Epoprostenol

Epoprostenol and pulmonary arterial hypertension: 20 years of clinical experience.[Pubmed:28096285]

Eur Respir Rev. 2017 Jan 17;26(143). pii: 26/143/160055.

Epoprostenol was the first therapy to be approved for the treatment of pulmonary arterial hypertension (PAH). In the 20 years since the introduction of this prostacyclin analogue, the outlook for patients with PAH has improved, with survival rates now double those from the era before the development of disease-specific treatments. Today, there are a large amount of data on the clinical role of prostacyclin treatments and a body of evidence attesting the efficacy of Epoprostenol in improving exercise capacity, key haemodynamic parameters and PAH symptoms, as well as in reducing mortality. The place of Epoprostenol in the therapeutic management of PAH continues to evolve, with the development of new formulations and use in combination with other drug classes. In this review, we provide a historical perspective on the first 20 years of Epoprostenol, a therapy that led to evidence-based study of PAH-specific treatments and the subsequent expansion of treatment options for PAH.

Refractory Cardiogenic Shock from Right Ventricular Infarction Successfully Managed with Inhaled Epoprostenol.[Pubmed:28298620]

Am J Case Rep. 2017 Mar 16;18:271-275.

BACKGROUND Recognition and appropriate management of right ventricular (RV) infarction is essential, as RV injury increases mortality and substantially alters management during acute coronary syndrome. We report a case of RV infarction presenting with new right bundle branch block (RBBB), and therapeutic use of inhaled Epoprostenol to reduce RV afterload and augment cardiac output during refractory cardiogenic shock. CASE REPORT A 53-year-old male presented to our institution in ventricular fibrillation with subsequent development of RBBB in the setting of proximal right coronary artery occlusion. Following percutaneous coronary intervention, the patient developed severe RV dysfunction with refractory cardiogenic shock. This was successfully managed with inhaled Epoprostenol with normalization of right ventricular systolic function. CONCLUSIONS Although typically associated with anterior myocardial infarction, new RBBB should be recognized as a potential presenting sign of acute RV infarction. The use of inhaled Epoprostenol in the setting of RV infarction has not been previously described, but it may augment right ventricular cardiac output via pulmonary vasodilatation.

Evidence for the Use of Epoprostenol to Treat Raynaud's Phenomenon With or Without Digital Ulcers.[Pubmed:27465880]

Ann Pharmacother. 2016 Dec;50(12):1060-1067.

OBJECTIVE: To review the evidence for using intravenous (IV) Epoprostenol to treat Raynaud's phenomenon (RP). DATA SOURCES: The databases MEDLINE (1946 to March 2016), PubMed, and International Pharmaceutical Abstracts were searched using the terms Epoprostenol, Flolan, Raynaud's disease, and CREST syndrome. Further literature sources were identified by reviewing article citations. STUDY SELECTION AND DATA EXTRACTION: All English-language, clinical trials and case series evaluating IV Epoprostenol for the management or treatment of RP were included. Lower-quality evidence were incorporated due to limited information. DATA SYNTHESIS: Seven small uncontrolled studies/case series, 1 small placebo controlled study, and 1 larger randomized trial were identified and included. There was no consistent measurement of efficacy utilized, but improvements in hand temperature, RP attack duration and frequency were commonly associated with IV Epoprostenol treatment (5 trials). There were conflicting data regarding effect sustainability, with 5 trials showing long-term effects and 3 showing immediate effects. Fewer ischemic ulcers developed during treatment with IV Epoprostenol in 1 trial compared to conventional treatment. Ulcer healing ocurred in 2 trials. Common adverse effects included hypotension, headache, flushing, gastrointestinal symptoms, and jaw pain. CONCLUSIONS: Available evidence supports the use of IV Epoprostenol for treatment of severe RP in patients refractory or intolerant to standard therapies. The dose, titration schedule, and duration of IV Epoprostenol utilized in studies varied, but a conservative approach to initiation should be considered. Patients who do not respond to intermittent infusions and have severe digital ischemia may require more aggressive regimens.

Comparison of anti-aggregatory effects of PGI2, PGI3 and iloprost on human and rabbit platelets.[Pubmed:11684817]

Cell Physiol Biochem. 2001;11(5):279-84.

In human, prostaglandin I3 (PGI3) is as potent inhibitor of platelet aggregation as prostacyclin (PGI2). However the data on the anti-aggregatiory effect of this prostaglandin is scanty on human and is absent on platelets of other species. The potency of PGI3 on other species may be different if there are differences in the structure of receptors. Comparison of the rank orders of the potency of the selective agonists in different species may provide evidence for the existence of such differences. The aim of this work was to study the anti-aggregatory effect of PGI3 on the platelets of human and rabbit and compare the rank orders of the potency of PGI2, PGI3, and iloprost, a synthetic analogue of PGI2, on the platelets of the two species. Experiments were performed in the suspensions of washed platelets prepared from the blood anticoagulated with trisodium citrate solution. A prostaglandin concentration causing 50% inhibition of ADP-induced platelet aggregation (IC50) was obtained from concentration-effect curves. On human platelets, PGI3 was as effective as PGI2, while on rabbit platelets, the value of IC50 for PGI3 (10.2 +/- 1.6 nM) was twofold higher than that of PGI2. The rank orders of agonist potency are different in rabbit compared to those of human. This indicates that the prostacyclin receptors of rabbit platelets are pharmacologically different from those of human.

Epoprostenol sodium (Prostaglandin I2 (sodium salt)), the synthetic form of the natural prostaglandin derivative prostacyclin (prostaglandin I2), is registered worldwide for the treatment of Pulmonary arterial hypertension (PAH). Epoprostenol sodium is used in pulmonary hypertension and transplantation as a potent inhibitor of platelet aggregation.

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