<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">2977</id>
  <title>T3D2935</title>
  <common-name>Diethylpropion</common-name>
  <description>Diethylpropion is only found in individuals that have used or taken this drug. It is a appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category. It is also considered to be among the safest for patients with hypertension. (From AMA Drug Evaluations Annual, 1994, p2290)Diethylpropion is an amphetamine that stimulates neurons to release or maintain high levels of a particular group of neurotransmitters known as catecholamines; these include dopamine and norepinephrine. High levels of these catecholamines tend to suppress hunger signals and appetite. Diethylpropion (through catecholamine elevation) may also indirectly affect leptin levels in the brain. It is theorized that diethylpropion can raise levels of leptin which signal satiety. It is also theorized that increased levels of the catecholamines are partially responsible for halting another chemical messenger known as neuropeptide Y. This peptide initiates eating, decreases energy expenditure, and increases fat storage.</description>
  <cas>90-84-6</cas>
  <pubchem-id>7029</pubchem-id>
  <chemical-formula>C13H19NO</chemical-formula>
  <weight>205.146660</weight>
  <appearance>White powder.</appearance>
  <melting-point>168°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>1.22e+00 g/L</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Diethylpropion is rapidly absorbed from the GI tract after oral administration.</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Diethylpropion is an amphetamine that stimulates neurons to release or maintain high levels of a particular group of neurotransmitters known as catecholamines; these include dopamine and norepinephrine. High levels of these catecholamines tend to suppress hunger signals and appetite. Diethylpropion (through catecholamine elevation) may also indirectly affect leptin levels in the brain. It is theorized that diethylpropion can raise levels of leptin which signal satiety. It is also theorized that increased levels of the catecholamines are partially responsible for halting another chemical messenger known as neuropeptide Y. This peptide initiates eating, decreases energy expenditure, and increases fat storage.</mechanism-of-toxicity>
  <metabolism>Extensively metabolized through a complex pathway of biotransformation involving N-dealkylation and reduction. Many of these metabolites are biologically active and may participate in the therapeutic action of diethylpropion.Route of Elimination: Diethylpropion is rapidly absorbed from the GI tract after oral administration and is extensively metabolized through a complex pathway of biotransformation involving N-dealkylation and reduction. Diethylpropion and/or its active metabolites are believed to cross the blood-brain barrier and the placenta. Diethylpropion and its metabolites are excreted mainly by the kidney.Half Life: Using a phosphorescence assay that is specific for basic compounds containing benzoyl group, the plasma half-life of the aminoketone metabolites is estimated to be between 4 to 6 hours.</metabolism>
  <toxicity>LD50: 600 mg/kg (Oral, Mouse) (A308)LD50: 50 mg/kg (Oral, Rat) (A308)LD50: 225 mg/kg (Oral, Dog) (A308)</toxicity>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>Used as an antidepressant. [Wikipedia]. Used in the management of exogenous obesity as a short-term adjunct (a few weeks) in a regimen of weight reduction based on caloric restriction. </use-source>
  <min-risk-level nil="true"/>
  <health-effects>Using large amounts of these drugs can result in a condition known as amphetamine psychosis -- which can result in auditory, visual and tactile hallucinations, intense paranoia, irrational thoughts and beliefs, delusions, and mental confusion.</health-effects>
  <symptoms>Manifestation of acute overdosage include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, and panic states.</symptoms>
  <treatment>Management of acute diethylpropion hydrochloride intoxication is largely symptomatic and includes lavage and sedation with a barbiturate. Experience with hemodialysis or peritoneal dialysis is inadequate to permit recommendation in this regard. Intravenous phentolamine (Regitine</treatment>
  <created-at type="dateTime">2009-07-21T20:27:59Z</created-at>
  <updated-at type="dateTime">2014-12-24T20:25:53Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Diethylpropion</wikipedia>
  <uniprot-id></uniprot-id>
  <kegg-compound-id>C06954</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>4530</chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>Diethylpropion</stitch-id>
  <drugbank-id>DB00937</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)C(C)C(=O)C1=CC=CC=C1</moldb-smiles>
  <moldb-formula>C13H19NO</moldb-formula>
  <moldb-inchi>InChI=1/C13H19NO/c1-4-14(5-2)11(3)13(15)12-9-7-6-8-10-12/h6-11H,4-5H2,1-3H3</moldb-inchi>
  <moldb-inchikey>InChIKey=XXEPPPIWZFICOJ-UHFFFAOYNA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">205.2961</moldb-average-mass>
  <moldb-mono-mass type="decimal">205.146664235</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>2.8</logp>
  <hmdb-id>HMDB15072</hmdb-id>
  <chembl-id>CHEMBL1194666</chembl-id>
  <chemspider-id>6762</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;Schutte, J.; U.S. Patent 3,001,910; September 26, 1961; assigned to Firma Ternmler-Werke&lt;br /&gt;
(W. Germany).&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
</compound>
