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Chemical Compound Review

Succinobucol     4-[4-[2-(4-hydroxy-3,5- ditert-butyl...

Synonyms: CHEMBL83626, AGI-1067, AGZ-1067, AG-K-57691, AGI1067, ...
 
 
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Disease relevance of AGI-1067

 

High impact information on AGI-1067

  • RECENT FINDINGS: AGI-1067, the mono-succinic acid ester of probucol, is a phenolic antioxidant member of a novel class of agents termed v-protectants [4].
  • The inhibitory effect of AGI-1067 on inducible VCAM-1 gene expression occurred at the transcriptional level, yet AGI-1067 had no effect on the activation of the redox-sensitive transcription factor NF-kappaB [5].
  • These studies suggest that the anti-inflammatory and antiatherosclerotic properties of AGI-1067 may be due to selective inhibition of redox-sensitive endothelial and monocyte inflammatory gene expression [5].
  • In ApoE -/- mice, AGI-1067 reduced atherosclerosis by 25, 41, and 49% in the arch, thoracic, and abdominal regions of the aorta [6].
  • AGI-1067 also inhibited atherosclerosis in LDL receptor-deficient (LDLr -/-) mice and apolipoprotein E-deficient (ApoE -/-) mice even in the absence of a lipid-lowering effect [6].
 

Biological context of AGI-1067

  • At the cellular level, AGI-1067 inhibited tumor necrosis factor-alpha-inducible expression of VCAM-1, MCP-1, and E-selectin in human aortic endothelial cells (IC50 values = 6, 10, and 25 microM, respectively) [6].
  • Considering that oxidative stress and inflammation may persist for a prolonged period after stent placement, treatment with AGI-1067 for the entire period of risk after percutaneous coronary intervention (PCI) [instead of only 4 weeks in CART-1] may result in enhanced protection against luminal renarrowing [7].
 

Anatomical context of AGI-1067

  • These data show that AGI-1067 can inhibit atherosclerosis not only via its lipid-lowering effects but also by having direct anti-inflammatory effects on the vessel wall and suggest that it may be a novel therapeutic agent for coronary artery disease [6].
 

Associations of AGI-1067 with other chemical compounds

 

Gene context of AGI-1067

  • AGI-1067 inhibited the TNF-alpha induction of redox-sensitive inflammatory proteins, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and Eselectin, in cell culture [8].
  • The nonintervened reference coronary segments of the PCI vessel demonstrated improvements with AGI-1067 in the Canadian Antioxidant Restenosis Trial-1 (CART-1), evidence supportive of a clinical effect on slowing atherosclerosis progression [9].
  • In the Canadian Antioxidant Restenosis Trial (CART-1) of AGI-1067 in percutaneous coronary interventions, AGI-1067 had no effect on LDL-cholesterol but lowered HDL-cholesterol [8].
  • The In Vitro Effects of a Novel Vascular Protectant, AGI-1067, on Platelet Aggregation and Major Receptor Expression in Subjects With Multiple Risk Factors for Vascular Disease [2].
 

Analytical, diagnostic and therapeutic context of AGI-1067

  • To explore the therapeutic efficacy and potential mechanisms of action of a new class of antiatherosclerotic drugs, AGI-1067 [mono[4-[[1-[[3,5-bis(1,1-dimethylethyl)-4-hydroxyphenyl]thio]-1-methylethyl]thio]-2,6-bis(1,1-dimethylethyl)phenyl] ester] (butanedioc acid) was tested in several animal models of atherosclerosis [6].
  • AGI-1067 is currently undergoing clinical trials as an antiatherosclerotic agent [10].

References

  1. Clinical results with AGI-1067: a novel antioxidant vascular protectant. Tardif, J.C. Am. J. Cardiol. (2003) [Pubmed]
  2. The In Vitro Effects of a Novel Vascular Protectant, AGI-1067, on Platelet Aggregation and Major Receptor Expression in Subjects With Multiple Risk Factors for Vascular Disease. Serebruany, V., Malinin, A., Scott, R. J. Cardiovasc. Pharmacol. Ther. (2006) [Pubmed]
  3. AGI-1067. AtheroGenics. Hatch, G.M. Current opinion in investigational drugs (London, England : 2000) (2002) [Pubmed]
  4. Pharmacologic prevention of both restenosis and atherosclerosis progression: AGI-1067, probucol, statins, folic acid and other therapies. Tardif, J.C., Grégoire, J., Lavoie, M.A., L'Allier, P.L. Curr. Opin. Lipidol. (2003) [Pubmed]
  5. Selective inhibition of endothelial and monocyte redox-sensitive genes by AGI-1067: a novel antioxidant and anti-inflammatory agent. Kunsch, C., Luchoomun, J., Grey, J.Y., Olliff, L.K., Saint, L.B., Arrendale, R.F., Wasserman, M.A., Saxena, U., Medford, R.M. J. Pharmacol. Exp. Ther. (2004) [Pubmed]
  6. AGI-1067: a multifunctional phenolic antioxidant, lipid modulator, anti-inflammatory and antiatherosclerotic agent. Sundell, C.L., Somers, P.K., Meng, C.Q., Hoong, L.K., Suen, K.L., Hill, R.R., Landers, L.K., Chapman, A., Butteiger, D., Jones, M., Edwards, D., Daugherty, A., Wasserman, M.A., Alexander, R.W., Medford, R.M., Saxena, U. J. Pharmacol. Exp. Ther. (2003) [Pubmed]
  7. Prevention of restenosis with antioxidants: mechanisms and implications. Tardif, J.C., Grégoire, J., L'Allier, P.L. American journal of cardiovascular drugs : drugs, devices, and other interventions. (2002) [Pubmed]
  8. Experimental and clinical studies show that the probucol derivative AGI-1067 prevents vascular growth. Doggrell, S.A. Expert opinion on investigational drugs. (2003) [Pubmed]
  9. Antioxidants: The good, the bad and the ugly. Tardif, J. The Canadian journal of cardiology. (2006) [Pubmed]
  10. Chemistry and pharmacology of vascular protectants: a novel approach to the treatment of atherosclerosis and coronary artery disease. Wasserman, M.A., Sundell, C.L., Kunsch, C., Edwards, D., Meng, C.Q., Medford, R.M. Am. J. Cardiol. (2003) [Pubmed]
 
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