PGE1 is not a major naturally occurring prostaglandin, but it is widely administered clinically for several indications including peripheral occlusive vascular disease, erectile dysfunction, and in neonatal cardiology. The metabolism of PGE1 is normally initiated by oxidation at C-15, resulting in 13,14-dihydro-15-keto PGE1 as the major metabolite. However, inhibition of this pathway or saturation by excess substrate could theoretically lead to enhanced production of 2,3-dinor metabolites, including 2,3-dinor PGE1. The biological activity of 2,3-dinor PGE1 has not been published.