General
Preferred name
PENTAERYTHRITOL TETRANITRATE
Synonyms
pentaerithrityl tetranitrate ()
Cardiacap ()
Pentaerithritol tetranitrate ()
Peritrate ()
Peritrate Sa ()
Tetranitrate de pentaerithrityle ()
Pentritol tempules ()
Pentalong ()
Tetranitrato de pentaeritritilo ()
Mycardol ()
Pentaerythrityl tetranitrate ()
P&D ID
PD014201
CAS
103842-90-6
78-11-5
Tags
drug
Drug indication
Angina pectoris
Cardiovascular disease
Drug Status
approved
investigational
Max Phase
3.0
Probe control
Probe control not defined
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
TOXICITY
The toxicity of nitrate drugs are the result of nitrate conversion to nitrite in the body. Nitrite leads to the autocatalytic oxidation of oxyhemoglobin to both hydrogen peroxide and methemoglobin. This increase in methemoglobin levels is a condition known as methemoglobinemia and is manifested by tissue hypoxia, as methemoglobin is unable to bind oxygen [L2402].; ; Dizziness, redness of the skin (due to vasodilatation), skin irritation and headache are common adverse effects of this drug. Postural hypotension can also occur, especially if this drug is taken at higher doses or while standing [L2395].; ; PETN - Oral LD50 (mouse) = 25,000 mg/kg [MSDS]
METABOLISM
Extensively metabolized in the liver [L2413].; ; Metabolites: pentaerythritol trinitrate, pentaerythritol dinitrate, pentaerythritol mononitrate, & pentaerythritol (inactive)[L2413]
PHARMACODYNAMICS
Organic nitrate which causes systemic vasodilation, decreasing cardiovascular preload [L2413].; ; Nitrate enters vascular smooth muscle and converted to nitric oxide (NO) which acts as a cellular messenger, leading to activation of cyclic GMP and, therefore, vasodilation [L2413].; ; The nitrovasodilator group of drugs relaxes most smooth muscles in the body, including those in the walls of arteries and veins, and selectively dilate large coronary vessels [L2398]. Lower doses of nitrates increase coronary blood flow without significantly affecting systemic arterial pressure. Higher doses, especially if repeated frequently, decrease systolic and diastolic blood pressure as well as cardiac output, which can result in a headache, weakness, dizziness, and the activation of compensatory sympathetic reflexes, including tachycardia and peripheral arteriolar vasoconstriction [A32651].; ; Smooth muscles in the bronchi, biliary tract, gastrointestinal tract, ureters, and uterus also can be relaxed by nitrovasodilators. PETN seems to be unique among the long-acting nitrovasodilators in that patients do not demonstrate tolerance to treatment, which results in sustained vasodilation in humans with continuous PETN treatment [L2412].; ; Important to note is that this drug is devoid of induction of oxidative stress and related side-effects such as endothelial dysfunction or tolerance to nitrates. Some of these effects are related to special pharmacokinetics of PETN, but upon chronic administration, PETN also induces antioxidative pathways at the genomic level, resulting in increased expression of heme _oxygenase-1 (HO-1)_ _and ferritin_, both possessing highly protective properties. There is good experimental evidence that at least part of the beneficial profile of long-term treatment with this drug is based on the activation of the _heme oxygenase-1/ferritin_ system [L2414].;
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Compound Sets
9
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
26
Molecular Weight
316.01
Hydrogen Bond Acceptors
12
Hydrogen Bond Donors
0
Rotatable Bonds
12
Ring Count
0
Aromatic Ring Count
0
cLogP
-1.19
TPSA
209.48
Fraction CSP3
1.0
Chiral centers
0.0
Largest ring
0.0
QED
0.31
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Source data
