2,3-dinor-6-keto-prostaglandin F1 alpha

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2,3-dinor-6-keto-prostaglandin F1 alpha
2D structure for 2,3-dinor-6-keto-prostaglandin F1 alpha
Chemical Name	(Z)-5-[(1R,2R,3S,5S)-3,5-dihydroxy-2-[(E,3S)-3-hydroxyoct-1-enyl]cyclopentyl]pent-3-enoic acid
Chemical Formula	C₁₈H₃₀O₅
CAS Number
Chemical Information	HMDB02277
Biochemical Taxonomy	Prostanoids
Functional Taxonomy	Not Available
Nutritional Taxonomy	Not Available
Metabolic Pathways	Not Available
Biofluid Location	Not Available
Tissue Location	Not Available
Normal Biofluid Concentrations	Not Available
Normal Tissue Concentrations	Not Available
Diseases / Conditions Related to Nutrition	Not Available
Other (Monogenic Disorders)	Not Available
Abnormal Biofluid Concentrations	Not Available
Abnormal Tissue Concentrations	Not Available
Physiological Processes	Not Available

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Introduction

guidelines
2,3-dinor-6-keto-prostaglandin F1 alpha is a major urinary prostacyclin metabolite, and is significantly higher in 9 patients with severe atherosclerosis and evidence of platelet activation. Prostacyclin is a potent vasodilator and platelet inhibitor produced by vascular endothelium. Endogenous production of prostacyclin under physiologic conditions is extremely low, far below the capacity of vascular tissue to generate this substance in response to stimulation in vitro. This may reflect a low frequency or intensity of stimulation of prostacyclin production. PGI2 synthase (PGIS), a catalyst of PGI2 formation from prostaglandin H2, is widely distributed and predominantly found in vascular endothelial and smooth muscle cells. PGI2 plays an important cardioprotective role increasingly appreciated in recent years in light of adverse effects of COX-2 inhibitors in clinical trials. This cardioprotection is thought to be mediated, in part, by prostacyclin inhibition of platelet aggregation. Multiple lines of evidence suggest that prostacyclin additionally protects from cardiovascular disease by pleiotropic effects on vascular smooth muscle. PGI2 inhibits proliferation of cultured vascular SMCs by inhibiting cell cycle progression from G1 to S phase. (PMID: 6231483, 7000774, 6231483, 16303599, 16533160, 17073611, 17164138)