Misoprostol is a prostaglandin E1 (PGE1) analogue used for the treatment and prevention of stomach ulcers. When administered, misoprostol stimulates increased secretion of the protective mucus that lines the gastrointestinal tract and increases mucosal blood flow, thereby increasing mucosal integrity. It is sometimes co-prescribed with non-steroidal anti-inflammatory drugs (NSAIDs) to prevent the occurrence of gastric ulceration, a common adverse effect of the NSAIDs. Misoprostol seems to inhibit gastric acid secretion by a direct action on the parietal cells through binding to the prostaglandin receptor. The activity of this receptor is mediated by G proteins which normally activate adenylate cyclase. The indirect inhibition of adenylate cyclase by Misoprostol may be dependent on guanosine-5’-triphosphate (GTP). The significant cytoprotective actions of misoprostol are related to several mechanisms. These include: 1. Increased secretion of bicarbonate, 2. Considerable decrease in the volume and pepsin content of the gastric secretions, 3. It prevents harmful agents from disrupting the tight junctions between the epithelial cells which stops the subsequent back diffusion of H+ ions into the gastric mucosa, 4. Increased thickness of mucus layer, 5. Enhanced mucosal blood flow as a result of direct vasodilatation, 6. Stabilization of tissue lysozymes/vascular endothelium, 7. Improvement of mucosal regeneration capacity, and 8. Replacement of prostaglandins that have been depleted as a result of various insults to the area. Misoprostol has also been shown to increase the amplitude and frequency of uterine contractions during pregnancy via selective binding to the EP-2/EP-3 prostanoid receptors. Misoprostol is indicated for the treatment of ulceration (duodenal, gastric and NSAID induced) and prophylaxis for NSAID induced ulceration. Misoprostol is also indicated for other uses that are not approved in Canada, including the medical termination of an intrauterine pregnancy used alone or in combination with methotrexate, as well as the induction of labour in a selected population of pregnant women with unfavourable cervices. This indication is avoided in women with prior uterine surgery or cesarean surgery due to an increased risk of possible uterine rupture. Misoprostol is also used for the prevention or treatment of serious postpartum hemorrhage. Misoprostol is sold under the brandname Cytotec among others.

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.

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.

The oil obtained from the seeds of the castor oil plant Ricinus communis is one of the oldest drugs known to man. Castor oil is known primarily as an effective laxative; however, it was also used in ancient times with pregnant women to induce labor. Aside from getting rid of acne, castor oil also helps detoxify the skin. It helps break up the oils that clog glands and pores on the face. Only now, have scientists at the Max Planck Institute for Heart and Lung Research succeeded in unravelling the mysteries of the action mechanism. Ricinoleic acid released from the oil in the intestine, is responsible for the analgesic and anti-inflammatory effects. It was discovered, that G protein-coupled receptors, a large group of receptors in the body involved primarily in transmitting signals in cells. Hundreds of receptors were systematically turned off, and then the reaction of the cells to ricinoleic acid was tested. Ultimately, was succeeded identified the key receptor with the name EP3. There was concluded that after being released from the castor oil, the ricinoleic acid is first of all absorbed by the body via the intestinal mucosa; the EP3 receptor then becomes active on the muscle cells of the intestine and uterus, which in turn stimulates intestinal activity.

Enprostil, a derivative of heptadienoic acid, is a prostaglandin E2 agonist. It is effective in the treatment of patients with duodenal or gastric ulcers.

Beraprost is a stable, orally active prostacyclin analogue. Beraprost acts by binding to prostacyclin membrane receptors ultimately inhibiting the release of Ca2+ from intracellular storage sites. This reduction in the influx of Ca2+ has been postulated to cause relaxation of the smooth muscle cells and vasodilation. Beraprost is indicated for the treatment of pulmonary hypertension and improvement of ulcers, pain & feeling of coldness associated with chronic arterial occlusion. In addition beraprost displays thyroid hormone receptor antagonistic properties.

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.

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.

The oil obtained from the seeds of the castor oil plant Ricinus communis is one of the oldest drugs known to man. Castor oil is known primarily as an effective laxative; however, it was also used in ancient times with pregnant women to induce labor. Aside from getting rid of acne, castor oil also helps detoxify the skin. It helps break up the oils that clog glands and pores on the face. Only now, have scientists at the Max Planck Institute for Heart and Lung Research succeeded in unravelling the mysteries of the action mechanism. Ricinoleic acid released from the oil in the intestine, is responsible for the analgesic and anti-inflammatory effects. It was discovered, that G protein-coupled receptors, a large group of receptors in the body involved primarily in transmitting signals in cells. Hundreds of receptors were systematically turned off, and then the reaction of the cells to ricinoleic acid was tested. Ultimately, was succeeded identified the key receptor with the name EP3. There was concluded that after being released from the castor oil, the ricinoleic acid is first of all absorbed by the body via the intestinal mucosa; the EP3 receptor then becomes active on the muscle cells of the intestine and uterus, which in turn stimulates intestinal activity.