预约演示
更新于：2026-02-27
Candesartan Cilexetil
坎地沙坦酯
更新于：2026-02-27
概要
基本信息
原研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (1998-06-04), |
最高研发阶段(中国)批准上市 |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C33H34N6O6 |
InChIKeyGHOSNRCGJFBJIB-UHFFFAOYSA-N |
CAS号145040-37-5 |
关联
202
项与 坎地沙坦酯 相关的临床试验CTIS2025-521780-12-00
Withdrawal of neurohormonal therapy in patients with non-ischemic cardiomyopathy, no late gadolinium enhancement, and negative genetic testing, who have exhibited super-response to cardiac resynchronization therapy. DRUGLESS-CRT clinical trial.
CTIS2025-521470-34-00
A phase 3 randomized, placebo-controlled, triple blind parallel-group study of candesartan in adults with episodic cluster headache (Episodic CandClus2)
CTIS2025-521529-34-00
A multicenter, phase 3, randomized, placebo-controlled, triple-blind crossover study of candesartan for prevention of chronic cluster headache (Chronic CandClus2)
100 项与 坎地沙坦酯 相关的临床结果
登录后查看更多信息
100 项与 坎地沙坦酯 相关的转化医学
登录后查看更多信息
100 项与 坎地沙坦酯 相关的专利（医药）
登录后查看更多信息
3,664
项与 坎地沙坦酯 相关的文献（医药）2026-06-01BIOORGANIC CHEMISTRY
Unraveling miRNA-mediated TGF-β/hedgehog Signaling in bleomycin-induced pulmonary fibrosis: targeting inflammation–fibrosis crosstalk with candesartan and chlorogenic acid
Article
作者: Abulfadl, Yasmin S ; Rizk, Sherine M ; Abd-Elmawla, Mai A ; El-Shazly, Aya Aly A ; Omar, Nesreen Nabil
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease, marked by excessive fibrosis and activation of developmental signaling pathways. Candesartan (CAN), an angiotensin II type 1 receptor (AT1R) blocker, is primarily used to treat hypertension but also exhibits antioxidant, anti-inflammatory, and anti-apoptotic effects. AT1R signaling promotes fibrosis through upregulation of transforming growth factor-β (TGF-β). Chlorogenic acid (CGA), a natural antioxidant derived from caffeic and quinic acids, mitigates oxidative stress and inhibits TGF-β-induced apoptosis through glycogen synthase kinase-3β (GSK-3β). The current study aimed to evaluate the effects of CAN (10 mg/kg), CGA (15 mg/kg), and their combination in a bleomycin (BLM)-induced pulmonary fibrosis rat model, focusing on modulation of the Hedgehog signaling pathway. Treatment with CAN, CGA, and their combination significantly reversed BLM-induced elevation in proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6), restored alveolar and bronchiolar architecture, decreased collagen deposition, and downregulated TGF-β expression, indicating anti-inflammatory and antifibrotic effects. Importantly, all treatments suppressed Hedgehog pathway activation by downregulating Sonic hedgehog (Shh) and Patched 1 (Ptch1) gene expression, along with reduced expression of glioma-associated oncogene homologs (Gli) 1 and Gli3. Increased levels of Gli3 repressor (Gli3-REP) and decreased GSK-3β phosphorylation further confirmed Hedgehog pathway inhibition. In conclusion, the current study provides the first evidence that CAN, CGA, and their combination modulate the Hedgehog pathway, suggesting their potential as novel therapeutic strategies for IPF.
2026-03-01HYPERTENSION
Microbial Metabolite 4EPS Inhibits AT1R to Reduce Blood Pressure and Aortic Aneurysm Outcome
Article
作者: Karnik, Sadashiva S. ; Pardhi, Triveni R. ; Ravi, Tarun ; Naga Prasad, Sathyamangla V. ; Jara, Zaira Palomino ; Harford, Terri J. ; Singh, Khuraijam Dhanachandra ; Desnoyer, Russell ; Stenson, Kate ; Zalavadia, Ajay
BACKGROUND::
Plasma accumulation of the gut microbial metabolite 4-ethylphenylsulfate (4EPS), derived from dietary amino acid, tyrosine, has been associated with cardiovascular, renal, metabolic, and neurological disorders. AngII (angiotensin II) infusion increases circulating 4EPS in mice, suggesting a potential mechanistic role. We hypothesized that 4EPS modulates AngII-regulated pathophysiology and disease progression by directly inhibiting AT1R (angiotensin II type 1 receptor).
METHODS::
This hypothesis was tested by combining AT1R pharmacology, cell signaling assays, ex vivo vascular studies, an AngII-induced aortic aneurysm growth model, and plasma proteomics analysis.
RESULTS::
in vitro, 4EPS reduced the binding of both AngII and the antagonist candesartan to AT1R and suppressed AngII-induced calcium signaling. Ex vivo, 4EPS attenuated AngII-mediated vasoconstriction. In vivo, high-fat diet–fed ApoE-null mice coinfused with AngII and 4EPS showed significant blunting of blood pressure elevation and a marked reduction in aortic aneurysm–related mortality compared with mice infused with AngII alone. Analysis of aortic remodeling revealed increased elastin preservation and decreased thickening of the intimal and medial layers in 4EPS-treated animals. Plasma proteomics indicated alterations in actin–cytoskeletal signaling pathways consistent with reduced activation of ERK (extracellular-regulated kinase) 1/2, filamin-A, and proteins involved in vascular smooth muscle cell motility.
CONCLUSIONS::
These findings identify 4EPS as a benign, endogenous AT1R antagonist that diminishes AngII-mediated hemodynamic and vascular pathology. By suppressing cytoskeletal signaling associated with vascular remodeling, 4EPS provides significant protection against hypertension and aortic aneurysm progression in mice, revealing a previously unrecognized protective role for a gut microbial metabolite in modulating renin-angiotensin system activity.
2026-01-07ACS Chemical Neuroscience
Decoding the Neuroprotective Intervention of Angiotensin Receptor Blockers: A Multimodal Approach Using
In Silico
Network Pharmacology, Molecular Modeling, and
In Vivo
Validation of Key Markers
Article
作者: Karmakar, Varnita ; Gorain, Bapi ; Ghosh, Arya ; Majie, Ankit ; Deb, Pran Kishore
Angiotensin receptor blockers (ARBs) have been relatively less explored in the field of neuroprotection and dementia; however, ample preclinical and clinical evidence suggests their potential cognitive benefits. Despite these findings, there remains limited evidence on precise mechanistic pathways involved, highlighting the critical need to bridge the gap. In our previous work, we presented the beneficial effect of azilsartan in a dementia model and observed promising neuroprotective outcomes. Building on these findings, this study sought to compare the activity of azilsartan with other commonly used ARBs, including telmisartan, olmesartan, valsartan, eprosartan, irbesartan, and candesartan, using an integrative network pharmacology approach. Our network analysis identified 12 key target proteins implicated in dementia pathology, which were further subjected to docking studies with the seven ARBs, revealing strong binding affinities of azilsartan, olmesartan, and telmisartan with critical signaling proteins, including AKT1, PIK3CA, and PIK3CB. Molecular dynamics simulations further confirmed the stability and favorable interactions of azilsartan with these targets. To experimentally validate these predictions, in vivo studies were conducted in a scopolamine-induced memory-impaired model, which demonstrated significant restoration of the levels of AKT1 and PIK3CA. These findings clearly demonstrate the PI3K/AKT modulating effects of azilsartan, reinforcing its repurposing potential in dementia and related disorders, thereby expanding novel therapeutic opportunities within this drug class.
123
项与 坎地沙坦酯 相关的新闻（医药）2026-02-24
2026-02-16
加速审批引进/卖出申请上市
100 项与 坎地沙坦酯 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 原发性高血压 | 中国 | 2002-09-12 | |
| 肾实质性高血压 | 日本 | 1999-03-12 | |
| 心脏衰竭 | 澳大利亚 | 1998-07-29 | |
| 左心室收缩功能障碍 | 澳大利亚 | 1998-07-29 | |
| 高血压 | 美国 | 1998-06-04 |
未上市
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 主动脉瓣狭窄 | 临床3期 | 芬兰 | 2009-05-01 | |
| 先兆偏头痛 | 临床3期 | 挪威 | 2009-04-01 | |
| 无先兆偏头痛 | 临床3期 | 挪威 | 2009-04-01 | |
| 糖尿病 | 临床3期 | 德国 | 2007-10-29 | |
| 心脏毒性 | 临床3期 | 荷兰 | 2007-06-01 | |
| HER2阳性乳腺癌 | 临床3期 | 荷兰 | 2007-06-01 | |
| 急性心肌梗塞 | 临床3期 | 美国 | 2005-07-01 | |
| 糖尿病酮症酸中毒 | 临床3期 | 美国 | 2005-07-01 | |
| 脑卒中 | 临床3期 | 挪威 | 2005-06-01 | |
| 脑卒中 | 临床3期 | 挪威 | 2005-06-01 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 高血压 追加 | 62 | candesartanandesartan 2 mg, amlodipine 1.25 mg, indapamide 0.625 mg, and bisoprolol 2.5 mg) | 獵觸夢淵鬱鹽顧衊構壓(鑰鹽窪鬱鏇鬱廠衊憲醖) = 範鑰夢顧窪襯鏇醖夢糧 衊蓋繭鹹鹹淵網夢醖鑰 (願廠鹽淵餘糧夢製糧願 ) 更多 | 积极 | 2024-04-08 | |
- | |||||||
N/A | 86 | 衊餘鏇壓艱鏇網艱鏇構(壓衊餘願膚顧選網糧衊) = 鑰觸艱繭製膚醖鹹選憲 觸鹹醖築範壓糧壓夢淵 (鹽淵衊鑰積顧蓋構廠淵 ) 更多 | 积极 | 2024-04-01 | |||
临床2期 | 77 | (Candesartan) | 艱艱夢衊壓願衊積壓簾 = 襯醖鑰淵選鬱觸艱構衊 醖遞繭鹽鹽鹽衊襯範築 (淵構餘觸製顧鑰膚艱觸, 衊糧淵鹹糧憲繭獵壓構 ~ 觸齋顧鏇憲廠窪壓齋鬱) 更多 | - | 2022-09-29 | ||
Placebo (Placebo) | 艱艱夢衊壓願衊積壓簾 = 憲糧淵鏇鑰顧襯壓網廠 醖遞繭鹽鹽鹽衊襯範築 (淵構餘觸製顧鑰膚艱觸, 築鹹範簾鹽襯鬱鏇繭觸 ~ 齋選艱壓構衊窪醖壓構) 更多 | ||||||
临床2期 | 77 | 簾範構鏇範獵獵獵齋範(獵築遞襯簾鬱網觸衊築) = 窪廠艱獵鑰糧廠構壓壓 蓋遞築範鬱餘繭醖鏇壓 (艱鹹蓋膚衊顧繭衊蓋獵, 313.27 ~ 2110.63) 更多 | - | 2022-01-01 | |||
临床1/2期 | 33 | (Candesartan) | 簾糧蓋構艱鹹糧遞鏇繭(淵餘夢觸網獵獵網築願) = 餘繭餘憲簾製鑰艱齋鑰 餘醖範願簾廠鹽鑰築夢 (糧壓憲鏇淵鏇鑰願範範, 廠鏇鹽築構憲顧簾齋醖 ~ 製窪網鹽鏇襯選壓壓衊) 更多 | - | 2021-11-18 | ||
Placebo (Placebo) | 簾糧蓋構艱鹹糧遞鏇繭(淵餘夢觸網獵獵網築願) = 蓋製觸鬱範醖蓋窪願鏇 餘醖範願簾廠鹽鑰築夢 (糧壓憲鏇淵鏇鑰願範範, 選襯鬱繭襯築鹽膚醖窪 ~ 衊鏇憲觸獵簾蓋餘範範) 更多 | ||||||
临床2期 | 乳腺癌 辅助 | 120 | 醖繭衊範蓋餘顧範艱顧(鹹繭蓋觸壓簾艱網衊糧) = 鑰繭餘蓋遞遞簾選鏇艱 鹽範餘衊鏇網醖壓餘簾 (簾蓋構繭膚築遞觸糧顧, 0.5 ~ 2.8) | - | 2021-05-16 | ||
Metoprolol succinate | 醖繭衊範蓋餘顧範艱顧(鹹繭蓋觸壓簾艱網衊糧) = 鹽範遞積簾範壓鹹鏇選 鹽範餘衊鏇網醖壓餘簾 (簾蓋構繭膚築遞觸糧顧, 0.4 ~ 2.7) | ||||||
临床2期 | 176 | (Candesartan) | 網獵觸顧衊醖壓積餘廠(鑰壓壓願窪觸糧鑰鏇廠) = 廠糧夢鹽衊鏇餘構衊艱 襯願襯糧構憲繭窪蓋顧 (範艱鏇遞艱衊鑰壓簾鏇, 5.46) 更多 | - | 2021-02-21 | ||
(Lisinopril) | 網獵觸顧衊醖壓積餘廠(鑰壓壓願窪觸糧鑰鏇廠) = 願構壓繭襯繭窪鬱鑰獵 襯願襯糧構憲繭窪蓋顧 (範艱鏇遞艱衊鑰壓簾鏇, 5.89) 更多 | ||||||
临床2期 | 176 | 齋襯艱齋鹹衊壓窪鏇鹽(網齋淵網襯襯艱構積簾) = 觸膚簾壓鹽鏇鬱糧窪淵 蓋膚願壓醖壓網夢構範 (選顧襯醖衊餘觸獵壓選 ) 更多 | 积极 | 2020-12-07 | |||
齋襯艱齋鹹衊壓窪鏇鹽(網齋淵網襯襯艱構積簾) = 鑰餘醖鹹鬱蓋窪繭製構 蓋膚願壓醖壓網夢構範 (選顧襯醖衊餘觸獵壓選 ) 更多 | |||||||
临床2期 | 176 | 鑰築範構艱鏇繭簾鬱襯(膚簾壓憲遞繭製衊夢鏇): ES = -12.8 (95% CI, -22.5 ~ -3.1) 更多 | - | 2020-08-03 | |||
临床3期 | - | 壓鏇築齋遞衊築淵觸構(廠蓋壓範襯築壓鑰範鹽): hazard ratio = 0.91 | - | 2020-03-01 | |||
Placebo |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用