ADR-001(ADR-001) - 药物靶点：ADAR_在研适应症：新型冠状病毒感染，失代偿性肝硬化，免疫球蛋白a肾病_专利_临床

概要

基本信息

药物类型

间充质干细胞疗法

别名

靶点

ADAR

作用机制

ADAR抑制剂(adenosine deaminase RNA specific inhibitors)

治疗领域

感染呼吸系统疾病消化系统疾病+ [2]

在研适应症

新型冠状病毒感染失代偿性肝硬化免疫球蛋白a肾病

非在研适应症-

原研机构

Rohto Pharmaceutical Co., Ltd.

在研机构

Rohto Pharmaceutical Co., Ltd.

非在研机构-

最高研发阶段临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

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关联

19

项与 ADR-001 相关的临床试验

JPRN-jRCT2033220602 / Not yet recruitingN/AIIT

Continuous observation study after administration of ADR-001 in patients with Compensated Liver Cirrhosis

开始日期2023-02-14

申办/合作机构-

JPRN-jRCT2073220005 / Recruiting临床1期IIT

ADR-001 in Patients with Comprehensive Advanced Chronic Leg Ischemia Phase I Study to Evaluate Safety and Efficacy - ADR-04

开始日期2022-04-23

申办/合作机构-

JPRN-jRCT2033210425 / Not yet recruiting临床2期IIT

A Phase II Study of ADR-001 in Patients with Compensated Liver Cirrhosis

开始日期2022-02-08

申办/合作机构-

100 项与 ADR-001 相关的临床结果

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100 项与 ADR-001 相关的转化医学

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100 项与 ADR-001 相关的专利（医药）

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6

项与 ADR-001 相关的文献（医药）

2008-11-28·Journal of Microbiology and Biotechnology4区 · 工程技术

Bacterial Community and Biological Nitrate Removal: Comparisons of Autotrophic and Heterotrophic Reactors for Denitrification with Raw Sewage

4区 · 工程技术

Article

作者: Lee, Jin Woo ; Choi, Euiso ; Park, Yong Keun ; Lee, Han Woong

An autotrophic denitrification reactor (ADR-1) and a heterotrophic denitrification reactor (HDR-2) were operated to remove nitrate and nitrite in an anoxic environment in raw sewage. The NO3-N removal rate of ADR-1 was shown to range from 52.8% to 78.7%, which was higher than the NO3-N removal rate of HDR-2. Specific denitrification rates (SDNR) of ADR-1 and HDR-2 were 3.0 to 4.0 and 1.1 to 1.2mgNO3- N/gVSS/h, respectively. From results of restriction fragment length polymorphism (RFLP) of the 16S rRNA gene, Aquaspirillum metamorphum, Alcaligenes defragrans, and Azoarcus sp. were beta-Proteobacteria that are affiliated with denitrifying bacteria in the ADR-1. Specifically, Thiobacillus denitrificans was detected as an autotrophic denitrification bacteria. In HDR-2, the beta-Proteobacteria such as Denitrifying- Fe-oxidizing bacteria, Alcaligenes defragrans, Acidovorax sp., Azoarcus denitrificans, and Aquaspirillum metamorphum were the main bacteria related to denitrifying bacteria. The beta-and alpha-Proteobacteria were the important bacterial groups in ADR-1, whereas the beta-Proteobacteria were the main bacterial group in HDR-2 based on results of fluorescent in situ hybridization (FISH). The number of Thiobacillus denitrificans increased in ADR-1 during the operation period but not in HRD-2. Overall, the data presented here demonstrate that many heterotrophic denitrifying bacteria coexisted with autotrophic denitrifying bacteria such as Thiobacillus denitrificans for nitrate removal in ADR-1. On the other hand, only heterotrophic denitrifying bacteria were identified as dominant bacterial groups in HDR-2. Our research may provide a foundation for the complete nitrate removal in raw sewage of low-COD concentration under anoxic condition without any external organic carbon or the requirement of post-treatment.

2003-04-01·The Canadian journal of cardiology

The protective effect of melatonin on adriamycin-induced acute cardiac injury.

Article

作者: Erbil, K Mine ; Tuncel, Mürvet ; Aydemir, Songül ; Sunar, Bülbin ; Atalay, Semra ; Koçak, Gülendam ; Ozdemir, Ilknur

BACKGROUNDCardiotoxicity is the main complication of adriamycin (ADR), which is a widely used chemotherapeutic agent.OBJECTIVETo examine the potential cardioprotective effect of melatonin (MEL) on acute ADR cardiotoxicity in a rat model.METHODSCardioprotection was assessed on the basis of myocardial lipid peroxidation and ultrastructure. Rats were given MEL at a daily dose of 5 mg/kg and ADR 15 mg/kg, intraperitoneally. The MEL-1 group rats received one dose and the MEL-7 group rats six daily doses of MEL and were sacrificed at the end of one and seven days, respectively. Rats in the ADR-1 and ADR-7 groups were each given a single dose of ADR, and were then sacrificed 24 h and seven days later, respectively. The MEL+ADR-1 group rats received one dose each of ADR and MEL simultaneously and were sacrificed 24 h later. The MEL+ADR-7 group received a single dose of ADR plus a daily MEL dose for six consecutive days, and were sacrificed seven days after the ADR injection.RESULTSLipid peroxidation products were elevated in both ADR-1 and ADR-7 groups, and this elevation was significantly inhibited by MEL treatment. Electron microscopy confirmed that ADR was positively cardiotoxic after one and seven days of exposure. The extent of ADR-induced myocardial damage was markedly reduced when MEL was combined with ADR (MEL+ADR-1 and MEL+ADR-7).CONCLUSIONThe results suggest that MEL is highly efficacious at reducing the acute cardiotoxic effects of high dose ADR, and that it acts by preventing lipid peroxidation.

1996-10-01·Biochemical Pharmacology2区 · 医学

Development of anthracenyl-amino acid conjugates as topoisomerase I and II inhibitors that circumvent drug resistance

2区 · 医学

Article

作者: Jeffrey Cummings ; John F. Smyth ; Ian Meikle ; Janet S. Macpherson

Anthracenyl-amino acid conjugates (AAC) represent a novel class of topoisomerase (topo) inhibitor. The relationship between mechanism of enzyme inhibition and in vitro cytotoxicity has been investigated in a panel of 5 Chinese hamster ovary (CHO) and 2 human ovarian cancer cell lines (A2780) shown to possess different drug resistance phenotypes associated with altered expression of topo I and topo II. From a total of 13 compounds, 4 displayed broad-spectrum activity (IC50 ranging from 3.5-29.7 microM). NU/ICRF 500 (topo II catalytic inhibitor) was 1.4-fold more active against CHO ADR-1, which overexpresses topo II and was essentially noncross-resistant in CHO ADR-r (13.9-fold resistant to doxorubicin (DOX)) and 2780AD (1,460-fold resistant to DOX). NU/ICRF 505, which stabilises topo I cleavable complexes, was noncross-resistant in CHO ADR-3 (3,4-fold resistant to camptothecin) and only 1.8-fold cross-resistant in 2780AD. Hypersensitivity was recorded in ADR-r that overexpresses topo I. The most active compound was NU/ICRF 506, a dual catalytic inhibitor of topo I and II. Hypersensitivity was observed in ADR-r (1.4-fold) but not ADR-1, indicating that topo I is the likely nuclear target, and a low level of resistance was seen in the CHO ADR-6 drug transport mutant and 2780AD. The topo II catalytic inhibitor NU/ICRF 513 only produced hypersensitivity in ADR-r. These data suggest that NU/ICRF 500, 505, and 506 induce cell death, at least partly, through topo inhibition. NU/ICRF 513 appears to be cytotoxic via a nontopo mechanism of action. In addition, NU/ICRF 505 significantly inhibited the growth of two human xenografts (HT-29 colon cancer and NX002 nonsmall-cell lung cancer) in nude mice after i.p. administration at a dose of 25 mg/kg. The important properties of noncross-resistance and in vivo antitumour activity merit further development of AAC as potential new anticancer drugs.

100 项与 ADR-001 相关的药物交易

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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
新型冠状病毒感染	临床2期	日本	Rohto Pharmaceutical Co., Ltd.	2021-06-15
失代偿性肝硬化	临床2期	日本	Rohto Pharmaceutical Co., Ltd.	2017-07-20
免疫球蛋白a肾病	临床1期	日本	Rohto Pharmaceutical Co., Ltd.	2020-06-15