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Drug-Target Interaction

Drug

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PubChem ID:3562
Structure:
Synonyms:
(+-)-2-Bromo-2-chloro-1,1,1-trifluoroethane
(R)-2-Bromo-2-chloro-1,1,1-trifluoroethane
1,1,1-Trifluoro-2-bromo-2-chloroethane
1,1,1-Trifluoro-2-chloro-2-bromoethane
1-Bromo-1-chloro-2,2,2-trifluoroethane
151-67-7
16730_FLUKA
2,2,2-Trifluoro-1-chloro-1-bromoethane
2-Brom-2-chlor-1,1,1-trifluorethan
2-BROMO-2-CHLORO-1,1,1-TRIFLUOROETHANE
4-01-00-00156 (Beilstein Handbook Reference)
51230-17-2
AC1L1G7T
Alotano
Alotano [DCIT]
Anestan
B4388_SIGMA
BCQZXOMGPXTTIC-UHFFFAOYSA-
BRN 1736947
Bromchlortrifluoraethanum
Bromochlorotrifluoroethane
C07515
C2HBrClF3
CCRIS 6244
Cf3chclbr
Chalothane
CHEBI:5615
CHEMBL931
D00542
D006221
DB01159
DB02330
EINECS 205-796-5
Ethane, 1-bromo-1-chloro-2,2,2-trifluoro-
Ethane, 2-bromo-2-chloro-1,1,1-trifluoro-
Ethane, 2-bromo-2-chloro-1,1,1-trifluoro-, (+-)-
Ethane, 2-bromo-2-chloro-1,1,1-trifluoro-, (R)-
Fluktan
Fluorotane
Fluorothane
Fluothane
Fluothane (TN)
Freon 123B1
Ftorotan
Ftorotan [Russian]
Ftuorotan
Halan
Halotan
Halotano
Halotano [INN-Spanish]
Halothan
Halothane
Halothane (JP15/USP/INN)
Halothane (JP16/USP/INN)
Halothane [Anaesthetics, volatile]
Halothane [BAN:INN:JAN]
Halothane [INN:BAN:JAN]
Halothanum
Halothanum [INN-Latin]
Halsan
HMS2094K17
HSDB 6753
LS-881
Narcotan
Narcotane
Narcotann ne-spofa
Narcotann NE-spofa [Russian]
Narkotan
NCGC00090868-01
NCGC00090868-02
NCGC00090868-03
NSC 143490
NSC143490
Phthorothanum
Rhodialothan
UNII-UQT9G45D1P
WLN: GYEXFFF
ATC-Codes:
Side-Effects:
Side-EffectFrequency
arrhythmia0
cardiac arrest0
hypotension0
nausea0
vomiting0
hepatic necrosis0
respiratory arrest0

Target

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Uniprot ID:NOS2_RAT
Synonyms:
Inducible NO synthase
Inducible NOS
iNOS
Nitric oxide synthase, inducible
NOS type II
EC-Numbers:1.14.13.39
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

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

References:

11506125
Halothane but not isoflurane attenuates interleukin 1beta-induced nitric oxide synthase in vascular smooth muscle.. H Maeda; H Iranami; M Yamamoto; K Ogawa; Y Morikawa; E Senba; Y Hatano (2001) Anesthesiology display abstract
BACKGROUND: Inducible nitric oxide synthase (iNOS) is induced by endotoxin or cytokines, such as interleukin (IL)-1, through a protein synthesis pathway. Halothane reportedly inhibits protein synthesis in various tissues. The aim of the current study was to examine the effect of halothane on the IL-1beta-evoked induction of NOS in vascular smooth muscle. METHODS: After removal of the endothelium, arterial rings of rat aorta were mounted in an isometric force recording system. The effects of halothane (1.0-3.0%) or isoflurane (3.0%) on IL-1beta (20 ng/ml)-induced inhibition of the contractile responses to KCl (30 mM) and phenylephrine (10(-9)-10(-5) M) were studied. The cyclic guanosine monophosphate and cyclic adenosine monophosphate contents were determined by radioimmunoassay. Expression of iNOS and iNOS mRNA were measured by Western or Northern blot analysis, respectively. RESULTS: Halothane (1.0-3.0%) but not isoflurane (3%) significantly reduced the ML-1beta-induced inhibition of contraction in a concentration-dependent manner. The cyclic guanosine monophosphate content of the vascular smooth muscle increased significantly after a 5-h exposure to IL-1beta. Halothane at 3.0% significantly inhibited the increase in cyclic guanosine monophosphate content induced by IL-1beta. Halothane had no effect on cyclic adenosine monophosphate content. IL-1beta-induced expression of iNOS and iNOS mRNA in the rat aorta were inhibited significantly by halothane. CONCLUSION: The current study demonstrated that halothane but not isoflurane inhibits IL-1beta-stimulated hyporesponsiveness to vasoconstrictive agents in vascular smooth muscle and that this inhibitory effect of halothane involves the inhibition of iNOS mRNA expression. Thus, these findings suggest that halothane may have some sites to affect nitric oxide-signaling pathway.