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Drug-Target Interaction

Drug

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PubChem ID:68876
Structure:
Synonyms:
68206-94-0
8-chloro-3-beta-diethylaminoethyl-4-methyl-7-ethyoxycarbonymethoxycoumarin
8-Chlorocarbochromen
8-chlorocarbochromen hydrochloride
8-monochloro-3-beta-diethylaminoethyl-4-methyl-7-ethoxycarboxylmethoxycoumarin
Acetic acid,
Acetic acid, ((8-chloro-3-(2-(diethylamino)ethyl)-4-methyl-2-oxo-2H-1-benzopyran-7-yl)oxy)-, ethyl ester
Acetic acid, ((8-chloro-3-(2-(diethylamino)ethyl)-4-methyl-2-oxo-2H-1-benzopyran-7-yl)oxy)-,ethyl ester
AD 6
AD 6 (pharmaceutical)
AD(6)
AD-6
AD6
C025945
C20H26ClNO5
Cloricromen
Cloricromen (INN)
Cloricromen [INN]
Cloricromene
Cloricromene [French]
Cloricromeno [Spanish]
Cloricromenum [Latin]
D07139
Ethyl ((8-chloro-3-(2-(diethylamino)ethyl)-4-methyl-2-oxo-2H-1-benzopyran-7-yl)oxy)acetate
LS-11267
NCGC00165769-01
NCGC00165769-02
Proendotel
ATC-Codes:

Target

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Uniprot ID:Q62710_RAT
Synonyms:
Nitric oxide synthase
EC-Numbers:-
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

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

References:

15322736
Cloricromene in endotoxemia: role of NF-kappaB.. A Ianaro; P Maffia; G Grassia; P Di Meglio; R Sorrentino; R d'Emmanuele di Villa Bianca; M Di Rosa; A Ialenti (2004) Naunyn-Schmiedeberg's archives of pharmacology display abstract
In this study we investigated, for the first time in vivo, the effect of cloricromene, a cumarine derivative, on NF-kappaB activation in endotoxin-treated rats. Endotoxemia was induced in male rats by the intravenous injection of Salmonella typhosa lipopolysaccharide (LPS; 2 mg/kg/i.v.). In vivo treatment with cloricromene (2 mg/kg/i.v.) 30 min before lipopolysaccharide administration reversed the LPS-induced loss in tone of the aortic rings, improved their reactivity to phenylephrine, decreased both nitric oxide (NO) and TNF-alpha serum levels by inhibiting LPS-induced inducible NO synthase and TNF-alpha mRNA expression, and interestingly inhibited LPS-induced NF-kappaB activation. Our data suggest that cloricromene protects rats from LPS by blocking LPS-induced NF-kappaB activation, leading to inhibition of NO and TNF-alpha overproduction and thereby reversing the LPS-induced vascular hyporeactivity.