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35

项与 R.W. Johnson Pharmaceutical Research Institute 相关的药物

Levofloxacin

左氧氟沙星

靶点

Bacterial DNA gyrase x Bacterial top IV

作用机制

Bacterial DNA gyrase 抑制剂 [+1]

在研机构

CHIESI Farmaceutici SpA [+5]

原研机构

Johnson & Johnson

在研适应症

外耳炎 [+31]

非在研适应症

脓肿 [+35]

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期1996-12-20

MC-02306

靶点-

作用机制

细胞壁抑制剂

在研机构-

原研机构

Essential Therapeutics, Inc.

在研适应症-

非在研适应症

粪肠球菌感染 [+1]

最高研发阶段终止

首次获批国家/地区-

首次获批日期-

RWJ-63556

靶点

5-LOX x COX-2

作用机制

5-LOX抑制剂 [+1]

在研机构-

原研机构

R.W. Johnson Pharmaceutical Research Institute

在研适应症-

非在研适应症

炎症

最高研发阶段终止

首次获批国家/地区-

首次获批日期-

3

项与 R.W. Johnson Pharmaceutical Research Institute 相关的临床试验

NCT00002249

/ Completed临床1期

A Double-Blind Study to Evaluate the Safety and Pharmacokinetics of L-Ofloxacin (RWJ 25213) in Subjects With HIV Infection

To determine the safety and pharmacokinetics of L-ofloxacin (RWJ 25213) in patients with HIV infection.

开始日期-

申办/合作机构

R.W. Johnson Pharmaceutical Research Institute

NCT00002022

/ CompletedN/A

Treatment Program for Anemia in AIDS Patients

The objective of the Eprex (erythropoietin) Treatment Program is to provide erythropoietin for the treatment of anemia in AIDS patients.

开始日期-

申办/合作机构

R.W. Johnson Pharmaceutical Research Institute

NCT02040311

/ Terminated临床4期

A Multicenter Randomized, Double-blind, Placebo-controlled, Parallel Group Study of the Efficacy and Safety of Topiramate in Weight Loss Maintenance in Obese Subjects Following Participation in an Intensive, Non-pharmacologic Weight Loss Program

The purpose of this study is to determine the efficacy and safety of topiramate (96 mg or 192 mg daily) as compared to placebo in maintaining weight loss in obese subjects who participated in an eight week intensive non-pharmacologic weight loss program.
The primary efficacy endpoint will be the percent change in body weight from enrollment visit to week 60.

开始日期2000-08-01

申办/合作机构

University of Copenhagen

[+1]

100 项与 R.W. Johnson Pharmaceutical Research Institute 相关的临床结果

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0 项与 R.W. Johnson Pharmaceutical Research Institute 相关的专利（医药）

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737

项与 R.W. Johnson Pharmaceutical Research Institute 相关的文献（医药）

2007-12-01·Antimicrobial Agents and Chemotherapy2区 · 医学

Drugs Designed To Inhibit Human p38 Mitogen-Activated Protein Kinase Activation TreatToxoplasma gondiiandEncephalitozoon cuniculiInfection

2区 · 医学

Article

作者: Zou, Weiping ; Daniel, Benjamin J. ; Siekierka, John ; Wadsworth, Scott ; Curiel, Tyler J. ; Brumlik, Michael J. ; Khan, Imtiaz A. ; Burow, Matthew E. ; Wei, Shuang

ABSTRACTWe recently showed that the pyridinylimidazoles SB203580 and SB202190, drugs designed to block human p38 mitogen-activated protein kinase (MAPK) activation, also inhibited replication of the medically important intracellular parasiteToxoplasma gondiiin cultured human fibroblasts through a direct effect on the parasite. We now show that additional pyridinylimidazole and imidazopyrimidine p38 MAPK inhibitors inhibit intracellularT. gondiireplication in vitro and protect mice against fatalT. gondiiinfection. Mice surviving infection following treatment with p38 MAPK inhibitors were resistant to subsequentT. gondiichallenge, demonstrating induction of protective immunity. Thus, drugs originally developed to block human p38 MAPK activation are useful for treatingT. gondiiinfection without inducing significant immunosuppression. MAPK inhibitors combined with either of the approved anti-Toxoplasmadrugs sulfadiazine and pyrimethamine resulted in improved survival among mice challenged with a fatalT. gondiiinoculum. A MAPK inhibitor also treated mice infected with theMicrosporidiumparasiteEncephalitozoon cuniculi, suggesting that MAPK inhibitors represent a novel class of agents that may have a broad spectrum of antiparasitic activity. Preliminary studies implicate aT. gondiiMAPK homologue as the target of drug action, suggesting possibilities for more-selective agents.

2004-12-01·Journal of Endotoxin Research

p38-MAPK inhibition and endotoxin induced tubular dysfunction in men

作者: Zijlstra, Jan G. ; Ligtenberg, Jack J.M. ; van der Werf, Tjip S. ; de Boer, Peter ; Tulleken, Jaap E.

Background: To evaluate the possibility of preventing endotoxin induced renal damage by p38-MAPK inhibition in a human model.Design and Methods: Twenty-one healthy young male volunteers received 4 ng/kg Escherichia coli endotoxin as a single dose. Four groups of volunteers received an oral dose of placebo or 350, 700 or 1400 mg RWJ-67657, a p38-MAPK inhibitor, 20 min before endotoxin infusion. Urine samples were collected at set time intervals. The urinary excretion rate of β2-microglobulin and N-acetyl-β-D-glucosaminidase, as indicators of tubular dysfunction was determined.Results: There was a significant increase of β2-microglobulin and N-acetyl-β-D-glucosaminidase urine excretion rate after endotoxin infusion in the placebo group. p38-MAPK inhibition prevented the increase of markers for tubulopathy.Conclusions: Endotoxin infusion induces measurable tubular damage. Blocking the p38-MAPK may prevent this damage. The mechanism is unclear, but blocking TNF-α release is a possible explanation.

2004-12-01·Journal of Endotoxin Research

p38-MAPK inhibition and endotoxin induced tubular dysfunction in men

Article

作者: Jaap E. Tulleken ; Jan G. Zijlstra ; Peter de Boer ; Tjip S. van der Werf ; Jack J.M. Ligtenberg

BACKGROUNDTo evaluate the possibility of preventing endotoxin induced renal damage by p38-MAPK inhibition in a human model.DESIGN AND METHODSTwenty-one healthy young male volunteers received 4 ng/kg Escherichia coli endotoxin as a single dose. Four groups of volunteers received an oral dose of placebo or 350, 700 or 1400 mg RWJ-67657, a p38-MAPK inhibitor, 20 min before endotoxin infusion. Urine samples were collected at set time intervals. The urinary excretion rate of beta(2)-microglobulin and N-acetyl-beta-D-glucosaminidase, as indicators of tubular dysfunction was determined.RESULTSThere was a significant increase of beta(2)-microglobulin and N-acetyl-beta-D-glucosaminidase urine excretion rate after endotoxin infusion in the placebo group. p38-MAPK inhibition prevented the increase of markers for tubulopathy.CONCLUSIONSEndotoxin infusion induces measurable tubular damage. Blocking the p38-MAPK may prevent this damage. The mechanism is unclear, but blocking TNF-alpha release is a possible explanation.

100 项与 R.W. Johnson Pharmaceutical Research Institute 相关的药物交易

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100 项与 R.W. Johnson Pharmaceutical Research Institute 相关的转化医学

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当前项目

药物(靶点)	适应症	全球最高研发状态

RWJ-22108 ( calcium channel )	哮喘更多	终止
RWJ-63556 ( 5-LOX x COX-2 )	炎症更多	终止
Perflubron Emulsion(Alliance)	输血反应更多	终止
MC-02306	葡萄球菌感染更多	终止
RWJ-46458 ( AT1R )	高血压更多	终止