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ONO AE 248

structure in first source

Also Known As:

ONO AE-248; ONO-AE-248

Networked: 9 relevant articles (0 outcomes, 0 trials/studies)

Bio-Agent Context: Research Results

Lipids: 114793
- Fatty Acids: 27405
  - Unsaturated Fatty Acids: 8236
    - Eicosanoids: 3262
      - Prostaglandins: 17100
        Prostaglandins E: 2673
        Dinoprostone: 10047
        ONO AE 248: 9
Biological Factors: 2472
- Inflammation Mediators: 1113
  - Autacoids: 276
    - Eicosanoids: 3262
      - Prostaglandins: 17100
        Prostaglandins E: 2673
        Dinoprostone: 10047
        ONO AE 248: 9

Experts

1.	Narumiya, Shuh: 2 articles (10/2009 - 03/2007)
2.	He, Hao: 2 articles (12/2007 - 09/2005)
3.	Zhang, Zi: 2 articles (12/2007 - 09/2005)
4.	Narumiya, S: 2 articles (08/2004 - 06/2001)
5.	Sugimoto, Y: 2 articles (08/2004 - 06/2001)
6.	Honda, Tetsuya: 1 article (10/2009)
7.	Kabashima, Kenji: 1 article (10/2009)
8.	Matsuoka, Toshiyuki: 1 article (10/2009)
9.	Miyachi, Yoshiki: 1 article (10/2009)
10.	Ueta, Mayumi: 1 article (10/2009)

Related Diseases

1.	Necrosis 12/01/2007 - "We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. " 09/01/2005 - "ONO-AE-248 rapidly caused a unique form of neutrophil death, showing morphological changes of nucleus, including fusion of the lobules, blebbing and rupture of the nuclear membrane, which were different from typical morphological changes of apoptosis and necrosis. " 08/01/2000 - "Induction of neutrophil death resembling neither apoptosis nor necrosis by ONO-AE-248, a selective agonist for PGE2 receptor subtype 3."
2.	Infarction (Infarctions) 03/01/2007 - "Treatment with the selective EP3 agonist ONO-AE-248 significantly and dose-dependently increased infarct size in the middle cerebral artery occlusion model. " 09/01/1999 - "The reduction in infarct size caused by ONO-AE-248 in the rabbit was also abolished by 5-hydroxydecanoate. " 09/01/1999 - "The reduction in infarct size caused by ONO-AE-248 in rats subjected to 25 minutes of ischemia and reperfusion was abolished by a selective inhibitor of ATP-sensitive potassium (K(ATP)) channels, 5-hydroxydecanoate (n=6), and the protein kinase C inhibitors staurosporine (n=6) and chelerythrine (n=6). "
3.	Middle Cerebral Artery Infarction (Middle Cerebral Artery Syndrome) 03/01/2007 - "Treatment with the selective EP3 agonist ONO-AE-248 significantly and dose-dependently increased infarct size in the middle cerebral artery occlusion model. "
4.	Myocardial Ischemia (Ischemic Heart Diseases) 09/01/1999 - "In anesthetized rats subjected to regional myocardial ischemia for 25 or 45 minutes and 2 hours of reperfusion, infusion of ONO-AE-248 (5 microg kg(-1). "
5.	Tachycardia (Tachyarrhythmias) 05/10/2002 - "An i.c.v. administration of the EP3 agonist ONO-AE-248 (50.0 nmol) resulted in an increase in RSNA with pressor and tachycardia responses, while administration of the EP2 agonist ONO-AE1-259 and the EP4 agonist ONO-AE1-329 caused transient hypotension and slight increases in HR and RSNA. "

Related Drugs and Biologics

1.	Staurosporine
2.	Dinoprostone (PGE2)
3.	Protein Kinase C
4.	Potassium
5.	Adenosine Triphosphate (ATP)
6.	9- deoxy- 9- chloro- 15- deoxy- 16- hydroxy- 17,17- trimethylene- 19,20- didehydroprostaglandin E2
7.	ONO-AE1-329
8.	5-hydroxydecanoic acid
9.	chelerythrine