<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">3094</id>
  <title>T3D3052</title>
  <common-name>Methamphetamine</common-name>
  <description>Methamphetamine is a psychostimulant and sympathomimetic drug. It is a member of the amphetamine group of sympathomimetic amines. Methamphetamine can induce effects such as euphoria, increased alertness and energy, and enhanced self-esteem. It is a scheduled drug in most countries due to its high potential for addiction and abuse.</description>
  <cas>537-46-2</cas>
  <pubchem-id>10836</pubchem-id>
  <chemical-formula>C10H15N</chemical-formula>
  <weight>149.120450</weight>
  <appearance>White powder.</appearance>
  <melting-point></melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>9.28e-01 g/L</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure>Methamphetamine is rapidly absorbed from the gastrointestinal tract with peak methamphetamine concentrations occurring in 3.13 to 6.3 hours post ingestion. Methamphetamine is also well absorbed following inhalation and following intranasal administration. It is distributed to most parts of the body. Because methamphetamine has a high lipophilicity it is distributed across the blood brain barrier and crosses the placenta.</route-of-exposure>
  <target nil="true"/>
  <mechanism-of-toxicity>Methamphetamine enters the brain and triggers a cascading release of norepinephrine, dopamine and serotonin. To a lesser extent methamphetamine acts as a dopaminergic and adrenergic reuptake inhibitor and in high concentrations as a monamine oxidase inhibitor (MAOI). The mechanism of action involved in producing the beneficial behavioral changes seen in hyperkinetic children receiving methamphetamine is unknown.</mechanism-of-toxicity>
  <metabolism>Hepatic. The primary site of metabolism is in the liver by aromatic hydroxylation, N-dealkylation and deamination. At least seven metabolites have been identified in the urine, with the main metabolites being amphetamine (active) and 4-hydroxymethamphetamine. Other minor metabolites include 4-hydroxyamphetamine, norephedrine, and 4-hydroxynorephedrine.Route of Elimination: Excretion occurs primarily in the urine, the rate of which is dependent on urine pH. Between 30-54% of an oral dose is excreted in urine as unchanged methamphetamine and 10-23% as unchanged amphetamine. Following an intravenous dose, 45% is excreted as unchanged parent drug and 7% amphetamine.Half Life: The biological half-life has been reported in the range of 4 to 5 hours.</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>For the treatment of Attention Deficit Disorder with Hyperactivity (ADHD) and exogenous obesity.</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>Manifestations of acute overdosage with methamphetamine include restlessness, tremor, hyperreflexia, rapid respiration, confusion, assaultiveness, hallucinations, panic states, hyperpyrexia, and rhabdomyolysis. Fatigue and depression usually follow the central stimulation. Cardiovascular effects include arrhythmias, hypertension or hypotension, and circulatory collapse. Gastrointestinal symptoms include nausea, vomiting, diarrhea, and abdominal cramps. Fatal poisoning usually terminates in convulsions and coma.</symptoms>
  <treatment>Management of acute methamphetamine intoxication is largely symptomatic and includes gastric evacuation, administration of activated charcoal, and sedation. Experience with hemodialysis or peritoneal dialysis is inadequate to permit recommendations in this regard. Acidification of urine increases methamphetamine excretion, but is believed to increase risk of acute renal failure if myoglobinuria is present. Intravenous phentolamine has been suggested for possible acute, severe hypertension, if this complicates methamphetamine overdosage. Usually a gradual drop in blood pressure will result when sufficient sedation has been achieved. Chlorpromazine has been reported to be useful in decreasing CNS stimulation and sympathomimetic effects. (L1712)</treatment>
  <created-at type="dateTime">2009-07-21T20:28:53Z</created-at>
  <updated-at type="dateTime">2026-03-26T18:30:50Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Methamphetamine</wikipedia>
  <uniprot-id></uniprot-id>
  <kegg-compound-id>C07164</kegg-compound-id>
  <omim-id></omim-id>
  <chebi-id>6809</chebi-id>
  <biocyc-id></biocyc-id>
  <ctd-id nil="true"/>
  <stitch-id>Methamphetamine</stitch-id>
  <drugbank-id>DB01577</drugbank-id>
  <pdb-id>B40</pdb-id>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-smiles>CN[C@@H](C)CC1=CC=CC=C1</moldb-smiles>
  <moldb-formula>C10H15N</moldb-formula>
  <moldb-inchi>InChI=1S/C10H15N/c1-9(11-2)8-10-6-4-3-5-7-10/h3-7,9,11H,8H2,1-2H3/t9-/m0/s1</moldb-inchi>
  <moldb-inchikey>MYWUZJCMWCOHBA-VIFPVBQESA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">149.2328</moldb-average-mass>
  <moldb-mono-mass type="decimal">149.120449485</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>2.07</logp>
  <hmdb-id>HMDB15517</hmdb-id>
  <chembl-id>CHEMBL1201201</chembl-id>
  <chemspider-id>10379</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;Nobuyuki Shigetoh, Hiroshi Nakayama, Jinsei Miyazaki, Tadayasu Mitsumata, &amp;#8220;Labelling colors for detecting cocaine or methamphetamine, method of preparing the same and detector for cocaine or methamphetamine.&amp;#8221; U.S. Patent US5571727, issued October, 1981.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM002399</chemdb-id>
  <dsstox-id>DTXSID8037128</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00000412</susdat-id>
  <iupac>methyl[(2S)-1-phenylpropan-2-yl]amine</iupac>
</compound>
