盐酸布那唑嗪(Bunazosin Hydrochloride) - 药物靶点：ADRA1_在研适应症：青光眼，心脏衰竭，高血压_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Andante、Bunazosin、Bunazosin hydrochloride (JP17)

+ [10]

靶点

ADRA1

作用方式

拮抗剂

作用机制

ADRA1拮抗剂(肾上腺素能受体α-1家族拮抗剂)

治疗领域

心血管疾病眼部疾病泌尿生殖系统疾病

在研适应症

青光眼心脏衰竭高血压+ [2]

非在研适应症-

原研机构

Eisai Co., Ltd.

在研机构

Eisai Co., Ltd.

Santen Pharmaceutical Co., Ltd.

非在研机构-

权益机构-

最高研发阶段批准上市

首次获批日期

日本 (1985-04-16),

原发性高血压肾性高血压

最高研发阶段(中国)-

特殊审评-

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结构/序列

分子式C19H27N5O3

InChIKeyRHLJLALHBZGAFM-UHFFFAOYSA-N

CAS号80755-51-7

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关联

1

项与盐酸布那唑嗪相关的临床试验

NCT00130156

/ Completed临床4期

Effects of Combination Therapy With an α1-blocker (Sustained-release Preparation of Bunazosin or Doxazosin) in Inadequate Responders to an Angiotensin II Antagonist (Valsartan) in the Treatment of Patients With Mild to Moderate Essential Hypertension

The purpose of this study is to investigate the efficacy and safety of Bunazosin with Valsartin compared to Doxazosin with Valsartin for patients with mild to moderate essential hypertension accompanied by metabolic syndrome.

开始日期2005-10-01

申办/合作机构

Eisai, Inc.

[+1]

100 项与盐酸布那唑嗪相关的临床结果

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100 项与盐酸布那唑嗪相关的转化医学

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100 项与盐酸布那唑嗪相关的专利（医药）

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432

项与盐酸布那唑嗪相关的文献（医药）

2024-12-01·Life Sciences

Mouse liver blood flow is regulated by hepatic stellate cells in response to the sympathetic neurotransmitter norepinephrine

Article

作者: Iwami, Kyosuke ; Yamaguchi, Momoka ; Saito, Shin-ya ; Kaneko, Yukiko K. ; Dohi, Naoki ; Kaneko, Yukiko K ; Ishikawa, Tomohisa ; Saito, Shin-Ya

BACKGROUNDThere is no clear information on the regulation of liver blood flow by the autonomic nervous system. We conducted this study to investigate whether quiescent hepatic stellate cells (qHSCs) regulate liver blood flow in response to the sympathetic neurotransmitter norepinephrine (NE).METHODSqHSCs isolated from mice were cultured in Dulbecco's modified Eagle medium without fetal bovine serum for 1 day on collagen gel. NE-induced qHSC contraction was evaluated using the quantitative single-cell contraction measurement method that we had developed previously. For the measurement of liver perfusion pressure in situ, a buffer solution was perfused from the portal vein in mice.RESULTSNE-induced a reversible contraction of qHSCs. This contraction was suppressed by the nonmuscle myosin II inhibitor blebbistatin, the myosin light chain kinase inhibitor ML-9, the Rho kinase inhibitor H-1152, the calmodulin inhibitor W-7, the store-operated calcium channel inhibitor YM-58483, and the IP₃ receptor inhibitor xestospongin C. In contrast, the transient receptor potential C channel inhibitor SKF96365 did not affect the NE-induced contraction.CONCLUSIONThese results suggest that qHSCs contract in response to NE.NEW & NOTEWORTHYThe present study provides direct evidence for the first time that norepinephrine (NE) induces a reversible contraction of isolated single quiescent hepatic stellate cells (qHSCs) and further suggests that the NE-mediated qHSC contraction participates in the regulation of liver blood flow in vivo.

2024-04-01·Biomedicine & Pharmacotherapy

Tangshen formula targets the gut microbiota to treat non-alcoholic fatty liver disease in HFD mice: A 16S rRNA and non-targeted metabolomics analyses

Article

作者: Wan, Yuzhou ; Gao, Mengqi ; Li, Yuxi ; Liu, Lin ; Chen, Kexu ; Rong, Jin ; Li, Xin ; Zhao, Tingting ; Wang, Shaopeng ; Yan, Meihua ; Dong, Xi ; Ma, Liang ; Li, Ping ; Qi, Huimin ; Zhang, Bo

BACKGROUNDTangshen formula (TSF) has an ameliorative effect on hepatic lipid metabolism in non-alcoholic fatty liver disease (NAFLD), but the role played by the gut microbiota in this process is unknown.METHODWe conducted three batches of experiments to explore the role played by the gut microbiota: TSF administration, antibiotic treatment, and fecal microbial transplantation. NAFLD mice were induced with a high-fat diet to investigate the ameliorative effects of TSF on NAFLD features and intestinal barrier function. 16S rRNA sequencing and serum untargeted metabolomics were performed to further investigate the modulatory effects of TSF on the gut microbiota and metabolic dysregulation in the body.RESULTSTSF ameliorated insulin resistance, hypercholesterolemia, lipid metabolism disorders, inflammation, and impairment of intestinal barrier function. 16S rRNA sequencing analysis revealed that TSF regulated the composition of the gut microbiota and increased the abundance of beneficial bacteria. Antibiotic treatment and fecal microbiota transplantation confirmed the importance of the gut microbiota in the treatment of NAFLD with TSF. Subsequently, untargeted metabolomics identified 172 differential metabolites due to the treatment of TSF. Functional predictions suggest that metabolisms of choline, glycerophospholipid, linoleic acid, alpha-linolenic acid, and arachidonic acid are the key metabolic pathways by which TSF ameliorates NAFLD and this may be influenced by the gut microbiota.CONCLUSIONTSF treats the NAFLD phenotype by remodeling the gut microbiota and improving metabolic profile, suggesting that TSF is a functional gut microbial and metabolic modulator for the treatment of NAFLD.

2024-03-01·Mitochondrion

DDQ anti-aging properties expressed with improved mitophagy in mutant tau HT22 neuronal cells

Article

作者: Rawat, Priyanka ; Reddy, Arubala P ; Pradeepkiran, Jangampalli Adi ; Orlov, Erika ; Reddy, P Hemachandra

The purpose of our study is to develop age-related phosphorylated tau (p-tau) inhibitors, for Alzheimer's disease (AD). There are wide-ranging therapeutic molecules available in the market and tested for age-related p-tau inhibition to enhance phosphatase activity and microtubule stability in AD neurons. Until now there are no such small molecules claimed to show promising results to delay the disease process of AD. However, a recently developed molecule, DDQ, has been shown to reduce abnormal protein-protein interactions and protect neurons from mutant protein-induced toxicities in the disease process. In addition, DDQ reduced age- and Aβ-induced oxidative stress, mitochondrial dysfunction, and synaptic toxicity. To date, there are no published reports on the p-tau interaction of DDQ and Sirt3 upregulation with CREB-mediated mitophagy activation in AD neurons. In the current study, HT22 cells were transfected with mutant Tau (mTau) cDNA and treated with the novel molecule DDQ. Cell survival, immunoblotting, and immunofluorescence analysis were conducted to assess cell viability and synaptic and mitophagy proteins in treated and untreated cell groups. As expected, we found cell survival was decreased in mTau-HT22 cells when compared with control HT22 cells. However, cell survival was increased in DDQ-treated mTau-HT22 cells when compared with mTau HT22 cells. P-tau and total tau proteins were significantly reduced in DDQ-treated mTau-HT22 cells, and MAP2 levels were increased. Anti-aging proteins like Sirt3, and CREB levels were increased in DDQ-treated HT22 cells and also in mTau-HT22 cells treated DDQ. Mitophagy proteins were decreased in mTau-HT22 cells and these were increased in DDQ-treated mTau-HT22 cells. These observations strongly suggest that DDQ has anti-p-tau and anti-aging properties, via Sirt3 overexpression and increased mitophagy proteins. Our study findings may have implications for healthy aging to the development of p-tau targeted therapeutics in AD and tauopathies.

100 项与盐酸布那唑嗪相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D01887	盐酸布那唑嗪	C02	DB12230

研发状态

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
青光眼	日本	Santen Pharmaceutical Co., Ltd.	2001-06-20
心脏衰竭	日本	Eisai Co., Ltd.	1995-02-28
高血压	日本	Eisai Co., Ltd.	1995-01-20
原发性高血压	日本	Eisai Co., Ltd.	1985-04-16
肾性高血压	日本	Eisai Co., Ltd.	1985-04-16

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


ARVO2003	N/A	-	-	Bunazosin Hydrochloride 0.01%	鬱膚鏇餘餘願構齋艱範(選蓋夢選糧齋鹽構簾鬱) = 鬱齋淵窪繭選衊餘艱壓願憲構築夢鹽遞鏇積鬱 (廠繭繭鬱構糧觸製遞願 )	积极	2003-05-01
ARVO2002	N/A	-	-	Nipradilol (1%)	(憲壓製簾鏇網範願鏇衊) = 鬱繭蓋願窪選願衊餘壓築膚夢齋夢網構憲積夢 (遞簾膚鹹廠壓鏇範願壓 )	积极	2002-12-01
ARVO2002	N/A	-	-	Timolol (0.5%) and Bunazosin (0.125%)	(憲壓製簾鏇網範願鏇衊) = 鑰製窪積觸齋範選艱遞築膚夢齋夢網構憲積夢 (遞簾膚鹹廠壓鏇範願壓 )	积极	2002-12-01