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Drug-Target Interaction

Drug

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PubChem ID:1647
Structure:
Synonyms:
(C11-C13)Branched alkyl aminoethylenenitrile
(C12-C18)Alkyl alkoxyethyleneaminonitrile
.beta.-Alaninenitrile
.beta.-Aminopropionitrile
.beta.-Cyanoethylamine
151-18-8
2-Cyanoethylamine
3-Aminopropanenitrile
3-Aminopropionitrile
3-Aminopropionitrile fumarate
3-Aminopropiononitrile
4-04-00-02530 (Beilstein Handbook Reference)
60585-38-8
68130-65-4
68130-66-5
A0408
AC1L1BX6
AC1Q548R
AGSPXMVUFBBBMO-UHFFFAOYSA-
AKOS000121388
Aminopropionitrile
BAPN
beta-Alaminenitrile
beta-Alaninenitrile
beta-AMINOETHYL CYANIDE
beta-Aminopropionitrile
beta-Cyanoethylamine
BRN 1698848
C05670
CCRIS 8134
CHEBI:27413
EINECS 205-786-0
EINECS 268-598-8
FR-0015
H2NCH2CH2CN
HSDB 2897
Lopac-A-3134
Lopac0_000055
LS-124897
NCGC00015048-01
NCGC00015048-02
NCGC00015048-03
NCGC00162054-01
NSC 40641
NSC40641
Propanenitrile, 3-amino-
Propanenitrile, 3-amino-, N-(3-(C12-18-alkyloxy)propyl) derivs.
Propanenitrile, 3-amino-, N-C11-13-isoalkyl derivs.
Propionitrile, 3-amino-
S05-0160
SBB007637
UNII-38D5LJ4KH2
WLN: Z2CN

Target

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Uniprot ID:A4TB13_MYCGI
Synonyms:
Amine oxidase (Copper-containing)
EC-Numbers:1.4.3.6
Organism:Mycobacterium flavescens (strain ATCC 700033 / PYR-GCK
Mycobacterium gilvum
strain PYR-GCK
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

10593505
The role of plasma semicarbazide-sensitive amine oxidase in allylamine and beta-aminopropionitrile cardiovascular toxicity: mechanisms of myocardial protection and aortic medial injury in rats.. D J Conklin; M B Trent; P J Boor (1999) Toxicology display abstract
Allylamine (AA; 3-aminopropene) and beta-aminopropionitrile (betaAPN) combined treatment (AA + betaAPN) results in myocardial protection from AA-induced subendocardial necrosis and a rapid and extensive aortic medial smooth muscle injury in rats. To determine the mechanisms of AA + betaAPN-induced vascular toxicity, cardiovascular parameters were monitored during a 10-day exposure by gavage in male Sprague-Dawley rats (180-200 g). Water intake and urine output were measured in rats treated with water, AA (100 mg kg(-1) body weight), betaAPN (1 g kg(-1) body weight), and AA + betaAPN for 10 days in metabolic cages. Plasma and urine samples were analyzed for blood urea nitrogen, CO2, creatinine, hematocrit, electrolytes (Na+, K+, Cl-), and osmolality. Heart and plasma semicarbazide-sensitive amine oxidase metabolic capacity (SSAO)was also measured following 1, 3 and 10 days of treatment. Following 10 day exposure to control or AA + betaAPN treatment, thoracic aortic rings (approximately 3 mm) were removed, and aortic reactivity to contractile and relaxant agonists was tested in vitro. In addition, cultured rat aorta vascular smooth muscle cells or rat heart beating myocytes were exposed to various concentrations of AA and betaAPN or AA metabolites and betaAPN to test for synergism in vitro. Several of the changes in in vivo cardiovascular parameters were shared, both in direction and magnitude, between the AA + betaAPN and the AA alone or the betaAPN alone treatments. This suggests that these effects (e.g. increased water intake and urine flow, decreased hematocrit, decreased heart and plasma SSAO metabolic capacity) were dependent on an AA alone or a betaAPN alone effect and were not AA + betaAPN specific effects. Significant inhibition of plasma and heart SSAO metabolic capacity occurred in the betaAPN alone and the AA + betaAPN treatments, but not in the AA alone treatment. Aortic rings from AA + betaAPN treated rats were contracted significantly less than anatomically-matched control rat aortic rings by 100 mM potassium chloride or by 10 microM norepinephrine. BetaAPN offered substantial protection against AA cytotoxicity in cultured vascular smooth muscle cells and beating myocytes, but did not alter the cytotoxicity of AA metabolites (i.e. acrolein, H2O2, or ammonia) in vascular smooth muscle cells as determined by the MTT viability assay. Overall, these data suggest that myocardial protection from AA injury that occurs in the combined AA + betaAPN treatment is likely due to inhibition of plasma SSAO. This may result in an increase in the AA dose accumulation and metabolism in the aorta leading to the severe aortic medial injury.