更新于：2024-11-04
Fasudil Hydrochloride Hydrate
盐酸法舒地尔
更新于：2024-11-04
概要
基本信息
非在研机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟) |
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结构
分子式C28H38Cl2N6O5S2 |
InChIKeyAACOJGPCMIDLEY-UHFFFAOYSA-N |
CAS号186694-02-0 |
关联
16
项与 盐酸法舒地尔 相关的临床试验A PLACEBO CONTROLLED, RANDOMIZED DOUBLE-BLIND PARALLEL GROUP 12-MONTH TRIAL OF FASUDIL FOR THE TREATMENT OF EARLY ALZHEIMER’S DISEASE (FEAD)
Safety, Tolerability and Symptomatic Efficacy of the ROCK-Inhibitor Fasudil in Patients With Parkinson's Disease (ROCK-PD)
Safety and Efficacy Exploratory Study of the Use of Fasudil hydrochloride for Vasospasm on arteriovenous fistula construction - SAEF-AVF study
100 项与 盐酸法舒地尔 相关的临床结果
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100 项与 盐酸法舒地尔 相关的转化医学
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100 项与 盐酸法舒地尔 相关的专利（医药）
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316
项与 盐酸法舒地尔 相关的文献（医药）2024-09-01No shinkei geka. Neurological surgery
[Postoperative Management of Aneurysmal Subarachnoid Hemorrhage].
Review
作者: Endo, Hidenori ; Sakata, Hiroyuki
Delayed cerebral ischemia(DCI) is one of the most significant complications of subarachnoid hemorrhage. Despite significant evolution in understanding DCI pathophysiology, vasospasm affecting cerebral vessels of large and moderate diameters remain the only clinically measurable component of DCI and is therefore the primary target for intervention in the postoperative management of subarachnoid hemorrhage. In Japan, fasudil hydrochloride and ozagrel sodium are widely used to prevent vasospasms; however, their effects are sometimes insufficient. Clazosentan, a selective endothelin receptor subtype A antagonist, reduces vasospasm-related morbidity and all-cause mortality following aneurysmal subarachnoid hemorrhage. This was demonstrated in a recent randomized phase 3 trial, leading to the approval of clazosentan by the Pharmaceuticals and Medical Devices Agency in Japan. Recent advances in our understanding of subarachnoid hemorrhage will facilitate improved management to reduce the incidence of DCI.
2024-09-01AGING CELL
Sevoflurane‐induced overexpression of extrasynaptic α5‐GABAAR via the RhoA/ROCK2 pathway impairs cognitive function in aged mice
Article
作者: Luo, Yuan ; Wang, Yongan ; Wang, Sixuan ; Wang, Shengran ; Wu, Jiangnan ; Wang, Zhun ; Zhang, Mengxue ; Yin, Yiqing ; Dong, Jinpeng
Abstract:
Perioperative neurocognitive disorder (PND) is a serious neurologic complication in aged patients and might be associated with sevoflurane exposure. However, the specific pathogenesis is still unclear. The distribution of α5‐GABAAR, a γ‐aminobutyric acid type A receptor (GABAAR) subtype, at extrasynaptic sites is influenced by the anchor protein radixin, whose phosphorylation is regulated via the RhoA/ROCK2 signaling pathway and plays a crucial role in cognition. However, whether sevoflurane affects the ability of radixin phosphorylation to alter extrasynaptic receptor expression is unknown. Aged mice were exposed to sevoflurane to induce cognitive impairment. Both total proteins and membrane proteins were extracted for analysis. Cognitive function was evaluated using the Morris water maze and fear conditioning test. Western blotting was used to determine the expression of ROCK2 and the phosphorylation of radixin. Furthermore, the colocalization of p‐radixin and α5‐GABAAR was observed. To inhibit ROCK2 activity, either an adeno‐associated virus (AAV) or fasudil hydrochloride was administered. Aged mice treated with sevoflurane exhibited significant cognitive impairment accompanied by increased membrane expression of α5‐GABAAR. Moreover, the colocalization of α5‐GABAAR and p‐radixin increased after treatment with sevoflurane, and this change was accompanied by an increase in ROCK2 expression and radixin phosphorylation. Notably, inhibiting the RhoA/ROCK2 pathway significantly decreased the distribution of extrasynaptic α5‐GABAAR and improved cognitive function. Sevoflurane activates the RhoA/ROCK2 pathway and increases the phosphorylation of radixin. Excess α5‐GABAAR is anchored to extrasynaptic sites and impairs cognitive ability in aged mice. Fasudil hydrochloride administration improves cognitive function.
2024-07-30BIOLOGICAL & PHARMACEUTICAL BULLETIN
Difference in Contractile Mechanisms between the Early and Sustained Components of Ionomycin-Induced Contraction in Rat Caudal Arterial Smooth Muscle
Article
作者: Aida, Kazuki ; Mita, Mitsuo ; Ishii-Nozawa, Reiko
We previously reported that the sustained component of contraction induced by depolarizing stimulation by high K+ concentration in rat caudal arterial smooth muscle involves a Ca2+-induced Ca2+ sensitization mechanism whereby Ca2+ entry through voltage-gated Ca2+ channels activates proline-rich tyrosine kinase 2 (Pyk2), leading to activation of RhoA/Rho-associated kinase (ROCK). In the present study, we investigated a potential role for Pyk2-mediated RhoA/ROCK activation in contraction mediated by elevation of cytosolic free Ca2+ concentration ([Ca2+]i) induced by a Ca2+ ionophore, ionomycin, rather than by depolarizing stimulation. Ionomycin (60 µM) induced slow and sustained contraction of rat caudal arterial smooth muscle due to influx of Ca2+. Pre-treatment with a myosin light chain kinase (MLCK) inhibitor, ML-9 (30 µM), inhibited both the early phase (4 min) and the sustained phase (30 min) of ionomycin-induced contraction. On the other hand, a ROCK inhibitor, HA-1077 (3 µM), and Pyk2 inhibitors, sodium salicylate (10 mM) and PF-431396 (3 µM), suppressed only the sustained phase of ionomycin-induced contraction. A calmodulin (CaM) inhibitor, W-7 (150 µM), but not W-5 (150 µM), suppressed the early phase of contraction. Early or sustained increase of ionomycin-induced 20 kDa light chain of myosin (LC20) phosphorylation was inhibited by each inhibitor in a manner similar to the attenuation of contraction. These results indicate that the early phase of ionomycin-induced contraction is mediated by MLCK activation by [Ca2+]i elevation, whereas the sustained phase of ionomycin-induced contraction involves RhoA/ROCK activation and inhibition of myosin light chain phosphatase (MLCP) through CaM-independent Pyk2 activation by [Ca2+]i elevation.
100 项与 盐酸法舒地尔 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 |
|---|---|---|---|
| 脑缺血 | 日本 | 1995-06-30 | |
| 颅内血管痉挛 | 日本 | 1995-06-30 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 肌萎缩侧索硬化 | 临床2期 | 美国 | 2021-12-22 | |
| 肌萎缩侧索硬化 | 临床2期 | 澳大利亚 | 2021-12-22 |
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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2期 | 肌萎缩侧索硬化 Neurofilament Light Chain | 31 | 憲膚齋憲齋鹹鬱鑰範製(廠網壓簾鑰醖壓壓廠鑰) = 遞積積膚網鹹繭憲簾繭 蓋醖膚構積願鹹膚築製 (鹽構糧遞鬱鹽鹹簾衊構 ) 更多 | 积极 | 2024-06-19 | ||
临床2期 | 31 | placebo (Young Saline) | 網襯顧簾憲鹹糧製構憲(淵衊窪範蓋鹹膚願積憲) = 鹹蓋鹹構構選獵鑰淵壓 範範醖淵鑰顧膚築淵獵 (簾築遞願顧廠醖蓋蓋襯, 鏇鹽餘膚夢夢鬱衊醖製 ~ 願築淵選醖襯廠築網築) 更多 | - | 2020-02-27 | ||
(Young Fasudil) | 網襯顧簾憲鹹糧製構憲(淵衊窪範蓋鹹膚願積憲) = 鹽醖醖選範鹹獵廠鬱製 範範醖淵鑰顧膚築淵獵 (簾築遞願顧廠醖蓋蓋襯, 糧窪餘觸衊鏇繭鹽窪糧 ~ 膚醖艱醖獵夢壓範觸襯) 更多 | ||||||
N/A | - | 觸衊簾築鑰鑰鑰構顧簾(顧蓋構艱遞鑰餘衊鹽艱) = 51% reduction 夢鹽醖觸淵襯齋廠衊窪 (鬱遞鏇窪蓋繭構構蓋餘 ) | - | 2017-05-07 | |||
临床2期 | 2 | (Drug: Fasudil Hydrochloride) | 餘醖淵網製醖醖淵鹽製(膚願憲餘窪窪醖繭鹽選) = 網糧夢願網構獵衊築簾 廠憲繭鹹壓顧鏇製簾憲 (夢壓襯遞艱簾夢齋網壓, 膚獵糧衊壓遞衊範繭糧 ~ 顧艱鏇鹹觸膚襯製鑰衊) | - | 2017-03-29 | ||
Placebo Oral Tablet (Drug: Placebo Oral Tablet) | 餘醖淵網製醖醖淵鹽製(膚願憲餘窪窪醖繭鹽選) = 範築觸鬱範選艱廠製淵 廠憲繭鹹壓顧鏇製簾憲 (夢壓襯遞艱簾夢齋網壓, 廠衊淵糧壓衊築餘觸鏇 ~ 膚製鬱壓鹽糧築鹹齋鏇) | ||||||
N/A | - | IVB/IVF group | 選簾醖簾簾糧鹽積齋襯(廠獵鑰範鏇齋鏇構壓製) = BCVA changes were consistent with CMT changes 窪糧壓繭鹹構遞廠構鬱 (獵鏇遞艱積獵鏇遞膚膚 ) | 积极 | 2016-10-17 | ||
IVB group | |||||||
N/A | 6 | 構鑰積淵網遞顧鬱遞獵(醖積鏇選艱襯餘鹽鏇顧) = 鹽醖醖衊顧鑰糧鑰鬱齋 觸艱餘夢簾獵壓範壓壓 (範網醖鹹選蓋壓壓積襯, 18.0) | 不佳 | 2013-09-01 | |||
構鑰積淵網遞顧鬱遞獵(醖積鏇選艱襯餘鹽鏇顧) = 餘鑰廠積蓋醖網夢範衊 觸艱餘夢簾獵壓範壓壓 (範網醖鹹選蓋壓壓積襯, 4.5) | |||||||
N/A | - | 顧鑰築網選製糧積願壓(膚艱鏇廠糧積鹽觸壓願) = 鹽廠繭淵繭憲構繭憲夢 淵鏇鑰憲鹽製衊窪觸齋 (構鑰鑰膚襯鑰製鏇膚鹽 ) 更多 | 积极 | 2009-04-01 | |||
Vehicle | 顧鑰築網選製糧積願壓(膚艱鏇廠糧積鹽觸壓願) = 鹹廠齋鹹構範壓顧夢淵 淵鏇鑰憲鹽製衊窪觸齋 (構鑰鑰膚襯鑰製鏇膚鹽 ) 更多 |
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