Ecraprost [AS 013, Circulase] is a prodrug of prostaglandin E(1) within lipid microspheres that is being developed in Japan by Mitsubishi Pharma Corporation and Asahi Glass. It was originally in development with Welfide Corporation. On 1 October 2001, Welfide Corporation (formerly Yoshitomi) merged with Mitsubishi-Tokyo Pharmaceuticals to form Mitsubishi Pharma Corporation. The new company is a subsidiary of Mitsubishi Chemical. Taisho and Seikagaku Corporation had been involved in the development of ecraprost but discontinued their licences to do so. The effects of ecraprost on reperfusion injury, in preclinical studies, had been reported by Taisho. Ecraprost is in phase II in Japan and was in phase II in Europe for the treatment of peripheral arterial disease. It was also in a phase II study in the treatment of diabetic neuropathies. However, this is no longer an active indication. A phase III trial using a lipid emulsion of ecraprost [Circulase] is underway with Mitsubishi Pharma Corporation in the US, using ecraprost for the treatment of patients with severe peripheral arterial disease, which, because of decreased blood flow to the extremities, can lead to painful ulcers on the legs and feet and subsequent amputation. Alpha Therapeutic Corporation (a former subsidiary of Mitsubishi Pharma) was initially involved in trials of ecraprost in the US, but this responsibility has been taken over by the parent company.

8-Iso-prostaglandin E2 (8-iso-PGE2) is one of the several isoprostanes produced from arachidonic acid during lipid peroxidation. Isoprostanes are a group of stable prostaglandin-like compounds produced by free radical-catalyzed, non-enzymatic peroxidation of arachidonic acid, which are used as markers of oxidative stress in several human diseases, including diabetes. In addition, 8-iso-prostaglandin E2 is biologically active compound involved in contraction of vascular smooth muscle and activation of platelets. 8-iso-PGE2 has been demonstrated to be the most potent vasoconstrictor isoprostane on the human umbilical artery and vein, activating the TPα isoform, which is present in the human umbilical vein and platelets. 8-iso-prostaglandin E2 stimulates human umbilical vein endothelial cells to specifically bind monocytes and this effect is mediated by cyclic AMP/protein kinase A- and p38 MAP kinase-dependent pathways and is independent of the classical inflammatory NFkappaB pathway.

15-Epi-prostaglandin E2 (15R-Prostaglandin E2) is the C-15 epimer of the naturally occurring 15S-Prostaglandin E2 (15S-PGE2) isomer. 15-Epi-prostaglandin E2 is the most physiologically abundant eicosanoid, which is produced predominantly from arachidonic acid by COX and PGES, and exists at some level in nearly all cell types. Prostaglandin E2 acts on four different receptors termed EP1 through EP4 yielding an astounding array of biological effects, but this compound shows much lower potency in most biological assays; however acid catalyzed epimerization can convert this compound to the active form - 15S-Prostaglandin E2. In the in vivo assay, 15R-PGE2 showed anti-inflammatory activity, as well as in vitro inhibition of elastase release from polymorphonuclear cells. In the from polymorphonuclear cells degranulation assay, 15R-PGE2, was the most active compound in the inhibition of myeloperoxidase release.

Dinoprostone is a naturally occurring prostaglandin E2 (PGE2). Dinoprostone is equivalent to prostaglandin E2 (PGE2). It stimulates labor and delivery by stimulating the uterine, and thus terminates pregnancy. Dinoprostone is also capable of stimulating the smooth muscle of the gastrointestinal tract of man. This activity may be responsible for the vomiting and/or diarrhea that is not uncommon when dinoprostone is used to terminate pregnancy. Dinoprostone administered intravaginally stimulates the myometrium of the gravid uterus to contract in a manner that is similar to the contractions seen in the term uterus during labor, resulting in the evacuation of the products of conception from the uterus. It is believed that dinoprostone exerts its uterine effects via direct myometrial stimulation. It is used for the termination of pregnancy during the second trimester (from the 12th through the 20th gestational week as calculated from the first day of the last normal menstrual period), as well as for evacuation of the uterine contents in the management of missed abortion or intrauterine fetal death up to 28 weeks of gestational age as calculated from the first day of the last normal menstrual period. Also used in the management of nonmetastatic gestational trophoblastic disease (benign hydatidiform mole). Other indications include improving the cervical inducibility (cervical "ripening") in pregnant women at or near term with a medical or obstetrical need for labor induction, and the management of postpartum hemorrhage.