General
Preferred name
ALPROSTADIL
Synonyms
PGE1 ()
Prostaglandin E1 ()
Prostaglandin E1 (PGE1) ()
Prostaglandin-E1, PGE1, Edex, Muse, Liprostin ()
PGE1 ()
VIRIDAL 5 ()
VIRIDAL 10 ()
VIRIDAL 20 ()
ONO-1608 ()
CAVERJECT IMPULSE ()
PROSTIN VR PEDIATRIC ()
VIRIDAL DUO ()
VITAROS ()
NSC-165559 ()
U-10136 ()
PROSTIN VR ()
EDEX ()
CAVERJECT ()
U-10,136 ()
Prostaglandin E1-d4 ()
P&D ID
PD002898
CAS
745-65-3
119314-69-1
211105-33-8
Tags
available
drug
Approved by
FDA
First approval
1981
Drug indication
Erectile dysfunction
Diabetic foot ulcer
Vasodilator
Drug Status
approved
investigational
Max Phase
4.0
Structure
Probe scores
P&D probe-likeness score
[[ v.score ]]%
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
PHARMACODYNAMICS 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.
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.
ROE Alprostadil must be infused continuously because it is very rapidly metabolized. As much as 80% of the circulating alprostadil may be metabolized in one pass through the lungs, primarily by β- and ω-oxidation. The metabolites are excreted primarily by the kidney, and excretion is essentially complete within 24 hours after administration.
TOXICITY Oral, mouse: LD50 = 186 mg/kg; Oral, rat: LD50 = 228 mg/kg. Apnea, bradycardia, pyrexia, hypotension, and flushing may be signs of drug overdosage.
METABOLISM Alprostadil must be infused continuously because it is very rapidly metabolized. As much as 80% of the circulating alprostadil may be metabolized in one pass through the lungs, primarily by beta- and omega-oxidation.
ABSORPTION The absolute bioavailability of alprostadil has not been determined.
HALF-LIFE 5 to 10 minutes (after a single dose), in healthy adults and neonates.
DESCRIPTION PGE1 is an endogenous prostaglandin. Synthetic PGE1 is known as alprostadil. PGE1 activates prostanoid family GPCRs. (GtoPdb)
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.
DESCRIPTION Positive allosteric modulator of mGlu5 receptors (Tocris Bioactive Compound Library)
DESCRIPTION Prostaglandin. Vasodilator and antiplatelet agent in vivo (Tocriscreen Total)
Cell lines
0
Organisms
2
Compound Sets
32
AdooQ Bioactive Compound Library
A11820
Axon Medchem Screening Library
2062
Cayman Chemical Bioactives
13010
313010
ChEMBL Approved Drugs
CHEMBL495
ChEMBL Drugs
CHEMBL495
Concise Guide to Pharmacology 2017/18
1882
Concise Guide to Pharmacology 2019/20
1882
Concise Guide to Pharmacology 2021/22
1882
Concise Guide to Pharmacology 2023/24
1882
CZ-OPENSCREEN Bioactive Library
Drug Repurposing Hub
DrugBank
DB00770
DrugBank Approved Drugs
DB00770
DrugCentral
138
DrugCentral Approved Drugs
138
DrugMAP
DMWH7NQ
DrugMAP Approved Drugs
DMWH7NQ
EU-OPENSCREEN Bioactive Compound Library
EOS102348
EUbOPEN Chemogenomics Library
EUB0000980
Guide to Pharmacology
1882
LSP-MoA library (Laboratory of Systems Pharmacology)
CHEMBL495
MedChem Express Bioactive Compound Library
HY-B0131
NCATS Inxight Approved Drugs
F5TD010360
NIH Clinical Collections (NCC)
NPC Screening Collection
Prestwick Chemical Library
ReFrame library
Selleckchem Bioactive Compound Library
Alprostadil(Caverject)
TargetMol Bioactive Compound Library
T1626
Tocris Bioactive Compound Library
1620
Tocriscreen Total
ZINC Tool Compounds
ZINC000003813088
External IDs
59
Properties
(calculated by RDKit )
Molecular Weight
354.24
Hydrogen Bond Acceptors
4
Hydrogen Bond Donors
3
Rotatable Bonds
13
Ring Count
1
Aromatic Ring Count
0
cLogP
3.48
TPSA
94.83
Fraction CSP3
0.8
Chiral centers
4.0
Largest ring
5.0
QED
0.35
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Pathway
GPCR/G protein
Metabolic Enzyme/Protease
Target
PGE
CATSPER1, CATSPER2, CATSPER3, CATSPER4, PTGDR, PTGER1, PTGER2, PTGER4, PTGIR
PGE receptor (EP 1-4) antagonist
Endogenous Metabolite
Prostaglandin Receptor
PGES
Primary Target
Prostanoid Receptors
Indication
congenital heart defects
MOA
prostanoid receptor agonist
Therapeutic Class
Vasodilator Agents
Recommended Cell Concentration
None
Source data