[2-n-butyl-1-{(4-carboxyphenyl)methyl}-1H-imidazol-5-yl]-2-(2-thienyl)methyl-2-propenoic acid、(E)-α{[2-butyl-1-[(4-carboxyphenyl)methyl]-1H-imidazole-5-yl]methylene}-2-thiopheneproprionic acid + [18] |
靶点 |
作用方式 拮抗剂 |
作用机制 AT1R拮抗剂(血管紧张素II-1型受体拮抗剂) |
治疗领域 |
非在研适应症- |
原研机构 |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 美国 (1997-12-22), |
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C24H28N2O7S2 |
InChIKeyDJSLTDBPKHORNY-XMMWENQYSA-N |
CAS号144143-96-4 |
关联
8
项与 依普沙坦 相关的临床试验NCT04606563
Host Response Mediators in Coronavirus (COVID-19) Infection - Is There a Protective Effect of Losartan and Other ARBs on Outcomes of Coronavirus Infection?
NCT01631227
A Prospective, Randomized Double-blind Parallel Group Study to Compare the Effect of Eprosartan and Eprosartan Mesylate on Blood Pressure in Subjects With Mild to Moderate Essential Hypertension
NCT01502904
Neointimal Coverage After Implantation of Biolimus Eluting Stent With Biodegradable Polymer: Optical Coherence Tomographic Assessment According to the Treatment of Dyslipidemia and Hypertension and the Types of Implanted Drug-eluting Stents
100 项与 依普沙坦 相关的临床结果
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100 项与 依普沙坦 相关的转化医学
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100 项与 依普沙坦 相关的专利（医药）
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698
项与 依普沙坦 相关的文献（医药）2025-12-01MOLECULAR AND CELLULAR NEUROSCIENCE
Eprosartan alleviates the traumatic brain injury-induced multi-organ dysfunction syndrome in mice via AT1R/SNS/HMGB1 blockade and PDL-1 modulation
Article
作者: Saini, Paras ; Lather, Deepika ; Deepak, Deepak ; Vasudeva, Neeru ; Sharma, Sunil ; Thakur, Manisha
Traumatic brain injury is not constrained only to the brain but delayed secondary events disturb the end organ functioning via intense response of three homeostatic mechanisms such as sympathetic activity, inflammation, and immunosuppression. Current study involved weight drop model to induce TBI in Swiss albino mice. Eprosartan was administered orally after 30-45 min post injury to mice in 0.35 mg/kg and 0.7 mg/kg doses. Mice were tested for neurobehavioral alterations and multiple organs, including brain, heart, lungs, liver, and kidney were excised for further edema, biochemical, inflammatory, catecholamine, gene expression and histopathological estimations at both acute and chronic phases of injury. Results highlighted that Epro improved neurobehavioral performance, maintained the BBB and lung integrity. It also ameliorated the oxidative stress as well as docking studies exhibited strong binding affinity of Epro for HMGB1 and PDL-1, that further supported by low tissue HMGB1 and serum IL-6 and TNF-α cytokines levels which halted the systemic hyperinflammation. Moreover, Epro treatment successfully restored the cardiac, hepatic and kidney function through stabilized serum biomarkers with declined plasma noradrenaline levels that subsides the sympathetic storm. Considerably, a bizarre cellular morphology was displayed by the organs in acute phase of injury whereas Epro reversed the morphological changes at chronic stage. Also, epro encouraged the PD-1/PDL-1 and IL-10 gene expression in the tissues that regulates immune response. Thus, it is concluded that Epro exerts its organ protective effect against MODS via AT1/SNS pathway inhibition.
2025-07-01CURRENT PHARMACEUTICAL DESIGN
Eprosartan Reduces Inflammation and Oxidative Stress in Ethanol-induced Hepatotoxicity
Article
作者: Mansourian, Mahboubeh ; Jahantab, Mohammad Bagher ; Karimi, Farzaneh ; Larki, Rozina Abbasi ; Mirghaed, Ali Taheri ; Azizi, Mahdokht ; Behrouj, Hamid ; Abdzadeh, Soroor ; Daryabor, Gholamreza ; Mehrabi, Sadrollah ; Doustimotlagh, Amir Hossein
Introduction::
Eprosartan is an effective blood pressure medication that blocks the Angiotensin
Type 1 (AT1) receptor. The studies conducted on Eprosartan showed anti-oxidative stress effects and modulating
inflammatory mechanisms. The current research is designed to clarify and examine the possible advantageous
impacts of Eprosartan against chronic ethanol-induced hepatic damage.
Methods::
Twenty-four male Sprague-Dawley rats were haphazardly separated into four groups. The control
group received normal saline 1 g/kg for 35 days (group 1). The EtOH group received 7 g/kg of 40% ethanol
orally for 35 days (group 2). The EtOH+ EP group was pretreated with 60 mg/kg of Eprosartan dissolved in
normal saline orally and, after 60 minutes, received 7 g/kg of 40% ethanol orally for 35 days (group 3). The
EP group received only Eprosartan 60 mg/kg dissolved in normal saline for 35 days (group 4). The levels of
biochemical parameters, oxidative stress markers, pro-inflammatory cytokines, and histopathological staining
were evaluated in serum and liver tissue. The interactive behavior of Eprosartan with Tumor Necrosis Factor-α
(TNF-α) protein was also explained by molecular docking.
Results::
Pre-treatment with Eprosartan (60 mg/kg) notably diminished the elevation in serum alanine aminotransferase
(ALT), aspartate aminotransferase (AST) and Gamma-Glutamyl Transferase (GGT) enzymes, total
triglyceride, cholesterol, total bilirubin, and inflammatory cytokines including TNF-α, Interleukin-1β (IL-1β)
and Interleukin-6 (IL-6) levels, which were induced by alcohol administration (P-value ≤ 0.05). In the Eprosartan
pre-treated group, malondialdehyde and protein carbonyl content of liver tissue were remarkably diminished,
as compared to the ethanol-induced rats. In addition, histopathological results approved the indicated
finding. Molecular docking research gives insights into potential interactions of Eprosartan with TNF-α protein.
Conclusion::
Our results revealed that the pre-treatment with Eprosartan (60 mg/kg) preserves against chronic
alcohol-induced hepatic damage.
2025-06-01INTERNATIONAL IMMUNOPHARMACOLOGY
Modulating the renin-angiotensin system by eprosartan or xanthenone drives microglial M2 polarization in a rat model of Parkinson's disease via regulating the interplay between MKP-1/ miR-155 /SOCS1 and PP2A signaling network
Article
作者: El-Tanbouly, Dalia M ; Alhadad, Maha A ; Zaafan, Mai A ; Elbrairy, Amany I ; Zaki, Hala F
Despite growing evidence for the renin-angiotensin system (RAS) involvement in Parkinson's disease (PD), its role in microglial polarization during disease progression remains unclear. This study explored the ability of modulating RAS using eprosartan, an AT1R antagonist, and xanthenone, an ACE2 activator, to support microglial M2 polarization in rats with PD highlighting the roles of miR-155, protein phosphatase 2 A (PP2A), and mitogen-activated protein kinase phosphatase 1 (MKP-1). Rotenone (1.5 mg/kg) was administered to Wistar rats to induce PD, with concurrent treatments of eprosartan (60 mg/kg/day) or xanthenone (2 mg/kg/day) for 28 days. Both agents improved motor function and neuronal damage, as evidenced by behavioral, histopathological, and immunohistochemical analyses. Eprosartan and xanthenone enhanced tyrosine hydroxylase activity and reduced α-synuclein accumulation in the substantia nigra. Eprosartan and xanthenone modulated the RAS axis by reducing angiotensin II level and increasing ACE2 activity and Ang 1-7 concentration in the striatum. Importantly, these agents induced a shift in microglial polarization from the M1 proinflammatory phenotype (marked by reduced IL-1β, iNOS, and CD86) to the M2 anti-inflammatory phenotype (marked by enhanced arginase1, Ym1, Fizz1 and CD163). This shift was associated with altered STAT signaling pathways, including decreased p-STAT1 and increased p-STAT6. Additionally, levels of miR-155 were decreased, and levels of SOCS1, MKP-1, and PP2A were increased. These findings address a critical gap in understanding how RAS modulation can influence neuroinflammation through microglial polarization via regulating the interplay between MKP-1/ miR-155 /SOCS1 and PP2A, offering a promising therapeutic strategy to mitigate neurodegeneration and inflammation in PD.
100 项与 依普沙坦 相关的药物交易
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研发状态
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 原发性高血压 | 澳大利亚 | 1998-06-15 | |
| 高血压 | 美国 | 1997-12-22 |
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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
临床3期 | 665 | Placebo Eprosartan mesylate+Eprosartan (Eprosartan) | 簾鹹鏇觸衊蓋遞憲顧繭(構糧鹽壓遞願網窪壓憲) = 簾衊膚窪網醖餘淵糧顧 觸繭淵鑰鬱製鏇顧願範 (衊醖膚範簾觸構壓衊膚, 7.7) 更多 | - | 2014-05-26 | ||
Placebo Eprosartan+Eprosartan Mesylate (Eprosartan Mesylate) | 簾鹹鏇觸衊蓋遞憲顧繭(構糧鹽壓遞願網窪壓憲) = 糧築壓蓋蓋淵夢積繭壓 觸繭淵鑰鬱製鏇顧願範 (衊醖膚範簾觸構壓衊膚, 7.5) 更多 | ||||||
临床4期 | 1,405 | 簾衊襯壓選築壓構壓構(餘築製窪餘範蓋夢衊選) = 構襯蓋願糧淵鏇願構獵 範鑰遞衊構鑰艱衊夢遞 (廠鏇餘顧廠築繭構糧選 ) | - | 2005-06-01 | |||
簾衊襯壓選築壓構壓構(餘築製窪餘範蓋夢衊選) = 憲製衊範廠淵齋蓋襯構 範鑰遞衊構鑰艱衊夢遞 (廠鏇餘顧廠築繭構糧選 ) |
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