DNB-001(DNB-001) - 药物靶点：SUR_专利_临床

概要

基本信息

药物类型

小分子化药

别名

+ [1]

靶点

SUR

作用机制

SUR激动剂(磺酰脲受体激动剂)

治疗领域

眼部疾病心血管疾病

在研适应症-

非在研适应症

青光眼高血压心肌缺血+ [3]

原研机构

Danube Technologies, Inc.

在研机构-

非在研机构

Danube Pharmaceuticals, Inc.

Charlesson LLC

最高研发阶段终止临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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结构/序列

分子式C22H27N5O4

InChIKeyOZHUPJHJQIEDFA-DXIQSLLYSA-N

CAS号335381-68-5

关联

2

项与 DNB-001 相关的临床试验

NCT00683501

/ Completed临床1/2期

A Phase II Study to Investigate the Safety, Efficacy, and Pharmacokinetic Profile of Twice-Daily DNB-001 in Previously Untreated Patients With Elevated Intraocular Hypertension

A Multi-Centre, Double-Blind, Randomised, Parallel-Group, Placebo-Controlled Phase 1I Study to Investigate the Safety, Efficacy, and Pharmacokinetic Profile of Twice-Daily DNB-001 in Previously Untreated Patients with intraocular Hypertension

开始日期2007-10-01

申办/合作机构

Danube Pharmaceuticals, Inc.

EUCTR2007-002208-17-NL

/ Unknown statusN/A

A Phase IIa, Multi-Center, Double Blind, Randomized, Placebo-Controlled Trial to Evaluate the Efficacy, Safety and Pharmacokinetics of DNB-001 in Patients with Angina Pectoris and Moderate Chronic Kidney Disease Undergoing Percutaneous Coronary Intervention

开始日期2007-08-14

申办/合作机构

Danube Pharmaceuticals, Inc.

100 项与 DNB-001 相关的临床结果

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100 项与 DNB-001 相关的转化医学

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100 项与 DNB-001 相关的专利（医药）

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19

项与 DNB-001 相关的文献（医药）

2020-03-08·Huan jing ke xue= Huanjing kexue

[Influence of Antibiotics on the Denitrification Process of Antibiotic Resistant Denitrifying Bacteria and the Analysis of Microbial Community Structure].

Article

作者: Shen, Gen-Xiang ; Liu, Yu-Xue ; Li, Peng ; Peng, Wu-Qing ; Hu, Shuang-Qing ; Dai, Sha ; Wang, Zheng ; He, Yi-Liang

The removal rate of some antibiotics in urban sewage by conventional treatment is low, which leads to an increase in antibiotic resistant bacteria in natural water environments. To reduce the ecological harm of antibiotics to the water in towns, a risk control technique for degradation of microantibiotics by the co-metabolism of antibiotic resistant denitrifying bacteria was proposed. Using sodium acetate as an electron donor and maintaining the concentration of ofloxacin (OFLX) at 1 μg·g^-1, gradually increasing the dominant growth of antibiotic degradation bacteria, denitrifying bacteria (DnB₁), trace antibiotics and sodium acetate, and denitrifying bacteria (DnB₂) with the presence of sodium acetate and nitrogen elements were cultured. The degradation effect of antibiotics through denitrification and the effects of antibiotics on denitrification of resistant denitrifying bacteria and the changes to the microbial community were investigated. The results showed that DnB₂ had a significant degradation effect on OFLX compared to DnB₁. The degradation to OFLX by DnB₁ and DnB₂ was 0.31 μg·g^-1 and 16.14 μg·g^-1, respectively. Increased OFLX concentration inhibited DnB₁ denitrification activity in the short term. The denitrification process of DnB₂ was less affected by OFLX. At the same time, high-throughput sequencing using the Illumina MiSeq platform was used. Based on the operational taxonomic unit information formed by the clustering of sequencing results, the diversity of each sample was compared and analyzed. The research results show that the relative abundance and diversity of the microbial community of DnB₁ are higher than those of DnB₂.

2009-01-01·Journal of Pharmacological Sciences

KR-31378, a Potassium-Channel Opener, Induces the Protection of Retinal Ganglion Cells in Rat Retinal Ischemic Models

Article

作者: Kyung-A Kim ; Yone-Jung Yoon ; Anho Choi ; Choun-Ki Joo ; Jun-Sub Choi

KR-31378 is a newly developed K(ATP)-channel opener. To investigate the ability of KR-31378 to protect retinal ganglion cells (RGC), experiments were conducted using two retinal ischemia models. Retinal ischemia was induced by transient high intraocular pressure (IOP) for acute ischemia and by three episcleral vein occlusion for chronic retinal ischemia. KR-31378 was injected intraperitoneally and administered orally in the acute and chronic ischemia models, respectively. Under the condition of chronic ischemia, RGC density in the KR-31378-treated group was statistically higher than that in the non-treated group, and IOP was reduced. In the acute retinal ischemia model, 90% of RGC were degenerated after one week in non-treated retina, but, RGC in KR-31378-treated retina were protected from ischemic damage in a dose-dependent manner and showed inhibited glial fibrillary acidic protein (GFAP) expression. Furthermore, the KR-31378 protective effect was inhibited by glibenclamide treatment in acute ischemia. These findings indicate that systemic KR-31378 treatment may protect against ischemic injury-induced ganglion cell loss in glaucoma.

2007-05-01·Xenobiotica4区 · 医学

Disposition and metabolism of (2S,3S,4R)-N′′-cyano-N-(6-amino-3,4-dihydro-3-hydroxy-2-methyl-2-dimethoxy methyl-2H-benzopyran-4-yl)-N′-benzylguanidine, a novel neuroprotective agent for ischemia-reperfusion damage, in rats

4区 · 医学

Article

作者: Kim, N. S. ; Kim, H. S. ; Kim, D. H. ; Lee, M. W. ; Yoo, H. H.

The metabolism and disposition of KR31378 (a benzopyran derivative and a novel neuroprotective agent) were investigated following single oral or intravenous administration of [(14)C]-KR31378 to rats. [(14)C]-KR31378 was rapidly absorbed after oral dosing with an oral bioavailability of greater than 71%. The maximum plasma concentration and area under the curve of total radioactivity in rat plasma increased proportionally to the administered dose. KR31378 was distributed over all organs and tissues except for brain, eyeball and testis, and declined by first order kinetics up to 24 h after dosing. Excretion of the radioactivity was 29.5% of the dose in the urine and 58.5% in the feces within 2 days after oral administration. Biliary excretion of the radioactivity in bile duct-cannulated rats was about 66.0% for the first 24 h. KR31378 was extensively metabolized by ring hydroxylation, O-demethylation, oxidation and reduction with subsequent N-acetylation and O-glucuronide conjugation. N-acetylated conjugates (M2, M10, M11, M12, M14, and M15) were identified as the predominant metabolites in rats.

100 项与 DNB-001 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB05757

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
青光眼	临床2期	英国	Danube Pharmaceuticals, Inc.	2007-10-01
高血压	临床2期	英国	Danube Pharmaceuticals, Inc.	2007-10-01
低眼压	临床2期	英国	Danube Pharmaceuticals, Inc.	2007-10-01
心肌缺血	临床2期	韩国	Danube Pharmaceuticals, Inc.	-
高眼压症	临床2期	捷克	Danube Pharmaceuticals, Inc.	-
围手术期缺血	临床2期	韩国	-	-

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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


NCT00683501 (DNB-001, ARVO2009)	临床1/2期	-	-	DNB-001	廠網鏇壓艱廠鬱鹹蓋餘(鏇鹽範窪膚繭範顧蓋膚) = 觸積遞選夢廠願繭鹽觸範網繭製築願夢壓餘齋 (觸獵蓋齋蓋衊襯壓鹹夢 )	-	2009-04-01