PG-116800(PG-116800) - 药物靶点：MMPs_专利_临床

概要

基本信息

药物类型

小分子化药

别名

+ [1]

靶点

MMPs

作用机制

MMPs抑制剂(基质金属蛋白酶家族抑制剂)

治疗领域

免疫系统疾病心血管疾病皮肤和肌肉骨骼疾病

在研适应症-

非在研适应症

心脏肥大心脏衰竭心肌梗塞+ [1]

原研机构

Procter & Gamble Co.

在研机构-

非在研机构

Procter & Gamble, Inc.

最高研发阶段无进展临床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

分子式C24H27N3O7S

InChIKeyJAYVKNDQKXUNOJ-UHFFFAOYSA-N

CAS号291533-11-4

关联

2

项与 PG-116800 相关的临床试验

NCT00067236 / Completed临床2期

A Multicenter, Randomized, Double-blind, Placebo-controlled Study of Oral PG-116800 Following a Heart Attack

The main purpose of the study is to test whether a possible new drug (called PG-116800) can prevent some of the damage to heart muscle in patients who have had a heart attack. The study will also supply information regarding possible uses of this compound in cardiovascular disease.

开始日期2003-09-01

申办/合作机构

Procter & Gamble, Inc.

NCT00041756 / Completed临床2期

Efficacy and Safety of PG-530742 in the Treatment of Mild to Moderate Knee Osteoarthritis

Matrix metalloproteinases (MMPs) have been implicated in the cartilage degradation. PG-530742 inhibits some MMPs, potentially limiting cartilage degradation and disease progression. This study will test the efficacy and safety of PG-530742 in the treatment of mild to moderate knee osteoarthritis.

开始日期2002-07-01

申办/合作机构

Procter & Gamble, Inc.

100 项与 PG-116800 相关的临床结果

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100 项与 PG-116800 相关的转化医学

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100 项与 PG-116800 相关的专利（医药）

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9

项与 PG-116800 相关的文献（医药）

2023-01-01·The archives of bone and joint surgery

The Current Role of Disease-modifying Osteoarthritis Drugs.

Review

作者: Rodriguez-Merchan, E Carlos

Contemporary treatments for osteoarthritis (OA) pursue only to alleviate the pain caused by the illness. Discovering disease-modifying osteoarthritis drugs (DMOADs) that can induce the repair and regeneration of articular tissues would be of substantial usefulness. The purpose of this manuscript is to review the contemporary role of DMOADs in managing OA. A narrative literature review on the subject, exploring the Cochrane Library and PubMed (MEDLINE) was performed. It was encountered that many publications have analyzed the impact of several DMOAD methods, including anti-cytokine therapy (tanezumab, AMG 108, adalimumab, etanercept, anakinra), enzyme inhibitors (M6495, doxycycline, cindunistat, PG-116800), growth factors (bone morphogenetic protein-7, sprifermin), gene therapy (micro ribonucleic acids, antisense oligonucleotides), peptides (calcitonin) and others (SM04690, senolitic, transient receptor potential vanilloid 4, neural EGFL-like 1, TPCA-1, tofacitinib, lorecivivint and quercitrin). Tanezumab has been demonstrated to alleviate hip and knee pain in individuals with OA but can cause major adverse events (osteonecrosis of the knee, rapid illness progression, augmented prevalence of total joint arthroplasty of involved joints, particularly when tanezumab is combined with nonsteroidal anti-inflammatory drugs. SM04690 (a Wnt inhibitor) has been demonstrated to be safe and efficacious in alleviating pain and ameliorating function as measured by the Western Ontario and McMaster Universities Arthritis Index. The intraarticular injection of lorecivivint is deemed safe and well tolerated, with no important reported systemic complications. In conclusion, even though DMOADs seem promising, their clinical effectiveness has not yet been demonstrated for managing OA. Until forthcoming studies can proved the medications' capacity to repair and regenerate tissues affected by OA, physicians should keep using treatments that only intend to alleviate pain.

2008-11-01·Journal of Cardiac Failure2区 · 医学

Matrix Metalloproteinase Inhibition Attenuates Atrial Remodeling and Vulnerability to Atrial Fibrillation in a Canine Model of Heart Failure

2区 · 医学

Article

作者: Xudong Hu ; Gordon W. Moe ; Liia Doumanovskaia ; Gabriel Laurent ; Paul Dorian ; Andrea Konig

BACKGROUNDAtrial structural remodeling occurs in evolving heart failure (HF) and is an important substrate for the development of atrial fibrillation (AF). The matrix metalloproteinases (MMPs) play a role in extracellular remodeling, and recent studies have demonstrated increased atrial MMP activity in HF. Whether increased MMP activity directly contributes to atrial remodeling and AF in the setting of HF remains unclear. The current study examined the effects of MMP inhibition on atrial structural remodeling and AF vulnerability during HF progression.METHODS AND RESULTSThree groups of dogs (n = 5 each)--control normal dogs (controls) and 10 dogs subjected to simultaneous atrioventricular pacing (SAVP) for 2 weeks to induce HF and randomly assigned to treatment with placebo (SAVP-placebo) or a MMP inhibitor PGE-7113313, a MMP-1-sparing MMP inhibitor, 6 mg/kg orally twice daily (SAVP-MMPi)--were studied. SAVP-MMPi dogs had less AF inducibility (percent of burst attempts leading to AF episodes: 1.7 +/- 2.9 seconds vs. 23+/-19 seconds, mean +/- SD, P < .05) and maintenance (AF duration: 253 [105 to 326] vs. 1932 [1296 to 2724] seconds, median [25th-75th quartile], P < .05) than SAVP-placebo dogs. The SAVP-MMPi dogs had significantly smaller increases in atrial myocyte cross sectional area, collagen area fraction, and MMP-9 activity relative to controls than SAVP-placebo. There were, however, no significant differences in the changes in chamber dimension and function in the left atrium.CONCLUSIONSThis unique finding of an attenuation of the vulnerability to AF in conjunction with reduced myocyte hypertrophy and fibrosis after MMP inhibition suggests that heightened MMP activity in the atria contributes to atrial structural remodeling and AF promotion during evolving HF.

2007-01-01·Arthritis Research & Therapy2区 · 医学

The quest for the Holy Grail: a disease-modifying osteoarthritis drug

2区 · 医学

OA

作者: Francis Berenbaum

The unfortunate story of the matrix metalloproteinase inhibitor PG116800, which had no effect on the osteoarthritic process but had unexpected side effects, highlights the following. First, reality does not always match the theory. Second, cell biology data must be interpreted within the context of a specific environment. Third, the specificity of an enzyme inhibitor is always relative. Finally, a critical evaluation of the benefit/risk ratio of a drug must be carefully conducted and checked before and after launch. Well designed post-marketing surveillance is mandatory.

100 项与 PG-116800 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB05495

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
心脏肥大	临床2期	美国	Procter & Gamble, Inc.	2003-09-01
心脏肥大	临床2期	波兰	Procter & Gamble, Inc.	2003-09-01
心脏肥大	临床2期	加拿大	Procter & Gamble, Inc.	2003-09-01
心脏衰竭	临床2期	加拿大	Procter & Gamble, Inc.	2003-09-01
心脏衰竭	临床2期	波兰	Procter & Gamble, Inc.	2003-09-01
心肌梗塞	临床2期	美国	Procter & Gamble, Inc.	2003-09-01
心肌梗塞	临床2期	波兰	Procter & Gamble, Inc.	2003-09-01
心肌梗塞	临床2期	加拿大	Procter & Gamble, Inc.	2003-09-01
膝关节炎	临床2期	英国	Procter & Gamble, Inc.	2002-07-01
膝关节炎	临床2期	匈牙利	Procter & Gamble, Inc.	2002-07-01

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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


NCT00041756 (CTgov)	临床2期	膝关节炎	395	PG-530742 (25 mg PG-530742)	廠窪蓋遞遞鹹憲網網遞(遞獵獵獵廠簾範膚齋簾) = 獵構鹽積獵鏇繭簾艱鑰糧膚夢壓顧願憲製鹽願 (構廠獵憲鬱壓網繭鏇齋, 壓襯廠鬱鏇簾衊醖襯鏇 ~ 糧淵觸網顧簾築觸襯網) 更多	-	2011-11-08
NCT00041756 (CTgov)	临床2期	膝关节炎	395	50 mg PG-530742 (50 mg PG-530742)	廠窪蓋遞遞鹹憲網網遞(遞獵獵獵廠簾範膚齋簾) = 醖範醖選窪餘網鹽夢襯糧膚夢壓顧願憲製鹽願 (構廠獵憲鬱壓網繭鏇齋, 鬱選選選選獵醖壓夢願 ~ 鑰製網醖糧鏇廠夢廠顧) 更多	-	2011-11-08
NCT00067236 (CTgov)	临床2期	心肌梗塞 \| 心脏肥大 \| 心脏衰竭	253	PG-116800 (given as PG-530742)	願鑰淵醖膚鹹範齋願衊(壓窪鏇夢廠壓齋壓廠鹹) = 廠襯齋鑰夢襯憲夢範衊選蓋遞醖餘選築獵製糧 (窪簾選齋衊淵範廠遞鹽, 醖繭淵襯壓夢製製艱蓋 ~ 衊簾獵構願鬱鑰憲鑰淵) 更多	-	2011-11-04