<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">2902</id>
  <title>T3D2860</title>
  <common-name>Flurazepam</common-name>
  <description>Flurazepam is only found in individuals that have used or taken this drug. It is a benzodiazepine derivative used mainly as a hypnotic. [PubChem]Flurazepam binds to an allosteric site on GABA-A receptors. Binding potentiates the action of GABA on GABA-A receptors by opening the chloride channel within the receptor, causing chloride influx and hyperpolarization.</description>
  <cas>17617-23-1</cas>
  <pubchem-id>3393</pubchem-id>
  <chemical-formula>C21H23ClFN3O</chemical-formula>
  <weight>387.151370</weight>
  <appearance>White powder.</appearance>
  <melting-point>190-220°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>500 mg/mL (HCl salt)</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Oral. Flurazepam hydrochloride is rapidly (30 minutes) absorbed from the gastrointestinal tract</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Benzodiazepines bind nonspecifically to bezodiazepine receptors BNZ1, which mediates sleep, and BNZ2, which affects affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABAA) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.</mechanism-of-toxicity>
  <metabolism>Flurazepam is rapidly metabolized and is excreted primarily in the urine. Both hydroxyethyl flurazepam (the major metabolite) and N-desalkyl flurazepam are active. The N-desalkyl metabolite is slowly excreted in the urine as the conjugated formRoute of Elimination: Flurazepam is rapidly metabolized and is excreted primarily in the urine. Less than 1% of the dose is excreted in the urine as N1-desalkyl-flurazepam.Half Life: The mean apparent half-life of flurazepam is 2.3 hours. The half life of elimination of N1-des-alkyl- flurazepam ranged from 47 to 100 hours</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>For short-term and intermittent use in patients with recurring insomnia and poor sleeping habits</use-source>
  <min-risk-level nil="true"/>
  <health-effects>They cause slurred speech, disorientation and "drunken" behavior. They are physically and psychologically addictive.</health-effects>
  <symptoms>Coma, confusion, low blood pressure, sleepiness</symptoms>
  <treatment>General supportive measures should be employed, along with immediate gastric lavage. Intravenous fluids should be administered and an adequate airway maintained. Hypotension and CNS depression may be combated by judicious use of appropriate therapeutic agents. If excitation occurs in patients following Flurazepam overdosage, barbiturates should not be used. Flumazenil, a specific benzodiazepine-receptor antagonist, is indicated for the complete or partial reversal of the sedative effects of benzodiazepines and may be useful in situations when an overdose with a benzodiazepine is known or suspected. (L1712)</treatment>
  <created-at type="dateTime">2009-07-21T20:27:25Z</created-at>
  <updated-at type="dateTime">2026-03-31T19:09:22Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Flurazepam</wikipedia>
  <uniprot-id></uniprot-id>
  <kegg-compound-id></kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>195929</chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>Flurazepam</stitch-id>
  <drugbank-id>DB00690</drugbank-id>
  <pdb-id></pdb-id>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>CCN(CC)CCN1C2=C(C=C(Cl)C=C2)C(=NCC1=O)C1=CC=CC=C1F</moldb-smiles>
  <moldb-formula>C21H23ClFN3O</moldb-formula>
  <moldb-inchi>InChI=1S/C21H23ClFN3O/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</moldb-inchi>
  <moldb-inchikey>SAADBVWGJQAEFS-UHFFFAOYSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">387.878</moldb-average-mass>
  <moldb-mono-mass type="decimal">387.151368285</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>3.8</logp>
  <hmdb-id>HMDB14828</hmdb-id>
  <chembl-id>CHEMBL968</chembl-id>
  <chemspider-id>3276</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference>&lt;p&gt;Fryer, R. and Sternbach, L.H.; U.S. Patent 3,567,710; March 2, 1971; assigned to Hoffman-La Roche, Inc.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM002248</chemdb-id>
  <dsstox-id>DTXSID1023071</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00010460</susdat-id>
  <iupac>7-chloro-1-[2-(diethylamino)ethyl]-5-(2-fluorophenyl)-2,3-dihydro-1H-1,4-benzodiazepin-2-one</iupac>
</compound>
