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Drug-Target Interaction

Drug

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PubChem ID:7853
Structure:
Synonyms:
107-11-9
145831_ALDRICH
2-Propen-1-amine
2-Propen-1-amine, homopolymer
2-Propen-1-amine, hydrochloride, homopolymer
2-Propen-1-ylamine
2-Propenamine
2-Propenamine homopolymer
2-Propenylamine
241075_ALDRICH
3 Aminopropylene
3-Amino-1-propene
3-Aminopropene
3-Aminopropylene
30551-89-4
4-04-00-01057 (Beilstein Handbook Reference)
479136_ALDRICH
479144_ALDRICH
71550-12-4
71550-12-4 (hydrochloride)
AB1002535
AC1L1PP9
AC1Q53PG
AG-D-22045
AI3-23214
AKOS000119634
Allylamine
Allylamine homopolymer
Allylamine [UN2334] [Poison]
Allylamine [UN2334] [Poison]
Allylamine, hydrochloride, homopolymer
Allylamine, polymers
BRN 0635703
CCRIS 4746
CHEBI:189472
CHEMBL57286
D000499
EINECS 203-463-9
HSDB 2065
I05-0242
Jsp000634
LS-427
LTBB002820
MolPort-001-779-877
Monoallylamine
NCGC00159381-02
NSC 7600
NSC7600
PAA 10C
PAA 10L
PAA 1LV
PAA-L
Poly(allylamine)
Poly(allylamine) solution
Polyallylamine
prop-2-en-1-amine
prop-2-en-1-amine hydrochloride
UN2334
WLN: Z2U1

Target

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Uniprot ID:A1TAK3_MYCVP
Synonyms:
Amine oxidase (Copper-containing)
EC-Numbers:1.4.3.6
Organism:Mycobacterium vanbaalenii
strain DSM 7251 / PYR-1
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.