Investigational Drug Details
Drug ID: | D223 |
Drug Name: | Alprostadil |
Synonyms: | |
Type: | small molecule |
DrugBank ID: | DB00770 |
DrugBank Description: | Alprostadil is produced endogenously and causes vasodilation by means of a direct effect on vascular and ductus arteriosus (DA) smooth muscle, preventing or reversing the functional closure of the DA that occurs shortly after birth. This results in increased pulmonary or systemic blood flow in infants. In infants, it is used for palliative, not definitive, therapy to temporarily maintain the patency of the ductus arteriosus until corrective or palliative surgery can be performed in neonates who have congenital heart defects and who depend upon the patent ductus for survival. In adults, it is used for the treatment of erectile dysfunction due to neurogenic, vasculogenic, psychogenic, or mixed etiology. |
PubChem ID: | 5280723 |
CasNo: | 745-65-3 |
Repositioning for NAFLD: | Yes |
SMILES: | CCCCC[C@H](O)\C=C\[C@H]1[C@H](O)CC(=O)[C@@H]1CCCCCCC(O)=O |
Structure: |
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InChiKey: | GMVPRGQOIOIIMI-DWKJAMRDSA-N |
Molecular Weight: | 354.487 |
DrugBank Targets: | Prostaglandin E2 receptor EP1 subtype; Prostaglandin E2 receptor EP2 subtype; Prostaglandin E2 receptor EP3 subtype; Prostaglandin E2 receptor EP4 subtype; Prostaglandin D2 receptor 2 |
DrugBank MoA: | Alprostadil causes vasodilation by means of a direct effect on vascular and ductus arteriosus (DA) smooth muscle, preventing or reversing the functional closure of the DA that occurs shortly after birth. This is because, as a form of prostaglandinE1 (PGE1) it has multiple effects on blood flow. This results in increased pulmonary or systemic blood flow in infants. In cyanotic congenital heart disease, alprostadil's actions result in an increased oxygen supply to the tissues. In infants with interrupted aortic arch or very severe aortic coarctation, alprostadil maintains distal aortic perfusion by permitting blood flow through the DA from the pulmonary artery to the aorta. In infants with aortic coarctation, alprostadil reduces aortic obstruction either by relaxing ductus tissue in the aortic wall or by increasing effective aortic diameter by dilating the DA. In infants with these aortic arch anomalies, systemic blood flow to the lower body is increased, improving tissue oxygen supply and renal perfusion. When administered by intracavernosal injection or as an intraurethral suppository, alprostadil acts locally to relax the trabecular smooth muscle of the corpora cavernosa and the cavernosal arteries. Swelling, elongation, and rigidity of the penis result when arterial blood rapidly flows into the corpus cavernosum to expand the lacunar spaces. The entrapped blood reduces the venous blood outflow as sinusoids compress against the tunica albuginea. |
DrugBank Pharmacology: | Alprostadil (prostaglandin E1) is produced endogenously to relax vascular smooth muscle and cause vasodilation. In adult males, the vasodilatory effects of alprostadil on the cavernosal arteries and the trabecular smooth muscle of the corpora cavernosa result in rapid arteriolar inflow and expansion of the lacunar spaces within the corpora. As the expanded corporal sinusoids are compressed against the tunica albuginea, venous outflow through the subtunical vessels is impeded and penile rigidity develops. This is referred to as the corporal veno-occlusive mechanism. In infants, the vasodilatory effects of alprostadil increase pulmonary or systemic blood flow. |
DrugBank Indication: | For palliative, not definitive, therapy to temporarily maintain the patency of the ductus arteriosus until corrective or palliative surgery can be performed in neonates who have congenital heart defects and who depend upon the patent ductus for survival. Also for the treatment of erectile dysfunction due to neurogenic, vasculogenic, psychogenic, or mixed etiology. |
Targets: | |
Therapeutic Category: | |
Clinical Trial Progress: | |
Latest Progress: |

Trial ID | Source ID | Phases | Status | Study Results | Start Date | Last Update Posted | |
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L0004 | NCT02381275 | UNKNOWN | NO | 2014-08-14 | 2018-06-07 | Details | |
L2740 | NCT05161429 | RECRUITING | NO | 2021-07-01 | 2023-06-22 | Details |
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