Identification

Name
ACCLAIM
Accession Number
DB05252
Type
Small Molecule
Groups
Investigational
Description

ACCLAIM (organic nitrate combined with L-arginine), is an oral proprietary nitrate therapeutic shown to induce coronary vasodilation while overcoming the significant problem of drug tolerance. ACCLAIM treat chronic angina, the chest pain that occurs from inadequate blood flow to the coronary arteries around the heart.

Structure
Thumb
Synonyms
Not Available
Categories
Not Available
UNII
Not Available
CAS number
Not Available
Weight
Average: 361.776
Monoisotopic: 361.071700334
Chemical Formula
C18H16ClNO5
InChI Key
PQKBPHSEKWERTG-UHFFFAOYSA-N
InChI
InChI=1S/C18H16ClNO5/c1-3-22-17(21)11(2)23-13-5-7-14(8-6-13)24-18-20-15-9-4-12(19)10-16(15)25-18/h4-11H,3H2,1-2H3
IUPAC Name
ethyl 2-{4-[(6-chloro-1,3-benzoxazol-2-yl)oxy]phenoxy}propanoate
SMILES
CCOC(=O)C(C)OC1=CC=C(OC2=NC3=C(O2)C=C(Cl)C=C3)C=C1

Pharmacology

Indication

Chronic angina and Coronary Artery Disease

Structured Indications
Not Available
Pharmacodynamics
Not Available
Mechanism of action

ACCLAIM is a proprietary combination of nitrate and L-arginine that provides the beneficial cardiovascular effects of nitrates. Combining L-arginine with organic nitrates prevents the endothelial cell's depletion of L-arginine and the associated problem of nitrate tolerance. By eliminating nitrate tolerance, ACCLAIM allows patients to receive the continuous, 24-hour benefit of a potent nitrate product, thus sustaining the desired vasodilation effect.

TargetActionsOrganism
UNitric oxide synthase, inducibleNot AvailableHuman
Absorption
Not Available
Volume of distribution
Not Available
Protein binding
Not Available
Metabolism
Not Available
Route of elimination
Not Available
Half life
Not Available
Clearance
Not Available
Toxicity
Not Available
Affected organisms
  • Humans and other mammals
Pathways
Not Available
Pharmacogenomic Effects/ADRs
Not Available

Interactions

Drug Interactions
Not Available
Food Interactions
Not Available

References

General References
Not Available
External Links
KEGG Compound
C11024
PubChem Compound
47938
PubChem Substance
175426962
ChemSpider
43609
ChEBI
5008
ChEMBL
CHEMBL37932

Clinical Trials

Clinical Trials
Not Available

Pharmacoeconomics

Manufacturers
Not Available
Packagers
Not Available
Dosage forms
Not Available
Prices
Not Available
Patents
Not Available

Properties

State
Solid
Experimental Properties
Not Available
Predicted Properties
PropertyValueSource
Water Solubility0.0273 mg/mLALOGPS
logP4.69ALOGPS
logP4.5ChemAxon
logS-4.1ALOGPS
pKa (Strongest Basic)-2.9ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count3ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area70.79 Å2ChemAxon
Rotatable Bond Count7ChemAxon
Refractivity89.8 m3·mol-1ChemAxon
Polarizability36.68 Å3ChemAxon
Number of Rings3ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleYesChemAxon
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+1.0
Blood Brain Barrier+0.9769
Caco-2 permeable-0.5126
P-glycoprotein substrateNon-substrate0.7053
P-glycoprotein inhibitor INon-inhibitor0.8633
P-glycoprotein inhibitor IINon-inhibitor0.5277
Renal organic cation transporterNon-inhibitor0.8806
CYP450 2C9 substrateNon-substrate0.8137
CYP450 2D6 substrateNon-substrate0.6952
CYP450 3A4 substrateSubstrate0.6476
CYP450 1A2 substrateInhibitor0.8903
CYP450 2C9 inhibitorNon-inhibitor0.5234
CYP450 2D6 inhibitorNon-inhibitor0.8759
CYP450 2C19 inhibitorInhibitor0.5851
CYP450 3A4 inhibitorNon-inhibitor0.633
CYP450 inhibitory promiscuityHigh CYP Inhibitory Promiscuity0.9045
Ames testNon AMES toxic0.5402
CarcinogenicityNon-carcinogens0.8986
BiodegradationNot ready biodegradable0.9962
Rat acute toxicity2.2173 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.9753
hERG inhibition (predictor II)Non-inhibitor0.8118
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSNot Available
1H NMR Spectrum1D NMRNot Applicable
13C NMR Spectrum1D NMRNot Applicable

Taxonomy

Description
This compound belongs to the class of organic compounds known as 2-phenoxypropionic acid esters. These are aromatic compounds hat contain a phenol ether attached to the C2-atom of a phenylpropionic acid ester.
Kingdom
Organic compounds
Super Class
Benzenoids
Class
Benzene and substituted derivatives
Sub Class
2-phenoxypropionic acid esters
Direct Parent
2-phenoxypropionic acid esters
Alternative Parents
Phenoxyacetic acid derivatives / Diarylethers / Benzoxazoles / Phenoxy compounds / Phenol ethers / Alkyl aryl ethers / Aryl chlorides / Oxazoles / Heteroaromatic compounds / Carboxylic acid esters
show 9 more
Substituents
2-phenoxypropionic acid ester / Diaryl ether / Phenoxyacetate / Benzoxazole / Phenoxy compound / Phenol ether / Alkyl aryl ether / Aryl chloride / Aryl halide / Azole
show 20 more
Molecular Framework
Aromatic heteropolycyclic compounds
External Descriptors
aromatic ether (CHEBI:5008)

Targets

Kind
Protein
Organism
Human
Pharmacological action
Unknown
General Function
Tetrahydrobiopterin binding
Specific Function
Produces nitric oxide (NO) which is a messenger molecule with diverse functions throughout the body. In macrophages, NO mediates tumoricidal and bactericidal actions. Also has nitrosylase activity ...
Gene Name
NOS2
Uniprot ID
P35228
Uniprot Name
Nitric oxide synthase, inducible
Molecular Weight
131116.3 Da

Drug created on November 18, 2007 11:09 / Updated on December 01, 2017 15:35