InChI key
ZIIJJOPLRSCQNX-UHFFFAOYSA-N
InChI
1S/C21H23ClFN3O.2ClH/c1-3-25(4-2)11-12-26-19-10-9-15(22)13-17(19)21(24-14-20(26)27)16-7-5-6-8-18(16)23;;/h5-10,13H,3-4,11-12,14H2,1-2H3;2*1H
SMILES string
Cl[H].Cl[H].CCN(CC)CCN1C(=O)CN=C(c2ccccc2F)c3cc(Cl)ccc13
drug control
USDEA Schedule IV; regulated under CDSA - not available from Sigma-Aldrich Canada, kontrollierte Droge in Deutschland
technique(s)
HPLC: suitable, gas chromatography (GC): suitable
solubility
2-hydroxypropyl-β-cyclodextrin: 6 mg/mL, H2O: soluble
format
neat
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Application
Refer to the product′s Certificate of Analysis for more information on a suitable instrument technique. Contact Technical Service for further support.
Biochem/physiol Actions
抗焦虑药;抗惊厥药;GABAA 受体苯二氮卓调控位点的配体。
苯二氮卓抗焦虑药;抗惊厥药;GABAA 受体苯二氮卓调控位点的配体。
Legal Information
German
Dieses Produkt fällt unter das Betäubungsmittelgesetz (BtMG). Für eine Bestellung dieses Produktes ist eine Erlaubnis nach § 3 BtMG zwingend erforderlich, es sei denn, es greift eine Ausnahme von der Erlaubnispflicht nach § 4 oder § 26 BtMG.
English
This product is subject to the German Narcotics Act. A permit under Section 3 of the German Narcotics Act is mandatory for ordering this product unless an exemption from the permit requirement under Section 4 or Section 26 of the German Narcotics Act applies.
Dieses Produkt fällt unter das Betäubungsmittelgesetz (BtMG). Für eine Bestellung dieses Produktes ist eine Erlaubnis nach § 3 BtMG zwingend erforderlich, es sei denn, es greift eine Ausnahme von der Erlaubnispflicht nach § 4 oder § 26 BtMG.
English
This product is subject to the German Narcotics Act. A permit under Section 3 of the German Narcotics Act is mandatory for ordering this product unless an exemption from the permit requirement under Section 4 or Section 26 of the German Narcotics Act applies.
signalword
Warning
hcodes
Hazard Classifications
Acute Tox. 4 Oral - STOT RE 2
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
E I Tietz et al.
Neuroscience, 91(1), 327-341 (1999-05-21)
The effect of prolonged benzodiazepine administration on GABA(A) receptor subunit (alpha1-6, beta1-3, gamma2) messenger RNAs was investigated in the rat hippocampus and cortex, among other brain areas. Rats were orally administered flurazepam for one week, a protocol which results in
Silent GABAA synapses during flurazepam withdrawal are region-specific in the hippocampal formation.
P Poisbeau et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 17(10), 3467-3475 (1997-05-15)
Whole-cell patch-clamp recordings were made from CA1 pyramidal and dentate gyrus granule cells (GCs) in hippocampal slices to assess the effects of withdrawal from chronic flurazepam (FRZ) treatment on the function of synaptic GABAA receptors. In slices from control rats
Guofu Shen et al.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 35(9), 1897-1909 (2010-05-07)
Benzodiazepine withdrawal anxiety is associated with potentiation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor (AMPAR) currents in hippocampal CA1 pyramidal neurons attributable to increased synaptic incorporation of GluA1-containing AMPARs. The contribution of calcium/calmodulin-dependent protein kinase II (CaMKII) to enhanced glutamatergic synaptic strength during withdrawal
Marie-Pierre Sylvestre et al.
Statistics in medicine, 28(27), 3437-3453 (2009-08-27)
Many epidemiological studies assess the effects of time-dependent exposures, where both the exposure status and its intensity vary over time. One example that attracts public attention concerns pharmacoepidemiological studies of the adverse effects of medications. The analysis of such studies
Stephen I Deutsch et al.
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 19(6), 398-401 (2009-02-05)
Stress induces changes in the endogenous tone of both GABA and NMDA receptor-mediated neurotransmission in the intact mouse. Because changes are observed 24 h after stress, epigenetically-regulated alterations in gene expression may mediate these effects. In earlier work, sodium butyrate
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