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.

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.

11-Epiprostaglandin E1 is a synthetic prostaglandin analogue. The activity of the racemic synthetic prostaglandin is approximately one-half that of the naturally occurring compound. 11-Epiprostaglandin E1 is 13%, 3.6% and 12%as potent as PGE1 in contracting the rat uterus, guinea pig ileum and rabbit jejunum, respectively. Nevertheless, this unnatural compound was proposed as a prostaglandin D2 receptor antagonist for use in the treatment of androgenic alopecia.

8-Epiprostaglandin E1 (8-iso-PGE1) arises by isomerization of PGE1. This isoprostane found in human semen. 8-iso-PGE1 has very low biological activity relative to PGE1. Intravenous administration of 8-iso-PGE1 decreased systemic arterial pressure slightly and increased heart rate and myocardial contractile force slightly. The magnitude of the systemic hypotensive effect of 8-iso-PGEl was equivalent to approximately 1/125 to 1/250 of that of PGE1 in dogs. On the other hand, the pulmonary hypertensive action of 8-iso-PGE1 was 5 times greater than that of PGE1. 8-iso-PGE1 is an agonist of prostanoid TP receptor. It was proposed as a prostaglandin D2 receptor antagonist for use in the treatment of androgenic alopecia.

15-Epiprostaglandin E1 is a synthetic prostaglandin analogue. The activity of the racemic synthetic prostaglandin is approximately one-half that of the naturally occurring compound. 15-Epiprostaglandin E1 is 4% and 6% as potent as PGE1 in contracting the rat uterus and guinea pig ileum. PGA1 is very potent vasodilator and hypotensive agent, whereas its epimer 15-Epiprostaglandin E1 has a little vasodilator or hypotensive effects in anaesthetized dogs. 15-Epiprostaglandin E1 is a non-competitive inhibitor of 15-hydroxyprostaglandin dehydrogenase from human placenta.

Triphenylphosphine oxide (TPPO) is a neurotoxic very stable polar compound present in waste organic solutions from the chemical and pharmaceutical industry. The acute toxicity of TPPO LC50=12.2µg/mL, LC90=29.5µg/mL is higher than triphenyltin acetate so that a correct management in the relationship with sustainable chemistry is strongly required. TPPO was identified as a selective and potent inhibitor of transient receptor potential melastatin-5 (TRPM5), but at the same moment, it had no effect (up to 100 μM) on the membrane potential responses of TRPA1, TRPV1, or TRPM4b.

ALPROSTADIL ETHYL ESTER is a prodrug of PGE1 with an improved transdermal permeation due to the esterification

The cyclopentenone prostaglandin A1 (PGA1) is considered as an antitumor agent. Its action basis on two distinct mechanisms: direct cytostatic/cytotoxic effects on cancer cells. In addition, the second one is the inhibitory activity of a tumor-associated enzymatic function (i.e., telomerase) that is responsible for cancer cell immortality. In addition, was shown, that PGA1 triggers apoptosis by a process that entails the specific activation of H- and N-Ras isoforms, leading to caspase activation. Rodent models with focal cerebral ischemia have shown that PGA1 has the neuroprotective potential.