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Drug-Target Interaction

Drug

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PubChem ID:3226
Structure:
Synonyms:
(+-)-2-Chloro-1,1,2-trifluoroethyl difluoromethyl ether
13838-16-9
2-Chloro-1,1,2-trifluoroethyl difluoromethyl ether
2-Chloro-1-(difluoromethoxy)-1,1,2-trifluoroethane
AC1L1FGH
AIDS-213020
AIDS213020
Alyrane
Anesthetic 347
Anesthetic Compound No. 347
BRN 1903921
C 347
C07516
C3H2ClF5O
CHEBI:4792
CHEMBL1257
Compound 347
D00543
DB00228
Efrane
EINECS 237-553-4
Enflurane
Enflurane (JP15/USP/INN)
Enflurane (JP16/USP/INN)
Enflurane [Anaesthetics, volatile]
Enflurane [USAN:BAN:INN:JAN]
Enflurano
Enflurano [INN-Spanish]
Enfluranum
Enfluranum [INN-Latin]
Ethane, 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-
Ethane, 2-chloro-1-(difluoromethoxy)-1,1,2-trifluoro-, (+-)-
Ether, 2-chloro-1,1,2-trifluoroethyl difluoromethyl
Ethrane
Ethrane (TN)
Etran
LS-7376
Methylflurether
NCGC00167422-01
NCGC00167422-02
NSC-115944
NSC115944
OHIO 347
ST51041446
UNII-91I69L5AY5
WLN: GYFXFFOYFF
ATC-Codes:
Side-Effects:
Side-EffectFrequency
hepatic necrosis0.0010
hepatic failure0.0010
arrhythmia0
vomiting0
seizures0
nausea0
malignant hyperthermia0
hypotension0
hyperkalemia0
hypoxia0

Target

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Uniprot ID:GRIA1_HUMAN
Synonyms:
AMPA-selective glutamate receptor 1
GluR-1
GluR-A
GluR-K1
Glutamate receptor 1
Glutamate receptor ionotropic, AMPA 1
EC-Numbers:-
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

11020764
Enflurane directly depresses glutamate AMPA and NMDA currents in mouse spinal cord motor neurons independent of actions on GABAA or glycine receptors.. G Cheng; J J Kendig (2000) Anesthesiology display abstract
BACKGROUND: The spinal cord is an important anatomic site at which volatile agents act to prevent movement in response to a noxious stimulus. This study was designed to test the hypothesis that enflurane acts directly on motor neurons to inhibit excitatory synaptic transmission at glutamate receptors. METHODS: Whole-cell recordings were made in visually identified motor neurons in spinal cord slices from 1- to 4-day-old mice. Excitatory postsynaptic currents (EPSCs) or potentials (EPSPs) were evoked by electrical stimulation of the dorsal root entry area or dorsal horn. The EPSCs were isolated pharmacologically into glutamate N-methyl-d-aspartate (NMDA) receptor- and non-NMDA receptor-mediated components by using selective antagonists. Currents also were evoked by brief pulse pressure ejection of glutamate under various conditions of pharmacologic blockade. Enflurane was made up as a saturated stock solution and diluted in the superfusate; concentrations were measured using gas chromatography. RESULTS: Excitatory postsynaptic currents and EPSPs recorded from motor neurons by stimulation in the dorsal horn were mediated by glutamate receptors of both non-NMDA and NMDA subtypes. Enflurane at a general anesthetic concentration (one minimum alveolar anesthetic concentration) reversibly depressed EPSCs and EPSPs. Enflurane also depressed glutamate-evoked currents in the presence of tetrodotoxin (300 nm), showing that its actions are postsynaptic. Block of inhibitory gamma-aminobutyric acid A and glycine receptors by bicuculline (20 micrometer) or strychnine (2 micrometer) or both did not significantly reduce the effects of enflurane on glutamate-evoked currents. Enflurane also depressed glutamate-evoked currents if the inhibitory receptors were blocked and if either D,L-2-amino-5-phosphonopentanoic acid (50 micrometer) or 6-cyano-7-nitroquinoxaline-2,3-dione disodium (10 micrometer) was applied to block NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-kainate receptors respectively. CONCLUSIONS: Enflurane exerts direct depressant effects on both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and NMDA glutamate currents in motor neurons. Enhancement of gamma-aminobutyric acid A and glycine inhibition is not needed for this effect. Direct depression of glutamatergic excitatory transmission by a postsynaptic action on motor neurons thus may contribute to general anesthesia as defined by immobility in response to a noxious stimulus.
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