163201
N,N′-Dicyclohexyl-4-morpholincarboxamidin
98%
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Alle Fotos(1)
About This Item
Empirische Formel (Hill-System):
C17H31N3O
CAS-Nummer:
Molekulargewicht:
293.45
EG-Nummer:
MDL-Nummer:
UNSPSC-Code:
12352100
PubChem Substanz-ID:
NACRES:
NA.22
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Assay
98%
mp (Schmelzpunkt)
105-107 °C (lit.)
Funktionelle Gruppe
amine
SMILES String
C1CCC(CC1)N\C(=N\C2CCCCC2)N3CCOCC3
InChI
1S/C17H31N3O/c1-3-7-15(8-4-1)18-17(20-11-13-21-14-12-20)19-16-9-5-2-6-10-16/h15-16H,1-14H2,(H,18,19)
InChIKey
OZNYZQOTXQSUJM-UHFFFAOYSA-N
Verwandte Kategorien
Allgemeine Beschreibung
N,N′-Dicyclohexyl-4-morpholinecarboxamidine is kidney-selective ATP-sensitive potassium blocker. It is an an orally effective nonkaliuretic diuretic in rats.
Anwendung
N,N′-Dicyclohexyl-4-morpholinecarboxamidine was used as reagent in the synthesis of alkoxyalkyl analogs of nucleotide phosphonates, cidofovir and cyclic cidofovir.
Signalwort
Warning
H-Sätze
Gefahreneinstufungen
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
Zielorgane
Respiratory system
Lagerklassenschlüssel
11 - Combustible Solids
WGK
WGK 3
Flammpunkt (°F)
Not applicable
Flammpunkt (°C)
Not applicable
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S C Perricone et al.
Journal of medicinal chemistry, 37(22), 3693-3700 (1994-10-28)
Random screening identified N,N'-dicyclohexyl-4-morpholinecarboxamidine (U-18177, 1) as an orally effective nonkaliuretic diuretic in rats. The diuretic profile of 1 and its 1-adamantyl analog (U-37883A, 4) was confirmed orally in dogs, when they were less potent than standard diuretics but showed
Earl R Kern et al.
Antimicrobial agents and chemotherapy, 46(4), 991-995 (2002-03-19)
The nucleotide phosphonates cidofovir (CDV) and cyclic cidofovir (cCDV) are potent antiviral compounds when administered parenterally but are not well absorbed orally. These compounds have been reported to have activity against orthopoxvirus replication in vitro and in animal models when
Yuji Kamata et al.
Hypertension research : official journal of the Japanese Society of Hypertension, 32(3), 220-226 (2009-03-06)
It is suggested that an ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein. We reported that glibenclamide, an ATP-sensitive potassium channel blocker, accelerated dose-dependent secretion of renal kallikrein in sliced kidney cortex and in vivo
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