This double-blind, placebo-controlled, dose-finding study is designed to identify the lowest AGI-1067 dose that improves glycemic control as measured by HbA1c and fasting glucose in subjects with Type 2 diabetes mellitus. Glycemic control will be measured during a 6-month treatment period in subjects who are on 1 or no antidiabetic drugs

Start Date01 Aug 2007

Sponsor / Collaborator

AtheroGenics, Inc.

NCT00066898

/ Unknown statusPhase 3

"Reduction of Vascular Inflammation and Coronary Atherosclerosis With AGI-1067, a V-Protectant, Reduces Cardiovascular Events in Patients With Coronary Artery Disease"

To assess the safety and efficacy of AGI-1067, as compared to placebo, in the treatment of vascular inflammation and atherosclerosis by assessing the reduction in cardiovascular events.

Start Date01 Jun 2003

Sponsor / Collaborator

AtheroGenics, Inc.

100 Clinical Results associated with Succinobucol

100 Translational Medicine associated with Succinobucol

100 Patents (Medical) associated with Succinobucol

Literatures (Medical) associated with Succinobucol

01 Jun 2022·BMJ open

Examining anti-inflammatory therapies in the prevention of cardiovascular events: protocol for a systematic review and network meta-analysis of randomised controlled trials

Article

Author: Geejo, Aishwarya ; Pearson, Alexander Liam ; Shin, Sheojung ; Beanlands, Rob ; Wells, George A ; Fehlmann, Christophe A ; Visintini, Sarah ; Shahab, Saba ; Bezzina, Kathryn A ; Boczar, Kevin Emery

Introduction:

Inflammation is emerging as an important risk factor for atherosclerotic cardiovascular disease and has been a recent target for many novel therapeutic agents. However, comparative evidence regarding efficacy of these anti-inflammatory treatment options is currently lacking.

Methods and analysis:

This systematic review will include randomised controlled trials evaluating the effect of anti-inflammatory agents on cardiovascular outcomes in patients with known cardiovascular disease. Studies will be retrieved from Medline, Embase, the Cochrane Central Register of Controlled Trials, as well as clinical trial registry websites, Europe PMC and conference abstract handsearching. No publication date or language restrictions will be imposed. Eligible interventions must have some component of anti-inflammatory agent. These include (but are not limited to): non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, prednisone, methotrexate, canakinumab, pexelizumab, anakinra, succinobucol, losmapimod, inclacumab, atreleuton, LP-PLA2(darapladib) and sPLA2(varespladib). The primary outcomes will include major adverse cardiac events (MACE), and each individual component of MACE (myocardial infarction, stroke and cardiovascular death). Key secondary outcomes will include unstable angina, heart failure, all-cause mortality, cardiac arrest and revascularisation. Screening, inclusion, data extraction and quality assessment will be performed independently by two reviewers. Network meta-analysis based on the random effects model will be conducted to compare treatment effects both directly and indirectly. The quality of the evidence will be assessed with appropriate tools including the Grading of Recommendations, Assessment, Development and Evaluation profiler or Confidence in Network Meta-Analysis tool.

Ethics and dissemination:

Ethics approval is not required for this systematic review. The findings will be disseminated through a peer-reviewed journal.

PROSPERO registration number:

CRD42022303289.

14 Apr 2021·Nano lettersQ1 · MATERIALS SCIENCE

Preferential Targeting Cerebral Ischemic Lesions with Cancer Cell-Inspired Nanovehicle for Ischemic Stroke Treatment

Q1 · MATERIALS SCIENCE

Article

Author: Sha, Xianyi ; Zhai, Yuting ; Zhang, Xiao-Yong ; Zhang, Zhiwen ; Mei, Qiyong ; Wang, Rui ; Chen, Yiting ; Lu, Enhao ; Li, Jie ; He, Wenxiu

The poor drug delivery to cerebral ischemic regions is a key challenge of ischemic stroke treatment. Inspired by the intriguing blood-brain barrier (BBB)-penetrating ability of 4T1 cancer cells upon their brain metastasis, we herein designed a promising biomimetic nanoplatform by camouflaging a succinobucol-loaded pH-sensitive polymeric nanovehicle with a 4T1 cell membrane (MPP/SCB), aiming to promote the preferential targeting of cerebral ischemic lesions to attenuate the ischemia/reperfusion injury. In transient middle cerebral artery occlusion (tMCAO) rat models, MPP/SCB could be preferentially delivered to the ischemic hemisphere with a 4.79-fold higher than that in the normal hemisphere. Moreover, MPP/SCB produced notable enhancement of microvascular reperfusion in the ischemic hemisphere, resulting in a 69.9% reduction of infarct volume and showing remarkable neuroprotective effects of tMCAO rats, which was superior to the counterpart uncamouflaged nanovehicles (PP/SCB). Therefore, this design provides a promising nanoplatform to target the cerebral ischemic lesions for ischemic stroke therapy.

30 Nov 2018·International heart journalQ4 · MEDICINE

Novel ASK1 Inhibitor AGI-1067 Attenuates AGE-Induced Fibrotic Response by Suppressing the MKKs/p38 MAPK Pathway in Human Coronary Arterial Smooth Muscle Cells

Q4 · MEDICINE

Article

Author: Shi, Shuang ; Zheng, Zhenzhong ; Liu, Zhongwei ; Zhu, Haitao ; Chen, Yunfei ; Zhang, Yong ; Wang, Xi

The phenotype shifting of vascular smooth muscle cells (VSMCs) was indicated to play a role during the initial stage of atherosclerotic plaque formation by facilitating extracellular matrix deposition. This study was aimed at investigating the involvement of the apoptosis signal-regulating kinase 1 (ASK1) /mitogen-activated protein kinase (MAPK) kinases (MKKs) /p38 MAPK pathway in the advanced glycation end product (AGE) -induced fibrotic response of VSMCs. The effect of the novel ASK1 inhibitor AGI-1067 was also studied.Cultured human coronary smooth muscle cells (HCSMCs) were exposed to AGEs. AGI-1067 and siRNAs silencing mkk3, mkk6, and p38 mapk were used to treat the cells. The activation of MKK3, MKK6, and p38 MAPK was assessed by immunoblotting. Fibrotic response was assessed by the fluorescence immunohistochemistry staining of collagen I and collagen VIII. Activation of immunoprecipitation determined the association of ASK1 and its inhibitor thioredoxin. A kinase assay was used to determine ASK1 activity.AGE incubation significantly activated ASK1, MKK3, and MKK6, which led to activation of p38 MAPK, resulting in upregulated fibrotic response in HCSMCs. However, siRNAs knocking down mkk3, mkk6, and p38 mapk impaired this fibrotic response. AGI-1067 administration not only dramatically inhibited the activation of ASK1/MKKs/p38 MAPK but also suppressed the expression of the downstream proteins, including transforming growth factor-β1, connective tissue growth factor, collagen I, and collagen VIII in HCSMCs exposed to AGEs.The ASK1/MKKs/p38 MAPK pathway was activated by AGEs, leading to the fibrotic response in VSMCs. AGI-1067 reversed this process by maintaining the inactive state of ASK1.

News (Medical) associated with Succinobucol

31 Jul 2007

·www.biospace.com

AtheroGenics Follows a New Route

Development-stage drugmakers rarely ever close up shop following a failed drug program so as long as they have cash in the bank to fund some sort of clinical trial development. This is the case with AtheroGenics (Nasdaq: AGIX) following the failed testing of its AGI-1067 drug compound earlier this year.AtheroGenics and partner AstraZeneca (NYSE: AZN) announced in March that AGI-1067 failed a large, 6,000 patient study testing the compound as a treatment for atherosclerosis. Even though the primary endpoints of the study were unsuccessful, AGI-1067 may have shown some efficacy in helping patients with diabetes control their blood glucose levels.

Clinical Study

15 Feb 2006

·www.biospace.com

AtheroGenics Schedules 2005 Fourth Quarter And Year-End Results Conference Call For February 28, 2006

ATLANTA, Feb. 15 /PRNewswire-FirstCall/ -- AtheroGenics, Inc. , a pharmaceutical company focused on the treatment of chronic inflammatory diseases, today announced that it expects to release its fourth quarter and fiscal 2005 year-end results of operations on Tuesday, February 28, 2006, before the U.S. financial markets open. (Logo: ) Company officials will provide a company update and discuss fourth quarter and 2005 year-end results via conference call and webcast on Tuesday, February 28, 2006, at 9:00 a.m. ET. The conference call may be accessed by dialing 1- 877-407-8031 (domestic) or 1-201-689-8031 (international), five minutes prior to the start time. A replay of the call will be available from 11:00 a.m. ET on February 28, until 11:59 p.m. ET on March 7, 2006. Rebroadcast numbers are 1-877-660-6853 (domestic) or 1-201-612-7415 (international), account number 286 and conference ID number 188890. To access the webcast, log on to the Company's Investor Relations Web site and click on the Webcast Access link. An archived version of this webcast will be available at the same location through April 21, 2006. About AtheroGenics AtheroGenics is focused on the discovery, development and commercialization of novel drugs for the treatment of chronic inflammatory diseases, including heart disease (atherosclerosis), rheumatoid arthritis and asthma. The Company has two drug development programs currently in the clinic. AtheroGenics' lead compound, AGI-1067, is being evaluated in the pivotal Phase III ARISE clinical trial as an oral therapy for the treatment of atherosclerosis, in collaboration with AstraZeneca. AGI-1096 is a novel, oral agent in Phase I that is being developed for the prevention of organ transplant rejection in collaboration with Astellas. AtheroGenics also has preclinical programs in rheumatoid arthritis and asthma utilizing its proprietary vascular protectant(R) technology. For more information about AtheroGenics, please visit . Photo: AP Archive: PRN Photo Desk, photodesk@prnewswire.comAtheroGenics, Inc. CONTACT: Corporate Communications, Donna Glasky of AtheroGenics, Inc.,+1-678-336-2517, or investor@atherogenics.com; or Investor Relations,Lilian Stern of Stern Investor Relations, +1-212-362-1200, orlilian@sternir.com; or Media Relations, Katie Brazel of Fleishman Hillard,+1-404-739-0150, or brazelk@fleishman.com Web site:

100 Deals associated with Succinobucol

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KEGG	Wiki	ATC	Drug Bank
D06648	-	-	DB05399

R&D Status

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Indication	Highest Phase	Country/Location	Organization	Date
Diabetes Mellitus	Phase 3	United States	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	Bosnia and Herzegovina	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	Georgia	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	India	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	Montenegro	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	North Macedonia	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	South Africa	AtheroGenics, Inc.	01 Aug 2007
Diabetes Mellitus	Phase 3	Ukraine	AtheroGenics, Inc.	01 Aug 2007
Acute myocardial infarction	Phase 3	United States	AtheroGenics, Inc.	01 Jun 2003
Acute myocardial infarction	Phase 3	Canada	AtheroGenics, Inc.	01 Jun 2003

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